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b. T reatment side effects are a potential threat from all three treatment modalities with the most common including: i. Bowel dysfunction. ii. Sexual dysfunction. iii. Genitourinary dysfunction. iv. Neuropathies. B. Acute care issues in colorectal cancer. 1. Colorectal cancer patients will be admitted to the hos-pital following surgical resection or for urgent situations including bowel obstructions or perforations. 2. Postoperative hospitalization varies by surgical approach. The average hospital stay is 2 to 7 days, with a shorter average stay for patients who have undergone a minimally invasive surgical approach. a. Postoperative management is focused on return of bowel function, ostomy care (if applicable), and pain control. 3. Patients admitted for complications such as bowel obstruction or perforation are managed based on the severity of the complication. a. Bowel obstruction. i. Nothing by mouth (NPO) and bowel rest. ii. Nasogastric tube. iii. Surgery: Exploratory laparotomy with possi-ble bowel resection. b. Perforation. i. NPO and bowel rest. ii. Surgery is indicated in the majority of cases to remove the area of perforation and to wash out the abdomen. iii. Antibiotics. Follow-Up A. Colon cancer recurrence typically occurs within 3 years of resection; therefore, patients should have routine follow-up for at least 5 years after resection. B. Colonoscopy is necessary after resection for surveillance. Consultation/Referral A. Gastroenterology referral for screening is critical in patients who are high risk for colorectal cancer. B. Any patient with suspected colon cancer should be referred to surgery immediately. Surgery is the only curative option for localized cancer and should not be delayed. C. Medical oncology referral for treatment and surveillance. D. Refer patients to support groups. Special/Geriatric Considerations A. Most patients with colorectal cancer are older than 70 years old. B. Elderly patients may be undertreated and are under-represented in clinical trials, making treatment guidelines difficult. C. Life expectancy, quality of life, and patient's functional status should be taken into consideration when determining a plan of action. Bibliography Jasperson, K. W., T uohy, T. M., Neklason, D. W., & Burt, R. W. (2010). Hereditary and familial colon cancer. Gastroenterology, 138 (6), 2044-2058. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Gastrointestinal Cancers: Gastric Cancer Cheryl Pfennig, Karen Beaty, Erin Michelle Dean, Rae Brana Reynolds, and Leigh A. Samp Definition A. A malignant tumor of the stomach. B. Most cancers of the stomach are adenocarcinomas: Malig-nant tumors that develop from the cells in the lining of the stomach. Incidence A. Gastric cancer is the third most common cause of cancer-related mortality worldwide. B. In the United States, approximately 22,220 patients are diagnosed annually, 10,990 of whom are expected to die from gastric cancer. C. The worldwide incidence of gastric cancer has declined over the past few decades, partly due to the recognition of risk factors such as Helicobacter pylori and dietary risks. D. The overall 5-year relative survival rate of all people with stomach cancer in the United States is about 30%. Pathogenesis A. Gastric cancer is a malignant neoplasm that arises anywhere between the gastroesophageal junction and pylorus. B. Most tumors are epithelial in origin and classified as ade-nocarcinomas. C. H. pylori infection is strongly associated with the presence of precancerous lesions that manifest into cancer prolifera-tion. Over 80% of gastric cancers are thought to be attributed to H. pylori infection. Predisposing Factors A. Chronic gastritis caused by: 1. Chronic H. pylori infection. 2. Pernicious anemia. 3. Diet. a. Diet high in salt and salt-preserved foods, nitrates, nitrites, fried foods, processed meats, alcohol. b. Diets low in vegetables (diets high in fruits, vegeta-bles, and fiber are protective against gastric cancer). B. Obesity. C. Smoking. D. Prior gastric surgery. E. Prior abdominal radiation. F. Male gender. G. African American race. H. Inherited germline mutations in TP53, BRCA2, and CDH1. Subjective Data A. Common complaints/symptoms. 1. Unintentional weight loss secondary to insufficient caloric intake caused by tumor related anorexia, nausea, abdominal pain, early satiet-, and/or dysphagia. 2. Bowel changes: Melena or black tarry stools, consti-pation if treating pain, nausea, anemia, change in nature or pattern of bowel habits if an obstructing tumor. 3. Persistent vague, epigastric abdominal pain. 4. Dysphagia, especially for tumors in the proximal stomach or gastroesophageal junction. 5. Fatigue secondary to anemia from bleeding tumors. Gastrointestinal Cancers: Gastric Cancer271	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
13. Oncology Guidelines272 Physical Examination A. Focused areas of the physical examination for suspected gastric cancer should include: 1. Vital signs. a. Evaluate weight and recent trends for uninten-tional weight loss. b. Heart rate: Tachycardia suggestive of dehydration secondary to poor oral intake. 2. Head, ear, eyes, nose, and throat (HEENT). a. Evaluate oral mucosa for paleness suggestive of anemia. b. Evaluate tongue for evidence of thrush. c. Quality of dentition. 3. Palpate neck and cervical nodal chains for adenopathy suggestive of metastasis. 4. Abdominal examination. a. Observe for contour of the abdomen and disten-tion, evidence of cachexia. b. Evaluate the skin, subcutaneous tissue, and umbilicus. c. Auscultate abdomen noting the frequency and character of bowel sounds, normally 5 to 30 gurgling sounds per minute. d. Palpation: Prior to palpation, ask about any tender areas and palpate this area last; commonly tender in the epigastric region secondary to reflux. e. Evaluate for abdominal firmness suggesting carci-nomatosis and ascites. f. Evaluate for nodularity in the umbilical area sug-gestive of a Sister Mary Joseph nodule demonstrating umbilical metastasis. g. Palpate for hepatosplenomegaly suggestive of metastasis. Diagnostic Tests A. Complete history and physical examination. B. Laboratory tests including complete blood count (CBC) with differential and comprehensive metabolic panel (CMP). C. Upper gastrointestinal (GI) series with barium swallow as initial screening for patients with dysphagia. D. CT of the chest, abdomen, and pelvis. E. Esophagogastroduodenoscopy (EGD) for tissue diagno-sis and anatomic location. F. Endoscopic ultrasound (EUS) if no evidence of distant metastatic disease. G. Diagnostic laparoscopy with biopsy and peritoneal lavage to evaluate for radiographically occult metastatic disease and carcinomatosis. H. Diagnosis: Tissue diagnosis and anatomic localization of the primary tumor are best obtained by upper GI endoscopy. I. Staging. 1. Gastric cancers that are 5 cm or more from the gas-troesophageal junction are staged using the tumor, node, metastasis (TNM) system as gastric cancers. 2. Gastric cancers that are less than 5 cm from the gas-troesophageal junction are staged using the TNM system as esophageal cancers. Differential Diagnosis A. Gastritis. B. Gastroenteritis. C. Esophagitis. D. Esophageal cancer. E. Peptic ulcer disease. F. Neoplasm. Evaluation and Management Plan A. General plan and treatment. 1. Tissue diagnosis and staging evaluation are required for treatment planning. 2. Surgical resection is required for cure of gastric cancer. 3. Surgery followed by chemotherapy +/-radiation is the mainstay of treatment. 4. Surgery. 5. Advanced metastatic disease (stage IV) is treated with palliative chemotherapy or on a clinical trial. B. Acute care issues in gastric cancer. 1. Gastric cancer patients are often only admitted for surgical resection. 2. Postoperative gastric surgery patients without com-plications will spend 7 to 10 days in the hospital after surgery. 3. The primary focus in the postoperative inpatient set-ting is nutrition, pain control, monitoring lab work, wound care, and early ambulation. a. Routine blood work including CBC with differ-ential, electrolyte panel, blood urea nitrogen (BUN), and creatinine must be monitored for anemia, infec-tion, electrolyte imbalance/need for replacement, and kidney function. b. The incision site will be monitored daily for signs of infection and proper healing. c. The postgastrectomy patient will have a nasogas-tric tube in place. Once there is no evidence of anas-tomotic leak, the nasogastric tube may be removed. d. Supplemental jejunostomy tube feedings will be initiated on postoperative day one and will continue until oral intake is adequate. e. Oral feeding is started 4 to 7 days postoperatively. f. Upper GI studies are done as indicated (fever, tachycardia, tachypnea, leukocytosis). g. Early ambulation reduces risk of postoperative pneumonia, ileus, and thrombosis. The goal is to have the patient out of bed the day after the procedure as tolerated. h. Postoperative cancer patients have a hypercoagu-lable state; prophylactic enoxaparin is initiated post-operatively and continued for 28 days. Follow-Up A. Postgastrectomy complications. 1. Duodenal stump or anastomotic leak. a. Anastomotic leak: Arises from any of the suture/ staple lines of the anastomosis. b. Duodenal stump leak: Most feared complication of gastrectomy. c. Symptoms: Severe abdominal pain, fever, tachycar-dia, hypotension. d. CT abdomen is indicated. i. Findings: Pneumoperitoneum, extraluminal contrast, fluid collection, and/or abscess. e. Upper GI series (with Gastrografin) may also be performed to assess leak. f. T reatment. i. Broad-spectrum antibiotics. ii. Consider percutaneous drainage of fluid col-lection/abscess by interventional radiology. iii. If leak persists or patient is hemodynamically unstable, patient should be taken to the operating room for exploration, drainage, and repair.	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2. Dumping syndrome. a. Postgastrectomy patients commonly have rapid transit and report diarrhea. b. Dumping syndrome is characterized by diaphore-sis, abdominal cramps, and watery diarrhea shortly after intake of concentrated sweets and hyperosmolar liquids. c. Diagnosis is based on clinical symptoms. i. Gastric emptying studies or upper GI series may be performed. d. T reatment. i. Primary goal includes dietary changes with frequent small meals that are high in fiber and low in carbohydrates. Avoid food triggers (e. g., simple sugar). ii. Octreotide may help but is not typically required. Consultation/Referral A. In patients with suspected gastric cancer, consults should be made to gastroenterology, radiation oncology, medical oncology, and surgery. Special/Geriatric Considerations A. Most cases of gastric cancer affect the elderly. B. Aggressive treatment and surgery should not be withheld from patients solely due to chronological age. C. Life expectancy, quality of life, and patient's functional status need to be taken into consideration in conjunction with patient wishes. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Siegel, R., Ma, J., Zou, Z., & Jemal, A. (2014). Cancer statistics, 2014. CA: A Cancer Journal for Clinicians, 64 (1), 9-29. Zhu, A. L., & Sonnenberg, A. (2012). Is gastric cancer again rising? Journal of Clinical Gastroenterology, 46,804-806. Gastrointestinal Cancers: Hepatic Cancer Cheryl Pfennig, Karen Beaty, Erin Michelle Dean, Rae Brana Reynolds, and Leigh A. Samp Definition A. Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer in adults. B. Other cancers that begin in the liver include intra-hepatic cholangiocarcinoma (about 10%-20%) and less common tumors such as angiosarcomas, hemangiosarcomas, hepatoblastomas, and malignant epithelioid hemangioen-dotheliomas. Incidence A. Liver cancer occurs primarily in people ages 55 to 64, with a median age of 63 at diagnosis. B. Liver and bile duct cancers are relatively rare when com-pared with other cancers. C. In 2016, an estimated 39,230 cases were diagnosed in the United States, and about 27,170 people died of liver and intrahepatic cholangiocarcinoma. D. The survival rate among individuals with liver cancer varies based on staging at the time of diagnosis. E. Surveillance, epidemiology, and end results (SEER) data estimates that 43% of patients present with localized disease (confined to the primary site), 27% have disease that has spread to regional lymph nodes, and 18% present with dis-tant metastases. F. The 5-year relative survival rates for each are 30. 9%, 10. 9%, and 3. 1%, respectively. G. The incidence and mortality rates of HCC are on the rise in the United States. Pathogenesis A. There is a strong association with inflammation, necrosis, fibrosis, and cirrhosis in the development of HCC. B. Some gene mutations have been identified as the cause of uncontrolled division of cells in the liver, leading to develop-ment of cancer. C. HCC has several different subtypes, each with different growth patterns. Predisposing Factors A. Male sex. B. Chronic hepatitis B and C virus infections. C. Alcohol-related cirrhosis. D. Nonalcoholic fatty liver disease (NAFLD). E. Exposure to certain chemicals (e. g., nitrites, hydrocar-bons, and polychlorinated biphenyls). F. Dietary intake of aflatoxins (toxic metabolites produced by certain fungi in foods and feeds). G. Metabolic disorders such as hemochromatosis, Wilson's disease, and Alpha-1 antitrypsin deficiency. Presence of hepatocellular adenoma (unclear risk of malig-nant transformation to HCC). Subjective Data A. The presentation of liver cancer is dependent upon the stage of disease. B. Common complaints/symptoms. 1. Fatigue. 2. Abdominal pain/bloating. 3. Palpable mass in the right upper quadrant. 4. Signs and symptoms of liver disease: Ascites, jaundice, splenomegaly, portal hypertension. 5. Nausea. 6. Decreased appetite and early satiety. 7. Unexplained weight loss. 8. Fever. Physical Examination A. Check vital signs. B. Head and neck. 1. Evaluate for scleral icterus. 2. Palpate the neck and supraclavicular area for adenopa-thy. Look for jugular venous distention. C. Pulmonary system. 1. Observe the patient for signs of dyspnea, increased work of breathing, or retractions. 2. Auscultate all lung fields. D. Cardiovascular system: Auscultate heart sounds. E. Gastrointestinal system. 1. Perform a thorough abdominal examination. 2. Pay close attention to the right upper quadrant. 3. Assess for a fluid wave/evidence of ascites, hep-atomegaly, an umbilical hernia, and caput medusae. F. Musculoskeletal system. 1. Observe for signs of muscle wasting and cachexia. Gastrointestinal Cancers: Hepatic Cancer273	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2. Evaluate lower extremities for pitting edema. G. Central nervous system: Assess cranial nerves II-XII. H. Skin: Assess for jaundice, palmar erythema, and spider angiomata. Diagnostic Tests A. Laboratory evaluation should include complete blood count (CBC), comprehensive metabolic panel (CMP), pro-thrombin time/partial thromboplastin time/international normalized ratio ( PT/PTT/INR), and prealbumin. B. T umor markers: Alpha fetoprotein (AFP) and cancer anti-gen 19-9 (CA 19-9). C. CT of the chest, abdomen, and pelvis with contrast. D. MRI of the abdomen and chest x-ray in patients with PO/IV contrast allergy. E. EKG if considering surgery. F. Liver tumor biopsy is generally not necessary when con-sidering surgery in the setting of classic imaging findings, ele-vated tumor markers, and the presence of known risk factors. Patients with fatty liver disease may be referred for biopsy of their underlying (nontumoral) liver to evaluate for percent steatosis and fibrosis, as this impacts their candidacy for sur-gical resection. G. Diagnosis. 1. Diagnosis typically requires a combination of labora-tory data, imaging, and biopsy results. 2. Laboratory data. a. T umor markers are often elevated in patients with liver cancer and can be followed to assess response to therapy or monitored for disease progression. b. AFP, while neither specific nor sensitive for HCC, is elevated in 50% to 90% of all patients with HCC. c. CA 19-9 is a useful tumor marker and often ele-vated in cholangiocarcinoma. 3. Imaging. a. Ultrasonography may be used as the initial screen-ing technique in patients being monitored for chronic hepatitis; however, surgical resectability and treat-ment planning is always based on dedicated, multi-phasic imaging of the chest, abdomen, and pelvis. b. T riple phase CT assesses the blood flow to liver tissue during early arterial, late arterial, and portal venous phases. c. CT imaging typically shows arterial phase enhancement in HCC due to increased vascular sup-ply of the tumor from the hepatic artery. d. Metastatic adenocarcinomas and cholangiocarci-nomas typically enhance during the portal phase on CT. 4. Biopsy. a. Tissue sampling/biopsy is recommended if the patient is not a candidate for surgery and targeted therapy or systemic chemotherapy is being consid-ered. b. Tissue for pathologic confirmation can be obtained through a percutaneous image-guided biopsy of the liver nodule/mass. H. Staging. 1. The staging of HCC, like the majority of cancers, fol-lows the American Joint Committee on Cancer (AJCC) tumor, node, metastasis (TNM) system. 2. Higher numbers indicate more advanced disease. Differential Diagnosis 1. Cirrhosis. 2. Hepatocellular adenoma. 3. Cholangiocarcinoma. Evaluation and Management Plan A. General plan. 1. Patients with HCC may be offered surgery, targeted therapy/chemotherapy, radiation therapy, liver-directed therapy, or referral for transplantation depending upon multiple factors present at diagnosis including: a. Geographic distribution of disease. b. The presence of metastatic disease. c. Age and comorbidities. d. Cirrhosis. e. Liver reserve. 2. Surgery. 3. Targeted therapy/chemotherapy. 4. Radiation therapy. 5. Liver-directed therapy includes percutaneous treat-ments. a. Radiofrequency/laser/microwave ablation. b. Cryotherapy. c. Ethanol injection. d. T ransarterial chemoembolization (TACE). e. Radioembolization. 6. Liver transplantation. B. Acute care issues in hepatic cancer. 1. Liver cancer patients are often only admitted to the hospital after surgical resection or transplantation. 2. Patients either undergo a partial hepatectomy (removal of a portion of the right or left liver, which may or may not require resection of an entire segment) or a complete right or left hepatectomy. These surgeries can be performed laparoscopically, open, or via a min-imally invasive approach. The gallbladder is sometimes removed at the time of liver resection. 3. Liver-directed therapies are generally performed in the outpatient setting but can occasionally require hospital admission. Follow-Up A. Postoperative liver surgery patients, without complica-tions, will spend an average of 3 to 7 days in the hospital, depending upon the type of surgery performed (laparoscopic vs. open). B. The primary focus in the postoperative inpatient setting is pain control, early ambulation, monitoring blood counts and liver function tests, wound/drain management, pulmonary toileting to avoid pneumonia, and prevention of blood clots. C. Patients are evaluated by the inpatient dietician who stresses the importance of adequate protein and fluid intake in the perioperative period and after discharge. Consultation/Referral A. Most patients are treated by a multidisciplinary team including both surgical and medical oncologists who formu-late a treatment plan based upon clinical staging. B. Radiation oncologists may be consulted if radiation ther-apy is being considered. C. Prior to surgery, patients are often referred to internal medicine to optimize and manage medical comorbidities in the perioperative period. D. Patients with active hepatitis virus infections are managed by either infectious disease or hepatology specialists. Special/Geriatric Considerations A. Surgical resection is the only potentially curative treat-ment for most hepatic cancers. B. Decisions to aggressively treat or not treat hepatic cancer in the geriatric population should not be based on age alone. 13. Oncology Guidelines274	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
C. Factors such as life expectancy, quality of life, and patient functional status should be taken into consideration. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Gastrointestinal Cancers: Pancreatic Cancer Cheryl Pfennig, Karen Beaty, Erin Michelle Dean, Rae Brana Reynolds, and Leigh A. Samp Definition A. Adenocarcinoma of the pancreas (referred to as pancreatic cancer) originates from the exocrine cells of the pancreas. B. Pancreatic cancer comprises more than 95% of pancreatic malignancies. Incidence A. Pancreatic cancer is the fourth leading cause of can-cer deaths in the United States with an estimated 53,070 new cases and 41,780 deaths from pancreatic cancer in 2016. B. The overall risk of developing pancreatic cancer increases after 50 years of age and the majority of patients with disease are between the ages of 60 and 80 years. C. The only potentially curative therapy for pancreatic can-cer is surgical resection of the involved portion of the pan-creas in patients with localized disease. Unfortunately, 80% of patients have metastatic and locally advanced disease at initial diagnosis, which precludes curative resection for the majority of patients. D. In patients who have undergone resection with curative intent, only 10% to 27% of patients survive at least 5 years after surgical resection. Meanwhile, the 5-year overall survival rate for all pancreatic cancer stages combined remains low at 8%. Pathogenesis A. Pancreatic cancer is caused by mutations to DNA. B. Insults to DNA can be hereditary or environmental such as alcohol, smoking, drugs, and obesity. C. Acute pancreatitis and recurrent acute pancreatitis can develop into chronic pancreatitis, which can convert to pan-creatic cancer. D. Most cases of pancreatic cancer are adenocarcinomas. Predisposing Factors A. Cigarette smoking. B. Alcoholism. C. Obesity. D. Chronic pancreatitis. E. Diabetes mellitus. F. Family history. G. Genetic mutations. Subjective Data A. Common complaints/symptoms. 1. Pain. 2. Jaundice. 3. Weight loss. 4. Steatorrhea. 5. Nausea. 6. Hyperglycemia. 7. Diabetes mellitus. B. Common/typical scenario. 1. The pancreas is located proximal to the stomach, small intestine, and bile duct so clinical manifestations of pan-creatic cancer usually affect the anatomy and function of these adjacent structures. For example: a. A pancreatic tumor obstructing the biliary system could cause jaundice. b. Nausea, digestive problems, and weight loss may result from obstruction of the upper digestive tract. c. Steatorrhea can result from an obstruction of the pancreatic duct that prevents the passage of digestive enzymes into the intestines. Physical Examination A. Head and neck: Inspect for scleral icterus and palpate for cervical and supraclavicular lymphadenopathy. B. Integumentary: Inspect for jaundice. C. Abdomen: Inspect and palpate for mass effect, ascites, hepatosplenomegaly, and pain. D. Weight assessment: Measure weight at each visit especially when nutritionally compromised. E. Complete a full examination including cardiopulmonary, musculoskeletal, and neurology assessment to evaluate the patient's overall fitness for oncology treatment. Diagnostic Tests A. Laboratory data. 1. Complete blood count (CBC). 2. Comprehensive metabolic panel (CMP). 3. Prealbumin for nutrition status assessment. 4. CA 19-9. B. Diagnostic imaging. 1. Multiphase helical CT scan. a. A CT scan with contrast can correctly predict resectability in pancreatic cancer with 80% to 90% accuracy. 2. Endoscopic evaluation. a. Esophagogastroduodenoscopy (EGD). b. Endoscopic retrograde cholangiopancreatography (ERCP). C. Staging: The American Joint Committee on Cancer (AJCC) has developed a staging system based on tumor, node, metastasis (TNM) status for pancreatic cancer. Differential Diagnosis A. Acute pancreatitis. B. Cholangitis. C. Cholecystitis. D. Gastric cancer. E. Peptic ulcer disease. Evaluation and Management Plan A. General plan. 1. Chemotherapy, radiation, and surgery are utilized in the treatment of pancreatic cancer. 2. The modalities employed and the sequence in which they are administered often depend on the clinical stage of disease. 3. Neoadjuvant therapy for pancreatic cancer refers to chemotherapy and/or radiation administered prior to surgery. 4. Surgery. Gastrointestinal Cancers: Pancreatic Cancer275	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
a. The majority of pancreatic cancers arise from the pancreatic head and these lesions, if resectable, are treated with a pancreaticoduodenectomy, commonly known as the Whipple procedure. b. Resectable pancreatic tail cancers are treated with a distal pancreatectomy which can also involve a splenectomy depending on the splenic vessel involve-ment of the tumor. 5. Chemotherapy. 6. Radiation. Follow-Up A. Routine follow-up is essential. B. Patients should have CT imaging at 3-to 6-month inter-vals for the first 2 years and then annually. Consultation/Referral A. Consults should be made to gastroenterology, medical oncology, radiation oncology, and general surgery. Special/Geriatric Considerations A. Prognosis for pancreatic cancer is very poor and largely incurable. B. The 5-year relative survival rate is 7% for all stages of pan-creatic cancer. Bibliography Bose, D., Katz, M. H., & Fleming, J. B. (2012). Pancreatic adenocarcinoma. In B. W. Feig & C. D. Ching (Eds. ), The MD Anderson cancer center sur-gical oncology handbook (5th ed., pp. ). Philadelphia, PA: Wolters Kluwer/ Lippincott Williams&Wilkins. Chatterjee, D., Katz, M. H., Rashid, A., Varadhachary, G. R., Wolff, R. A., Wang, H.,... Wang, H. (2012). Histologic grading the extent of residual carcinoma following neoadjuvant chemoradiation in pancreatic ductal adenocarcinoma: A predictor for patient outcome. Cancer,118(12),3182-3190. Fernandez-del Castillo, C. (2019, January 18). Clinical manifestations, diagnosis, and staging of exocrine pancreatic cancer. In D. M. F. Savarese & K. M. Robson (Eds. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clinical-manifestations-diagnosis-and-staging-of-exocrine-pancreatic-cancer Karmazanovsky, G., Fedorov, V., Kubyshkin, V., & Kotchatkov, A. (2005). Pancreatic head cancer: Accuracy of CT in determination of resectability. Abdominal Imaging, 30 (4),488-500. Katz, M. H., Wang, H., Fleming, J. B., Sun, C. C., Hwang, R. F., Wolff, R. A.,... Evans, D. B. (2009). Long-term survival after multidisciplinary management of resected pancreatic adenocarcinoma. Annals of Surgical Oncology, 16 (4),836-847. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Gynecologic Cancers: Cervical Cancer Valerie F. Villanueva, Amelita B. Marzan, Annamma Sam, and Cynae Johnson Definition A. Types of cervical cancer. 1. The most common type of invasive cervical cancer is squamous cell carcinoma (about 70%-80%). 2. The second most common subtype is adenocarcinoma (10%-15%). 3. Other types include adenosquamous carcinoma, adenoid cystic carcinomas, neuroendocrine tumors of the cervix, undifferentiated cervical cancer, and mixed epithelial and mesenchymal tumors. Incidence A. Cervical cancer remains the fourth most common cancer of women worldwide with a mortality rate of ∼52%. B. Approximately 86% of deaths from cervical cancer are in the developing world. C. Cervical cancer is the third most common gynecologic cancer (after uterine and ovarian cancer) and the 12th most common cancer of women in the United States. D. An estimated 12,990 new cases of invasive cervical cancer were diagnosed in 2016 and approximately 4,120 deaths from cervical cancer occurred in the United States in 2016. Pathogenesis A. Caused by an abnormal growth of cells. Human papil-lomavirus (HPV) must be present for cervical cancer to develop. Predisposing Factors A. Early age of sexual activity: The relative risk of having cer-vical cancer is 2. 5 if the age of first sexual exposure is less than 18 years of age. B. Multiple sexual partners: Relative risk is 2. 8 if the number of partners is five or more. C. Lower socioeconomic status. D. Promiscuous sexual partners. E. Tobacco use. F. Immunocompromised conditions. G. In utero exposure to diethylstilbestrol (DES) increases the risk of clear cell carcinoma of the cervix. H. HPV infection. 1. HPV is a double-stranded DNA virus that belongs to the Papillomaviridae family. 2. There are more than 100 different types of HPV iden-tified, and they are divided into two groups. a. Low-risk HPV. b. High-risk HPV. Subjective Data A. Common complaints/symptoms. 1. At early stages, many patients are asymptomatic. 2. Postcoital bleeding (most common). 3. Thin, clear, or blood-tinged vaginal discharge. 4. Abnormally heavy or prolonged menses. 5. Vaginal bleeding becomes heavier, frequent, and may become continuous with progressive disease. 6. Pelvic pain, often seen with advanced disease. B. Common/typical scenario. 1. The most common cervical lesions are exophytic and friable, arising from the ectocervix. 2. Endocervical lesions are more commonly ade-nocarcinomas arising from the mucus-producing glands. 3. Cervix may be firm with or without mass or ulcera-tion. 4. May find an ulcerated tumor eroding through the cervix. Physical Examination A. When patients present with symptoms suggestive of cer-vical cancer, they should undergo complete physical exami-nation including a pelvic examination. 13. Oncology Guidelines276	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
B. It is important to determine if the disease has spread into the parametria or the pelvic sidewalls. C. Rectovaginal examination is also important to assess the spread. Diagnostic Tests A. Pelvic examination, including Pap smear. B. If no lesions are noted, perform a colposcopy to identify any abnormalities. C. Histologic confirmation is important for accurate diag-nosis. If a visible lesion is noted, obtain a biopsy. The best site to take the biopsy is from the edge of the tumor, where the transition from invasive to noninvasive can be clearly seen. D. Once diagnosis is confirmed by biopsy, the following tests may be beneficial. 1. Laboratory data: Complete blood count (CBC) and comprehensive metabolic panel (CMP). 2. Chest x-ray. 3. CT imaging to assess extrauterine spread and adenopathy. 4. MRI (best imaging modality to assess extent of disease). 5. PET scan to assess for lymphatic metastasis. 6. Cystoscopy. 7. Proctoscopy. 8. Exam under anesthesia (EUA) may be needed for a thorough examination. E. Staging. 1. Cervical cancer is staged clinically. 2. Staging is used to determine the treatment and prog-nosis. Differential Diagnosis A. Cervicitis. B. Endometrial carcinoma. C. Vaginitis. D. Pelvic inflammatory disease. Evaluation and Management Plan A. General plan. 1. T reatments for cervical cancer depend on the age of the patient, type of cervical cancer, stage, and desire for children. 2. Prognostic factors. a. Pathologic types. b. T umor size. c. Depth of invasion. d. Lymphovascular invasion. e. Nodal metastases. 3. Surgery is the treatment of choice for stage I-IIA1 cer-vical cancer. 4. Most patients with stage I disease do not require fur-ther treatment if they do not have adverse prognostic fac-tors (see following). 5. Surgical options depend on the stage of cancer and/or are based on the fertility needs. a. Simple hysterectomy. b. Radical hysterectomy. c. Fertility preserving surgeries. d. Pelvic exenteration surgery: Type of radical surgery that removes organs from urinary, gastrointestinal, and gynecological systems. 6. Chemotherapy. 7. Radiation therapy. B. Acute care issues in cervical cancer. 1. Cervical cancer patients are only admitted for certain types of surgeries. a. Radical hysterectomy. b. Pelvic exenteration. c. Other surgeries, including simple hysterectomy and fertility preserving surgical procedures, can be done as outpatient. 2. Radiation therapy. 3. Other situations where cervical cancer patients may need inpatient admission include postoperative compli-cations or due to chemotherapy side effects including nausea, vomiting, and neutropenic fever. Follow-Up A. The goals of postoperative management include pain con-trol, fluid and electrolyte balance, early ambulation, and return of bowel and bladder function. B. Follow-up care should focus on identifying, prevent-ing, and controlling long-term and late effects of cervical cancer. C. Coordination of all the patient's providers should be nav-igated by the primary/leading care provider. D. Follow-up standards for frequency of follow-up have not been established. Consultation/Referral A. Gynecologist, gynecologic oncology, radiation oncology, and surgery. Special/Geriatric Considerations A. Cervical cancer is common in elderly women, and treat-ment disparities are significantly associated with mortality in this population. B. Despite evidence that elderly women tolerate treatment well, they are less likely to be offered surgery and adjuvant radiation. Bibliography Bruni, L., Barrionuevo-Rosas, L., Albero, G., Serrano, B., Mena, M., Gómez,D,... de Sanjosé,S(2016,December15). ICOInformation Centre on HPV and Cancer (HPV Information Centre). Human Papillo-mavirus and Related Diseases in the World. Eskander, R. N., & Bristow, R. E. (Eds. ). (2014). Gynecologic oncology: A pocketbook. New York, NY: Springer Science +Business Media. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Noor, R., Tay, E. H., & Low, J. (2014). Gynaecologic cancer: A handbook for students and practitioners. Boca Raton, FL : Pan Stanford. Siegel, R., Naishadham, D., & Jemal, A. (2013). Cancer statistics, 2013. CA: A Cancer Journal for Clinicians, 63 (1), 11-30. Gynecologic Cancers: Endometrial Cancer Valerie F. Villanueva, Amelita B. Marzan, Annamma Sam, and Cynae Johnson Definition A. Endometrial cancer develops in the uterus and is the most common type of malignancy of the female reproductive sys-tem. B. The majority of all uterine cancers arise from the endometrium (the inner layer) of the uterus. However, uter-ine leiomyosarcoma is a type of endometrial cancer that develops in the myometrium (the muscle layer) of the uterus. Gynecologic Cancers: Endometrial Cancer277.	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
13. Oncology Guidelines278 Incidence A. It is estimated that 60,050 new uterine cancer cases were diagnosed in 2016, with 10,470 deaths resulting from the disease. B. Uterine sarcomas are rare, accounting for approximately 9% of all uterine malignancies. C. A woman's lifetime risk of developing endometrial cancer is approximately 2. 8%. D. Endometrial cancer represents 3. 6% of all new cancer cases in the United States. E. The majority of women are diagnosed between ages 45 and 74, with a median age of 62. Pathogenesis A. Endometrial cancer is usually preceded by endome-trial hyperplasia, which is an overgrowth of the uterine lining. B. Adenocarcinomas comprise 80% of endometrial cancers. Predisposing Factors A. Major risk factors. 1. Obesity. 2. Diabetes. 3. Hypertension. B. Other risk factors. 1. Increased levels of unopposed estrogen. 2. Early age at menarche. 3. Nulliparity. 4. Late age at menopause. 5. Older age of 55 or more. 6. Tamoxifen use for greater than 5 years. 7. Previous pelvic radiation therapy. 8. A personal family history of breast or ovarian cancer. 9. Family history of hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome). Subjective Data A. Common complaints/symptoms. 1. About 90% of women diagnosed with endome-trial cancer have abnormal uterine bleeding (i. e., postmenopausal bleeding, recurrent metrorrhagia, or menorrhagia). 2. Asymptomatic women can present with an abnormal Pap smear showing atypical or malignant endometrial cells. B. Common/typical scenario: Endometrial cancer can be discovered incidentally on ultrasonography, CT, or MRI with a thickened endometrial lining. C. Family and social history: An accurate history of present illness as well as past medical conditions, family, and social history should be taken. Physical Examination A. The physical examination should involve a general inspec-tion of the body for abnormalities, palpation of the inguinal and supraclavicular nodes, and inspection of the vulva, anus, vagina, and cervix to evaluate for metastatic lesions. B. Bimanual and rectovaginal examination should be per-formed to evaluate the uterus, cervix, adnexa, parametria, and rectum. C. The size, mobility, and axis of the uterus should be assessed. D. A biopsy should be performed for any suspicious genital tract lesions detected on examination. Diagnostic Tests A. Histologic evaluation of endometrial tissue is required for diagnosis. B. Once endometrial cancer is confirmed, additional studies are needed for treatment planning. 1. Complete blood count (CBC) with differential. 2. Serum electrolytes. 3. Kidney and liver function tests. 4. EKG. 5. T ransvaginal ultrasound. 6. CT chest, abdomen, and pelvis with intravenous (IV) and oral contrast to rule out extrauterine spread in high-grade malignancies. 7. MRI of the abdomen and pelvis. 8. Chest x-ray (can be used as alternative to CT). 9. CA-125—can be elevated in some uterine subtypes. 10. Colonoscopy, sigmoidoscopy, or barium enema. 11. Genetic testing. C. Staging: Staging of endometrial cancer is defined by the International Federation of Gynecology and Obstetrics (FIGO) criteria. Differential Diagnosis A. Determine source of bleeding. 1. Cervix. 2. Vulva. 3. Vagina. B. Bleeding can be caused by: 1. Polyps. 2. Endometritis. 3. Neoplasm. 4. Atrophic changes. Evaluation and Management Plan A. General plan. 1. T reatment is determined based on disease stage and histologic features. a. Stage I. b. Stage II or III. c. Stage IV. 2. T reatment can continue as long as treatment response is favorable. 3. There are four basic types of treatment for women with endometrial cancer. a. Surgery: The standard of care for treatment of endometrial cancer is hysterectomy. b. Radiation therapy. c. Hormone therapy. d. Chemotherapy. 4. Fertility-sparing therapy—may be initiated in pre-menopausal patients with Grade 1 well-differentiated tumor; stage FIGO IA tumor without involvement of myometrium on MRI, absence of lymphovascular inva-sion, and without intraabdominal disease or adnexal mass. a. Hormone therapy with megestrol and medrox-yprogesterone (most common). b. Levonorgestrel. B. Acute care issues in endometrial cancer. 1. Endometrial cancer patients are often admitted for surgical management. Surgery can be performed either open laparotomy or minimally invasive via laparoscopic or robotic approach. 2. Postoperative laparotomy patients without complica-tions will spend 3 to 5 days in the hospital after surgery, compared to 1 to 2 days recovery for patients undergoing minimally invasive surgery (MIS).	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Follow-Up A. Follow-up should occur every 3 to 4 months for the first 2 years and then every 6 months for 5 years. B. PET/CT has been shown to be more sensitive or spe-cific than CT alone for recurrence but further investigation is being evaluated. C. Pap smears for detection of local recurrence has not been demonstrated. Consultation/Referral A. Gynecology oncology, medical oncology, radiation oncology, and surgery. Special/Geriatric Considerations A. Prognosis is favorable for endometrial cancer. B. Diagnosis at an early stage of the disease process is a key factor for good prognosis. C. Surgery is a safe option for elderly women, which signif-icantly extends life with a low rate of complications. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Nordal, R. R., & Thoresen, S. O. (1997). Uterine sarcomas in Norway 1956-1992: Incidence, survival, and mortality. European Journal of Can-cer, 33 (6), 907-911. Pecorelli, S. (2009). Revised FIGO staging for carcinoma of the vulva, cervix and endometrium. International Journal of Gynecology and Obstetrics, 105(2), 103-104. doi:10. 1016/j. ijgo. 2009. 02. 012 Pecorelli, S. (2010). Corrigendum to “Revised FIGO staging for carcinoma of the vulva, cervix, and endometrium”. International Journal of Gyne-cology and Obstetrics, 108 (2), 176. doi:10. 1016/j. ijgo. 2009. 08. 009 Gynecologic Cancers: Ovarian Cancer Valerie F. Villanueva, Amelita B. Marzan, Annamma Sam, and Cynae Johnson Definition A. Ovarian cancers are classified by cells they are derived from. B. There are three main types of ovarian cancer: Epithelial tumors (accounting for 95%), germ cell tumors, and sex cord stromal tumors. Incidence A. It is the second most common cancer among women, with endometrial cancer being first, but it is the most lethal of all gynecologic malignancies. B. In a woman's lifetime, there is a 1. 3% risk of developing ovarian cancer and 1 in 100 risk of dying from ovarian cancer. C. Approximately 22,280 new cases were reported in 2016. Pathogenesis A. The origin and pathogenesis of epithelial ovarian cancer are poorly understood though dedifferentiation of cells over-lying the ovary is thought to be an important source. B. Ovarian cancer typically spreads by local extension with significant dissemination within the peritoneal cavity. C. Ovarian cancer often goes undetected as symptoms are vague and there is no approved screening test. Therefore, patients are typically diagnosed with advanced stages. Predisposing Factors A. Age. B. Family history of ovarian, breast, or colon cancer. C. Genetic predisposition. D. Reproductive and endocrine abnormalities. 1. Infertility. 2. Endometriosis. 3. Hormonal replacement therapy. E. Obesity (body mass index of ≥30). Subjective Data A. Common complaints/symptoms. 1. Abdominal bloating. 2. Increase in abdominal girth. 3. Pelvic/abdominal pain. 4. Early satiety. 5. Difficulty eating. 6. Nausea and vomiting. 7. Fatigue. B. Common/typical scenario. 1. Ovarian cancer was dubbed the “silent killer” due to women presenting with vague symptoms. 2. Additionally, there are no approved screening meth-ods for ovarian cancer. 3. Because of the vague symptoms, the majority of women are not diagnosed until they have advanced stage disease. Physical Examination A. In patients with early disease, physical examination find-ings are uncommon. B. Ovarian/pelvic mass, fluid in the abdomen (ascites), pleu-ral effusion, and abdominal mass or a bowel obstruction may be present in advanced disease. C. Physical examination includes, and is not limited to: 1. General assessment. 2. Survey of the lymphatic system. 3. Abdomen: Assess for pain, palpable masses, fluid waves, bowel sounds. 4. Pelvic examination: Assess for bleeding, masses, posi-tion of cervix if present, uterine size. 5. Rectovaginal examination: Assess for bleeding, masses, uterosacral ligaments, and cul-de-sac. Diagnostic Tests A. Ultrasound, CT, or MRI of the abdomen/pelvis. B. T umor markers. C. Complete blood count and comprehensive metabolic panel. D. Urinalysis to rule out other causes of pain (urinary tract infection [UTI], kidney stones). E. Diagnosis. 1. Final diagnosis is based on the pathologic review of tissue specimen obtained through surgery or biopsy. 2. Initial surgery (exploratory laparotomy vs. laparo-scopic). If there is a strong clinical suggestion for ovar-ian cancer, laparotomy is preferred for diagnosis and staging. 3. Fine needle aspiration (FNA) or diagnostic paracen-tesis should be performed in patients with diffuse carci-nomatosis or ascites without an obvious ovarian mass. F. Staging: Ovarian cancer is clinically staged based on the Federation International de Gynecologue et d'Obstetrique (FIGO) staging system. Differential Diagnosis 1. Adnexal tumors. 2. Ectopic pregnancy. Gynecologic Cancers: Ovarian Cancer279	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
3. Cysts. 4. Endometriosis. 5. Cervicitis. 6. Cancer of surrounding structures. 7. Pelvic inflammatory disease. 8. Uterine leiomyomas. Evaluation and Management Plan A. General plan. 1. All women diagnosed with ovarian, fallopian tube, or peritoneal cancer should have genetic counseling and be considered for genetic testing. 2. Surgery. 3. Chemotherapy. 4. Radiation therapy: Not used as first-line treatment; however, it may be used occasionally to treat small, local-ized recurrent tumors. 5. Hormonal therapy. 6. Targeted therapy. 7. Biotherapy/immunotherapy. Follow-Up A. Follow-up for ovarian cancer is based on National Com-prehensive Cancer Network (NCCN) guidelines for tumor type and stage. B. Many providers recommend pelvic examination every 2 to 4 months for the first 4 years after resection and every 6 months for 3 years thereafter. Consultation/Referral A. Gynecological oncologist: Typically will involve surgery, medical oncology, and radiation oncology. B. Gastroenterologist: Patients may present with primarily gastrointestinal complaints. C. Palliative care: Due to the very poor prognosis, may be beneficial early on. Special/Geriatric Considerations A. Ovarian cancer increases with advancing age, peaking in the seventh decade of life. B. Discuss aggressive treatment with the patient, based on life expectancy, quality of life goals, and functional status. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Prat, J. (2014). Staging classification for cancer of the ovary, fallopian tube, and peritoneum. International Journal of Gynaecology and Obstetrics, 124(1), 1-5. Head and Neck Cancers Susan Varghese Definition A. Head and neck cancers can arise in the oral cavity, pharynx, larynx, nasal cavity, paranasal sinuses, and salivary glands and include a variety of histopathologic tumors. Incidence A. In the United States, head and neck cancer accounts for 3% of malignancies, with approximately 63,030 Americansdeveloping head and neck cancer annually and 13,000 dying from the disease. B. Head and neck squamous cell carcinoma (HNSCC) com-prises more than 90% of head and neck cancers. Pathogenesis A. Pathophysiology of cancers of the head and neck usually begin in squamous cells of the mucosal lining of the aerodi-gestive tract. B. Viral infection, smoking, and alcohol consumption can encourage differentiation of squamous cells. Predisposing Factors A. Tobacco products. B. Alcohol. C. Viral infections. 1. Epstein-Barr virus (nasopharyngeal cancers). 2. Human papilloma virus (HPV; oropharyngeal can-cers). a. HPV is accepted as a risk factor in the develop-ment of squamous cell carcinomas of the oropharynx, especially cancers of the lingual and palatine tonsil and base of tongue. b. HPV vaccine reduces HPV oral infection, but the impact on HNSCC incidence is yet unknown. D. Betel nut use: Combination of areca palm nuts, betel leaf, slaked lime, +/-tobacco commonly used in South Asia. E. Radiation exposure. F. Periodontal disease. G. Immunodeficiency (immunosuppressant use, HIV/AIDS, bone marrow, or organ transplantation). H. Occupational exposure. I. Genetic factors (polymorphisms, Fanconi anemia, etc. ). J. Iron deficiency (Plummer-Vinson) associated with ele-vated risk of squamous cell carcinoma. K. Gastroesophageal reflux or laryngopharyngeal reflux (laryngeal cancers). Subjective Data A. Common complaints/symptoms. 1. Symptoms and signs vary depending on the subtype and location of the tumor. 2. Patient may be asymptomatic, but common symp-toms include: a. Oral mass. b. Dsyphagia. c. Pain: Odynophagia and/or otalgia. d. Dysarthria. e. Cervical adenopathy. f. Hoarseness. g. Hearing loss. h. Facial numbness, paresthesias, or paralysis. i. T rismus. j. Loose teeth. 3. Patients may present with precursor lesions that trans-form into oral cancer. a. Can develop from area of leukoplakia or erythro-plakia. b. T ransformation of severe dysplasia or carcinoma in situ. Physical Examination A. Identify the key elements of the mass: The size, firmness, associated pain, and overlying skin changes. 13. Oncology Guidelines280	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
B. Head and neck: Assess for dysarthria, tongue mobility; visual examination and palpation of mucous membranes, floor of the mouth, tongue, buccal and gingival mucosa, palates, and posterior pharyngeal wall. C. Ears: Inspect ear canal for drainage and tympanic mem-brane; grossly assess hearing. D. Lymphatics: Palpate the neck for cervical lymphadenopa-thy. E. Neurological: Assess cranial nerves II through XII; assess for facial twitching. Diagnostic Tests A. History and physical examination. B. Direct laryngoscopy and biopsy of the primary site. C. CT or MRI of the head and neck. D. PET/CT (optional, preferred in lymph node positive dis-ease). E. Chest imaging as clinically indicated. F. Fine needle aspiration (FNA) and/or biopsies of primary tumor and/or nodal disease. G. Videostroboscopy for patients with dysphonia. H. Epstein-Barr virus (EBV) quantitative polymerase chain reaction (PCR; for nasopharyngeal cancers). I. Dental, nutrition, speech/swallowing evaluation, and audiogram if indicated. J. Staging. 1. Staging for all oral cancers utilizes the tumor, node, metastasis (TNM) staging outlined by the American Joint Committee on Cancer (AJCC). 2. TNM staging varies depending on the primary tumor site. Differential Diagnosis A. Inflammatory process. Evaluation and Management Plan A. General plan: Subtypes and treatment. 1. T reatment for all head and neck cancers depends on TNM stage at diagnosis. 2. T reatment recommendations vary depending on pri-mary site of tumor. However, generalized guidelines are outlined here. a. Early stage (localized) disease (stage I or II): Definitive radiation therapy (RT) and/or localized resection may be all that is indicated. b. Advanced disease (stage III or IV) or resections without clear margins. i. Adjuvant or neoadjuvant chemotherapy or radiation may also be indicated in addition to surgery. ii. High risk of local recurrence and distant metastasis. B. Acute care issues in head and neck cancers. 1. Patients with HNSCC are rarely admitted except for postoperative management. 2. RT sequelae. a. Sore throat. b. Dry mouth. c. Alteration in taste. d. Swelling in the neck. e. Soft tissue necrosis leading to chondritis ( <1%). f. Sensation of lump in the throat. 3. Xerostomia. a. Due to salivary gland destruction/injury. b. May be prevented by administering amifostine during RT. c. Management. i. Submandibular gland transfer. ii. Pilocarpine. iii. Hyperbaric oxygen. 4. Mucositis. a. Frequent severe complication of RT and chemora-diotherapy. b. Management. i. Avoid acidic or spicy foods. ii. Monitor closely for infections (e. g., oral can-didiasis or herpes simplex virus). iii. Topical anesthetics. iv. Doxepin rinse. v. Palifermin (keratinocyte growth factor). 5. Weight loss and malnutrition. a. Due to difficulty eating, mucositis, trismus, and difficult mastication. b. Management. i. Consider parenteral, enteral, or oral nutri-tional support. ii. Refer to nutritionist. Follow-Up A. Follow-up should occur every 1 to 2 months for the first 6 months after the completion of treatment and every 2 to 3 months in the next 6 months, then every 3 to 4 months during the second year and then every 6 months from years 3 to 5. Consultation/Referral A. Otolaryngology, medical oncology, and radiation oncology. B. Nutritionist for weight loss and malnutrition. Special/Geriatric Considerations A. Patients older than 70 years should not be denied chemotherapy based solely on age. B. Discuss aggressive treatment with the patient. C. Take life expectancy, quality of life, and patient's func-tional status into consideration. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Poon, C. S., & Stenson, K. M. (2018, November 19). Overview of the diag-nosis and staging of head and neck cancer. In R. F. Connor (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/overview-of-the-diagnosis-and-staging-of-head-and-neck-cancer Popescu, C. R., Bertesteanu, S. V., Mirea, D., Grigore, R., Ionescu, D., & Popescu, B. (2010). The epidemiology of hypopharynx and cervical esophagus cancer. Journal of Medicine and Life, 3,396-401. Leukemias: Acute Leukemias Alexis C. Geppner Definition A. Acute leukemias are a group of rare clonal hematopoiet-ic/stem cell neoplasms involving myeloid or lymphoid pre-cursor cells. B. These malignant clones replace the normal bone mar-row causing ineffective hematopoiesis, resulting in granulo-cytopenia, anemia, and thrombocytopenia. Leukemias: Acute Leukemias281	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
C. Acute leukemia is categorized broadly into acute myeloid/myelogenous leukemia (AML) and acute lym-phoblastic leukemia (ALL). Incidence A. AML. 1. An estimated 19,950 people were diagnosed with AML in the United States in 2016. 2. The incidence of AML is similar to that of solid tumors with an exponential rise after age 40. The median age of patients is roughly 67 years. 3. Approximately 83% of patients with newly diagnosed AML are greater than 45 years old. B. ALL. 1. An estimated 6,590 people were diagnosed with ALL in the United States in 2016. 2. Approximately 57% of new cases are diagnosed before age 20, indicating that ALL is primarily a disease of younger patients. Pathogenesis A. Leukemia develops as a series of genetic changes within a single hematopoietic precursor cell, resulting in alteration of normal hematopoietic growth and differentiation. Accu-mulation of large numbers of abnormal, immature cells incapable of differentiating into mature hematopoietic cells results. B. AML. 1. Thought to be related to the transformation of a single hematopoietic stem cell into a malignant undifferentiated cell with endless proliferation; results in accumulation of abnormal, immature myeloid cells in the bone marrow, and peripheral blood. 2. Can occur de novo or secondary to previous cytotoxic therapy (therapy-related or secondary AML). C. ALL. 1. Thought to be the result of genetic insults that block lymphoid differentiation and drive aberrant cell prolifer-ation and survival. 2. T wo subtypes depending on lymphocyte lineage affected: T-lymphocytes (T-ALL) or B-lymphocytes (B-ALL). Predisposing Factors A. Gender: Male to female ratio is 4. 1 to 1. B. Race and ethnicity: Slightly higher in European descent; acute promyelocytic leukemia (APL) more common in His-panic population. C. Chemical or pesticide exposure: Particularly benzene, petroleum products, and ionizing radiation. D. Smoking: Most significant controllable risk factor. E. Prior chemotherapy or high-dose radiation exposure: Alkylating agents, topoisomerase II inhibitors, anthracy-clines, and taxanes. F. Genetic disorders: Down syndrome, Bloom syndrome, Fanconi anemia, Diamond-Blackfan anemia, Shwachman-Diamond syndrome, Li-Fraumeni syndrome, Kline-felter syndrome, Neurofibromatosis type 1, Kostmann syndrome (severe congenital neutropenia), ataxia-telangiectasia, Wiskott-Aldrich syndrome. G. Blood disorders: Myelodysplastic syndrome (MDS), polycythemia vera (PV), and myelofibrosis (MF). H. Viruses: RNA retroviruses, parvovirus B19. Subjective Data A. Common complaints/symptoms. 1. Patients are often symptomatic due to the disease's impact on normal hematopoiesis, causing pancytopenia and/or leukocytosis; however, patients can be initially asymptomatic. a. Thrombocytopenia: Easy bruising and bleeding (especially of the mucosal surfaces), epistaxis, petechi-ae/purpura. b. Anemia: Dyspnea, orthopnea, headaches, pallor. c. Fatigue often precedes diagnosis for a number of months. d. Leukopenia/dysfunctional white blood cells: Fever, persistent infections not responsive to antibi-otics. 2. Bone pain/joint pain (due to marrow proliferation). 3. Altered mental status, intermittent/persistent cranial nerve palsies, priapism (due to leukostasis or leukemia infiltrating the central nervous system [CNS]). 4. Ocular, cardiac, pulmonary, or cerebral dysfunction (due to hyperleukocytosis). 5. Palpable lymphadenopathy and/or abdominal disten-tion/bloating. 6. Unexplained weight loss. 7. Loss of appetite. 8. Night sweats (possibly due to the release of cytokines). Physical Examination A. Check vital signs including pulse oximetry, height, and weight. B. Head and neck. 1. Evaluate conjunctiva for pallor (anemia) and ocular fundus for hemorrhage or white plaques (related to nerve fiber ischemia). 2. Evaluate pupils for symmetry and reactivity to light and accommodation (acute brain bleed or CNS infiltra-tion). 3. Carefully examine oropharynx for bleeding, her-petic lesions/aphthous ulcers, oral candidiasis, or gingival hypertrophy (leukemic involvement of the gums: Com-mon in monocytic variants of AML). 4. Evaluate neck/cervical area for lymphadenopathy due to leukemic infiltration, often seen in ALL rather than AML. C. Cardiovascular system. 1. Auscultate heart sounds in all four quadrants. Tachy-cardia may be present if the patient is profoundly anemic or septic. 2. Assess for signs of pericardial effusion or cardiac tam-ponade (hypotension, muffled heart sounds, pericardial friction rub, jugular venous distension [JVD]). D. Pulmonary system. 1. Inspect and observe for signs of dyspnea, retractions, and work of breathing. 2. Auscultate and percuss all lung fields for signs of infec-tion/leukostasis to include pneumonia, pleural effusion, pulmonary embolism, mediastinal mass, or pneumotho-rax. 3. Mediastinal adenopathy is found in 80% of cases of T-cell ALL. E. Gastrointestinal system. 1. Inspect abdomen for distention. 2. Auscultate for bowel sounds in all four quadrants. 3. Palpate for hepatosplenomegaly (HSM) due to infil-tration of the liver and spleen with leukemia cells. HSM13. Oncology Guidelines282	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
is often found in ALL rather than AML. Massive HSM is rare in de novo acute leukemia and should raise the suspi-cion of leukemia evolving from a prior hematologic dis-order (e. g., chronic myeloid leukemia [CML] or MDS) or ALL. F. Integumentary system. 1. Inspect skin for pallor (anemia), petechiae and ecchy-mosis (thrombocytopenia or disseminated intravascular coagulopathy [DIC]), or infiltrative lesions (leukemia cutis/myeloid sarcoma). a. Leukemic involvement of the skin occurs in 13% or more of patients and is often found in AML with a monocytic of myelomonocytic component. b. Cutis lesions are often nodular and violaceous/blue-gray in color. 2. Erythematous to violaceous tender nodules and plaques suggest acute neutrophilic dermatosis (Sweet syn-drome). G. CNS. 1. Perform a full neurological examination to evalu-ate for focal neurological deficits secondary to leukemic involvement. 2. CNS involvement occurs in 3% to 5% of adult ALL and is rare in AML, but can be seen. 3. CNS involvement is usually restricted to the lep-tomeninges. Diagnostic Tests A. Complete history, including family history. B. Physical examination. C. Laboratory data: Complete blood count (CBC), com-prehensive metabolic panel (CMP), lactate dehydrogenase (LDH), prothrombin time/international normalized ratio (PT/INR), partial thromboplastin time (PTT), thyroid-stimulating hormone and free T4 levels (TSH/T4), fib-rinogen, vitamin B12, reticulocyte count, ferritin, total iron-binding capacity (TIBC), D-Dimer, erythropoietin, B-type natriuretic peptide (BNP), type and screen, and infec-tious disease screening (hepatitis B/C and HIV). D. Chest x-ray or CT imaging of the chest. E. Bone marrow aspiration and biopsy: Morphology, immunohistochemistry, flow cytometry, molecular, and cytogenetic analysis. F. PET/CT if staging for ALL or myeloid sarcoma or clini-cal suspicion for extramedullary disease. G. Lymph node biopsy if necessary for staging of ALL. H. CT chest with mediastinal biopsy for T-ALL. I. Lumbar puncture in patients with neurological symptoms. J. CT or MRI with contrast if neurological symptoms and/or suspicion of leukemic meningitis. K. Human leukocyte antigen (HLA) typing if a potential allogeneic stem cell transplant candidate. L. Echocardiogram for patients with a history or symptoms of cardiac disease, or prior exposure to cardiotoxic agents, such as anthracyclines. M. Central venous access: Peripheral intravenous central catheter (PICC) or central venous catheter (CVC). N. Diagnosis. 1. Bone marrow aspiration/biopsy required for diagnosis of all types of acute leukemia. 2. Lymph node biopsy may be necessary to aid in diag-nosis of ALL. 3. Perform lumbar puncture at diagnosis in all pedi-atric patients with ALL and all patients with neurological symptoms. O. Classification of acute leukemia. 1. Diagnosis of acute leukemia requires ≥20% blasts (myeloblasts or lymphoblasts) in the bone marrow or peripheral blood. 2. T wo main classification systems. a. French-American-British (FAB). b. World Health Organization (WHO). Differential Diagnosis A. Acute myeloid leukemia. B. Lymphomas. C. Aplastic anemia. D. Idiopathic thrombocytopenic purpura. Evaluation and Management Plan A. General plan. 1. The general approach is based on the subtype of leukemia, age, and performance status. 2. T reatment for all patients with acute leukemia (AML and ALL) can be subdivided into two or three phases. a. Induction chemotherapy. b. Consolidation chemotherapy. c. Maintenance chemotherapy. Follow-Up A. Supportive care. 1. Myelosuppression is anticipated as a consequence of both leukemia and the treatment of leukemia with chemotherapy. 2. Blood work required two to three times weekly with transfusional support. 3. Broad-spectrum prophylactic antimicrobial therapy during myelosuppression, which increases susceptibility to opportunistic infections. B. Disease monitoring. 1. Bone marrow aspirate/biopsy 14 to 21 days following start of therapy to document hypoplasia. 2. Repeat in 7 to 14 days if hypoplasia is indeterminate or not documented. If documented, repeat at the time of hematologic recovery. Consultation/Referral A. Hematology oncology once ALL is suspected. Special/Geriatric Considerations A. Elderly patients tend to have a poor overall prognosis compared to younger patients, which may be related to some intrinsic poorly understood aspects of the tumor or even host factors. B. Despite poor prognosis, treatment options should not be based on chronological age alone and should be discussed in detail with the patient. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Stock, W. S., & Thirman, M. J. (2017, August 4). Pathogenesis of acute myeloid leukemia. In A. G. Rosmarin (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/pathogenesis-of-acute-myeloid-leukemia Zuckerman, T., & Rowe, J. M. (2014). Pathogenesis and prognostication in acute lymphoblastic leukemia. F1000Prime Reports, 6,59. Leukemias: Acute Leukemias283	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Leukemias: Chronic Leukemias Allyson Price Definition A. Chronic leukemias are blood cancers that arise from hematopoietic stem cells in the bone marrow. B. T wo general subtypes. 1. Chronic myeloid leukemia (CML): Myeloprolifera-tive neoplasm (MPN) characterized by uncontrolled pro-liferation of mature and maturing granulocytes. 2. Chronic lymphocytic leukemia (CLL): Monoclonal disease characterized by accumulation of mature B-cell lymphocytes. Incidence A. CML. 1. Approximately 14% of newly diagnosed leukemia in the United States. 2. Approximately 1 in every 555 persons will develop CML in a lifetime within the United States. 3. Average age of diagnosis is approximately 64 years old; rarely seen in children. 4. Approximately 1,070 people died of CML in 2016. B. CLL. 1. Most common type of adult leukemia in the United States with approximately 30% of adults diagnosed with leukemia. 2. Mean age of diagnosis is approximately 70 years old. Pathogenesis A. CML. 1. Caused by a reciprocal translocation of chromosome 22 (BCR) and chromosome 9 (ABL) resulting in fusion gene BCR-ABL1, also known as the Philadelphia chro-mosome. a. Results in expression of an oncoprotein leading to elevated and uncontrolled kinase activity, allowing unregulated cell division (i. e., proliferation of mature and maturing granulocytes). b. Overall promotes leukemogenesis. 2. Three phases. a. Chronic. b. Accelerated. c. Blast. 3. CLL. a. Heterogeneous disease. b. Incidental diagnosis often seen on imaging or rou-tine complete blood count (CBC). c. Can remain indolent, not requiring treatment for years. d. Aggressive disease requires more upfront treat-ment; can have complications such as hemolytic anemia, hypogammaglobulinemia, or progression to Richter's transformation. Predisposing Factors A. Exposure to ionizing radiation. B. Family history. C. Exposures to certain chemicals: Agent orange, herbicides, pesticides. D. Gender: More common in males. E. Race/ethnicity: More common in North America and Europe in comparison to Asia. Subjective Data A. Common complaints/symptoms. 1. Typically asymptomatic. 2. Fatigue and malaise. 3. Weight loss. 4. Excessive sweating or night sweats. 5. Abdominal fullness/discomfort with or without early satiety. 6. Bleeding or bruising easily. 7. Bone pain. 8. B symptoms: Fevers, drenching night sweats, or unintentional weight loss. 9. Lymphadenopathy. 10. Organomegaly. B. Common/typical scenario. 1. Presentation varies. 2. Most common symptom in majority of cases is pres-ence of enlarged lymph nodes. 3. Patients frequently complain of petechiae, tiredness, and fatigue. 4. Staging. a. Prognostic factors for CLL: Advanced age, increased number of prolymphocytes, diffuse pattern of bone marrow infiltration, short time of lymphocyte doubling. b. T wo staging systems. i. Rai (see Table 13. 2). ii. Binet (see Table 13. 3). Physical Examination A. Monitor vitals to ensure hemodynamic stability. B. Routine physical examination. C. Abdomen: Evaluation for organomegaly. D. Skin: Assess for petechiae or bruising. E. Lymphatics: Assess for cervical, axillary, and inguinal adenopathy. Diagnostic Tests A. CML. 1. CBC. a. White count normal or elevated. TABLE 13. 2 Rai Staging for CLL Rai Staging Stage Risk Defining Characteristics 0 Low risk Lymphocytosisain blood and marrow only. I Intermediate risk Lymphocytosisaand presence of ymphadenopathy. II Intermediate risk Lymphocytosisaand presence of splenomegaly and/or hepatomegaly. III High risk Lymphocytosisaand presence of anemia. IV High risk Lymphocytosisaand presence of thrombocytopenia. Note:a Defined as greater than 15,000 lymphocytes/mm3. CLL, chronic lymphocytic leukemia. Source: Adapted from Rai, K. R., Sawitsky, A., Cronkite, E. P., Chanana, A. D., Levy, R. N., & Pasternack, B. S. (1975). Clinical staging of chronic lymphocytic leukemia. Blood, 46 (2),219-23413. Oncology Guidelines284	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
TABLE 13. 3 Binet Staging for CLL Binet Staging Stage Risk/Survival All Criteria Must Be Met A Low risk Up to two areas of enlarged lymph nodes >1 cm in diameter Platelets >100×109/L Hemoglobin ≥10 g/d L B Intermediate risk Three or more areas of enlarged lymph nodes >1 cm in diameter Platelets >100×109/L Hemoglobin ≥10 g/d L C High risk Three or more areas of enlarged lymph nodes >1 cm in diameter Platelets <100×109/L Hemoglobin <10 g/d L CLL, chronic lymphocytic leukemia. Source: Adapted from Desai, S., & Pinilla-Ibarz, J. (2012). Front-line therapy for chronic lymphocytic leukemia. Cancer Contr ol,19,26-3. b. Absolute basophilia and absolute eosinophilia on blood smear. c. Leukemia hiatus—finding in peripheral blood from CBC showing greater percent of myelocytes ver-sus more mature metamyelocytes. d. Platelets normal or elevated. e. Normocytic, normochromic anemia. 2. Peripheral blood quantitative polymerase chain reac-tion (q PCR) for BCR-ABL1. 3. Bone marrow aspiration and biopsy. B. CLL. 1. CBC with differential: ≥5,000 monoclonal B lym-phocytes/ μL. 2. Comprehensive metabolic panel (CMP), immunoglobulins, direct antiglobulin test, infectious disease panel including HIV, hepatitis B, and hepatitis C; lactate dehydrogenase (LDH), beta-2 microglobulin. 3. Clonality of circulating B lymphocytes confirmed by flow cytometry on peripheral blood. 4. Fluorescent in situ hybridization (FISH) and con-ventional cytogenetics performed on peripheral blood or bone marrow aspiration. 5. Bone marrow aspiration/biopsy. 6. Chest x-ray or CT imaging to assess for lym-phadenopathy. 7. PET/CT scan. Differential Diagnosis 1. Acute leukemias. Evaluation and Management Plan A. General plan: Goal of treatment for CML is to prohibit the disease from progressing to accelerated or blast phase. B. Therapy. 1. CML. a. Tyrosine kinase inhibitors (TKIs): Gold standard treatment of CML. b. Stem cell transplant. 2. CLL. a. Indications for initiating therapy include: i. Constitutional symptoms referable to relating to CLL; also known as tumor burden. ii. Progressive marrow failure; depicted through suppression of counts or progression of anemia and thrombocytopenia. iii. Autoimmune anemia +/-thrombocytopenia poorly responsive to steroids. iv. Splenomegaly ( >6 cm) or progressing in size. v. Lymphadenopathy ( >10 cm) or progressing in size. vi. Progressive lymphocytosis, greater than 50% increase in 2 months or lymphocyte doubling time (LDT) less than 6 months. b. Observation is acceptable if all of the following are met. i. Absolute monoclonal B lymphocyte count less than 5,000/mm3. ii. All lymph nodes less than 1. 5 cm. iii. No anemia. iv. No thrombocytopenia. c. Frontline therapy: Monoclonal antibodies used in CLL. 3. CML response to therapy. a. Typically patients are monitored for cytogenetic and molecular responses with repeat bone marrow aspirations every 3 to 6 months for the first year or once a complete cytogenetic remission has been achieved. b. Hematologic response. i. Normalization of CBC including white blood cell (WBC) less than 10k and platelets less than 450. ii. No immature cells in peripheral blood. iii. Goal to achieve hematologic response within 1 month of starting therapy. c. Cytogenetic response: Goal is to achieve com-plete cytogenetic remission within 1 year of start-ing therapy. If not obtained, change of therapy is indicated. d. Molecular response: No indication to switch ther-apy if molecular response is not obtained. C. Acute care issues in leukemias. 1. Neutropenic fever. a. Fever (temperature ≥100. 5ºF) in the setting of absolute neutrophil count (ANC) less than 500/mm3. b. Common in patients undergoing cytotoxic sys-temic chemotherapy causing profound neutropenia or patients receiving immunosuppressive agents like IV steroids. c. Assess vital signs for hemodynamic stability: Fever, tachycardia, and hypotensive or altered mental status. d. Need full assessment on physical examination. e. Diagnostic tests: Blood and urine cultures, chest x-ray, discontinue peripheral line (i. e., peripheral intravenous central catheter [PICC] line); stool cul-ture for Clostridium difficile and vancomycin-resistant enterococci (VRE), respiratory panel via nasal or throat swab. f. T reatment: Tylenol PRN, initiate broad-spectrum antimicrobials while awaiting culture results, IV flu-ids, supplemental oxygen. Leukemias: Chronic Leukemias285	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
i. Most commonly isolated organisms are gram-positive organisms such as Staphylococcus epider-midis and gram-negative organisms such as Pseu-domonas aeruginosa, Escherichia coli, and Klebsiella. ii. Empiric antibiotic options include intravenous cefepime/ceftazidime, piperacillin-tazobactam, vancomycin, and/or imipenem/meropenem. iii. Antibiotics should be continued until the patient is no longer neutropenic. iv. If the infection persists despite antibiotic ther-apy, consider removal of an indwelling catheter. v. If the neutropenic patient remains febrile for greater than 1 week while on broad-spectrum antibiotics, a fungal infection should be suspected. 2. Hyperleukocytosis. a. Medical emergency seen in patients experiencing CML blast crisis or CLL in more aggressive settings. b. It is defined by a WBC greater than 100,000k caused by rapid, uncontrolled leukemic cell prolifera-tion; however, this value is an arbitrary threshold. c. Three main complications: Disseminated intravas-cular coagulation (DIC), tumor lysis syndrome (TLS), leukostasis. i. DIC. ii. TLS. 1)Most common disease-related emergency in adults with hematologic cancers. 2)Classically: Hyperuricemia, hyper-kalemia, hyperphosphatemia, and hypocal-cemia. a)Hyperuricemia: Gout attacks, renal insufficiency. b)Hyperkalemia: Cardiac arrhythmias (peaked T waves on EKG), muscle cramps, paresthesia, nausea, vomiting, diarrhea. c)Hyperphosphatemia/hypocalcemia: Hypotension, arrhythmias, tetany/muscle cramps, confusion, seizures. 3)Management. a)Goals are to prevent moderate to severe metabolic abnormalities and subse-quent clinical complications. b)Monitor: Serum electrolytes, renal function, urine output, neurological sta-tus, EKG. c)Avoid: Nephrotoxic agents, exogenous electrolyte supplementation. d)Hydration is the most important fac-tor for renal perfusion; rate is dependent on risk factors and subsequent comorbidi-ties. 3. Leukostasis. a. “Symptomatic hyperleukocytosis”; medical emer-gency. b. Characterized by extremely high WBC ( >100× 106/L) resulting in decreased tissue perfusion sec-ondary to increased blood viscosity and inflammation from cytokine release. c. Pulmonary signs and symptoms: Dyspnea, short-ness of breath, hypoxia demonstrated through pulse oximetry; imaging revealing diffuse or alveolar infil-trates; increased oxygen supplementation needs. d. Neurological signs and symptoms: Headache, con-fusion, altered mental status, visual changes, gait instability; imaging demonstrating intracranial hem-orrhage or areas of ischemia. e. Approximately 80% of patients with leukostasis are febrile; typically treated with empiric antibiotics. f. Diagnosis is made empirically when a patient presents with a high white count manifesting in res-piratory or neurological distress. g. T reatment. i. Hemodynamic stabilization with rapid cytore-duction in conjunction with prophylaxis for TLS due to rapid cessation of leukocytosis. ii. Cytoreduction. 1)Achieved with hydroxyurea (Hydrea), induction chemotherapy, and leukapharesis. 2)Prophylactic platelet transfusions and cor-rection of coagulopathy dependent on clinical presentation. 3)Adequate fluid restoration and prophylac-tic treatment of TLS with reduction in uric acid level and restoring electrolyte balance. 4. Autoimmune hemolytic anemia and autoimmune thrombocytopenia. a. Autoimmune hemolytic anemia. i. Laboratory findings. 1)Positive Coombs test. 2)Decreased hemoglobin. 3)Increased reticulocyte count. 4)Elevated LDH. 5)Elevated indirect bilirubin. ii. First-line treatment is steroids. iii. Consider intravenous immunoglobulin (IVIG), Rituxan, or splenectomy in steroid-refractory patients. b. Immune thrombocytopenia (ITP). i. Characterized by rapid decrease in platelet count. ii. Laboratory findings. 1)Decreased platelet count. 13. Oncology Guidelines e)T reating electrolyte imbalance. i) Hyperuricemia. Allopurinol: Hypoxanthine analog. Rasburicase: Guidelines for administration include high LDH, high WBC, large tumor mass, significantly elevated serum uric acid level. ii) Hyperkalemia. Kayexalate or other sodium polystyrene sulfonate. Calcium gluconate (if EKG changes). Lasix, Regular insulin +D50W, Albuterol via nebulizer. iii) Hyperphosphatemia. Phosphate binders: Seve-lamer, aluminum hydroxide. Dialysis in severe cases. iv) Hypocalcemia. Correct hyperphosphatemia first! Caution with additional cal-cium supplementation. v) Hemodialysis in severe cases. vi) Cardiac monitoring for dysrhyth-mias.---------286	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2)Hemoglobin and WBC within expected ranges (may be low due to disease or chemotherapy). 3)Normal coagulation studies (prothrom-bin time [PT]/partial thromboplastin time [PTT]). 4)Peripheral smear to rule out platelet clumping (pseudothrombocytopenia). iii. Diagnosis of exclusion. Must rule out other causes of thrombocytopenia (e. g., medications, microangiopathy, infections). iv. T reatment. 1)Frontline treatment is IV steroids tapered to PO steroids. 2)IVIG raises platelet count more rapidly than steroids. 3)Rituxan and/or splenectomy can be con-sidered in steroid-refractory patients. 5. Central nervous system (CNS) disease. a. Evaluation for CNS disease both in CML blast cri-sis and CLL. i. Signs/symptoms: Headaches, visual changes, unexplained neuropathy, altered mental status. b. Imaging including CT head/brain or MRI brain. c. Lumbar puncture to assess cell count and differ-ential and flow cytometry; cerebrospinal fluid (CSF) cytology. d. T reatment: Intrathecal chemotherapy until CNS clears of malignant cells. 6. Differentiation syndrome. a. Often seen in patients with acute promyelocytic leukemia (APL). b. Fever often associated with increasing WBC, shortness of breath, hypoxemia, and pleural or peri-cardial effusions. c. T reatment. i. Initiate dexamethasone (10 mg twice daily x 3-5 days tapering over 2 weeks) at first sign of res-piratory compromise. ii. Interrupt administration of all-trans-retinoic acid (ATRA) until hypoxia resolves. iv. With difficult to treat patients, may begin cytoreduction, hydroxyurea, or anthracycline. Follow-Up A. Routine follow-up for all patients should occur once every 6 to 12 months and include a physical examination and CBC. B. Patients with CLL have a higher risk of developing other types of cancer. Follow-up should occur if patients notice any new or worsening symptoms. Consultation/Referral A. Hematology oncology. B. Additional referrals to surgery for port access or infectious disease may be made at the discretion of the team. Special/Geriatric Considerations A. CLL primarily affects the elderly population. B. A careful assessment of the elderly patient should be taken into consideration when determining a plan of action. C. Chronological age should not be the sole determinant of treatment options. Life expectancy, quality of life, and patient functional status should be considered as well. Bibliography Baccarani, M., Pileri, S., Steegmann, J., Muller, M., Soverini, S., & Dreyling, M. (2012). Chronic myeloid leukemia: ESMO Clinical Prac-tice Guidelines for diagnosis, treatment, and follow-up. Annals of Oncol-ogy, 23 (Suppl. 7), vii72-vii77. Desai, S., & Pinilla-Ibarz, J. (2012). Front-line therapy for chronic lympho-cytic leukemia. Cancer Control, 19,26-36. Elinoff, J. M., Salit, R. B., & Ackerman, H. C. (2011). The tumor lysis syndrome. The New England Journal of Medicine, 365 (6),571-572. Greenberg, E. M., & Probst, A. (2013). Chronic leukemia. Critical Care Nursing Clinics, 25,459-470. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Rai, K. R., Sawitsky, A., Cronkite, E. P., Chanana, A. D., Levy, R. N., & Pasternack, B. S. (1975). Clinical staging of chronic lymphocytic leukemia. Blood, 46 (2),219-234. Schiffer, C. A. (2017, November 27). Hyperleukocytosis and leukosta-sis in hematologic malignancies. In A. G. Rosmarin (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ hyperleukocytosis-and-leukostasis-in-hematologic-malignancies Woessner, D., & Lim, C. (2013). Disrupting BCR-ABL in combina-tion with secondary leukemia-specific pathways in CML cells lead to enhanced apoptosis and decreased proliferation. Molecular Pharmaceu-tics, 10,270-277. Leukemias: Myelodysplastic Syndromes Madeleine Nguyen-Cao Definition A. Myelodysplastic syndromes (MDS) encompass an array of myeloid clonal hemopathies with a wide range of clinical presentations. B. They are characterized by the morbidities of their cytope-nias and the ominous potential to evolve into acute myeloid leukemia (AML). Incidence A. The incidence rate of MDS is approximately 4. 9 per 100,000 people per year. B. MDS is a disease of older individuals (median age at diag-nosis: 70-75 years of age) with incidence peaking at 59. 8 per 100,000 people among those who are 80 years of age and older. Pathogenesis A. MDS develops when a clonal population of dysplas-tic hematopoietic stem cells overtakes healthy bone marrow cells. B. MDS can be characterized as primary (de novo) or sec-ondary to a prior potent chemotherapy regimen for other cancers. Predisposing Factors A. More common in males. B. Increases with age. C. Exposure to chemotherapy or radiation therapy. Subjective Data A. Common complaints/symptoms: Patient presentation is typically related to cytopenias and may include: Leukemias: Myelodysplastic Syndromes287 iii. For those at high risk for differentiation syn-drome, begin prophylaxis with corticosteroids (prednisone 0. 5 mg/kg on day 1 or dexametha-sone 10 mg every 12 hours) tapered over several days.	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
1. Fever. 2. Cough. 3. Malaise. 4. Fatigue. 5. Bruising. 6. Gingival bleeding. 7. Epistaxis. 8. Recurrent infections. B. Medical history. 1. Timing, severity, and pace of abnormal cytopenias. 2. T ransfusion history. 3. Pneumonias, urinary tract, and other frequent infections. Physical Examination A. Vital signs: Assess for tachycardia due to anemia or weight. B. General: Assess for pallor or weakness. C. Head, ear, eyes, nose, and throat ( HEENT): Assess oral cavity for hemorrhagic bullae or gingival bleeding and eyes for hemorrhagic conjunctiva. D. Cardiopulmonary: Assess for signs of heart failure and adventitious breath sounds consistent with infection. E. Gastrointestinal: Assess for hepatosplenomegaly and hematochezia. F. Skin: Assess for petechiae. Diagnostic Tests A. Laboratory. 1. Complete blood count (CBC) with differential. 2. Peripheral blood smear. 3. Comprehensive metabolic panel (CMP) with serum uric acid and lactate dehydrogenase (LDH). 4. Thyroid function tests. 5. Serum erythropoietin, vitamin B12, folate, and iron studies. 6. Fluorescence in situ hybridization (FISH) to detect BCR-ABL fusion transcript to exclude chronic myeloid leukemia (CML) diagnosis. 7. Human leukocyte antigen (HLA)—typing for high-risk patients being considered for allogeneic hematopoi-etic cell transplantation. B. Bone marrow aspirate and biopsy. C. Diagnostic criteria. 1. MDS diagnostic criteria is primarily based on the fol-lowing World Health Organization (WHO) guidelines correlated with the clinical presentation (see Table 13. 4). 2. Risk stratification and prognostic scoring system. Differential Diagnosis 1. Anemias. 2. Neutropenia. Evaluation and Management Plan A. General plan. 1. T reatment of MDS is based on the stage and mecha-nism of the disease that predominates the particular phase of the disease process. 2. In the early phases, when increased bone marrow apoptosis results in ineffective hematopoiesis, retinoids and hematopoietic growth factors are indicated. 3. T reatment is focused on supportive management of cytopenias (e. g., blood and platelet transfusions, growth factors) and prolonging the time to disease progression (i. e., transformation to AML). 4. Supportive care pharmacotherapy. a. Thrombocytopenia: Romiplostim (Nplate), eltrombopag (Promacta). b. Anemia: Darbepoetin (Aranesp). c. Neutropenia: Neupogen (Filgastrim) and antimi-crobial prophylaxis. d. Iron overload from repeated transfusions: Iron chelation therapy. B. Pharmacotherapy. 1. Hypomethylating agents. 2. Biologic response modifiers. 3. High-intensity idarubicin-, cytarabine-, fludarabine-, and topotecan-based regimens. C. Other treatments: Allogeneic hematopoietic stem cell transplant. D. Disease progression to AML is defined by the presence of 20% or more myeloid blasts in bone marrow or peripheral blood. This is associated with poor prognosis and response to standard treatment options. Follow-Up A. Focus on response to therapy and monitor for signs or symptoms of disease progression. B. Frequency of visits determined by the oncologist; will include CBCs to monitor hematological response. C. A bone marrow aspirate may be warranted if concern for disease progression. Consultation/Referral A. Patients with MDS need to be referred to hematology-oncology. Special/Geriatric Considerations A. Management of the disease in the elderly population presents a challenge due to concomitant morbidities, which preclude toleration of intensive chemotherapy regimens. B. Patients with MDS have high utilization rates of EDs and require frequent transfusions. Comorbidities, including dia-betes, liver disease, and infections, tend to be higher in elderly MDS patients. Bibliography Arber, D. A., Orazi, A., Hasserjian, R., Thiele, J., Borowitz, M., Le Beau, M., & Vardiman, J. W. (2016). The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood, 127 (20), 2391-2405. Gerds, A. T., Gooley, T. A., Estey, E. H., Appelbaum, F. R., Deeg, H. J., & Scott, B. L. (2012). Pretransplantation therapy with azacitadine vs induction chemotherapy and posttransplantation outcome in patients with MDS. Biology of Blood and Marrow Transplantation, 18, 1211-1218. Germing, U., Kobbe, G., Hass, R., & Gatterman, N. (2013). Myelodysplas-tic syndromes: Diagnosis, prognosis, and treatment. Deutsches Ärzteblatt International, 110 (46), 783-790. Greenberg, P. L. (1997). The role of hemopoietic growth factors in the treat-ment of myelodysplastic syndromes. International Journal of Pediatric Hematology/ Oncology, 4,231-238. Ma, X. (2012). Epidemiology of myelodysplastic syndromes. Amer-ican Journal of Medicine, 125 (7 Suppl), S2-S5. doi:10. 1016/ j. amjmed. 2012. 04. 014 Ma, X., Does, M., Raza, A., & Mayne, S. T. (2007). Myelodysplastic syn-dromes: Incidence and survival in the United States. Cancer, 109,1536-1542. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Thiele, J., Kvasnicka, H. M., Facchetti, F., Franco, V., van der Walt, J., & Orazi, A. (2005). European consensus on grading bone marrow fibrosis and assessment of cellularity. Haematologica, 90 (8),1128-1132. 13. Oncology Guidelines288	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
TABLE 13. 4 2008 and 2016 WHO Classifications of MDS 2008 WHO Classification 2016 WHO Classification Refractory cytopenia with unilineage dysplasia (RCUD) encompassing refractory anemia (RA), refractory neutropenia (RN), and refractory thrombocytopenia (RT)MDS with single lineage dysplasia (MDS-SLD) Refractory cytopenia with multilineage dysplasia (RCMD) MDS with multilineage dysplasia (MDS-MLD) Refractory anemia with ringed sideroblasts (RARS) MDS with ringed sideroblasts (MDS-RS) MDS-RS with single lineage dysplasia (MDS-RS-SLD) MDS-RS with multilineage dysplasia (MDS-RS-MLD) MDS associated with isolated del(5q) MDS with isolated del(5q) MDS with excess blasts (MDS-EB) Refractory anemia with excess blasts-1 (RAEB-1) MDS-EB-1 Refractory anemia with excess blasts-2 (RAEB-2) MDS-EB-2 MDS, unclassified (MDS-U) MDS, unclassifiable (MDS-U) With 1% blood blasts With single lineage dysplasia and pancytopenia Based on defining cytogenetic abnormality Refractory cytopenia of childhood Refractory cytopenia of childhood MDS, myelodysplastic syndrome; WHO, World Health Organization. Leukemias: Myeloproliferative Neoplasms Shannon B. Holloway Definition A. Myeloproliferative neoplasms (MPNs) are charac-terized by clonal myeloproliferation without dysplastic features. B. Essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF) result in clonal pro-liferation of hematopoietic stem cells. Incidence A. The reported worldwide annual incidence rate of MPNs ranges from 0. 44 to 5. 87 per 100,000 with the lowest inci-dence rates being reported in Japan and Israel. B. PV is the most prevalent Philadelphia-negative MPN in the United States and is estimated to affect about 148,000 people. Pathogenesis A. MPNs are characterized by the overproduction of mature blood cells deriving from the three primary myeloid lineages. B. Typically predominate in one lineage depending on the disease. Predisposing Factors A. Age greater than 65. B. History of thrombosis. Subjective Data A. Common complaints/symptoms. 1. Most patients with MPNs are typically asymptomatic and abnormal blood counts (e. g., thrombocytosis or ele-vated hematocrit) often prompt further evaluation. 2. Common symptoms according to the myeloprolifer-ative neoplasm symptom assessment form (MPN-SAF) include: a. Abdominal pain. b. Early satiety. c. Abdominal discomfort. d. Inactivity. e. Vasomotor symptoms: Headaches/lightheaded-ness. f. Difficulty concentrating/sleeping. g. Night sweats. h. Pruritus (particularly after warm showers). i. Bone pain. j. Fever. k. Unintentional weight loss that lasts greater than 6 months. l. Depressed mood. B. Common/typical scenario. 1. Some patients present with bleeding or thrombosis. If there are small vessel disturbances due to thrombosis, patients may experience headaches, migraines, dizziness, lightheadedness, coldness of the fingers and toes, and/or burning and erythema of the smaller extremities. 2. There can be life-threatening presentations associ-ated with thrombosis, such as transient ischemic attack, myocardial infarction, stroke, deep vein thrombosis (DVT), pulmonary embolism (PE), or clotting in usual areas such as abdominal veins. 3. Patients with a platelet count of 1. 5 million or more are at risk for spontaneous bleeding and may experience frequent epistaxis, easy bruising, menorrhagia, or gas-trointestinal bleeding. Leukemias: Myeloproliferative Neoplasms289	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Physical Examination A. Skin: Facial plethora (flushed face), excoriations from scratching secondary to pruritus, petechiae. B. Abdomen: Splenomegaly, hepatomegaly, abdominal dis-tention, tenderness to palpation typically in the left upper quadrant. C. Head and neck: Epistaxis, hemorrhagic bullae, or gingival bleeding in oral cavity. Diagnostic Tests A. Complete blood count (CBC) with differential. B. Comprehensive metabolic panel (CMP) with serum uric acid and lactate dehydrogenase (LDH). C. Erythropoietin level and iron studies. D. Vitamin B12level. E. Evaluate for acquired Von Willebrand disease. 1. Prothrombin time/international normalized ratio (PT/INR) and partial thromboplastin time (PTT). 2. Factor VIII. 3. Gold standard: Ristocetin activity test. F. Peripheral blood smear. G. Bone marrow aspiration and biopsy. H. Abdominal ultrasound to assess splenomegaly/hep-atomegaly. I. CT scan of abdomen and pelvis with contrast to assess splenomegaly/hepatomegaly and for obscure venous throm-bosis. J. Diagnosis: According to the World Health Organization (WHO) diagnostic criteria, laboratory findings and a bone marrow aspiration and biopsy are necessary to confirm a diag-nosis of ET, PV, and PMF. Differential Diagnosis A. Acute lymphoblastic leukemia. B. Acute myeloid leukemia (AML). C. Chronic lymphocytic leukemia. D. Chronic myelogenous leukemia. E. Non-Hodgkin lymphoma. Evaluation and Management Plan A. General plan. 1. The overall goal of treatment for patients with ET and PV is to prevent thrombosis and bleeding. 2. The most frequent complication of ET/PV is throm-bosis, which can include myocardial infarction, PE, DVT, or cerebrovascular accident. 3. There is a risk stratification process that assesses a patient's risk for thrombohemorrhagic complications. B. T reatment of ET. 1. Low-risk patients. a. Managed with observation. b. Low-dose aspirin can be added to a low-risk patient's regimen on a case-by-case basis. 2. High-risk patients. a. T reated with a cytoreductive agent. b. In addition, all high-risk patients must be on low-dose aspirin. c. Patients with a history of thrombosis should be treated with anticoagulant therapy. C. T reatment of PV. 1. Low-risk patients. a. Therapeutic phlebotomy and daily low-dose aspirin are indicated for low-risk patients. 2. High-risk patients. a. Initially treated with phlebotomy to attain hema-tocrit goal of less than 45% and are then placed on acytoreductive agent such as hydroxyurea or interferon alpha. b. The recommendation is for these patients to take a daily low-dose aspirin. 3. Common complaints/symptoms: Pruritus is a com-mon symptom of PV and can be treated with proper hematocrit control and the use of antihistamines or antipruritic agents such as hydroxyzine. 4. Patients with preexisting thrombus must be treated with anticoagulation. D. Staging of myelofibrosis (MF). 1. Risk stratification. a. Three main prognostic scoring systems are used for MF risk stratification. i. International Prognostic Scoring System (IPSS) is used at initial diagnosis and scores are based on age, hemoglobin level, leukocyte count, and circulating peripheral blasts. ii. Diagnostic International Prognostic Scoring System (DIPSS) is used if karyotyping is not avail-able during the course of treatment. iii. Diagnostic International Prognostic Scoring System-plus (DIPSS-plus) is used if karyotyping is available during the course of treatment and includes platelet count and transfusion needs, as well as unfavorable karyotype. 2. MF grading based on bone marrow biopsy. E. T reatment of MF. 1. The treatment approach for PMF, post-PV, or post-ET MF is the same. 2. Referral to specialized centers with experts in MF and stem cell transplantation is recommended. 3. Watch and wait approach is appropriate for low-risk patients. 4. Immunotherapy and targeted therapy. 5. Allogeneic hematopoietic stem cell transplant is the only curative option. 6. Disease progression to AML is defined by the pres-ence of 20% or more myeloid blasts in bone marrow or peripheral blood. This is associated with poor prognosis and response to standard treatment options. Follow-Up A. Changes in symptom status should be reported immedi-ately to providers; prompt evaluation should include a CBC at a minimum. B. Follow-up to monitor response to treatment should occur every 3 to 6 months, or more frequently if there is a change in symptoms. Consultation/Referral A. Refer to an oncologist specializing in MPNs. B. MPNs are relatively rare, and smaller community type oncologists may not have extensive experience in treatment options or access to major clinical trials that could benefit patients. Special/Geriatric Considerations A. Supportive care should be an integral part of treatment. B. MPNs are more prevalent in the elderly, who are at increased risk for cardiovascular and other comorbidities, such as congestive heart failure, peripheral vascular disease, stroke, thromboembolism, renal disease, liver disease, and infections. 13. Oncology Guidelines290	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Bibliography Barbui, T., Thiele, J., Gisslinger, H., Finazzi, G., Vannucchi, A. M., & Tef-feri, A. (2016). The 2016 revision of WHO classification of myeloprolif-erative neoplasms: Clinical and molecular advances. Blood Review, 30 (6), 453-459. Cervantes, F., Dupriez, B., Pereira, A., Passamonti, F., Reilly, J. T., Morra, E., & Tefferi, A. (2009). New prognostic scoring system for based on a study of the International Working Group for Myelofibrosis Research and T reatment. Blood, 113 (13), 2895-2901. Choi, C. W., Bang, S., Jang, S., Jung, C. W., Kim, H. J., Kim, H. Y.,... Won, J. H. (2015). Guidelines for the management of myeloproliferative neoplasms. Korean Journal of Internal Medicine, 30 (6), 771-788. Mesa, R., Jamieson, C., Bhatia, R., Deininger, M. W., Gerds, A. T., Gojo, I.,... Sundar, H. (2016). Myeloproliferative neoplasms. Journal of the National Comprehensive Cancer Network, 14 (2), 1572-1611. Passamonti, F., Cervantes, F., Vannucchi, A. M., Morra, E., Rumi, E., Pereira, A.,... Tefferi, A. (2010). A dynamic prognostic model to pre-dict survival in primary myelofibrosis: A study by the IWG-MRT. Blood, 115,1703-1708. Thiele, J., Kvasnicka, H. M., Facchetti, F., Franco, V., van der Walt, J., & Orazi, A. (2005). European consensus on grading bone marrow fibrosis and assessment of cellularity. Haematologica, 90 (8), 1128-1132. Vainchenker, W., & Constantinescu, S. N. (2013). JAK/STAT signaling in hematologic malignancies. Oncogene, 32,2601-2613. Vannucchi, A. M., Barbui, T., Cervantes, F., Harrison, C., Kiladjian, J. J., Kröger, N.,... Buske, C. (2015). Philadelphia chromosome-negative chronic myeloproliferative neoplasms: ESMO clinical practice guide-lines for diagnosis, treatment and follow-up. Annals of Oncology, 26 (5), 85-99. Lung Cancer Courtney Robb Definition A. Lung cancer is the uncontrolled growth of abnormal cells that form in tissues of one or both lungs, usually in the cells lining air passages. These abnormal cells divide rapidly to form tumors. B. The two main types are non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). 1. NSCLC. a. NSCLC is the most common type of lung cancer, comprising 85% of the lung cancer diagnoses. b. There are three histologic subtypes of NSCLC aris-ing from different lung cells, which have similar prog-nosis and treatment. i. Adenocarcinoma. 1)Most common subtype of NSCLC, mak-ing up roughly 40% of lung cancers, and it is the most common type of lung cancer found in nonsmokers. 2)Originates in glandular cells that typically secrete mucus. ii. Squamous cell carcinoma. 1)Typically linked to a history of smoking. 2)T umors are often located in the central area of the lungs near the main bronchus. 3)Comprises 25% to 30% of lung cancer diagnoses. 4)Originates in the flat cells that coat the inside of the airways called squamous cells. iii. Large cell (undifferentiated) carcinoma. 1)Accounts for 10% to 15% of lung cancers. 2)Can occur anywhere in the lung but often appears as a large peripheral mass on chest radiograph. 3)Tends to grow and spread quickly. 4)Due to its tendency for rapid growth and metastasis, it is more difficult to treat. 2. SCLC. a. SCLC, previously known as oat cell lung cancer, accounts for 15% to 20% of all lung cancers. b. Associated with a poor prognosis due to the advanced stage (usually metastatic) at the time of diag-nosis. Incidence A. Lung cancer is the second most common cancer among both women and men, accounting for approximately 14% of all new cancer diagnoses. However, it is the number one cause of cancer deaths among both women and men each year. B. More individuals die annually from lung cancer than of breast, prostate, and colon cancer combined. C. Lung cancer primarily occurs in people over the age of 65 with less than 2% being younger than age 45. D. The average age at diagnosis is 70 years old. E. The survival rate among individuals with lung cancer varies based on staging at the time of diagnosis. However, if diagnosed and treated early it can be cured. F. Five-year overall survival rate is 17. 7% for all patients or 55. 2% for patients presenting with localized disease (i. e., early detection). Pathogenesis A. Lung cancer can be divided into two broad categories: Small cell and non-small cell carcinoma. 1. Small cell carcinoma is almost exclusively caused by exposure to cigarette smoking. 2. Non-small cell carcinoma (adenocarcinoma, squa-mous cell and large cell carcinoma) can be caused by other environmental factors such as: a. Smoking. b. Radon gas. c. Pollution. d. Asbestos. e. Radiation. f. Toxic dust. g. Coal. h. Diesel. i. Arsenic. Predisposing Factors A. History of smoking (cigarette/cigar/pipe/marijuana). This is dose dependent, meaning the increased quantity and duration of smoking increase the risk of lung cancer. B. Exposure to radon or asbestos. C. History of lung cancer in the immediate family. D. Exposure to Agent Orange or other carcinogens. E. Diagnosis of another respiratory disease such as chronic obstructive pulmonary disease (COPD), emphysema, chronic bronchitis, or pneumonia. F. Contact with secondhand smoke. Subjective Data A. Common complaints/symptoms. 1. Cough, especially if persistent (the most common). 2. Shortness of breath. 3. Hemoptysis. 4. Pain in the chest, back, or shoulder unrelated to cough. 5. Changes in voice or becoming hoarse. 6. Recurrent lung problems, like bronchitis or pneu-monia. Lung Cancer291	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
7. Wheezing. 8. Bone pain (with bone metastasis). 9. Headaches (with intracranial metastasis). 10. Unexplained weight loss. 11. Fatigue. B. Common/typical scenario. 1. Patients are frequently asymptomatic with symptoms only developing once the disease is well advanced. 2. Often, lung cancer is discovered incidentally on chest imaging. Physical Examination A. Check vital signs including pulse oximetry. B. Head and neck. 1. Evaluate pupils for symmetry and reaction to light. T umor in the lung apex can cause compression of the cervical sympathetic plexus, which can cause Horner syn-drome (ptosis, miosis, and anhidrosis). 2. Palpate the neck and supraclavicular area for adenopathy. 3. Evaluate the neck for facial edema, facial cyanosis, or jugular vein distention (JVD), which could indicate supe-rior vena cava (SVC) syndrome if the tumor is obstructing the SVC. C. Pulmonary system. 1. Observe for signs of dyspnea, increased work of breathing, or retractions. 2. Auscultate lung sounds in all lung fields. Lung tumor can lead to obstruction and collapse of a lobe or entire lung or postobstructive pneumonia. Pleural effusions may develop as well. All of these scenarios would lead to decreased breath sounds in those areas of the lung affected. 3. Percussion of the lung will be dull with collapsed lobes of the lung or pleural effusion. D. Cardiovascular system. 1. Auscultate heart sounds, which should be normal. If the tumor has direct cardiac involvement, or pericardial effusion has developed, the heart sounds may be affected. 2. Assess for signs of cardiac tamponade, such as hypotension, distant/muffled heart sounds, pericardial rub, or JVD. E. Gastrointestinal tract. 1. Auscultate for bowel sounds in all four quadrants. 2. Palpate for hepatomegaly. One of the most common sites of lung metastasis is the liver, which can manifest as tender hepatomegaly. F. Musculoskeletal system. 1. Bone is another area of common metastasis. 2. Patients may report bone pain or tender spots on examination, including the spine. 3. Lung cancers that arise in the lung apex, called Pan-coast tumors, can cause shoulder or scapula pain that radiates down the arm. G. Central nervous system. 1. A neurological examination should be performed to evaluate for any focal neurological deficits that may be produced by intracranial metastases or spinal cord com-pression. 2. Evaluation for neuropathy, decreased sensation, or decreased strength should be performed. Diagnostic Tests A. Laboratory data. 1. Complete blood count (CBC). 2. Comprehensive metabolic panel (CMP). 3. Prothrombin time/international normalized ratio (PT/INR) and partial thromboplastin time (PTT). B. Imaging and procedures. 1. Chest x-ray. 2. CT of the chest with contrast. 3. PET/CT scan to assess for metastatic disease. 4. Endobronchial ultrasound (EBUS) to evaluate medi-astinal lymph nodes. 5. Brain MRI to complete staging. C. Biopsy: Interventional radiology (IR) CT guided biopsy. D. Ancillary tests prior to surgery. 1. EKG. 2. Pulmonary function test (PFT). E. Diagnosis: Tissue sample or biopsy is required for diagno-sis; these are typically obtained through a CT-guided biopsy of the lung nodule/mass. 1. Staging is one of the most important elements in determining therapeutic options and prognosis. The stag-ing for NSCLC and SCLC differ as noted in the follow-ing. a. NSCLC. i. Like the majority of cancers, NSCLC is staged by the tumor, node, metastasis (TNM) system. ii. Higher numbers indicate more advanced lung cancer. iii. Staging determines the approach to treatment (i. e., surgery, chemotherapy, radiation, or combi-nation of treatment modalities). b. SCLC: SCLC has a two-stage system: Limited ver-sus extensive stage. i. Limited stage: Localized to one hemithorax. Lymph nodes may be involved but they too must be located in the ipsilateral hemithorax in relation to the primary tumor. ii. Extensive stage involves lung cancer in both hemithoraces and/or metastasis to other organs and/or contralateral nodal metastasis. Staging determines the approach to treatment (chemora-diation vs. chemotherapy alone). Differential Diagnosis A. Adenocarcinoma. B. Squamous cell carcinoma. C. Large cell carcinoma. D. Small cell carcinoma. E. Pulmonary nodule. Evaluation and Management Plan A. General plan. 1. Based on staging, patients will be offered chemother-apy+/-radiation, stereotactic body radiation therapy (SBRT), and/or surgery. 2. Targeted therapies. B. Acute care issues in lung cancer. 1. Lung cancer patients are often only admitted for sur-gical resection. a. Pneumonectomy: Removal of the entire lung. b. Lobectomy: The most common surgical procedure in lung cancer patients, with removal of a single lobe of the lung. c. Segmental resection: Removal of a segment/ portion of the involved lobe. d. Sleeve resection: Consider when the cancer is confined to the bronchus or pulmonary artery and requires bronchoplastic reconstruction. 13. Oncology Guidelines292	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
e. Wedge resection: Removal of a small peripheral nodule; performed only on lung cancer patients with limited pulmonary reserve. 2. Postoperative lung surgery patients, without compli-cations, will spend 3 to 5 days in the hospital after surgery. 3. The primary focus in the postoperative inpatient set-ting includes the following: Pain control, monitoring lab work, wound care, chest tube management, pulmonary toileting to avoid pneumonia, and early ambulation. a. Pain control. i. May be managed by epidural, intercostal nerve block, and/or PO/IV pain medications. ii. Optimizing pain control leads to faster recov-ery as pain control allows the patient to deep breathe, deep cough, and ambulate, thereby reducing the risk of pneumonia. b. Monitoring laboratory data: Routine blood work including CBC with differential, electrolyte panel, blood urea nitrogen (BUN), and creatinine must be monitored for anemia, infection, electrolyte imbal-ance/need for replacement, and kidney function. c. Infection. i. The incision site will be monitored daily for signs of infection and proper healing. ii. Pulmonary toileting with the incentive spirometer and acapella apparatuses are crucial to prevent pneumonia in the postoperative lung resection patient. iii. Early ambulation is also crucial for reducing the risk of postoperative pneumonia. d. Pneumothorax prevention/monitoring. i. The postlung surgery patient will have any-where from one to two chest tubes placed in the operating room and managed in the recovery unit. ii. Chest tubes are placed on wall suction to help reinflate the lung and allow for fluid drainage. iii. The chest tube is a closed system that will need to be monitored for air leak and fluid drainage daily. iv. Daily chest x-rays should also be performed. v. Once there is evidence of no air leak and the chest x-ray shows an inflated lung, the chest tube may be removed. Follow-Up A. Five-year survival remains poor in this patient population. B. Perform surveillance to manage complications and symptoms. C. Follow-up visits recommended every 6 months for first 2 years. D. In NSCLC: Perform CT chest every 6 months for first 2 years after resection and every year thereafter. E. Assess for health-related quality of life at baseline and dur-ing follow-up visits. Consultation/Referral A. Most lung cancer patients are seen by: 1. Medical oncologist, who orders chemotherapy. 2. Radiation oncologist, who offers radiation therapy. 3. Cardiothoracic surgeon to formulate a treatment plan based on clinical staging. Special/Geriatric Considerations A. Much evidence exists to suggest that elderly adults with good functional status can tolerate combination chemother-apy in the treatment of lung cancer. B. Chronological age alone should not dictate treatment options. C. Providers should work with patients to decide on the best alternatives of management. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Lymphomas: Hodgkin Lymphoma Melissa Timmons Definition A. Malignancies that develop from lymph nodes and lym-phoid tissues are broadly classified into Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). B. HL, which originates in germinal center or postgerminal center B-lymphocytes, is characterized by the presence of a distinctive type of giant cell called a Reed-Sternberg cell in a background of reactive cells. Incidence A. HL accounts for approximately 10% of all lymphomas and approximately 0. 6% of all cancers diagnosed annually in the developed world. B. Median age at diagnosis is 39 years. C. In 2016, an estimated 8,500 patients were diagnosed with HL, and an estimated 1,120 patients died of HL. D. In the United States, the most common subtype of HL is classical HL, followed by mixed cellularity, lymphocyte-rich, and lymphocyte-depleted. Pathogenesis A. HL occurs due to the clonal proliferation of malignant Hodgkin/Reed-Sternberg cells in a background of reactive cells. B. The proliferation of these malignant cells causes lym-phadenopathy and enlargement of lymphoid tissue/organs (e. g., spleen). C. Lymphoma generally spreads to contiguous lymph nodes following lymph vessels. Predisposing Factors A. Epstein-Barr virus (EBV) infection. B. Immunosuppression (e. g., patients with HIV infection or long-term immunosuppressant use). C. Family history of HL. D. Most patients who develop HL have no identifiable risk factors. Subjective Data A. Common complaints/symptoms. 1. Painless lymphadenopathy, most commonly in the neck, axilla, or groin, is the most common presenting complaint. Occasionally, lymph nodes can become painful after consuming alcohol. Lymphomas: Hodgkin Lymphoma293	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2. B-symptoms: Unintentional weight loss, fever, and night sweats. B. Common/typical scenario. 1. Other signs and symptoms. a. Generalized pruritus. b. Fatigue. c. Lack of appetite. d. Cough, difficulty breathing, or chest pain sec-ondary to large mediastinal mass or lymphadenopa-thy. Often a mediastinal mass will be discovered incidentally on a routine chest radiograph. C. Family and social history. 1. Elicit presence or absence and duration of symptoms. 2. Ask about previous malignancy, prior treatment with chemotherapy or radiation therapy, history of immuno-suppressive illnesses such as HIV, and family history of malignancy. D. Review of systems: Determine the patient's performance status, as this can impact future treatment options. Physical Examination A. A complete physical examination, including vital signs, should be performed. B. Special attention should be paid to the size and number of palpable peripheral lymph nodes and presence or absence of hepatosplenomegaly. C. Comprehensive neurological examination should be per-formed to assess for central nervous system (CNS) involve-ment. Diagnostic Tests A. Definitive diagnosis is made by lymph node biopsy. An excisional biopsy is preferred for diagnosis but often core biopsy of an involved node is sufficient. B. Complete workup should include complete blood count (CBC), erythrocyte sedimentation rate (ESR), comprehen-sive metabolic panel (CMP), lactate dehydrogenase (LDH), pregnancy test in women with childbearing potential, and HIV serology. C. Clinical staging, including the following evaluations, should also be completed. 1. Full-body PET/CT scan. 2. Bilateral bone marrow biopsy/aspiration should be considered if the patient has pancytopenia. 3. Lumbar puncture and/or dedicated brain imaging, only if CNS involvement is suspected. D. HL is staged per the Ann Arbor Staging. E. Other important tests to consider include pulmonary function tests and echocardiogram, as they will likely be needed for assessment prior to chemotherapy or radiation therapy. Differential Diagnosis A. HIV. B. Other solid tumors. C. NHL D. Any disease with lymphadenopathy needs to be consid-ered. Evaluation and Management Plan A. General plan. 1. T reatment based on the stage of the disease at diagno-sis, but can involve chemotherapy, radiation therapy, and immunotherapy, either alone or in combination. 2. Several chemotherapy regimens exist for the initial treatment of HL. 3. High-dose chemotherapy followed by autologous or allogeneic stem cell transplant may be indicated for refractory or recurrent disease. Follow-Up A. Based on individual needs and individual oncologists. B. Basic schedule includes: 1. Visits every 3 to 6 months for first 2 years, every 6 to 12 months in years 3 to 5, and annually after year 5. 2. Usual tests are physical examination, blood work, imaging as indicated, and surveillance of symptom changes. Consultation/Referral A. Immediate referral to an oncologist should be made when HL is suspected or diagnosed. Special/Geriatric Considerations A. HL is one of the most curable malignancies in adults; however, survival rates in elderly patients are significantly lower than in younger patients. Bibliography Cheson, B. D., Fisher, R. I., Barrington, S. F., Cavalli, F., Schwartz, L. H., Zucca, E., & Lister, T. A. (2014). Recommendations for initial evalua-tion, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: The Lugano classification. Journal of Clinical Oncology, 32(27), 3059-3068. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Siegel, R., Ma, J., Zou, Z., & Jemal, A. (2014). Cancer statistics, 2014. CA: A Cancer Journal for Clinicians, 64 (1),9-29. Lymphomas: Non-Hodgkin Lymphoma Megan Krug Definition A. Malignancies that develop from lymph nodes and lym-phoid tissues are broadly classified into Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). B. NHL encompasses a diverse group of diseases with more than 50 distinct subtypes, which are further classified by his-tology and clinical presentation. These various subtypes are determined based on the cells from which they arise (B-cells, T-cells, natural killer cells) or by their degree of indolence versus aggressiveness. C. Patients with indolent lymphomas typically survive for several years even without therapy. However, patients with aggressive lymphomas may only have months to live. Incidence A. NHL is relatively common in the United States with greater than 70,000 new cases each year (accounting for 4. 3% of all cancer diagnoses), as compared to approximately 8,000 cases of HL each year. B. The majority of NHL cases are B-cell neoplasms (85%), whereas T-cell/NK-cell neoplasms account for only 15% of NHLs. C. The median age at diagnosis is 66, although it is seen in all age groups. 13. Oncology Guidelines294	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
D. Between the years 2004 and 2013, rates of new cases have remained stable, though the rate of mortality has decreased an average of 2. 4% each year. Pathogenesis A. T umors associated with NHL originate from lymphoid tissues. B. Most NHLs come from B-cell expansion. Predisposing Factors A. Immunodeficiency states. B. Epstein-Barr virus (EBV) infection. C. HIV infection. D. Human T lymphotropic virus type 1 (HTLV-1) infection. E. Autoimmune rheumatoid diseases (lupus, Sjögren's, rheumatoid arthritis). F. Herbicide/pesticide exposure. Subjective Data A. Common complaints/symptoms. 1. Rapidly enlarging lymph nodes (most commonly in neck or abdomen). 2. B Symptoms : Fever greater than 38∘C, drenching night sweats, unintentional weight loss of greater than 10% body weight. B. Common/typical scenario. 1. Other nonspecific symptoms: Malaise, fatigue, chronic pain, early satiety, cough/chest discomfort (seen with mediastinal involvement). 2. Approximately 34% of all patients present with pri-mary extranodal lymphoma at the time of diagnosis; the gastrointestinal (GI) tract is the most common site, fol-lowed by the skin. Physical Examination A. Vital signs. B. Head and neck: Facial edema/jugular venous distention (JVD) can indicate superior vena cava syndrome (most com-monly seen in primary mediastinal lymphoma). C. Lymphatics: Cervical, axillary, inguinal, Waldeyer's ring (tonsils, base of tongue, nasopharynx). D. Cardiopulmonary: Evaluate for signs of dyspnea/air-way obstruction, evidence of malignant pleural effusion (decreased breath sounds/crackles), and signs of pericardial effusion/tamponade. E. Abdomen: Evaluate for hepatomegaly/splenomegaly and ascites. F. Neurological: Evaluate for signs of spinal cord compres-sion, altered mental status, memory impairment, or cranial nerve dysfunction. Diagnostic Tests A. Laboratory data. 1. Complete blood count (CBC) with differential. 2. Comprehensive metabolic panel (CMP). 3. Magnesium. 4. Phosphorus. 5. Lactate dehydrogenase (LDH). 6. Uric acid. 7. Coagulation studies: Prothrombin time/international normalized ratio (PT/INR) and partial thromboplastin time ( PTT). B. Lymph node biopsy. C. PET/CT scan. D. Bone marrow biopsy. E. Lumbar puncture and brain/spine MRI if at risk for central nervous system (CNS) involvement. F. Formal ophthalmologic examination if at risk for/con-firmed CNS involvement (can also rarely be seen in mantle cell lymphoma and marginal zone lymphoma). G. Hepatitis B and C serologies (risk of reactivation due to Rituxan). H. HIV screen. I. +/-serum protein electrophoresis (SPEP). J. +/-echocardiogram (for patients who will receive an anthracycline). K. Diagnosis/staging. 1. Definitive diagnosis is confirmed with excisional or core needle biopsy (not fine needle aspiration [FNA]). 2. The Lugano classification system, based on Ann Arbor Staging, is the most widely used classification system employed in NHL. Differential Diagnosis A. Solid tumors. B. Hematological malignancies. C. Hodgkin's lymphoma. Evaluation and Management Plan A. General plan/therapy. 1. The indicated treatment varies greatly depending on the type of NHL, staging, and age/performance status/-comorbidities. 2. A majority of NHL is treated with chemotherapy alone, though there are variants of indolent lymphoma in which watchful waiting is appropriate. 3. For some subtypes, radiation therapy is indicated as monotherapy. 4. Infrequently, surgery is employed for excision of lym-phoid tumors. 5. Stem cell transplant (autologous or allogenic) is typ-ically reserved for aggressive/late-stage disease, or for relapsed/refractory NHLs. B. Acute care issues in lymphomas. 1. Neutropenic fever (see sections on Leukemias). 2. T umor lysis syndrome (TLS; see sections on Leukemias). 3. Superior vena cava (SVC) syndrome. a. The obstruction of blood flow through the SVC caused by external lymph node compression or by thrombus within the vena cava, and is most com-monly seen associated with cases of primary mediasti-nal B-cell lymphoma. b. Clinical presentation most commonly reveals dys-pnea, cough, facial swelling, upper extremity edema, or chest pain. c. T reatment should be initiated after the cause of the obstruction is clarified, so as not to confound accu-rate diagnosis; and is focused on treating the underly-ing cause with chemotherapy and/or radiation. Stent placement or surgical bypass are reserved for severe cases, and are rarely utilized. 4. Spinal cord compression. a. Involvement of the spinal cord is not an unusual finding in patients with NHLs, and spinal cord com-pression typically manifests as severe back pain at the level of involvement, weakness (typically involving lower extremities), or paresthesia below the level of Lymphomas: Non-Hodgkin Lymphoma295	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
spinal involvement, bladder/bowel dysfunction (late finding). b. Diagnosis is confirmed with MRI. c. High-dose steroids and radiation therapy are the mainstays of treatment. Follow-Up A. Based on individual needs and individual oncologists. B. Basic schedule includes: 1. Visits every 3 to 6 months for the first 2 years, every 6 to 12 months in years 3 to 5, and annually after year 5. 2. Usual tests are physical examination, blood work, imaging as indicated, and surveillance of symptom changes. Consultation/Referral A. Hematology oncology to manage patients with NHL. B. Radiation oncology and surgery for placement of ports should be initiated. C. Infectious disease is often consulted to manage neu-tropenic fevers. Special/Geriatric Considerations A. Elderly patients with NHL show similar features and prognostic factors as younger patients, suggesting similar treatment strategies should be offered to both groups. B. Chronological age should not be the main determinant in treatment options, even in elderly patients older than 80 years. Bibliography National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Krol, A. D. G., le Cessie, S., Snijder, S., Kluin-Nelemans, J. C., Kluin, P. M., & Noordijk, E. M. (2003). Primary extranodal non-Hodgkin's lym-phoma (NHL): The impact of alternative definitions tested in the Com-prehensive Cancer Centre West population-based NHL registry. Annals of Oncology, 14 (1), 131-139. doi:10. 1093/annonc/mdg004 Multiple Myeloma Jerrad M. Stoddard Definition A. Plasma cell dyscrasias are a group of heterogeneous disorders that stem from the malignant proliferation of mon-oclonal plasma cells. Incidence A. Multiple myeloma (MM) is primarily a disease of the elderly, and the median age at diagnosis is 69. B. MM represents approximately 1% of all cancers and approximately 10% of all hematologic malignancies. Pathogenesis A. Plasma cell dyscrasias arise from the monoclonal prolifer-ation of plasma cells. Predisposing Factors A. Although not considered an inherited disease, the risk of developing MM is approximately 3. 7-fold higher for persons with a first-degree relative with MM. B. T wice as common in black persons. C. Family history increases risk 2-to 4-fold. D. Occupational exposures may contribute, such as: 1. Pesticides. 2. Petroleum workers. 3. Woodworkers. 4. Leather workers. 5. Ionizing radiation. Subjective Data A. Common complaints/symptoms. 1. The clinical presentation for plasma cell dyscrasias is quite variable. 2. Patients with MM often present with signs/symptoms related to plasma cell proliferation in the bone marrow and/or renal dysfunction. a. Elevated total protein—due to hypersecretion of monoclonal immunoglobulin and light chains; often associated with decreased albumin. b. Bone involvement—osteolytic lesions, pathologic fractures, hypercalcemia. c. Anemia. d. Renal failure. e. Recurrent infections. B. Common/typical scenario. 1. Patients may also present with an extramedullary plas-macytoma (soft tissue mass comprised of clonal plasma cells) that can cause spinal cord compression, cauda equina syndrome, severe back pain, paresthesia, and/or radiculopathy. 2. AL amyloidosis can lead to amyloid deposition in any organ, and patients can present with congestive heart failure, renal failure, skin changes, neuropathy, gastro-paresis, or diarrhea depending on the organ system(s) involved. Physical Examination A. Head and neck: Conjunctival pallor due to anemia; macroglossia. B. Musculoskeletal: Bone tenderness. C. Lymphatics: Assess for lymphadenopathy. D. Neurological: Vertebral compression fractures and/or plasmacytomas can cause neurological deficits if there is spinal cord or nerve compression. Diagnostic Tests A. Laboratory data. 1. Complete blood count (CBC) with differential. 2. Comprehensive metabolic panel (CMP) and calcium level. 3. Serum protein electrophoresis with immunofixation electrophoresis (SPEP/IFE). 4. 24-hour urine protein electrophoresis with immunofixation electrophoresis (UPEP/IFE)—Bence Jones proteinuria. 5. Serum free light chain assay (kappa and lambda). 6. Serum immunoglobulin levels (Ig A, Ig G, Ig M, Ig D). 7. 𝛽2-microglobulin for staging and prognostication. 8. Lactate dehydrogenase (LDH) for staging and prog-nostication. B. Imaging. 1. Bone survey with plain films to assess for axial and appendicular lytic bone lesions. 2. Consider PET/CT to assess for subtle bone lesions and/or plasmacytomas. 13. Oncology Guidelines296	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
3. Consider MRI of the cervical, thoracic, and lumbar (C/T/L) spine if there is concern for spinal cord com-pression from extramedullary plasmacytoma or vertebral compression fracture. C. Bone marrow aspiration and biopsy. D. Diagnosis. 1. CRAB criteria for symptomatic myeloma. a. Calcium (hypercalcemia)—serum calcium greater than 11 mg/d L. b. Renal insufficiency—serum creatinine greater than 2 mg/d L or Cr Cl less than 40 m L/min. c. Anemia—hemoglobin less than 10 g/d L. d. Bone lesions—one or more osteolytic lesions on bone survey, MRI, CT, or PET/CT. E. Staging. 1. Staging systems for newly diagnosed myeloma patients. a. Revised International Staging System (R-ISS). b. Durie-Salmon staging (more subjective and less commonly utilized). Differential Diagnosis A. Non-Hodgkin lymphoma (NHL). B. Amyloidosis. C. Plasmacytoma. Evaluation and Management Plan A. General plan. 1. T reatment depends on the plasma cell dyscrasia. 2. Therapy options for MM and amyloidosis. a. Patients typically receive two to six cycles of induction systemic chemotherapy followed by autol-ogous stem cell transplant (if eligible) or maintenance chemotherapy (if ineligible for transplant). b. Systemic chemotherapy. c. Autologous stem cell transplant. d. Allogeneic stem cell transplant. i. Not commonly utilized for MM. ii. Can be considered for patients with plasma cell leukemia, refractory myeloma, relapsed myeloma, or young patients with high-risk dis-ease (based on fluorescent in situ hybridization [FISH] data). e. Maintenance chemotherapy. f. Radiation therapy. g. Surgical intervention. i. Vertebroplasty or kyphoplasty may be indi-cated for patients with vertebral compression fractures. ii. Excisional biopsy may be performed to con-firm plasmacytomas. B. Supportive care. 1. Bone disease. a. All patients with osteolytic lesions and/or patho-logic fractures should be initiated on IV bisphospho-nates. b. Prior to initiation of bisphosphonate, patients must be evaluated by a dentist to assess for periodontal disease and risk for jaw osteonecrosis. 2. Infectious prophylaxis. 3. Thromboembolic prophylaxis. 4. Pain management. C. Emergencies and inpatient management. 1. Pain management. a. Pain is primarily due to skeletal fractures and bone pain from lytic lesions. b. Pharmacologic therapy. i. Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) due to nephrotoxicity. ii. Oral or IV analgesics. c. Surgical intervention for collapsed vertebral body. i. Vertebroplasty—injection of bone cement (methyl methacrylate) under fluoroscopy. ii. Kyphoplasty—placement of inflatable bone tamp prior to injection of bone cement. 2. Hypercalcemia. a. Due to osteolysis and/or renal failure. b. Corrected calcium =serum calcium +0. 8 (nor-mal albumin-serum albumin). c. Rule out other causes (e. g., hyperparathyroidism, thyrotoxicosis, medications, hypervitaminosis D). d. If asymptomatic and corrected calcium less than 12 mg/d L, patient may not require immediate treatment. e. Therapeutic intervention. i. Simultaneous administration of: 1)Hydration—isotonic saline for volume expansion. 2)Calcitonin—dose of 4 international units/kg (IU/kg). 3)Bisphosphonates (e. g., zoledronic acid). ii. Consider dialysis for patients with severe hypercalcemia. iii. Repeat serum calcium. 3. Renal failure. a. Due to light chain deposition in renal tubules (light chain cast nephropathy). b. Correct electrolyte abnormalities. c. Careful review of medications and discontinue or dose-adjust nephrotoxic agents. d. Consider kidney biopsy—stain for Congo red to rule out amyloidosis. e. IV hydration. f. Consider dialysis. 4. T umor lysis syndrome (see sections on Leukemias). 5. Spinal cord compression. a. Due to vertebral compression fracture and/or plas-macytoma. b. Symptoms vary depending on the location of com-pression and may include: i. Back pain. ii. Motor deficits. iii. Paresthesia. iv. Bowel/bladder incontinence or dysfunction. v. Gait ataxia. c. Emergent evaluation with MRI of cervical, tho-racic, and/or lumbar spine. d. If a mass is present, arrange biopsy of lesion for diagnosis. e. Requires emergent steroids, radiation therapy, and/or neurosurgical decompression. 6. Hyperviscosity syndrome. a. Symptoms and signs include: i. Blurred vision. ii. Papilledema. iii. Headache. iv. Neurological symptoms. v. Oral/nasal bleeding. vi. Stupor/coma. b. Obtain Ig M and serum viscosity levels. c. Requires emergent plasmapheresis if symptomatic (not based on serum viscosity level). Multiple Myeloma297	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Follow-Up A. Typically includes blood tests, radiologic testing, and bone marrow evaluation every 1 to 3 months. B. Long-term surveillance varies on a case-by-case basis. Consultation/Referral A. Consult medical oncologists and surgical oncologists spe-cializing in MM. Special/Geriatric Considerations A. Long-term and late effects of treatment can develop in survivors months or even years after treatment. 1. These effects can be physical and/or emotional. 2. Teach patients to identify and report them to their providers. B. Elderly patients older than 70 years should not be denied chemotherapy based solely on age. 1. Aggressive treatment should be discussed with the patient. 2. Life expectancy, quality of life, and functional status should be taken into consideration. Bibliography Lynch, H. T., Sanger, W. G., Pirruccello, S., Quinn-Laquer, B., & Weisen-burger, D. D. (2001). Familial multiple myeloma: A family study and review of the literature. Journal of National Cancer Institute, 93 (19), 1479-1483. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Palumbo, A., Avet-Loiseau, H., Oliva, S., Lokhorst, H. M., Goldschmidt, H., Rosinol, L., & Moreau, P. (2015 ). Group Revised International Staging System for Multiple Myeloma: A report from International Myeloma Working. Journal of Clinical Oncology, 33 (26), 2863-2869. Sarcoma Siji Thomas Definition A. Sarcomas are divided into two broad categories. 1. Soft tissue sarcoma. 2. Bone sarcoma. B. Soft tissues include adipose, muscle, tendinous, fibrous, and vascular tissues, and there are approximately 60 subtypes of soft tissue sarcoma. Examples include: 1. Osteosarcoma. 2. Ewing's sarcoma. 3. Liposarcoma. 4. Rhabdomyosarcoma. 5. Leiomyosarcomas. Incidence A. In 2016, there was an estimated 12,310 new cases of soft tissue sarcomas and 4,990 patients died of the disease. B. In 2016, there was an estimated 3,260 new cases of bone sarcomas and 1,550 patients died of the disease. C. Although very rare in adults, sarcomas comprise ∼15% of all pediatric cancers. D. Males are affected more frequently than females. Pathogenesis A. Sarcomas, as with many cancers, are often associated with cytogenetic abnormalities or molecular mutations. B. Sarcomas have a wide range of clinical behaviors and out-comes depending on the subtype and extent of disease. C. Expert pathological review is necessary to determine the specific subtype. Differentiation patterns can be difficult to ascertain, as there are approximately 60 different histologic subtypes. D. Classification of sarcomas depends on tissue appearance, histologic grade, and cell of origin. Predisposing Factors A. Genetic factors. B. Exposure to radiation. C. Exposure to chemical carcinogens (e. g., Agent Orange or polyvinyl chloride). Subjective Data A. Common complaints/symptoms. 1. Sarcomas can occur in any anatomic area: About 46% occur in lower extremities, 18% occur in the torso, 13% occur in the upper extremities, 13% occur in the retroperitoneum, and 9% occur in the head and neck. 2. The clinical presentation depends on the tumor's loca-tion. 3. Patients often present with: a. Swelling. b. Palpable soft tissue or bone mass. c. Sometimes pain. 4. Patients may present with: a. Constitutional symptoms such as fever, weight loss, and night sweats. b. Neurological symptoms if there is involved nerve compression. 5. Patients with a mass increasing in size or a mass greater than 5 cm should undergo evaluation for possible sar-coma with imaging (x-rays, CT, and/or MRI). Physical Examination A. Vital signs. B. Musculoskeletal: Evaluate location, size, and mobility of palpable mass. C. Neurological: Assess for any sensory/motor deficits, gait abnormality, and strength. D. Evaluate for metastatic disease. 1. Lymphatics: Assess for adenopathy. 2. Cough: Assess for metastatic spread to the lung. 3. Ascites: Retroperitoneal sarcomas can metastasize to the liver producing fluid wave. Diagnostic Tests A. General plan. 1. Imaging. a. CT or MRI for suspected soft tissue sarcoma. b. Conventional x-ray imaging should be performed for suspected bone sarcoma followed by CT and/or MRI. c. Consider PET scan. 2. Biopsy. a. Definitive diagnosis is based on biopsy of the mass. Core needle biopsy is typically sufficient to make an accurate diagnosis. b. Fine needle aspiration (FNA) is not recom-mended. 3. Molecular/cytogenetic markers. 13. Oncology Guidelines298	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
4. Metastatic evaluation. a. May include MRI with gadolinium to evaluate for bone metastasis. b. CT of the chest and/or abdomen to assess for lung or liver metastasis. c. Consider whole body PET. B. Staging. 1. Complete staging includes chest x-ray, CT scan of the chest, and bone scan to assess for metastatic disease. 2. For Ewing sarcoma, an MRI of the spine should be performed to assess for bone marrow metastases. 3. Soft tissue sarcomas (except retroperitoneal sarcomas): The tumor, node, metastasis (TNM) staging system is used. 4. Bone sarcomas: The Musculoskeletal T umor Society (MSTS) staging system is used. Differential Diagnosis A. Lipoma. B. Carcinoma. C. Neuroma. Evaluation and Management Plan A. General plan. 1. T reatment and prognosis vary depending on the subtype, location, and extent of disease. 2. Therapy includes a combination of systemic therapy, radiation, surgery, and in some cases targeted therapy. 3. For localized sarcomas, surgical excision is the main-stay of treatment. 4. For metastatic disease, unresectable disease, large tumors ( >5 cm), and tumors that are located in deeper tissues or have visceral involvement, systemic chemother-apy+/-radiation is often given followed by debulking surgery if indicated. 5. Chemosensitivity and choice of treatment differs based on histologic subtype. B. Acute care issues in sarcoma. 1. Local surgical resections can be attempted as outpatient. 2. Patients are usually admitted for extensive debulking or cytoreductive surgery or chemotherapy. 3. Postoperative management usually focuses on pain control, wound care, pulmonary toileting, and early ambulation. 4. Complex aggressive chemotherapy usually requires inpatient admission. a. High-dose chemotherapeutic combinations are employed depending on the type of sarcoma. b. T wo-dimensional echocardiography. c. Routine blood work including electrolyte panel, blood urea nitrogen (BUN), and creatinine must be monitored for electrolyte imbalance/need for replace-ment and kidney function. Follow-Up A. Complete within first 6 weeks. B. Surveillance in first year should occur at 3 months, 6 months, and then annually. C. If patients have higher grade cancer, more frequent visits should be scheduled. An MRI of the primary site may be indicated. Consultation/Referral A. Referrals for patients with suspected sarcoma should be referred to a cancer center so they can be followed by a surgical oncologist, medical oncologist, and radiation oncologist. B. Orthopedics should be consulted as well. Special/Geriatric Considerations A. Sarcomas are rare, but malignant tumors. Elderly patients are more often diagnosed with high stage sarcomas and have a higher mortality rate. Bibliography Lawrence, W., Jr., Donegan, W. L., Natarajan, N., Mettlin, C., Beart, R., & Winchester, D. (1987). Adult soft tissue sarcomas. A pattern of care survey of the American College of Surgeons. Annals of Surgery, 205 (4), 349-359. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Skin Cancer Sijimol Mathew Definition A. T wo main types. 1. Melanoma (most aggressive). 2. Nonmelanoma. a. Basal cell carcinoma (most common). b. Squamous cell carcinoma (second most common). B. Other types of less common nonmelanoma skin cancers include Merkel cell carcinoma or trabecular cancer, Kaposi sarcoma (associated with HIV), cutaneous lymphoma, and skin adnexal tumors. Incidence A. Skin cancer is the most common cancer in the United States. B. Each year there are more new cases of skin cancer than the combined incidence of cancers of the breast, prostate, lung, and colon. C. Melanoma is one of only three cancers with an increasing mortality rate for men, along with liver cancer and esophageal cancer. D. An estimated 76,380 new cases of melanoma were diag-nosed in 2016 with 10,130 deaths. E. Males are affected more than females, and non-Hispanic whites have higher incidence rates compared to other ethnic-ities. F. The incidence and mortality rates in the United States are 19. 9% and 2. 7%, respectively. G. The rates of new cases of melanoma have risen ∼1. 4% each year over the past 10 years. Pathogenesis A. Pathophysiology of skin cancer comes from damage to the DNA base. B. Ultraviolet (UV) radiation from sunlight is an important risk factor for skin cancer. C. UV sunlight appears to disable a tumor suppressor gene called p53. Skin Cancer299	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Predisposing Factors A. Male with age greater than 60 years. B. Excess sun exposure and ultraviolet-based artificial tanning. C. Family history of skin cancer. D. Personal history of skin cancer. E. History of sunburns, especially early in life. F. History of indoor tanning. G. Patients receiving immunosuppressive drugs. H. Individuals with dysplastic or atypical nevi, with several large nondysplastic nevi, with many small nevi, or with mod-erate freckles. I. Chemical exposure to arsenic, chromium, polycyclic aro-matic hydrocarbons, or benzene. J. Associated genetic syndromes; basal cell nevus syndrome, xeroderma pigmentosum, oculocutaneous albinism, epider-molysis bullosa, and Fanconi anemia are associated with an increased risk of skin cancer. Subjective Data A. Common complaints/symptoms. 1. There are some general physical characteristics of malignant skin lesions but the appearance may vary with each skin cancer. 2. The most common sign of skin cancer is a change in the skin including: a. A new growth. b. Nonhealing sore: Basal cell carcinomas often ulcerate and have an eczematous appearance. c. A change in appearance of a mole. d. Scar elevation (thickening or rising of a previously flat mole). e. Surface changes (scaling, erosion, oozing, bleed-ing, or crusting). f. Surrounding skin changes (redness, swelling, or small new patches of color around a larger lesion [satellite pigmentations]). g. Sensory changes (itching, tingling, or burning). h. Changes in consistency (friability). 3. Metastatic melanoma signs and symptoms include: a. Unexplained weight loss or fatigue. b. Swollen or painful lymph nodes: This may be the first presenting sign in metastatic melanoma of unknown primary. c. Shortness of breath or persistent cough. d. Bone pain. e. Headaches, numbness, weakness, or decreased sensation. f. Seizures. g. Anorexia, abdominal pain, dysphagia, small bowel obstruction, hematemesis, and melena. h. Intraocular melanoma may present with altered vision. Physical Examination A. Integumentary system. 1. Total body skin should be examined including scalp, dorsal feet, soles, toe webs, and nails. 2. Assess the total number of nevi present on patient's skin and differentiate between typical and atypical lesions using the ABCDE criteria. 3. Melanoma lesions are more likely to be asymmetrical, have irregular borders, appear very dark black or blue or have more variation in color than a benign mole and may be greater than 6 mm in diameter. B. Lymphatic system. 1. Melanoma may disseminate through the lymphatics. 2. Palpate for hard and swollen lymph nodes. C. Pulmonary system. 1. Observe for tachypnea, dyspnea, or labored breathing. 2. Auscultate all lung fields for lung sounds. 3. Melanoma metastasis to lungs may cause persistent cough, shortness of breath, pain in the chest, or pleural effusion. D. Cardiovascular system. 1. Auscultate heart sounds for abnormal findings to eval-uate the presence of a tumor that has direct cardiac involvement. 2. Assess for signs of hypotension, jugular venous disten-sion, or pericardial rub. 3. Cardiac symptoms, pericardial effusion, and cardiac tamponade are associated with cardiac metastasis of melanoma. E. Gastrointestinal tract. 1. Auscultate bowel sounds in four quadrants. 2. Palpate for hepatomegaly or tenderness to palpation. 3. Liver metastases also may cause ascites. F. Musculoskeletal system. 1. Bone metastasis of melanoma can cause bone pain and discomfort. 2. Examine for any tender area including spine. G. Central nervous system. 1. A neurological examination is essential to evaluate for any intracranial metastases. 2. Evaluate for decreased strength, altered sensation, and/or neuropathy. H. A complete eye examination is necessary to test the pres-ence of intraocular melanoma. 1. Uveal melanomas can arise in the iris or in the poste-rior uveal tract, and initially may be asymptomatic. 2. Iris melanoma may cause distortion of the pupil; ciliary body melanoma may cause blurred vision. 3. Choroidal melanoma may result in retinal detach-ment and decreased visual acuity. Diagnostic Tests A. Biopsy. B. Nodal basin ultrasound and/or lymphoscintigraphy. C. Imaging (if a sentinel lymph node is positive or symptoms warrant). 1. CT of the chest/abdomen/pelvis with intravenous contrast. 2. Consider whole body PET/CT. 3. Consider brain MRI with IV contrast. 4. If clinically indicated, perform a neck CT with IV contrast. D. Staging. 1. Staging for melanoma determines the degree of sever-ity, treatment options, and prognosis. 2. The American Joint Commission of Cancer staging system tumor, node, metastasis (TNM) classification of melanoma is similar to any other cancers. Differential Diagnosis A. Basal cell carcinoma. B. Squamous cell carcinoma. C. Malignant melanoma. D. Benign lesions. 13. Oncology Guidelines300	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Evaluation and Management Plan A. General plan. 1. Based on staging, the treatment options include surgery, immunotherapy, targeted therapy, and chemotherapy and/or radiation therapy (e. g., stereotactic radio surgery or whole brain radiation). 2. For metastatic and unresectable disease, systemic ther-apy is indicated. 3. Surgery. 4. Radiation therapy. 5. Immunotherapy and targeted therapy. B. Acute care issues in skin cancers. 1. Most of the surgical procedures are done on an outpa-tient basis; however, hospitalization is indicated for com-plex surgeries and depends on reconstructive techniques. 2. Wound care, JP drain management and pain manage-ment, and monitoring for infection are the main areas of focus during postoperative management. Follow-Up A. Perform physical and skin examinations every 3 to 6 months for the first 2 to 3 years, then once a year after that. B. Follow-up scans may be recommended. Consultation/Referral A. Patients with suspected skin cancer should be referred to dermatology, medical oncology, radiation oncology, and sur-gical oncology. Special/Geriatric Considerations A. The white skinned elderly population represents the largest patient group at risk for developing skin cancer. B. T reatment of skin cancer in the elderly population should be based on life expectancy, quality of life, and patient functional status, and not solely on chronological age. Bibliography Aerts, B., Kock, M., Kofflard, M., & Plaisier, P. (2014). Cardiac metastasis of malignant melanoma: A case report. Netherlands Heart Journal, 22 (1), 39-41. National Cancer Institute. (2016, September 12). Surveillance, epidemiol-ogy, and end results program. Retrieved from https://seer. cancer. gov/ faststats/selections. php?series=cancer Skin Cancer301	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
14Immune System, Connective Tissue, and Joints Guidelines Joanne Elaine Pechar Back Pain Joanne Elaine Pechar Definition A. Pain in the lower back region, which may, or may not, have a radicular component. B. Low back pain (LBP) is categorized into three groups, based on duration of symptoms. 1. Acute LBP: Pain that is 6 weeks or less in duration. 2. Sub-acute LBP: Pain that continues between 6 and 12 weeks. 3. Chronic LBP: Pain that is more than 3 months in duration. C. Types of LBP. 1. Benign back pain is a dull, aching pain that generally worsens with movement but improves with rest and lying. 2. T umor-or infection-related back pain typically presents with constant and dull pain. This pain is unre-lieved by rest and is worse at night, therefore often awak-ening the patient. 3. Disc herniation is worsened by coughing, valsalva maneuver, and sitting and is relieved by lying in the supine position. 4. Spinal stenosis is associated with bilateral (and occa-sionally unilateral) sciatic pain that is worsened by activ-ities such as walking, prolonged standing, and back extension. Pain is relieved by rest and forward flexion. Incidence A. The lifetime incidence of LBP is 70% and has an inci-dence of 5% per year. B. The peak incidence of LBP is in the age range of 40s to 50s. C. LBP is the second most common reason for physician visits in the United States. D. For approximately 90% of the patients, the most com-mon cause of LBP is related to disc degeneration. Pathogenesis A. LBP presents suddenly from an accident, fall, whiplash injury, or heavy lifting. B. LBP develops gradually as a result of age-related changes to the spine. C. Bony overgrowth (osteophytes) or disc herniation may directly impinge on spinal nerve roots or the spinal cord itself and can lead to instability and misalignment of the spine, which produces pain and neurological deficits. D. Radiculopathy is caused by compression, inflammation, or injury to a spinal nerve root. E. Sciatica is a form of radiculopathy caused by compression of the sciatic nerve, the large nerve that travels through the buttocks and extends down the back of the leg. F. Spondylolisthesis is a condition in which a vertebra of the lower spine slips out of place, pinching the nerves exiting the spinal column. G. Spinal stenosis is the narrowing of the spinal column, which then leads to pressure on the spinal cord and nerves. 1. The spinal cord pressure can cause pain or numbness with walking and may, over time, lead to leg weakness and sensory loss. 2. This is also known as neurogenic claudication. Predisposing Factors A. The first attack typically occurs between ages 30 and 40. B. African American female. C. Diet high in calories and fat. D. Inactive lifestyle. E. Obesity. F. Cigarette smoking. G. Occupation: Job that requires heavy lifting, pushing, pulling, or twisting. Subjective Data A. Common complaints/symptoms. 1. LBP with radiation to buttocks, legs, or feet. 2. Paraspinal muscle spasms. 3. Muscle stiffness. 4. Paresthesias. 5. Gait disturbances. 6. Numbness. B. Common/typical scenario. 1. Neurogenic claudication (low back, buttock, or leg pain, which may be relieved by sitting or with rest, induced by walking or standing). 2. Fecal or urinary incontinence. 3. Large post void residual greater than 100 m L and overflow incontinence. 4. Perianal or perineal sensory loss. 5. Dermatomal sensory loss. 6. Focal leg weakness, paralysis, and hyporeflexia in the legs. 7. Elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and human leukocyte anti-gen (HLA), if infection is present. 8. Fever. Back Pain303	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
C. Family and social history. 1. Family history is typically noncontributory. 2. Social history. a. Smoking, which is associated with LBP. b. Dietary and eating habits. c. Obesity is a major cause of LBP. d. Elicit drug use. D. Review of systems. 1. Elicit onset, frequency, duration, and location of symptoms. 2. Inquire if pain is worse during activity, at rest, or at night. 3. Inquire about exacerbating factors. 4. Inquire if pain radiates to lower extremities. 5. Inquire about associated symptoms, such as numb-ness, tingling, weakness, and sensory deficits. 6. Determine if there is any recent loss or change in bowel or bladder function. 7. Check if there is symptom improvement after taking pain medications. 8. Determine whether patient has a history of trauma and chronic infection. 9. Check for signs of systemic disease, which include his-tory of cancer, age greater than 50 years, unexplained weight loss, duration of pain greater than 1 month, night-time pain, and unresponsiveness to previous therapies. Physical Examination A. Check vital signs: Blood pressure, heart rate, respirations, and temperature. B. Inspect. 1. Examine the back for any warmth, erythema, swelling, purulent drainage, or abscess. 2. Inspect the curvature of the spine. 3. Observe for signs of previous surgery. C. Check for tenderness or pain using palpation along the spine. D. Check for radicular pain associated with straight-leg test. 1. Straight-leg raise test is positive if test causes radicular pain of the affected leg radiating below the knee. E. Complete neurological examination including : 1. Motor strength. 2. Sensation. 3. Deep tendon reflexes. F. Check back range of motion (ROM): Flexion, extension, side bending, and rotation. G. Check hip ROM: Possible referred pain from hip pathology. H. Assess gait. I. Perform digital rectal examination to assess rectal sphinc-ter tone or anal sphincter laxity. Diagnostic Tests A. Spine x-rays or films. 1. Anteroposterior and lateral views. 2. Demonstrates fractures, disc space narrowing, osteo-phyte formation, tumor, or instability. B. MRI scan. 1. Provides axial and sagittal views, which demonstrate normal and pathologic discs, ligaments, nerve roots, epidural fat, and shape and size of the spinal canal. 2. Gold standard study in cases of suspected spinal infec-tion, neoplasm, and epidural compression syndromes. C. CT scan. 1. Useful in evaluating vertebral fractures, facet joints, and posterior elements of the spine. 2. When MRI scan is unavailable, CT myelography is the best substitute for conditions, such as epidural abscess or cord compression. D. Nuclear medicine bone scan. 1. Can also be used if infection and tumor are suspected. E. Laboratory tests: ESR, CRP, c omplete b lood count (CBC), blood cultures, and urinalysis. Differential Diagnosis A. Degenerative disc disease. B. Spinal stenosis. C. Spondylosis and spondylolisthesis. D. Discitis. E. Vertebral osteomyelitis. F. Spinal cord or cauda equina compression. G. Herniated intervertebral disc. H. Spinal epidural abscess. I. Ankylosing spondylitis. J. Spine-related bone tumors. K. Metastatic cancer. L. Scoliosis and hyperkyphosis. M. Vertebral compression fracture. N. Myofascial pain syndrome. O. Fibromyalgia pain syndrome. Evaluation and Management Plan A. General plan. 1. General intervention. a. Bed rest for a few days. Limit bending, lifting, and twisting. b. Physical therapy and aerobic exercise. c. Local application of heat and ice. d. Brace is indicated for adolescents with spine cur-vature between 20∘C and 40∘C. 2. Adjunct therapy. a. T ranscutaneous electrical nerve stimulation (TENS). b. Biofeedback. c. Acupuncture. 3. Red flags: Indications for imaging. a. Concern for malignancy: Age 50 or older, previous history of cancer, unexplained weight loss, pain unre-lieved by bed rest, pain lasting more than a month, or LBP failure to improve in 1 month. b. Concern for infection: Elevated ESR greater than 20, intravenous drug abuse, urinary tract infection, skin infection, or fever. c. Concern for compression fracture: Corticosteroid use and/or age 50 or older. d. Concern for neurological problem: Sciatica. e. New fecal or urinary incontinence. 4. Surgical intervention. a. Indications for surgery when allthree criteria are met. i. Evidence of disc herniation as demonstrated by an imaging study. ii. Worsening clinical picture with neurological deficit. iii. Failed improvement after 4 to 6 weeks of con-servative treatment. iv. NOTE: Cauda equina and spinal cord com-pression syndromes need urgent surgical decom-pression in 24 to 48 hours of symptom onset. v. Imaging demonstrates compressive abscess or epidural collection. 14. Immune System, Connective Tissue, and Joints Guidelines304	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
b. Types of spine surgery. i. Vertebroplasty and kyphoplasty are minimally invasive treatments to repair compression frac-tures of the vertebrae. ii. Spinal laminectomy or spinal decompression is used to treat spinal stenosis. 1)Lamina or bony walls of the vertebrae and bone spurs are removed. The goal of the pro-cedure is to open up the spinal column to remove pressure on the nerves. iii. Discectomy or microdiscectomy is recom-mended to remove herniated discs from pressing on nerve roots or the spinal cord. iv. Foraminotomy is an operation that enlarges the foramen, which is where a nerve root exits the spinal canal. The enlargement removes the block-age and relieves pressure, caused by bulging discs, on the nerve. v. Spinal fusion is used to treat degenerative disc disease and spondylolisthesis. 1)The disc between two or more vertebrae is removed and the adjacent vertebrae are fused together by bone grafts or metal devices secured by screws. 2)Spinal fusion can be performed through the abdomen with a procedure known as an anterior lumbar interbody fusion or it may be performed through the back in a procedure called posterior lumbar fusion. B. Patient/family teaching points. 1. Counsel in regards to exercise therapy. 2. Counsel about smoking cessation and weight loss. 3. Counsel about ergonomic interventions for preven-tion of occupational LBP. C. Pharmacotherapy. 1. First-line agents: N onsteroidal anti-inflammatory drugs (NSAIDs) and Tylenol. Avoid NSAIDs after fusion. 2. Muscle relaxants: Cyclobenzaprine, diazepam, or tizanidine. 3. Opioids or narcotics. 4. Antidepressants and anticonvulsants. 5. T ransforaminal or epidural steroid injections. D. Discharge instructions. 1. Patients should participate in physical therapy and start with first-line pharmacological agents for pain man-agement. 2. If the pain does not get better with treatment or it worsens, the patient should call the healthcare provider. 3. Patients should also call if they suddenly feel some-thing pop or snap in the back or if they have questions or concerns about their condition or care. 4. Patients should seek urgent attention if change in bowel or bladder habits are observed. Follow-Up A. Patients who have not improved after 4 to 6 weeks of con-servative therapy and who did not receive imaging during ini-tial evaluations require follow-up. B. Patients presenting with persistent and worsening symp-toms should have an MRI for further evaluation. Consultation/Referral A. Patients without concerns for a particular etiology who have not improved after 12 weeks need imaging andreferral to orthopedic spine surgery or neurosurgery special-ists for further evaluation and treatment. B. Patients with symptoms of spinal cord compression or severe neurological deficits should have immediate MRIs for further evaluation and also receive urgent specialist referrals. Special/Geriatric Considerations A. When performing a pain assessment in a cognitively impaired older adult, the American Geriatrics Society encourages the integration of the following six behavioral domains: 1. Facial expressions. 2. Verbalizations or vocalizations. 3. Body movements. 4. Changes in interpersonal interactions. 5. Changes in activity patterns or routines. 6. Mental status changes. B. Clinicians should be mindful of older patients with dementia and chronic LBP and should accordingly adjust pain management. 1. Dementia can alter pain reporting, pain behaviors, and pain coping. 2. Older patients may not reliably communicate the need for analgesic medications. C. Due to harmful side effects in older patients with non cancer pain, nonopioid medications are preferred to opioids. D. Doses of opioid medications should be reduced in older adults and also titrated slowly. 1. Decrease initial dose by 25% for a 60-year-old patient and by 50% for an 80-year-old patient. Bibliography Deyo, R. A., & Tsui-Wu, Y. (1987). Descriptive epidemiology of low-back pain and its related medical care in the United States. Spine, 12 (3), 264-268. doi:10. 1097/00007632-198704000-00013 Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine (19th ed. ). New York, NY: Mc Graw-Hill. Knight, C. Deyo, R., Staiger, T., & Wipf, J. (2017, December 6). T reatment of acute low back pain. In L. Kunins (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/?source=search_ result&search=acute%20low%20back%20pain&selected Title=1 Parvizi, J. (2010). High yield orthopaedics. Philadelphia, PA: Saunders/Else-vier. Swiontkowski, M. F., & Stovitz, S. D. (2006). Manual of orthopaedics (6th ed. ). Philadelphia, PA: Lippincott Williams & Wilkins. Wheeler, S. G., Wipf, J. E., Staiger, T. O., Deyo, R. A., & Jarvik, J. G. (2018, July 12). Evaluation of low back pain in adults. In L. Kunins & S. I. Lee (Eds. ), Up To Date. Retrieved from https://www. uptodate. com/contents/evaluation-of-low-back-pain-in-?source=search_result &search =acute%20low%20back%20pain&selected Title =2 26 Wright, R., Malec, M., Shega, J. W., Rodriguez, E., Kulas, J., Morrow, L.,... Weiner, D. K. (2016). Deconstructing chronic low back pain in the older adult—Step by step evidence and expert-based recommendations for evaluation and treatment: Part XI: Dementia. Pain Medicine, 17 (11), 1993-2002. doi:10. 1093/pm/pnw247 Compartment Syndrome of the Lower Leg Joanne Elaine Pechar Definition A. A surgical emergency, which refers to a build-up of pres-sure within a muscle compartment (surrounded by a closed fascia) leading to a decline in tissue perfusion in the injured extremity; causes permanent damage to muscle and nerves. B. A serious complication typically resulting from a crush injury to a large bone. There is an increase in closed Compartment Syndrome of the Lower Leg305	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
compartmental pressure causing ischemic changes and diminished microcirculation within the soft tissues. Incidence A. The average annual overall incidence of acute compart-ment syndrome (ACS) is 3. 1 cases per 100,000 people. B. Due to relatively larger muscle mass in men, ACS is more prevalent in men compared to women. C. Tibial fractures caused by trauma account for approx-imately 75% of ACS cases; blunt soft tissue injury is the second-leading cause. D. The most common sites of ACS are (in descending order of prevalence): Calf, forearm, thigh, upper arm, hand, and foot. Pathogenesis A. ACS develops when the intracompartmental pressure (ICP) exceeds venous capillary pressure. B. Arteriovenous pressure gradient theory. 1. Ischemia begins when local blood flow cannot meet the metabolic demands of surrounding affected tissue. 2. As compartment pressure rises, venous outflow is reduced and venous pressure rises, leading to a decrease in the arteriovenous pressure gradient. 3. Without intervention, due to arteriolar compression, microcirculation is compromised, and blood is shunted away from intracompartmental tissues, which ultimately reduces tissue perfusion. 4. Inadequate tissue perfusion and oxygenation results in soft tissue ischemia, cellular necrosis, anoxia, and irre-versible death of the cells. C. Anatomy of the lower leg. 1. There are four compartments in the lower leg: Ante-rior, lateral, superficial posterior, and deep posterior. 2. Each individual compartment encloses specific mus-cles, nerves, arteries, veins, and bones. Predisposing Factors A. T rauma-related closed tibial shaft fracture is the major contributing factor to ACS and accounts for one-third of all ACS cases. B. List of traumatic and nontraumatic ACS etiologies. 1. Vascular: Reperfusion therapy, arterial puncture or injury, hemorrhage, and deep vein thrombosis. 2. Soft tissue: Crush injury, contusion, fall, direct blow, burn, and snake bite. 3. Latrogenic: Drugs such as anticoagulants, bleeding disorders, circumferential wraps, casts or splints, constric-tive dressings, tourniquets, long leg brace, extravasations of drugs and fluids, prolonged lithotomy positioning, viral myositis, and diabetic muscle infarction. Subjective Data A. Common complaints/symptoms. 1. The cardinal symptom of ACS is pain out-of-proportion. 2. Persistent burning pain at rest. 3. Pain reproduced with passive stretch of the affected muscle compartment. B. Common/typical scenario. 1. Massive swelling of the limb with firm and tense feel-ing on deep palpation. 2. Reduced two-point discrimination or vibration sense. 3. Loss of light touch sensation. C. Family and social history. 1. Family and social history are noncontributory, as the cause of ACS is typically related to injury or surgery. D. Review of systems. 1. Pain out of proportion to injury is often an early and sensitive sign of ACS. a. Most patients at risk for ACS have sustained trauma, fracture, or injury to the nerve or soft tissue, which may be the source of pain. b. The injured extremity becomes swollen and tense as ACS develops. Increasing ICP builds up on nerve fibers and injured components within the compart-ment. c. Obtunded patients, patients emerging from anes-thesia, or patients receiving nerve blocks may not accurately report pain. d. In the late stages of ACS, pain may not be a subjec-tive clinical finding, as pain receptors and nerve fibers are at high risk of ischemic necrosis and death. 2. Paresthesia. a. Onset, which suggests the first signs of ischemic nerve dysfunction, is within approximately 30 min-utes to 2 hours following injury. Physical Examination A. Paralysis is found in the late stages of ACS. 1. A higher ICP leads to ischemic neuronal tissues and nerve dysfunction and subsequent paresthesia, paresis, and, ultimately, complete paralysis. 2. Motor function may deteriorate within 4 hours of muscle tissue ischemia. 3. At 8 to 24 hours of ischemia, motor and sensory loss is irreversible. B. Pulselessness is a late finding, which is a poor indicator of ACS. 1. As ICP rises, a loss of limb pulses indicates a decline in arterial perfusion. C. Pallor. 1. Presence of pallor and longer capillary time in the injured limb indicates direct arterial injury. D. Poikilothermia. 1. Presence of coolness or a change in the temperature in the affected extremity. Diagnostic Tests A. High index of clinical suspicion and the “6 Ps” cardinal symptoms: Pain, pallor, poikilothermia, paresthesia, paraly-sis, and pulselessness. B. Measuring limb ICP. 1. Stryker pressure monitoring device: A hand-held dig-ital monitor for single tissue fluid pressure readings. To measure, the clinician injects 0. 3 m L of saline solution into each of the four leg compartments (see Figure 14. 1). 2. An ICP of 30 mm Hg or above is considered a critical threshold for diagnosis of ACS, and, if ICP is elevated, emergent decompression should be considered. 3. Normal pressure of a tissue compartment falls between 0 and 8 mm Hg in resting stage. 4. ICP should be measured in each compartment of interest but within 5 cm from the injured or fractured site. C. Delta pressure. 1. Delta pressure is the difference between the diastolic pressure and the measured ICP. 2. Delta pressure of less than, or equal to, 30 mm Hg is diagnostic of ACS. 14. Immune System, Connective Tissue, and Joints Guidelines306	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
FIGURE 14. 1 Advancedpractice provider(APP) monitoring for compartment syndrome. Differential Diagnosis A. Deep vein thrombosis. B. Thrombophlebitis. C. Cellulitis. D. Necrotizing fasciitis. E. Peripheral vascular injury. F. Rhabdomyolysis. G. Shin splints. H. Stress fractures. Evaluation and Management Plan A. General plan. 1. Standard treatment: Emergent fasciotomy is a surgical limb-saving procedure to decompress the affected com-partments and prevent critical limb ischemia. a. T wo types of surgical technique: Single or double incision. i. Single-incision technique involves a single long incision made from the head of the fibula to the lateral malleolus. ii. Double-incision technique is the most com-mon fasciotomy method: Four-compartment technique incorporating two longitudinal antero-lateral and posteromedial incisions. 2. In 48 to 72 hours, return to surgery is needed for reevaluation of muscle viability and wound debridement of nonviable tissues. 3. Once ACS is completely resolved within 7 to 10 days, the fasciotomy wound is left open for delayed primary closure or skin grafting. 4. To prevent bacterial colonization, improve circu-lation, and approximate wound edges, a negative pressure wound therapy is used for assisted closure of fasciotomy wounds. 5. Nonoperative treatment measures. a. Loosening compression dressings, “bi-valving” casts, and complete removal of splints and casts. b. Elevation of the affected extremity to facilitate venous drainage, reduce edema, and maximize tissue perfusion. B. Patient/family teaching points. 1. ACS is a surgical emergency that can develop quickly. 2. Permanent damage to muscles and nerves can occur within hours, which can necessitate amputation if not addressed immediately. 3. Keep the affected limb propped up on pillows so the limb is level with the heart. 4. Do not put any compressive bandages over the site. C. Pharmacotherapy. 1. There is no pharmacological treatment for ACS, only surgery will reduce the pressure in the compartment. D. Discharge instructions. 1. Seek care immediately if the pain or swelling does not improve, fever or rash develops, or the injured limb becomes cold or numb. 2. Contact the provider with questions or concerns. Follow-Up A. Follow-up is needed in 1 to 2 weeks for neurovascular examination, control of swelling, and wound check to ensure complete wound healing. Consultation/Referral A. Early consultation and collaboration with orthopedic or vascular surgery is critical for limb salvage and to prevent pos-sible devastating complications, such as the following. 1. Wound infection. 2. Paralysis. 3. Permanent nerve damage. 4. Contractures. 5. Amputation. 6. Rhabdomyolysis. 7. Multiorgan failure. 8. Sepsis. 9. Death. Special/Geriatric Considerations A. Diagnosis of ACS may be delayed with older patients who received epidural anesthesia and who sustained neurovascular injuries following total knee arthroplasty (TKA). 1. Continuous epidural analgesia can mask pain associ-ated with passive stretching, therefore delaying diagnosis. 2. Older patients may develop foot drop or peroneal nerve injury following TKA. Bibliography Asprey, D. P., & Dehn, R. W. (2013). Essential clinical procedures. Philadel-phia, PA: Elsevier Health Sciences. Azar, F. M., Canale, S. T., & Beaty, J. H. (2017). Campbell's operative orthopaedics. Philadelphia, PA: Elsevier. Donaldson, J., Haddad, B., & Khan, W. S. (2014). The patho-physiology, diagnosis and current management of acute compart-ment syndrome. The Open Orthopaedics Journal, 8 (1), 185-193. doi:10. 2174/1874325001408010185 Gahtan, V., & Costanza, M. J. (Eds. ). (2015). Essentials of vascular surgery for the general surgeon. New York, NY: Springer. Murdock, M., & Murdoch, M. M. (2012). Compartment syndrome: A review of the literature. Clinics in Podiatric Medicine and Surgery, 29 (2), 301-310. doi:10. 1016/j. cpm. 2012. 02. 001 Pechar, J., & Lyons, M. M. (2016). Acute compartment syndrome of the lower leg: A review. The Journal for Nurse Practitioners, 12 (4), 265-270. doi:10. 1016/j. nurpra. 2015. 10. 013 Raza, H., & Mahapatra, A. (2015). Acute compartment syndrome in ortho-pedics: Causes, diagnosis, and management. Advances in Orthopedics, 2005, 1-8. doi:10. 1155/2015/543412 Stahel, P. F., Mauser, N., Gissel, H., Henderson, C., Hao, J., & Mauffrey, C. (2013). Acute lower-leg compartment syndrome. Orthopedics, 36 (8), 619-624. doi:10. 3928/01477447-20130724-07 Vegari, D. N., Rangavajjula, A. V., Dilorio, T. M., & Parvizi, J. (2014). Fasciotomy following total knee arthroplasty: Beware of terrible outcome. The Journal of Arthroplasty, 29 (2), 355-359. doi:10. 1016/j. arth. 2013. 05. 013 Compartment Syndrome of the Lower Leg307	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Joint Pain Laura A. Santanna Lonergan Definition A. Joint pain can be discomfort, pain, or inflammation aris-ing from any part of a joint including cartilage, bone, liga-ments, tendons, or muscles. B. Acute joint pain is defined as pain resolving within 6 weeks of onset. C. Chronic joint pain extends past 6 weeks from onset of symptoms. D. Many joint pain complaints stem from self-limiting con-ditions, but there are many causes that require immediate and ongoing care. E. Osteoarthritis (OA) or degenerative joint disease (DJD), which presents with pain and swelling resulting in decreased joint mobility, is the most common form of joint disease. It may affect any joint in the body, notably the hips and knees. F. OA can affect the cartilage that cushions the ends of bones and allows for easy movement of joints. Incidence A. It is estimated that approximately 5% of primary care office visits are for joint pain with OA being the most com-mon diagnosis. Pathogenesis A. Sources of pain within the joint include the joint capsule, periosteum, ligaments, subchondral bone, and synovium, but not the articular cartilage, which lacks nerve endings. B. The basic pathophysiologic types of joint disease and pain stem from synovitis, enthesopathy, crystal deposition, infec-tion, and structural or mechanical derangements. Predisposing Factors A. A combination of clinical, laboratory, and imaging data can help to differentiate patients likely to have self-limited disease from those likely to have persistent arthritis. B. Prediction models based upon patients with early arthritis have identified a number of features associated with persistent and/or erosive disease, including: 1. Duration of symptoms prior to presentation. 2. Older age. 3. Male gender. 4. High body mass index (BMI). 5. Duration of morning stiffness. 6. Number of tender or swollen joints. 7. Involvement of lower extremities. 8. Elevated acute phase reactants. 9. Rheumatoid factor. 10. Anti-cyclic citrullinated peptide (anti-CCP) anti-body. 11. Erosive change on baseline radiograph. 12. Human leukocyte antigen (HLA)-DRB1 shared epi-tope alleles. Subjective Data A. Common complaints/symptoms. 1. Knee pain. 2. Shoulder pain. 3. Hip pain. 4. Hand pain. 5. Ankle and foot pain. 6. Soft tissue swelling or effusion. 7. Joint erythema and warmth. 8. Joint tenderness. 9. Joint contractures or deformity. 10. Joint stiffness. 11. Myalgias and muscle spasms. 12. Muscle weakness. B. Common/typical scenario. 1. Rash. 2. Fever. 3. Crepitus. C. Family and social history. 1. Family history may have a role in joint pain. Specific questions inquiring about autoimmune diseases in the family should be addressed. 2. Patient's daily routine may provide insight into causes of repetitive injuries. 3. Smoking can also contribute to joint pain. D. Review of systems. 1. Specific symptoms to ask patients with joint pain. 2. Joint pain may represent a vast number of problems. The following questions can help direct clinical decision making and narrow down differential diagnosis. a. Is one joint affected or many joints affected? E. Is inflammation present or absent? F. What joints are involved? G. Are there systemic symptoms? Physical Examination A. A complete history and physical examination is appro-priate for all patients presenting with joint pain, since this symptom may be the initial manifestation of a systemic illness. B. The following findings on physical examination could indicate a more serious pathogenesis of joint pain. 1. General survey: Level of patient's pain, ability to carry out activities of daily living (ADL). 2. Vital signs: Fever. 3. Eye: Keratoconjunctivitis sicca, uveitis, conjunctivi-tis, episcleritis. 4. Neck: Lymphadenopathy. 5. Mouth: Parotid enlargement, oral ulcerations. 14. Immune System, Connective Tissue, and Joints Guidelinesa. Fever. b. Weight loss. c. Night sweats. d. Rash. e. Nodules. f. Neuropathy. g. Joint swelling. h. Joint erythema. i. Tenderness. j. Warmth around joint. k. Inability to use joint. l. Eye pain. m. Eye dryness. n. Recent infection. o. Recent tick bite. p. Recent exposure to sexually transmitted infection (STI). q. Recent joint injection or surgery. r. History of immunosuppression. i. One joint =monoarticular. ii. T wo to four joints =oligoarticular. iii. Greater than five joints =polyarticular. 308	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
6. Cardiovascular (CV): Murmur, pericardial, or pleu-ral friction rubs. 7. Lungs: Fine inspiratory rales (secondary to intersti-tial lung disease). 8. Skin: Skin lesions may suggest that the joint symp-toms are due to psoriatic arthritis, systemic lupus erythe-matosus (SLE), viral infection, or Still's disease. 9. Musculoskeletal: Swollen, erythematous, warm joints, joint deformities, range of motion of joints. 10. Neurovascular: Muscle tone, muscle strength, sen-sory perceptions, gait. Diagnostic Tests A. Arthrocentesis and examination of synovial fluid to include a cell count, gram stain, crystal analysis, and culture. B. Laboratory tests. a. Complete blood count (CBC). b. Basic metabolic panel (BMP). c. Liver function test (LFTs). d. Erythrocyte sedimentation rate (ESR). e. C-reactive protein (CRP). f. Uric acid. g. Antinuclear antibody (ANA). h. Rheumatoid factor. i. Anti-CCP antibody. C. Radiologic imaging of affected joint(s). a. X-rays. b. CT scan. c. MRI. D. Tissue biopsy. Differential Diagnosis A. Adult Still's disease. B. Ankylosing spondylitis. C. Avascular necrosis. D. Bone cancer. E. Certain types of arthritis. 1. OA. 2. Juvenile rheumatoid arthritis. 3. Psoriatic arthritis. 4. Reactive arthritis. 5. Rheumatoid arthritis. 6. Septic arthritis. F. Fractured bone. G. Bursitis. H. Complex regional pain syndrome. I. Dislocation. J. Gonococcal arthritis. K. Gout. L. Hypothyroidism. M. Leukemia. N. Lupus. O. Lyme disease. P. Osteomyelitis. Q. Paget's disease of bone. R. Polymyalgia rheumatica. S. Pseudogout. T. Rickets. U. Sarcoidosis. V. Sprains and strains. W. Tendinitis. Evaluation and Management Plan A. General plan. 1. Avoid using affected joint if doing so causes pain. 2. Use ice to area 15 to 20 minutes of each hour. 3. Specific treatment targeted to each individual diagno-sis that may include but not be limited to: a. Physical therapy. b. Surgical management. c. Pharmacologic intervention (noted in the follow-ing section). B. Patient/family teaching points. 1. Exercise and weight loss are highly effective in reliev-ing joint pain. 2. Start with low-impact exercises that don't irritate the joint such as swimming or cycling. 3. Short-term joint pain can be relieved with rest, ice, compressing with a wrap, and elevating the joint above the level of the heart. C. Pharmacotherapy. 1. Analgesic medications: N onsteroidal anti-inflammatory drugs (NSAIDs), Tylenol. 2. Steroids. 3. COX-2 inhibitors. 4. Disease-modifying antirheumatic drugs (DMARDs). 5. Intra-articular injections. D. Discharge instructions. 1. Total hip arthroplasty (THA) and total knee arthro-plasty (TKA) are highly effective elective procedures for patients who suffer from hip and knee pain, which is mainly due to joint deterioration from OA. a. THA and TKA can relieve pain, restore function, and improve quality of life by replacing the diseased articular surfaces with synthetic material. b. Discharge criteria. i. Stable vital signs and afebrile for more than 24 hours postoperatively. ii. Wound incision clean, dry, and intact. iii. Hip and knee pain well managed and con-trolled. iv. No signs and symptoms of infection, such as fever, hip erythema, and warmth. v. No signs and symptoms of blood clot, such as hip or leg swelling, and calf tenderness. c. Activity. i. Full weight-bearing status with physical ther-apy. ii. Walker and crutch training will be provided prior to hospital discharge. iii. Patient can resume most daily activities within a few weeks after surgery. iv. After a THA, patients may need to adhere to hip precautions for 6 weeks. v. Avoid bending and flexing hips greater than 90∘C. vi. Avoid twisting leg in or out. vii. Avoid crossing legs at the knee or ankle. viii. Avoid allowing legs to cross midline. ix. Avoid raising knee higher than the hip. x. Avoid allowing toes to point inward (pigeon-toe) or to rotate outward (duck-walking). xi. Always lie on the back while resting in bed, and place a pillow between the thighs if laying on one's side. xii. Sit in chairs higher than knee height. xiii. Avoid low beds. xiv. Avoid pivoting on the operated leg, and take small steps when turning. xv. Before standing, scoot to the edges of beds and chairs. Joint Pain309	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
xvi. After a TKA, the following measures are needed to protect a new knee joint. 1)Place pillow between the thighs if laying on one's side. 2)Avoid kneeling or squatting. 3)Avoid twisting the new knee. d. Diet. i. Patients are not able to eat or drink until fully recovered from anesthesia. ii. To avoid nausea after surgery, start patients slowly on a clear liquid diet. iii. Once clear liquid diets are tolerated, patients may be offered solid foods. iv. Since narcotics should not be mixed with alco-hol, limit alcohol consumption. v. Eat healthy foods and watch weight. vi. Obesity can add more stress to the new joint. e. Medications. i. Used for postoperative pain management, the multimodal perioperative pain protocol (MP3) consists of short-and long-acting opioids, oral nonsteroidal anti-inflammatory cyclooxygenase-2 inhibitor NSAIDs, intravenous NSAIDs, and anticonvulsants. ii. Percocet 5/325 mg 1 to 2 tablets every 4 to 6 hours as needed. iii. Gabapentin 100 mg twice a day for 2 weeks. iv. Celebrex 200 mg twice a day for 6 weeks. v. Toradol 7. 5 mg intravenous every 6 hours as needed (do not exceed 5 days). vi. Morphine 2 mg intravenous every 2 hours as needed. f. Wound care. i. Always keep the surgical wound clean and dry. ii. Unless instructed to do otherwise, do not apply any lotions, creams, oils, ointments, or powders to the surgical wound area. iii. Leave the dressing in place for 7 days postop-eratively. iv. Dressing will be removed by a provider at rehab or by a home health nurse. v. T wo weeks from the day of surgery, at the first orthopedic follow-up appointment, staples or sutures will be removed. vi. Patient may shower but the incision must be well covered. Do not scrub the incision. g. Follow-up. i. Patients are instructed to follow-up with the surgeon in 6 weeks or immediately for any con-cerning signs or symptoms. ii. Discuss with patient. 1)Concerning signs or symptoms to moni-tor. 2)Difficulty breathing, shortness of breath, dyspnea, or pleuritic chest pain. 3)Persistent nausea or vomiting. 4)Persistent fever over 101∘F, chills, and sweating. 5)Signs of a blood clot. iii. Pain in the operative leg and calf tenderness. iv. Tenderness and erythema of the operative leg. v. Unexplained swelling, which does not dissi-pate with elevation, of the operative limb. 1)Pain with rotation of the limb and wors-ening pain even after taking pain medicine. 2)Unexplained limb shortening or extreme rotation. 3)Wound drainage soaking through the ban-dage over the incision. 4)Intermittent claudication, which is walking-based thigh pain that clears quickly with sitting. 5)Signs of wound infection. a)Increased pain, swelling, warmth, or erythema around the incision. b)Pus fluid draining from the incision. h. Intraoperative complications. i. Fracture. ii. Nerve injury. iii. Vascular injury. i. Postoperative complications and readmission con-cerns. i. Deep vein thrombosis. ii. Pulmonary embolism. iii. Septic hip. iv. Cellulitis. v. Hematoma. vi. Hip dislocation. vii. Periprosthetic fracture. viii. Hip fractures. 1)Femoral head fracture. 2)Femoral neck fracture. 3)Intertrochanteric fracture. 4)Subtrochanteric fracture. 5)Femoral shaft fracture. 6)Distal femur fracture. ix. Knee fractures and tendon ruptures. 1)Patella fracture. 2)Quadriceps tendon rupture. 3)Patella tendon rupture. 4)Tibial plateau fracture. 5)Tibia and fibula shaft fracture. a)Septic knee. b)Knee dislocation. c)Aseptic loosening. d)Heterotrophic ossification. e)Leg length discrepancy. f)Foot drop and peroneal nerve palsy. Follow-Up A. Follow-up with provider when joint pain begins. Do not wait until the pain is intense and the joint becomes stiff. B. Physical therapy can assist patients in relieving joint pain with exercises. Consultation/Referral A. Based off of patient diagnosis, but may include: 1. Primary care. 2. Orthopedist. 3. Rheumatologist. 4. Infectious disease. Special/Geriatric Considerations A. Certain joint pain diagnoses are more frequent in older adults over age 60. B. OA. C. Gout and pseudogout. D. Polymyalgia rheumatica. E. Osteoporotic fracture. F. Septic arthritis. 14. Immune System, Connective Tissue, and Joints Guidelines310	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Bibliography Baer, A. N. (2016, December 26). The approach to the painful joint. In H. S. Diamond (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/336054-overview Harrison, T. R., Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (2015). Harrison's principles of internal medicine. New York, NY: Mc Graw Hill Education. Joint Pain. (2016, February 26). Mayo clinic. Retrieved from http://www. mayoclinic. org/symptoms/joint-pain/basics/definition/sym-20050668 Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (Eds. ). (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw-Hill. Plamer, T., & Toombs, J. D. (2004). Managing joint pain in primary care. Journal of the American Board of Family Medicine, 17 (Suppl. 1), 32-42. doi:10. 3122/jabfm. 17. suppl_1. S32 Shmerling, R. H. (2019, March 7). Evaluation of the adult with polyartic-ular pain. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/evaluation-of-the-adult-with-polyarticular-pain Osteoarthritis Joanne Elaine Pechar Definition A. Osteoarthritis (OA) is defined as evident cartilage loss without inflammatory or crystal arthropathy, irrespective of whether the patient has symptoms. Incidence A. OA is the most common type of joint disease, affecting more than 20 million individuals in the United States alone. B. Ninety percent of all people have radiographic evidence of OA in weight-bearing joints by age 40. C. Symptomatic disease increases with age. D. Develops in women more frequently than in men. Pathogenesis A. OA is characterized by degeneration of cartilage and by hypertrophy of bone at the articular margins. B. Cartilage, subchondral bone, and synovium have been found to all have key roles in disease pathogenesis. Predisposing Factors A. Hereditary and mechanical factors may be involved. 1. Mechanical factors. a. Excessive weight, causing additional pressure. b. Repetitive movements or overuse, which causes damage to joints, tendons, and ligaments. i. Can break down cartilage over time. B. Obesity is a risk factor for OA of the knee, hand, and hip. C. Playing competitive contact sports increases the risk for developing OA. D. Jobs requiring frequent bending and carrying increase the risk of knee OA. Subjective Data A. Common complaints/symptoms. 1. The onset is insidious. 2. The disease process may start with articular stiffness or deep aching joint pain lasting less than 30 minutes; may be most prominent upon awakening. B. Common/typical scenario. 1. Reduced range of motion and crepitus of affected joint is frequently present. 2. There are no systemic manifestations. C. Family and social history. 1. May have genetic component. 2. Repetitive use and jobs requiring heavy lifting and bending may contribute. 3. Obesity. D. Review of systems. 1. Elicit onset, frequency, duration, and location of symptoms. 2. Inquire if pain is worse during activity or at rest. 3. Inquire about exacerbating factors. 4. Inquire about presence and duration of morning stiff-ness. 5. Determine if there are any systemic signs such as fever. Physical Examination A. Comprehensive musculoskeletal examination may reveal: 1. Flexion contracture or varus deformity of the knee. 2. Palpable osteophytes of the distal interphalangeal (DIP; Heberden nodes) and proximal interphalangeal (PIP; Bouchard) nodes. 3. Limited range of motion of the affected joint or joints. 4. Crepitus felt over the knee joint. 5. Joint effusion and other articular signs of inflamma-tion. Diagnostic Tests A. Laboratory test. 1. E rythrocyte sedimentation rate (ESR)—OA does not cause elevation of the ESR or other laboratory signs of inflammation. 2. Synovial fluid—tends to be noninflammatory. B. Imaging. 1. Plain film radiographs of the affected joint may reveal. a. Narrowing of the joint space. b. Osteophyte formation. c. Lipping of marginal bone. d. Thickened, dense subchondral bone. e. Bone cysts. Differential Diagnosis A. Gout. B. Pseudogout. C. Rheumatoid arthritis. D. Psoriatic arthritis. E. Reactive arthritis. F. Septic arthritis. G. Fibromyalgia. H. Tendonitis. I. Avascular necrosis. J. Charcot joint. K. Lyme disease. L. Patellofemoral syndrome. M. Prepatellar bursitis. Evaluation and Management Plan A. General plan. 1. Nonpharmacologic. a. OA of the hand may benefit from assistive devices and instruction on techniques for joint protection. 2. OA of the first carpometacarpal joint may benefit from splinting. 3. OA of the knee or hip may benefit from a regular exer-cise program. 4. If patient is overweight, he or she should be instructed to lose weight. Osteoarthritis311	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
5. The use of assistive devices (e. g., a cane on the con-tralateral side) can improve functional status. 6. Surgical intervention. a. Total hip and knee replacements provide excel-lent symptomatic and functional improvement when involvement of that joint severely restricts walking or causes pain at rest. b. Arthroscopic surgery for knee OA is ineffective. B. Patient/family teaching points. 1. General education of patients regarding benefits of exercise and weight loss. 2. Exercise can strengthen muscles and reduce pain and potentially help patients to avoid surgery. 3. Weight loss will reduce pressure on joints and slow down destruction of cartilage. 4. Avoid repetitive movements of an affected joint. 5. Use protective gear such as joint padding when play-ing sports to avoid injury. C. Pharmacotherapy. 1. Acetaminophen is first-line analgesic therapy (2. 6-4 g/day orally). 2. N onsteroidal anti-inflammatory drugs (NSAIDs) provide more pain relief but have greater side effects of toxicity. 3. Chondroitin sulfate and glucosamine, alone or in combination, are no better than placebo in reducing pain in patients with knee or hip OA. 4. Intra-articular injections. a. T riamcinolone (20-40 mg) for patients with OA of the knee or hip may reduce the need for oral anal-gesics and can be repeated up to four times a year. The American College of Rheumatology does not recommend corticosteroid injections for OA of the hand. b. Sodium hyaluronate produces moderate reduc-tion in symptoms in some patients with OA of the knee. Follow-Up A. Follow-up with your provider on a regular basis until your pain and mobility level are optimized. B. The patient should call once joint pain starts for better management. C. Follow-up at least once a year with your provider once your symptoms are controlled. Consultation/Referral A. Refer to an orthopedic surgeon when pain, loss of func-tion, or both warrant consideration of hip or knee joint replacement surgery. Special/Geriatric Considerations A. OA may account for up to 70% of the geriatric popula-tion's joint pain. B. This places geriatric patients at a higher risk for falls. C. Nonsurgical candidates may be considered for physical reconditioning and pharmacologic pain control. Bibliography Egol, K. A., Koval, K. J., & Zuckerman, J. D. (2015). Handbook of frac-tures. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins Health. Glyn-Jones, S., Palmer, A. J. R., Agricola, R., Price, A. J., Vincent, T. L., Weinans, H., & Carr, A. J. (2015). Osteoarthritis. The Lancet, 368(9991), 376-387. doi:10. 1016/S0140-6736(14)60802-3Lozada, C. J. (2016, November 30). Arthritis. Medscape. Retrieved from http://emedicine. medscape. com/article/330487 Maxey, L., & Magnusson, J. (2013). Rehabilitation for the postsurgical ortho-pedic patient. St. Louis, MO: Elsevier/Mosby. Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Peters, C. L., Shirley, B., & Erickson, J. (2006). The effect of a new multimodal perioperative anesthetic regimen on postoperative pain, side effects, rehabilitation, and length of hospital stay after total joint arthroplasty. The Journal of Arthroplasty, 21 (6), 132-138. doi:10. 1016/j. arth. 2006. 04. 017 Scott, W. N. (2012). Insall & Scott surgery of the knee (5th ed. ). Philadelphia, PA: Elsevier/Churchill Livingstone. Rheumatoid Arthritis Dana Cafaro Definition A. Rheumatoid arthritis (RA) is a chronic, inflammatory, symmetric polyarthritis that can have systemic effects on mul-tiple organ systems with no clear etiology. Incidence A. Prevalence 1% with female to male ration of 3:1. B. Peak onset for women is fourth to fifth decade. C. Peak onset for men is sixth to eighth decade. D. Annual incidence is 40 per 100,000. E. Increased frequency of the disease in first-degree relatives and monozygotic twins. Pathogenesis A. No clear cause has been identified for RA; however, genetics and environment appear to contribute to the devel-opment of RA. The best characterized genetic risk factor is inheritance of the HLA DRB1 alleles encoding a “shared epitope. ” B. Chronic synovitis and joint destruction are characteristic of RA. C. Pannus, destructive vascular granulation tissue, is a dis-tinctive feature of RA and destroys adjacent cartilage, bone, ligaments, and tendons. Predisposing Factors A. Gender-specific risk factors. 1. Women: Nulliparity and postpartum state can increase acute flare. 2. Men: Below normal testosterone levels. B. Genetic predisposition. C. Cigarette smoking, heavy caffeine consumption, and oral contraception, particularly in patients carrying the shared epitope. D. Infection (both bacterial and viral) has been hypothesized to trigger RA but no specific bacterial or viral pathogens have been identified. E. Autoantibody carriers, specifically rheumatoid fac-tor (RF) and anti-citrullinated peptide/protein antibodies (ACPA), increase the risk for development of RA. F. Occupational exposures including dust and silica. Subjective Data A. Common complaints/symptoms. 1. Insidious onset of polyarticular inflammation and complaints of joint pain and stiffness is the most common presentation but some patients may present with acute symptoms. 14. Immune System, Connective Tissue, and Joints Guidelines312	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2. Joint stiffness will last more than 30 minutes and is prominent in the morning, after periods of inactivity and after strenuous activity. 3. Systemic manifestations can also be present. 4. Symptoms tend to be reported in the small joints of the hands, wrist, and forefoot. All joints of the extremities can be affected. Typically, the axial skeleton except for the cervical spine will not be involved. B. Common/typical scenario. 1. Systemic symptoms include dryness of the eyes and mucous membranes, presence of rheumatoid nodules, pulmonary symptoms including cough and dyspnea, weight loss, fatigue, and depression. 2. Felty syndrome is seen in advanced disease and is char-acterized by splenomegaly and neutropenia. (C). C. Family and social history. 1. Family history of RA. 2. Social history. a. Smoking. b. Caffeine intake. c. Occupational exposures. D. Review of systems. 1. Joint pain and stiffness. 2. Swelling. 3. Presence of skin nodules. 4. Changes in skin color. 5. Dryness of mucous membranes. 6. Cough. 7. Dyspnea. Physical Examination A. Symmetrical, polyarticular swelling with pain, and ten-derness is characteristic. B. “Boggy” feeling over the affected joints due to synovial thickening or effusion. C. Palmar erythema may be present in acute flares. D. Deformities are common in late disease and may be asym-metrical. E. Decreased grip strength is noted in disease affecting the hands and can be an early indicator of disease. F. Ulnar deviation, swan neck deformities (flexion of the distal interphalangeal [DIP] joint with extension of the prox-imal interphalangeal [ PIP] joint) and Boutonniere deformi-ties (hyperextension of the DIP joint with flexion of the PIP joint) of the fingers are common in chronic RA. G. Tendon ruptures can occur. H. Rheumatoid nodules are subcutaneous nodules found over bony prominences (most commonly), bursae, and ten-don sheaths and are found in 20% of patients. I. Ocular findings include scleritis and episcleritis. Diagnostic Tests A. Radiographs (most specific testing): Early images may be normal or show evidence of soft tissue swelling and juxta-articular demineralization. Later images will reveal joint space narrowing and erosions. B. Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein levels: Elevated in acute phases. C. Anti-cyclic citrullinated peptide (anti-CCP) antibodies and RF: present in about 3/4 of patients with RA. D. Synovial fluid analysis: Inflammatory effusion often per-formed to rule out septic arthritis. Differential Diagnosis A. Fibromyalgia. B. Lyme disease. C. Myelodysplastic syndrome. D. Osteoarthritis. E. Sarcoidosis. F. Systemic lupus erythematosus. Evaluation and Management Plan A. General plan. 1. Goals. a. Reduce pain and inflammation. b. Preserve function. c. Prevent deformity. 2. Nonpharmacologic. a. Physical and occupational therapy. b. Diet and exercise. c. Smoking cessation. d. Osteoporosis screening and treatment. e. Immunizations to reduce risk of immunosuppres-sive therapies. B. Patient/family teaching points. 1. Similar to nonpharmacological management. 2. Diet. 3. Exercise. 4. Smoking cessation. 5. Physical and occupational therapy. 6. Routine screening and immunizations. C. Pharmacotherapy. 1. N onsteroidal anti-inflammatory drugs (NSAIDs): For symptomatic relief, but not to be used as monotherapy. 2. Corticosteroids. a. Used to bridge until d isease-modifying antirheumatic drugs (DMARDs) are effective or dur-ing active disease. b. Will decrease inflammation and slow articular ero-sion. c. Recommended dose is prednisone 5 to 10 mg po daily. i. Higher doses may be needed to treat extra-articular manifestations and should be tapered when discontinuing. d. Intra-articular corticosteroids may be helpful to treat one to two symptomatic joints but may not be administered more than four times per year. e. Recommended dose is triamcinolone 10 to 40 mg based on size of joint being treated. 3. DMARDs. a. Begin as soon as RA is confirmed. b. More efficacious when used in combination than as a monotherapy. c. Most commonly used combination is methotrex-ate with a t umor necrosis factor (TNF) inhibitor. i. Methotrexate: Initial synthetic DMARD of choice (7. 5 mg po weekly); can see improvement in 2 to 6 weeks. ii. TNF inhibitors: Added when patients do not respond to methotrexate. Follow-Up A. Patients should follow-up after starting or changes are made to medications. Consultation/Referral A. Rheumatology as early as possible to confirm diagnosis and manage disease. Special/Geriatric Considerations A. RA can be a debilitating disease that makes activities of daily living very difficult. Rheumatoid Arthritis313	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
B. Geriatric patients may have increased risk associated with RA, such as: 1. Cognitive impairment. 2. Depression. 3. Falls. 4. Urinary incontinence. 5. Malnutrition. Bibliography Firestein, G. S. (2017, August 30). Pathogenesis of rheumatoid arthritis. In P. L. Romain (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/pathogenesis-of-rheumatoid-arthritis Hannon, R. A., & Porth, C. M. (Eds. ). (2017). Porth pathophysiology: Con-cepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Moreland, L. W., & Cannella, A. (2018, May 31). General princi-ples of management of rheumatoid arthritis in adults. In P. L. Romain (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/ contents/general-principles-of-management-of-rheumatoid-arthritis-in-adults?source=search_result&search=treatment%20rheumatoid% 20arthritis&selected Title=1 Papadakis, M. A. (2017). Current medical diagnosis & treatment 2017 (56th ed. ). New York, NY: Mc Graw-Hill Education/Medical. Venables, P. J. W. (2017, October 12). Clinical manifestations of rheumatoid arthritis. In P. L. Romain (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clinical-manifestations-of-rheumatoid-arthritis?source=search_result&search=rheumatoid% 20arthritis&selected Title=2 Spondyloarthropathies Dana Cafaro Definition A. Spondyloarthropathies are a group of inflammatory con-ditions that affect the axial skeleton and also may have mul-tisystem effects. B. Inflammatory arthritis of the spine and sacroiliac joints, asymmetric oligoarthritis of the peripheral joints, and inflam-mation at sites where tendon and ligament insert into bone (enthesopathy) characterize spondyloarthropathies. C. Spondyloarthropathies include ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and arthritis associated with inflammatory bowel disease. D. Also known as seronegative spondyloarthropathies. E. Clinical presentation and diagnostic evaluation are simi-lar for the seronegative spondyloarthropathies. Incidence A. Males are more often affected. B. Onset is typically before age 40. C. Ankylosing spondylitis is common to manifest in late teens and early 20s. Pathogenesis A. The cause of spondyloarthropathies is not well under-stood. B. It appears to be a genetic relationship to human leukocyte antigen (HLA)-B27. C. Some theories exist that attribute microbial exposure as a possible cause; for example, chlamydia-induced arthritis, pso-riatic arthritis, and the development of arthritis in patients with Crohn's disease and ulcerative colitis. Predisposing Factors A. Male. B. Genetic predisposition. C. Bacterial infections. Subjective Data A. Common complaints/symptoms. 1. Low back pain more than 3 months' duration. a. Back pain may also have an “inflammatory pat-tern,” which is insidious onset often before age 40. It improves with exercise, but not rest and nocturnal pain. b. Also characteristic can be relief of pain within 24 to 48 hours of taking nonsteroidal anti-inflammatory drugs (NSAIDs). 2. Peripheral arthritis will affect the knees and ankles pre-dominantly, and will often be asymmetrical, affecting one to three joints. 3. Ocular complaints include redness, pain, and photo-phobia. These may be the first presenting symptoms of spondyloarthropathy. B. Common/typical scenario. 1. Ankylosing spondylitis will progress in cephalad direc-tion with limited chest expansion. 2. Heart disease characterized by atrioventricular con-duction defects and aortic regurgitation will manifest in severe disease. 3. Constitutional symptoms are typically absent. 4. Psoriatic arthritis may present with symmetric pol-yarthritis similar to rheumatoid arthritis. Pitting of the nails and onycholysis is common. 5. Reactive arthritis (formerly Reiter syndrome) will present with oligoarthritis, conjunctivitis, urethritis, and mouth ulcers. Patients will often report a history of gas-trointestinal (GI) or sexually transmitted infections. Sys-temic symptoms such as fever and weight loss are more common. C. Family/social history. 1. Family history. a. Spondyloarthropathies. b. Inflammatory bowel disease. 2. Social history. a. Sexual activity. b. Exercise. D. Review of systems. 1. Back pain. 2. Joint pain. 3. Swelling. 4. Eye pain. 5. Eye redness. 6. Mucosal ulcers. 7. Rashes. 8. Changes in nails. 9. Vomiting. 10. Bowel changes. 11. Diarrhea. 12. Dysuria. 13. Genital discharge. 14. Fever. 15. Weight loss. Physical Examination A. Musculoskeletal findings include the following. 1. Decreased range of motion in the back over time. 2. Edema in peripheral arthritis. 3. Enthesitis most commonly in the heel or Achilles ten-don, but can be seen at the following. a. Iliac crests. b. Greater trochanters. c. Epicondyles, tibial plateaus. d. Costochondral junctions of the sternum. 14. Immune System, Connective Tissue, and Joints Guidelines314	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
e. Humeral tuberosities, manubrial-sternal joints. f. Occiput. g. Spinous processes. 4. Dactylitis is a characteristic feature of spondy-loarthropathies, especially psoriatic arthritis and less fre-quently reactive arthritis. The physical finding is also known as “sausage toe or sausage finger” and is charac-terized by swelling of the entire digit without pain or ten-derness. 5. Ocular findings include nonpurulent conjunctivitis and anterior uveitis. 6. Dermatologic findings include psoriasis and pitting nails, particularly in patients with peripheral joint mani-festations. Diagnostic Tests A. No laboratory tests are specific for spondyloarthropathies. B. HLA-B27: 90% of patients with ankylosing spondylitis and 50% to 70% of patients with other types of spondy-loarthropathies will be positive. C. Negative rheumatoid factor. D. Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are elevated in 35% to 50% of patients. They are also used to assess radiographic progression and response to therapy. E. Uric acid levels may be high with psoriatic arthritis. F. Synovial fluid cultures in reactive arthritis are negative. G. Axial radiographs: Findings of sacroiliitis including ero-sions, ankylosis, changes in joint width, or sclerosis, are spe-cific for spondyloarthropathies; however, it takes several years to be visible on radiograph. Syndesmophytes can develop on the spine. H. MRI can be useful in patients with nonradiographic evi-dence of spondyloarthropathies. I. Ultrasound has been used to confirm enthesitis. Differential Diagnosis A. Degenerative disc disease. B. Kyphosis. C. Spine fractures, dislocations. D. Osteoarthritis. E. Spinal stenosis. Evaluation and Management Plan A. General plan. 1. Reduce swelling and pain. 2. T reat infectious processes and skin disorders. B. Patient/family teaching points. 1. Encourage exercise. C. Pharmacotherapy. 1. NSAIDs (use in caution in patients with inflamma-tory bowel disease). 2. T umor necrosis factor (TNF) inhibitors have been used for NSAID refractory cases for ankylosing spondyli-tis and methotrexate refractory cases of psoriatic arthritis. Both may also be used for reactive arthritis. 3. Methotrexate is used in psoriatic arthritis to treat both cutaneous and arthritic manifestations. 4. Monoclonal antibody therapy has been used in pso-riatic arthritis patients who do not respond to TNF inhibitors. 5. Sulfasalazine for peripheral arthritis. 6. Psoralen and ultraviolet A (PUVA) therapy for psori-asis skin lesions. 7. Antibiotics may be needed to treat GI or genitouri-nary infections in patients with reactive arthritis. Follow-Up A. Interval follow-up is necessary to monitor medication safety and patient's response to therapy. Consultation/Referral A. Physical therapy for exercise regimens. B. Dermatology for skin manifestations. C. Gastroenterology for GI manifestations. D. Ophthalmology for ocular manifestations. E. Infectious disease for sexually transmitted infections or other infectious diseases. Special/Geriatric Considerations A. Markers of disease progression and treatment do not appear to be age-related. B. Standard precautions in the elderly related to pharma-cokinetics still apply. Bibliography Hannon, R. A., & Porth, C. M. (2017). Porth pathophysiology: Concepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Yu, D. T., & van T ubergen, A. (2018, September 7). Overview of the clinical manifestations and classification of spondyloarthritis. In P. L. Romain (Ed. ), Up To Date. Retrieved from https://www. uptodate. com /contents/overview-of-the-clinical-manifestations-and-classification-of-spondyloarthritis?source =search_result&search =spondyloarthropathy &selected Title =1 Yu, D. T., & van T ubergen, A. (2019, January 1). Pathogene-sis of spondyloarthritis. In P. L. Romain (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/pathogenesis-of-spondyloarthritis?source =search_result& Systemic Lupus Erythematosus Monica Richey Definition A. Systemic lupus erythematosus (SLE) is a chronic inflam-matory disorder characterized by: 1. Multisystem involvement. 2. Presence of antinuclear antibodies. B. It has a chronic relapsing nature. C. The course of the disease is variable, alternating between periods of stable disease (remission) and/or flares with high disease activity. Incidence A. The incidence of SLE in the United States ranges from 2. 0 to 7. 6 cases per 100,000 persons per year. B. Prevalence ranges from 14. 6 to 68 cases per 100,000 persons. Pathogenesis A. SLE can be set off by a combination of predisposing genetic traits, hormonal and environmental factors, or infec-tious agents. B. These result in an abnormal immune response with dysregulation of B and T cells, resulting in the following. 1. Production and formation of autoantibodies. 2. Complement fixing. 3. Immune complexes that promote inflammation and tissue damage. Systemic Lupus Erythematosus315	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Predisposing Factors A. Affects more females than males with a ratio of 9:1, with a higher incidence among women of childbearing age. B. Disproportionately affects more black women with a three to four times higher prevalence than whites. C. There is also a higher incidence of SLE among the Afro-Caribbean, Asian, American Indian, and Hispanic descent populations as compared to the white population. Subjective Data A. Common complaints/symptoms. 1. Malar rash. 2. Arthritis. 3. Fatigue. 4. Fever. 5. Pleurisy. 6. Edema. 7. Anemia. 8. Lymphadenopathy. B. Common/typical scenario. 1. Patients typically present with fever, joint pain, and rash in women of childbearing age. C. Family and social history. 1. Lupus may run in families. 2. There is currently no screening or genetic tests avail-able. D. Review of systems. 1. Common questions. a. Onset of symptoms. b. Length of symptoms. c. New onset or previously experienced. d. Any triggers. e. Recent infections. 2. Constitutional. a. Fevers. b. Chills. c. Malaise. d. Weight loss. e. Photosensitivity. 3. Skin. a. Rashes. b. Does the patient have a diagnosis of Raynaud's phenomenon, which is periodic cold and numbness to fingers and toes? 4. Head, ear, eyes, nose, and throat (HEENT). a. Lymphadenopathy. b. Dry mouth/eye. 5. Cardiovascular. a. Chest pain. b. Palpitations. 6. Pulmonary. a. Shortness of breath. b. Pleuritic chest pain. 7. Peripheral vascular. a. Edema. b. Raynaud's. c. Wounds. 8. Musculoskeletal. a. Arthritis. b. Arthralgias. c. Joint deformities. 9. Gastrointestinal. a. Nausea. b. Vomiting. c. Changes in stools. d. Abdominal pain. Physical Examination A. Physical examination for SLE requires a full head-to-toe examination. B. Cutaneous manifestations. 1. Cutaneous vasculitis: Palpable petechiae in dependent areas, cutaneous necrosis, ulceration, and gangrene. 2. Raynaud's phenomenon: Red, white, and blue, inde-pendent of disease activity, ulceration, atrophy, and gan-grene. 3. Livedo reticularis: Antiphospholipid s yndrome (APS), blanchable red-purple ring, lace like. 4. Photosensitivity: Rashes, fever, malaise, adenopathy, arthritis. 5. Malar rash: Erythematous, edematous, spares nasolabial folds. 6. Mucocutaneous lesions: Upper palate, maybe pain-less, sharply marginated. 7. Alopecia: Diffuse or patchy, reversible, or permanent. C. Musculoskeletal manifestations. 1. Arthralgias. 2. Arthritis. 3. Myalgia and myositis. D. Pulmonary manifestations—add imaging as needed. 1. Pleurisy. 2. Acute lupus pneumonitis: 80% mortality rate. 3. Interstitial lung disease ground glass or honeycomb. 4. Pulmonary embolus. 5. Pulmonary hemorrhage. 6. Pulmonary hypertension. 7. Shrinking lung syndrome. E. Cardiac/peripheral vascular manifestations—add imag-ing as needed. 1. Pericarditis (echo). 2. Myocarditis and myocardial dysfunction. 3. M yocardial infarction (MI). 4. Deep vein thrombosis (DVT). 5. Edema. F. Central nervous system (CNS) manifestations (19 differ-ent manifestations). 1. Central. a. Aseptic meningitis. b. Cardiovascular disease. c. Demyelinating syndrome. d. Headache. e. Movement disorder. f. Myelopathy. g. Seizure disorder. h. Acute confusional state. i. Anxiety disorder. j. Cognitive dysfunction. k. Mood disorder. l. Psychosis. m. CNS vasculitis: Fevers, seizures, meningismus, altered behavior patterns. 2. Peripheral. a. Guillain-Barre syndrome, autonomic neuropathy. b. Mononeuropathy. c. Myasthenia gravis. d. Cranial neuropathy. e. Plexopathy. f. Polyneuropathy. 3. Hematological manifestations. a. b. c. d. 14. Immune System, Connective Tissue, and Joints Guidelines Anemia. Thrombocytopenia. Leukopenia. Pancytopenia. 316	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Diagnostic Tests A. The diagnosis of lupus is based on clinical presentation and laboratory analysis. B. The clinician should suspect lupus if 2 +organ systems are involved. 1. Positive laboratory workup only with no symptoms does not give the diagnosis and does not require treat-ment. C. Drug-induced SLE should be ruled-out if there is a pres-ence of the following medications. 1. Anti-tumor necrosis factor (TNF). 2. Hydralazine. 3. Anticonvulsants. 4. Isoniazid. 5. Thorazine. 6. Procainamide. 7. Penicillamine. 8. Minocycline. D. Laboratory workup for diagnosis. 1. Complete b lood count (CBC)/comprehensive metabolic panel (CMP)/e levated erythrocyte sedimen-tation rate (ESR)/C-reactive protein (CRP)/antinuclear antibody (ANA). 2. Anti-histone (if applicable). 3. ANA. 5. C3. 6. C4. 7. Anti-Smith antibody. 8. Ribonucleoprotein (RNP). 9. Anti ro (SSa). 10. Anti La (SSb). 11. Urine with microscopy. E. Laboratory workup for flares: 1. CBC/CMP/ESR/CRP. 2. C3. 3. C4. 4. Ds DNA. 5. Urine with microscopy. F. Diagnostic criteria. 1. The American College of Rheumatology (ACR) has established 11 criteria for classification of SLE. 2. These criteria are used mostly in clinical trials and population studies rather than for diagnostic purposes. 3. A minimum of four criteria out of 11 are necessary to participate in clinical trials. The 11 criteria are divided into four cutaneous, four systemic, and three lab compo-nents. Differential Diagnosis A. Malignancies. B. Infectious processes (c ytomegalovirus [ CMV], Epstein-Barr virus (EBV), HIV, and hepatitis). C. Rheumatoid arthritis. D. Scleroderma. E. Fibromyalgia. F. Thrombotic thrombocytopenia purpura (TTP). G. Multiple sclerosis. H. Myositis/dermatomyositis. Evaluation and Management Plan A. General plan. 1. If previously diagnosed with SLE. a. Assess and treat urgent symptoms (rashes, infec-tions, arthritis, s hortness of breath [ SOB], chestpain)—will likely need corticosteroid and/or anti-inflammatory. b. Infectious process must be rule-out—antibiotics as needed. c. Pain medications as needed in a short course. 2. If newly diagnosed. a. Start corticosteroids. b. Refer to specialist ASAP. 3. Associated conditions. a. Lupus nephritis (LN). i. Persistent proteinuria of greater than 0. 5g/day, measured by a spot urine protein/creatinine ratio and/or 24-hour protein urine collection. ii. Urine dipstick of 3 +and/or presence of active urinary sediment, such as: 1)More than five red blood cells (RBCs) or more than five white blood cells (WBCs) in the absence of infection. iii. All patients with clinical evidence of active but previously untreated LN should undergo renal biopsy (unless contraindicated). iv. The indications for renal biopsy are: 1)Increase in serum creatinine level without compelling causes (e. g., sepsis). 2)Confirmed proteinuria ( ≥1. 0 g per 24 hours [either 24-hour specimens or spot pro-tein/creatinine ratio]). 3)Combinations of the following, con-firmed in at least two tests done in a short period of time and in the absence of alterna-tive cause. a)Proteinuria of 0. 5 g or more per 24 hours plus hematuria. b)Proteinuria of 0. 5 g or more per 24 hours plus cellular cast. b. APS. i. Primary APS: Occurs in 1% to 6% of popu-lation; 8% of primary APS patients later develop SLE. ii. Secondary APS: 30% of SLE patients could develop APS (50% risk of thrombosis). 1)Laboratory criteria. a)Anticardiolipin antibody or Ig G and/or Ig M; medium or high titer on 2+occasion at least 12 weeks apart. b)Positive lupus anticoagulant test on 2+occasions at least 12 weeks apart. 2)Definite APS: One clinical +one labora-tory criteria. 3)Antiphospholipid antibodies (Ap L): Only laboratory criteria—DO NOT TREAT. 4)Catastrophic APS (CAPS). a)Multiple organs over a short period of days. Multiple thrombosis of small and medium size vessel may occur despite anticoagulation. 50% mortality. c. Management of lupus flares. i. Glucocorticoids: Patients with organ disease require high doses of prednisone (1mg/kg—up to 60 mg daily) or equivalent for 4 to 6 weeks fol-lowed by taper of 10% per week. ii. Flares presenting with synovitis, fevers, rashes, or serositis are managed with lower doses (10-20mg daily) with quick taper. iii. Long-term therapy with corticosteroids can lead to myopathy, osteoporosis, hyperten-sion, diabetes, cataracts, atherosclerotic vascular Systemic Lupus Erythematosus317 4. Anti-double-strandeddeoxyribonucleicacid (Ds DNA).	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
disease, avascular necrosis of the bone, and infec-tions. B. Patient/family teaching points. 1. Exercise and healthy lifestyle may be important factors in mitigating symptoms. 2. The disease is lifelong and the goal of care is to reduce flare-ups. C. Pharmacotherapy. 1. Antimalarial drugs: Hydroxychloroquine, quinacrine for joint pain, rash, and fatigue. 2. Glucocorticoids: Prednisone, methylprednisolone, solumedrol. 3. Topical steroid: Hydrocortisone, triamcinolone, fluo-cinolone for rash, skin lesions. 4. N onsteroidal anti-inflammatory drugs (NSAIDs): Many forms; arthralgias, polyarthritis, add p roton p ump inhibitor (PPI) as needed. 5. Immunosuppressive agents: Azathioprine, mycophe-nolate, belimumab, cyclophosphamide, methotrexate, rituximab, dapsone, thalidomide. Follow-Up A. Patient should always be referred to a rheumatologist as soon as possible for follow-up and further treatment deci-sions. Consultation/Referral A. Rheumatologist. B. Other specialties as needed, including dermatology, nephrology, and cardiology. C. Social work. D. Physical/occupational therapy. Special/Geriatric Considerations A. Infections. 1. Patients with SLE/LN are at increased risk for infec-tions. 2. They should be encouraged to receive all inactivated vaccines, following Centers for Disease Control and Pre-vention (CDC) recommendations for patients who are immunosuppressed. B. Heart disease. 1. SLE patients have a 7. 5-fold increase in coronary artery disease (CAD). 2. Routine care for patients with SLE should include: a. Screening for cardiovascular risk factor. b. Counseling for lifestyle modification, such as smoking cessation, encouraging physical activity, and weight loss. c. Screening for symptoms suggestive of heart dis-ease. C. Contraception. 1. Contraceptive options and education should be offered to all women with SLE. 2. Intrauterine devices containing levonorgestrel are among the safest and most effective options. 3. Also, progesterone-only pills are effective in long-term contraception. 4. Intense screening of risk factors for thrombotic events in women with SLE is important when prescribing con-traceptives. D. Osteoporosis. 1. Recommendations for patients taking glucocorti-coid for more than 3 months include smoking cessa-tion, regular exercise, and the administration of calcium(1,200-1,500 mg) and vitamin D (800-1,000 interna-tional units). 2. All patients starting on chronic treatment with gluco-corticoid for more than 5 mg/day should be started on a bisphosphonate if there are no contraindications. E. Pregnancy concerns. 1. SLE patients have worse outcomes with increased rates of the following. a. Preeclampsia. b. Fetal loss. c. Preterm delivery (higher rates of delivery <34 weeks). d. Fetal growth retardation (fgr). e. Infants small for gestational age. 2. Blood pressure control is of utmost importance in managing SLE/LN patients during pregnancy. 3. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are contraindicated during all three trimesters of pregnancy. a. Switch patients to other agents safer to use (if the potential benefits justify the potential risk to the fetus), such as methyldopa, labetalol, or nifedipine. 4. Because of immunosuppressant's fetal toxicity, only glucocorticoids, azathioprine, and hydroxychloroquine can be used safely during pregnancy. 5. They should be managed by a high-risk obstetrician in a tertiary center with a multidisciplinary team approach. Bibliography American College of Rheumatology Ad Hoc Committee on Systemic Lupus Erythematosus Guidelines. (1999). Guidelines for referral and manage-ment of systemic lupus erythematosus in adults. Arthritis and Rheuma-tology, 42 (9), 1785-1796. Bailey, T., Rowley, K., & Bernknopf, A. (2011). A review of systemic lupus erythematosus and current treatment options. Formulary, 46, 178-194. Bramham, K., Hunt, B. J., Bewley, S., Germain, S., Calatayud, I., Khamashta, M. A., & Nelson-Piercy, C. (2011). Pregnancy outcomes in systemic lupus erythematosus with and without previous nephritis. The Journal of Rheumatology, 38 (9), 1906-1913. Chakravarty, E. F. (2008). What we talk about when we talk about contra-ception. Arthritis & Rheumatology, 59 (6), 760-761. Faurschou, M., Mellemkjaer, L., Starklint, H., Kamper, A. L., Tarp, U., Voss, A., & Jacobsen, S. (2011). High risk of ischemic heart disease in patients with lupus nephritis. The Journal of Rheumatology, 38 (11), 2400-2405. Grossman, J. M., Gordon, R., Ranganath, V. K., Deal, C., Caplan, L., & Chen, W. (2010). American College of Rheumatology 2010 recom-mendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Care & Research (Hoboken), 62 (11), 1515-1526. Hahn, B. H., Mc Mahon, M. A., Wilkinson, A., Wallace, W. D., Daikh, D. I., & Fitzgerald, J. D. (2012). American College of Rheumatology guidelines for screening, treatment, and management of lupus nephritis. Arthritis Care & Research (Hoboken), 64 (6), 797-808. Hahn, B. H., & Wallace, D. J. (Eds. ). (2013). Dubois' lupus erythematosus and related syndromes. Philadelphia, PA: Elsevier/Saunders. Hochberg, M. C. (1997). Updating the American College of Rheumatol-ogy revised criteria for the classification of systemic lupus erythematosus. Arthritis and Rheumatism, 40 (9), 1725. doi:10. 1002/art. 1780400928 Märker-Hermann, E., & Fischer-Betz, R. (2010). Rheumatic diseases and pregnancy. Current Opinion in Obstetrics & Gynecology, 22 (6), 458-465. doi:10. 1097/GCO. 0b013e3283404d67 Michalski, J. P., & Kodner, C. (2010). Systemic lupus erythematosus: Safe and effective management in primary care. Primary Care, 37 (4), 767-778. doi:10. 1016/j. pop. 2010. 07. 006 Mosca, M., Tani, C., Aringer, M., Bombardieri, S., Boumpas, D., & Brey, R. (2010). European League against rheumatism recommendations for monitoring patients with systemic lupus erythematosus in clinical prac-tice and in observational studies. Annals of the Rheumatic Diseases, 69 (7), 1269-1274. doi:10. 1136/ard. 2009. 117200 Podymow, T., August, P., & Akbari, A. (2010). Management of renal disease in pregnancy. Obstetrics and Gynecology Clinics of North America, 37 (2), 195-210. doi:10. 1016/j. ogc. 2010. 02. 012 Rahman, A., & Isenberg, D. A. (2008). Systemic lupus erythemato-sus. The New England Journal of Medicine, 358 (9), 929-939. doi:10. 1056/NEJMra07129714. Immune System, Connective Tissue, and Joints Guidelines318	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Richey, M. (2014). The management of lupus nephritis. The Nurse Practi-tioner, 39 (3), 1-6. doi:10. 1097/01. NPR. 0000443229. 10476. 61 Tan, E. M., Cohen, A. S., Fries, J. F., Masi, A. T., Mc Shane, D. J., & Roth-field, N. F. (1982). The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis and Rheumatism, 25 (11), 1271-1277. doi:10. 1002/art. 1780251101 T unnicliffe, D. J., Singh-Grewal, D., Kim, S., Craig, J. C., & Tong, A. (2015). Diagnosis, monitoring, and treatment of systemic lupus ery-thematosus: A systematic review of clinical practice guidelines. Arthritis Care & Research, 67 (10), 1440-1452. doi:10. 1002/acr. 22591 T urano, L. (2013). Premature atherosclerotic cardiovascular dis-ease in systemic lupus erythematosus: Understanding manage-ment strategies. Journal of Cardiovascular Nursing, 28 (1), 48-53. doi:10. 1097/JCN. 0b013e3182363e3b Wallace, D. J. (2008). Lupus: The essential clinician's guide (1st ed., pp. 78-80). New York, NY: Oxford University Press. Vasculitis-Variable Vessel Dana Cafaro Definition A. Part of a group of disorders that result from inflammatory changes to walls of veins and arteries, causing damage to the mural structures which ultimately may cause tissue ischemia and necrosis. B. Nomenclature is changing for the specific forms of vas-culitis based on the Chapel Hill Consensus Conference (CHCC). C. T wo main types. 1. Behçet disease. 2. Essential cryoglobulinemia. Incidence A. More common in patients of Asian, T urkish, and Middle Eastern descent. B. Prevalence similar in men and women. C. Commonly afflicts patients ages 20 to 40 years old. D. Disease is more severe in young male patients from Mid-dle East or Far Eastern Asia. Pathogenesis A. Vasculitis can be a primary pathology or can be secondary to another underlying disease process (Table 14. 1). B. Direct injury to the vessel, infectious agents, or immune processes are known to cause vasculitis. C. Secondary vascular injury may occur from physical agents such as cold and irradiation, mechanical injuries, and toxins. 1. Behçet disease. a. Affects both arteries and veins of all sizes. 2. Essential cryoglobulinemia. a. Cold-precipitated, immune-complex mediated. b. Occurs in chronic underlying infection (hepatitis C most commonly), connective tissue disease, lym-phoproliferative disorders. Predisposing Factors A. First degree relative with Behçet disease increases the risk for the disease. B. Essential cryoglobulinemia is associated with chronic hepatitis C infection. Subjective Data A. Common complaints/symptoms. 1. Constitutional symptoms are common with all size vessel vasculitis and include fever, weight loss, malaise, and arthralgias/arthritis. 2. Behçet disease. a. Aphthous lesions of mouth and genitals. b. Tender, erythematous popular lesions which ulcerate. c. Knee and ankle arthritis. d. Posterior uveitis, hypopyon. e. Neurological conditions including sterile meningi-tis, cranial nerve palsies, seizures, encephalitis, mental status changes, and spinal cord lesions. f. Hypercoagulable states. 3. Essential cryoglobulinemia. a. Palpable purpura. b. Peripheral neuropathy. c. Abdominal pain. d. Digital gangrene. e. Pulmonary disease. f. Glomerulonephritis. B. Common/typical scenario. 1. Essential cryoglobulinemia. a. Purpura. b. Weakness. c. Arthralgia. 2. Behçet disease. a. Recurrent, painful ulcers of mouth and genitals. b. Follicular rash. c. Uveitis. d. Sterile pustules at needlestick sites. e. Arthritis. C. Family and social history. 1. Essential cryoglobulinemia. a. Sexual history. b. I ntravenous (IV) drug use. c. Family history of Behçet disease. D. Review of systems. 1. Essential cryoglobulinemia. a. Abdominal pain. TABLE 14. 1 Classification of Vasculitis Variable Vessel Large Vessel Medium Vessel Small Vessel Behçetdisease Essential cryoglobulinemia Takayasuarteritis Giantcell/temporal arteritis Polyarteritis nodosa Kawasaki disease Buergerdisease Primary angiitis of the central nervoussystem Granulomatosiswith polyangiitis Microscopicpolyangiitis Eosinophilicgranulomatosis with polyangiitis ANCA, antineutrophilcytoplasmic antibodies. Vasculitis-Variable Vessel Henöch Schonlein purpura ANCA associated disorders:319	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
b. Sensitivity to cold. c. Skin changes. d. Paresthesias. e. Weakness. 2. Behçet disease. a. Mucosal ulcers. b. Skin nodules. c. Skin rashes. d. Joint pain. e. Eye pain. f. Photophobia. g. Eye redness. h. Visual changes. i. Headache. j. Weakness. k. Mental status changes. l. Chest pain. m. Dyspnea. Physical Examination A. Behçet disease. 1. Aphthous ulcers of mouth and genitals. 2. Follicular rash. 3. Erythema nodosum-like lesions. 4. Hypopyon. B. Essential cryoglobulinemia. 1. Palpable purpura. 2. Peripheral sensorimotor deficits. 3. Raynaud's phenomenon. Diagnostic Tests A. Behçet disease. 1. Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). 2. No definitive tests. 3. Positive pathergy test: At least a 2 mm papule will develop 24 to 48 hours after needle insertion to the skin. B. Essential cryoglobulinemia. 1. Elevated liver enzymes. 2. Positive cryoglobulins. 3. Low C4 level. Differential Diagnosis A. Hepatitis B. B. Hepatitis C. C. HIV. D. Connective tissue disease. E. Lymphoproliferative disorders. F. Other types of vasculitis. Evaluation and Management Plan A. General plan. 1. Based on cause and severity of the vasculitis. 2. Alleviation of symptoms. B. Patient/family teaching points. 1. Regular follow-up is necessary to monitor condition. 2. Patients should also be educated on side effects of medications used for treatment. C. Pharmacotherapy. 1. Behçet disease. a. Colchicine 0. 6 mg 1 to 3 times per day and thalidomide 100 mg daily. b. Apremilast for oral ulcers. c. Corticosteroids or azathioprine for severe disease. d. Infliximab, cyclosporine, or cyclophosphamide for ocular and neurological disease. 2. Essential cryoglobulinemia. a. Corticosteroids and rituximab or cyclophos-phamide for 2 to 4 months. b. Hepatitis C treatment. Follow-Up A. Regular follow-up determined based on severity and cause of vasculitis. Consultation/Referral A. Based on cause and course of disease. B. Consider: 1. Ophthalmology. 2. Dermatology. 3. Infectious disease. Special/Geriatric Considerations A. Progression of these diseases is unpredictable and can affect basically all body systems. B. T reatment is symptomatic alleviation. Bibliography Hannon, R. A., & Porth, C. M. (2017). Porth pathophysiology: Concepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Merkel, P. A. (2019, March 1). Overview of and approach to the vas-culitides in adults. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-and-approach-to-the-vasculitides-in-adults/print Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Smith, E. L., & Yazici, Y. (2018, November 13). Clinical manifes-tations and diagnosis of Behçet syndrome. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ clinical-manifestations-and-diagnosis-of-behcets-syndrome Vasculitis-Small Vessel Dana Cafaro Definition A. Part of a group of disorders that result from inflammatory changes to walls of veins and arteries, causing damage to the mural structures that ultimately may cause tissue ischemia and necrosis. B. Nomenclature is changing for the specific forms of vas-culitis based on the Chapel Hill Consensus Conference (CHCC). C. There are several main types of small vessel vasculitis. 1. Henöch-Schonlein purpura (Ig A vasculitis). 2. Antineutrophil cytoplasmic antibodies (ANCA)-associated disorders. a. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). b. Microscopic polyangiitis. i. Most common cause of pulmonary-renal syn-dromes. ii. Does not cause chronic upper respiratory tract disease. iii. Does not have granulomatous inflammation on biopsy. c. Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome). 14. Immune System, Connective Tissue, and Joints Guidelines320	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Incidence A. Henöch-Schonlein purpura (Ig A vasculitis). 1. 90% of cases occur in pediatric population. B. ANCA-associated disorders. 1. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). a. 12 cases in 1 million people annually. b. Not gender specific. c. Age of onset commonly fourth to fifth decades. 2. Microscopic polyangiitis. a. Most common cause of pulmonary-renal syn-dromes. 3. Eosinophilic granulomatosis with polyangiitis (for-merly Churg-Strauss syndrome). a. Mean age of onset is 40. b. No gender specificity. c. Possibility of genetic predisposition. Pathogenesis A. Vasculitis can be a primary pathology or can be secondary to another underlying disease process. B. Direct injury to the vessel, infectious agents, or immune processes are known to cause vasculitis. C. Secondary vascular injury may occur from physical agents such as cold and irradiation, mechanical injuries, and toxins. D. Small vessel vasculitis may also be associated with ANCA. 1. Henöch-Schonlein purpura (Ig A vasculitis): Associ-ated with Ig A subclass 1 deposition in vessel walls. 2. ANCA-associated disorders. a. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). i. Characterized by upper and lower respiratory tract disease and glomerulonephritis. ii. Fatal if not treated. b. Microscopic polyangiitis: Caused by necrotizing vasculitis. c. Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome): Idiopathic in patients with asthma. Predisposing Factors A. Henöch-Schonlein purpura (Ig A vasculitis): Recent infection such as group A streptococcus. B. ANCA-associated disorders: Systemic diseases such as systemic lupus erythematosus, rheumatoid conditions, and polychondritis can predispose patients. 1. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). 2. Microscopic polyangiitis. 3. Eosinophilic granulomatosis with polyangiitis (for-merly Churg-Strauss syndrome). Subjective Data A. Common complaints/symptoms. 1. Small vessel vasculitis will often present with pur-pura, vesiculobullous lesions, urticaria, glomerulonephri-tis, alveolar hemorrhage, cutaneous extravascular necro-tizing granulomas, splinter hemorrhages, uveitis, episcle-ritis, and scleritis. a. Henöch-Schonlein purpura (Ig A vasculitis). i. Palpable purpura usually on lower extremities, arthralgias of knees and ankles, and hematuria. b. ANCA-associated disorders. i. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). 1)Upper respiratory tract: Nasal congestion, crusting, ulceration, bleeding, septal perfo-ration, “saddle nose,” sinusitis, otitis media, mastoiditis, gingival edema, stridor, subglot-tic stenosis. 2)Lower respiratory tract: Cough, dyspnea, hemoptysis. 3)Renal system: Hematuria, often not evi-dent until disease is advanced (UTD). 4)Other systems: Arthritis, ocular manifes-tations such as proptosis, scleritis, episcleritis, conjunctivitis, skin lesions, neuropathy. 5)Deep vein thrombosis (DVT)s and pul-monary embolism (PE)s are also common. ii. Microscopic polyangiitis. 1)Palpable purpura. 2)Ulcers. 3)Splinter hemorrhages. 4)Vesicular bullous lesions. 5)Interstitial lung fibrosis. 6)Pulmonary-renal syndromes. iii. Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome). 1)Allergic rhinitis. 2)Asthma. B. Review of systems. 1. Fever. 2. Fatigue. 3. Weight loss. 4. Arthralgias. 5. Respiratory symptoms (rhinorrhea, cough). 6. Skin changes. 7. Eye pain. 8. Eye redness. 9. Hematuria. Physical Examination A. Henöch-Schonlein purpura (Ig A vasculitis). 1. Palpable purpura in lower extremities and buttock. B. ANCA-associated disorders. 1. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). a. Nasal examination will reveal the following. i. Congestion. ii. Crusting. iii. Ulceration. iv. Bleeding. v. Septal perforation. b. “Saddle nose” deformity is a late finding. c. Otitis media. d. Proptosis. e. Conjunctivitis. f. Scleritis. g. Episcleritis. h. Signs of DVT. i. Calf swelling. ii. Erythema. iii. Tenderness. 2. Microscopic polyangiitis. a. Palpable purpura. b. Ulcers. c. Splinter hemorrhages. d. Vesiculobullous lesions. e. Pneumonitis. 3. Eosinophilic granulomatosis with polyangiitis (for-merly Churg-Strauss syndrome). Vasculitis-Small Vessel321	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
a. Skin and lung involvement. i. Wheezing. ii. Rhinitis. iii. Macular rash. iv. Urticaria. v. Palpable purpura. Diagnostic Tests A. Henöch-Schonlein purpura (Ig A vasculitis). 1. Biopsy will reveal leukocytoclastic vasculitis with Ig A deposition. B. ANCA-associated disorders. 1. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). a. Leukocytosis, thrombocytosis, normocytic, nor-mochromic anemia. b. Elevated creatinine. c. Elevated C-reactive protein (CRP) and elevated erythrocyte sedimentation rate (ESR). d. Positive ANCA. e. Red cell casts and proteinuria. f. Lung biopsy more likely to show granulomas. g. Chest CT. 2. Microscopic polyangiitis. a. 75% will be positive. b. Microscopic hematuria, proteinuria, red blood cell casts. c. Renal biopsy for necrotizing glomerulonephritis. 3. Eosinophilic granulomatosis with polyangiitis (for-merly Churg-Strauss syndrome). a. Eosinophilia in peripheral blood smear. b. Positive ANCA. Differential Diagnosis A. Other types of vasculitis. B. Infection. C. Malignancy. D. Atherosclerosis. E. Thromboembolic disease. F. Congenital/hereditary disorders. G. Hypercoagulable states. H. Inflammatory disorders (you may want to consider mak-ing this a general differential diagnosis for all forms of vas-culitis). Evaluation and Management Plan A. General plan. 1. Henöch-Schonlein purpura (Ig A vasculitis). a. Corticosteroids have been controversial and have not demonstrated reduction in long-term complica-tions. 2. ANCA-associated disorders. a. The disease process involves multiple systems. T reatment is symptomatic. B. Patient/family teaching points. 1. Requires regular examinations and tests to monitor for complications of the disease process. 2. Take medications as indicated. C. Pharmacotherapy. 1. Henöch-Schonlein purpura (Ig A vasculitis). a. Nonsteroidal anti-inflammatory drugs (NSAIDs) and Tylenol for treatment of pain; corticosteroids are reserved for refractory pain. 2. ANCA-associated disorders. a. Granulomatosis with polyangiitis (formerly Wegener's granulomatosis). i. Induction of remission. 1)Cyclophosphamide (2 mg/kg/day orally adjusted for renal disease and age >70) plus corticosteroids (1 mg/kg/day). 2)Rituximab and corticosteroids. 3)Bactrim for prophylaxis of opportunistic infections if using cyclophosphamide. ii. Maintenance of remission. 1)Azathioprine (up to 2 mg/kg/day orally) if no evidence of thiopurine methyltransferase deficiency is confirmed. 2)Methotrexate (20-25 mg/week orally or IM) if no renal insufficiency. 3)Rituximab (500 mg intravenous [IV]) at remission, repeat day 14 and then every 6 months three times. b. Microscopic polyangiitis (treatment is the same as granulomatosis with polyangiitis [formerly Wegener's granulomatosis]). c. Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome). i. Prednisone 0. 5 to 1. 5 mg/kg/day. ii. Cyclophosphamide for severe disease. Follow-Up A. Interval follow-up based on severity of disease. Consultation/Referral A. Refer to rheumatology. B. Consider consultation based on course of illness. 1. Nephrology for renal disease. 2. Pulmonology for pulmonary disease. Special/Geriatric Considerations A. The presence of comorbid diseases as commonly found in the geriatric population can impact care or obscure diagnosis. B. Infection is a prominent cause of morbidity and mortality in vasculitis patients and particularly with geriatric patients whose immune system may be compromised by other condi-tions and age. C. Influenza can be potentially life-threatening and there is no evidence that immunization has a negative impact on vas-culitis patients. D. Recommend all geriatric vasculitis patients receive annual influenza vaccination. E. Use of glucocorticoids as a treatment for vasculitis can cause osteoporosis and may lead to increased risk of falls and fractures. Bibliography Dedeoglu, F., & Kim, S. (2017, October 16). Ig A vasculitis (Henoch-Schönlein purpura): Management. In E. Te Pas (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/henoch-schonlein-purpura-immunoglobulin-a-vasculitis-management Falk, R. J., Merkel, P. A., & King, T. E., Jr. (2019, January 23). Granulomatosis with polyangiitis and microscopic polyangi-itis: Clinical manifestations and diagnosis. In A. Q. Lam, & & M. Ramirez Curtis (Eds. ), Up To Date. Retrieved from https:// www. uptodate. com/contents/clinical-manifestations-and-diagnosis-of-granulomatosis-with-polyangiitis-and-microscopic-polyangiitis Hannon, R. A., & Porth, C. M. (2017). Porth pathophysiology: Concepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. King, T. E., Jr. (2018, November 29). T reatment and progno-sis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss). In H. Hollingsworth (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/treatment-and-prognosis-of-eosinophilic-granulomatosis-with-polyangiitis-churg-strauss14. Immune System, Connective Tissue, and Joints Guidelines322	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Merkel, P. A. (2019, March 1). Overview of and approach to the vas-culitides in adults. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-and-approach-to-the-vasculitides-in-adults Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Vasculitis-Medium Vessel Dana Cafaro Definition A. Part of a group of disorders that result from inflammatory changes to walls of veins and arteries, causing damage to the mural structures, which ultimately may cause tissue ischemia and necrosis. B. Nomenclature is changing for the specific forms of vas-culitis based on the Chapel Hill Consensus Conference (CHCC). C. Several different types. 1. Polyarteritis nodosa. 2. Kawasaki disease (more common in peds). 3. Buerger disease (thromboangiitis obliterans). 4. Primary angiitis of the central nervous system. Incidence A. Polyarteritis nodosa. 1. Not common: 30 cases per 1 million people. 2. Males affected more than females; common age pre-sentation is in sixth decade. B. Buerger disease (thromboangiitis obliterans). 1. Typical patient is a young, male smoker using raw tobacco. C. Primary angiitis of the central nervous system. 1. Rare disorder with male predominance. 2. Can occur at any age, with median age being 50 years old. Pathogenesis A. Vasculitis can be a primary pathology or can be secondary to another underlying disease process. B. Direct injury to the vessel, infectious agents, or immune processes are known to cause vasculitis. C. Secondary vascular injury may occur from physical agents such as cold and irradiation, mechanical injuries, and toxins. D. Polyarteritis nodosa. 1. First form of vasculitis reported. 2. Predilection for vessels of skin, peripheral nerves, mesenteric vessels, renal vessels, heart, and brain. 3. 10% of cases caused by hepatitis B infection. E. Buerger disease (thromboangiitis obliterans). 1. Highly cellular and inflammatory occlusive thrombus affecting the extremities. F. Primary angiitis of the central nervous system. 1. Vasculitis affecting brain and spinal cord. Predisposing Factors A. Male gender. B. Use of raw tobacco for Buerger disease. Subjective Data A. Common complaints/symptoms. 1. Polyarteritis nodosa. a. Arthralgia, myalgia, and neuropathy. b. Skin manifestations include lower extremity malleoli skin ulcerations (most common), digital gangrene, livedo reticularis, and subcutaneous nod-ules. c. Acute abdomen presentation when abdominal vessels are affected including abdominal pain, nausea, and vomiting. d. Hypertension when renal vessels are affected. 2. Buerger disease (thromboangiitis obliterans). a. Distal extremity ischemia, ischemic digit ulcers, digit gangrene, migratory phlebitis. 3. Primary angiitis of the central nervous system. a. Weeks to months of headaches, encephalopathy, and multifocal strokes. B. Common/typical scenario. 1. Patients will complain of various symptoms upon pre-sentation that may be mistaken for other diseases. 2. In polyarteritis nodosa, patients commonly present with acute abdominal pain. 3. In Buerger disease, patients present with pain in their extremities; in primary angiitis, patients may present with strokes. C. Family and social history. 1. Buerger disease: Use of raw tobacco. D. Review of systems. 1. Arthralgias. 2. Myalgias. 3. Paresthesias. 4. Skin changes. 5. Abdominal pain. 6. Nausea, vomiting. 7. Headaches. 8. Ataxia. Physical Examination A. Polyarteritis nodosa. 1. Ulcerations on malleoli. 2. Motor and sensory deficits. 3. Digital gangrene. B. Kawasaki disease (more common in peds). 1. Bilateral conjunctivitis without exudate. 2. Lip and oral erythema. 3. Cervical lymphadenopathy. 4. Rash. 5. Edema of hands and feet. C. Buerger disease (thromboangiitis obliterans). 1. Superficial phlebitis. 2. Digit ischemia. D. Primary angiitis of the central nervous system. 1. Motor and sensory deficits. Diagnostic Tests A. Polyarteritis nodosa. 1. Anemia and leukocytosis. 2. Antineutrophil cytoplasmic antibodies (ANCA) neg-ative. 3. Elevated C-reactive protein (CRP) and elevated ery-throcyte sedimentation rate (ESR). 4. Hepatitis B screening. 5. Biopsy and angiogram of vessels and organs. B. Buerger disease (thromboangiitis obliterans). 1. Normal CRP, ESR, immunologic panel, hypercoagu-lability screen, and toxicology screen. 2. Positive anticardiolipin antibodies. 3. Consider arteriogram of upper and lower extremities and aorta. Vasculitis-Medium Vessel323	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
C. Primary angiitis of the central nervous system. 1. Cerebrospinal fluid (CSF): Leukocytosis with increased protein. 2. Angiograms: String of beads pattern. 3. Positive brain biopsy. 4. Clinical diagnosis made by ruling out infection, neo-plasm, metabolic disorder, and cocaine use. Differential Diagnosis A. Other forms of vasculitis. B. Thromboembolic events. Evaluation and Management Plan A. General plan. 1. Symptom management. 2. Exercise and healthy lifestyle changes. 3. Buerger disease (thromboangiitis obliterans). a. Smoking cessation is the cornerstone of treatment. b. Local wound care. c. Pneumatic compression and spinal cord stimula-tion for pain due to ischemia. B. Patient/family teaching points. 1. T reatment of vasculitis with corticosteroids or other immunocompromising medications causes an immuno-compromised state. 2. Corticosteroids can lead to complications with dia-betes, weight gain, or osteoporosis. C. Pharmacotherapy. 1. Polyarteritis nodosa. a. Prednisone 60 mg orally daily. b. Methylprednisolone 1,000 mg intravenous (IV) daily for 3 days for the critically ill. c. Immunosuppressive agents for moderate to severe disease. 2. Buerger disease (thromboangiitis obliterans). a. Calcium channel blockers for vasospasm. 3. Primary angiitis of the central nervous system. a. Corticosteroids and cyclophosphamide. Follow-Up A. Interval follow-up based on severity of disease. Consultation/Referral A. Refer to rheumatology. Special/Geriatric Considerations A. There are no specific age-related considerations in vasculitis-medium vessel. Bibliography Hajj-Ali, R. A., & Calabrese, L. H. (2017, July 3). Primary angi-itis of the central nervous system in adults. In M. Ramirez Cur-tis (Ed. ), Retrieved fromhttps://www. uptodate. com/contents/primary-angiitis-of-the-central-nervous-system-in-adults Hannon, R. A., & Porth, C. M. (2017). Porth pathophysiology: Concepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Merkel, P. A. (2019, March 1). Overview of and approach to the vas-culitides in adults. In MRamirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-and-approach-to-the-vasculitides-in-adults Olin, J. W. (2018, September 20). Thromboangiitis obliterans (Buerger's disease). In K. A. Collins (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/thromboangiitis-obliterans-buergers-disease Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Sundel, R. (2018, November 13). Kawasaki disease: Clinical fea-tures and diagnosis. In E. Te Pas (Ed. ), Up To Date. Retrieved fromhttps://https://www. uptodate. com/contents/kawasaki-disease-clinical-features-and-diagnosis Vasculitis-Large Vessel Dana Cafaro Definition A. Part of a group of disorders that result from inflammatory changes to walls of veins and arteries, causing damage to the mural structures which ultimately may cause tissue ischemia and necrosis. B. Nomenclature is changing for the specific forms of vas-culitis based on the Chapel Hill Consensus Conference (CHCC). C. T wo main types. 1. Takayasu arteritis. 2. Giant cell arteritis/temporal arteritis. Incidence A. Takayasu arteritis. 1. Common in Asian descent. 2. Women are typically more affected than men. 3. Age of onset tends to be early adulthood. B. Giant cell arteritis/temporal arteritis. 1. Most common vasculitis (UTD). 2. Afflicts more females than males; age greater than 50 with the most common presenting age between 70 and 79. 3. Common in Scandinavian descent. Pathogenesis A. Vasculitis can be a primary pathology or can be secondary to another underlying disease process. B. Direct injury to the vessel, infectious agents, or immune processes are known to cause vasculitis. C. Secondary vascular injury may occur from physical agents such as cold and irradiation, mechanical injuries, and toxins (P). D. Takayasu arteritis. E. Granulomatous vasculitis of aorta and its major branches (C). F. Possible immunogenetic predisposition (U). G. Giant cell arteritis/temporal arteritis. 1. Chronic inflammatory disease of cranial branches of carotid arteries. Predisposing Factors A. Female gender, age typically over 60 years old. B. Some familial pattern. Subjective Data A. Common complaints/symptoms. 1. Constitutional symptoms are common with all size vessel vasculitis and include fever, weight loss, malaise, and arthralgias/arthritis. 2. Large vessel vasculitis will often present with limb claudication, asymmetric blood pressures, absence of pulses, bruits, and aortic dilatation. 3. Takayasu arteritis. a. Decreased pulses. b. Unequal upper extremity blood pressures. c. Carotid and subclavian artery bruits. d. Limb claudication and hypertension. 14. Immune System, Connective Tissue, and Joints Guidelines324	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
4. Giant cell arteritis/temporal arteritis. a. Headache, scalp tenderness. b. Visual changes, such as amaurosis fugax. c. Jaw claudication. d. Throat pain. e. Temporal artery tenderness. B. Common/typical scenario. 1. See previous sections for common/typical scenario. C. Family and social history. 1. Inquire about family history of vasculitis. D. Review of systems. 1. See previous sections for review of systems. Physical Examination A. Cardiology. 1. Decreased pulses. 2. Unequal upper extremity blood pressures. 3. Carotid and subclavian artery bruits. B. Limb claudication and hypertension. C. Headache, scalp tenderness. D. Visual changes, such as amaurosis fugax. E. Jaw claudication. F. Throat pain. G. Temporal artery tenderness. Diagnostic Tests A. Takayasu arteritis. 1. Elevated C-reactive protein (CRP) and elevated ery-throcyte sedimentation rate (ESR). 2. MRI or CT angiography (CTA) of affected vessels. B. Giant cell arteritis/temporal arteritis. 1. Normochromic anemia, normal leukocytes, decreased serum albumin, elevated liver enzymes, and elevated CRP and ESR. 2. Best diagnostic test to confirm is temporal artery biopsy (UTD). 3. In patients with normal temporal artery biopsy, con-sider magnetic resonance angiography (MRA) or CTA for confirmation. Differential Diagnosis A. Other forms of vasculitis. B. Nonarteritic anterior ischemic optic neuropathy (NAAION). Evaluation and Management Plan A. General plan. 1. Giant cell arteritis: Early intervention is necessary to prevent blindness, which can become permanent. B. Patient/family teaching points. C. Pharmacotherapy. 1. Takayasu arteritis. a. Prednisone 1 mg/kg orally for 1 month; then tapered over several months to 10 mg orally daily. b. Methotrexate and mycophenolate mofetil may also be helpful. 2. Giant cell arteritis/temporal arteritis. D. Must be initiated quickly to avoid permanent blindness; therefore, if clinically suspected begin treatment. E. Visual loss present at time of diagnosis: Intravenous (IV) methylprednisone 1,000 mg IV daily for 3 days followed by oral steroids (UTD). F. Prednisone 60 mg po daily ×1 month then taper dose. G. Low dose aspirin—81 mg po daily. Follow-Up A. Giant cell arteritis. 1. Follow-up should be monthly for 6 months if possible and then spaced accordingly. 2. Consider ophthalmology consult for visual symp-toms. B. Takayasu arteritis. 1. Requires regular monitoring. Consultation/Referral A. Refer to rheumatology. Special/Geriatric Considerations A. Chronic steroid use can cause osteoporosis, so considera-tion should be made to treat osteoporosis. Bibliography Docken, W. P. (2018, August 13). T reatment of giant cell arteri-tis. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/treatment-of-giant-cell-temporal-arteritis?source=see_link Docken, W. P. (2018, October 5). Diagnosis of giant cell arteri-tis. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/diagnosis-of-giant-cell-arteritis? topic Ref=8240&source=related_link#H18 Docken, W. P., & Rosenbaum, J. T. (2017, December 8). Clin-ical manifestations of giant cell arteritis. In M. Ramirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ clinical-manifestations-of-giant-cell-temporal-arteritis Hannon, R. A., & Porth, C. M. (2017). Porth pathophysiology: Concepts of altered health states (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Merkel, P. A. (2019, March 1). Overview of and approach to the vas-culitides in adults. In MRamirez Curtis (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-and-approach-to-the-vasculitides-in-adults Papadakis, M. A., Mc Phee, S. J., & Rabow, M. W. (2016). Current medical diagnosis & treatment 2016. New York, NY: Mc Graw Hill Education. Vasculitis-Large Vessel325	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
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327 15 Dermatology Guidelines Amber Tran Atopic Dermatitis Amber Tran Definition A. Dermatitis means inflammation of the skin. It is a broad description describing an abnormal finding of the skin. Causes may be mechanical, environmental, allergic, viral, bacterial, fungal, parasitic, inflammatory, autoimmune (drug, lupus, psoriasis), neoplastic, and occasionally a com-bination. Treatment requires removing the offending agent and decreasing the inflammation to allow the skin to repair. B. The most important thing for the new acute care advanced practice provider (APP) is to differentiate and determine whether a skin finding is acute, chronic, and/or emergent. If it is emergent, decide whether it is a condition you can treat yourself or if it requires a consult for dermatol-ogy, or if other hospital team specialists are needed. C. Chronic pruritic inflammatory skin disease is common on flexural areas; this is associated with allergic rhinoconjunc-tivitis, asthma, and food allergies. D. Most develop rash after scratching. Incidence A. May occur at any age. 1. Typically starts in childhood and may continue through adulthood. 2. About 1% to 3% of adults. B. In past few decades, it has increased to around 30% for most industrialized countries versus around 10% in other countries. C. High latitude. D. Peaks during cold dry weather. Pathogenesis A. Thought to be caused by defective skin barrier for heal-ing and maintaining skin integrity, but true cause remains unknown. Predisposing Factors A. Family history of atopic dermatitis (AD). B. Breakdown of skin. 1. Dry skin. 2. Abrasion or injury. 3. Contact dermatitis (allergies, irritants). C. Seasonal, environmental, or food allergies. D. Dry weather. E. Heat. F. Stress. Subjective Data A. Common complaints/symptoms. 1. Itch. 2. Dry skin patches. 3. Burning. B. Common/typical scenario. 1. Chronic rash that comes and goes. a. Worse in cooler months; better in summer. b. Flares with different exposures and seasons. C. Family and social history. 1. Family history of AD. 2. Frequent hand washer or bather. D. Review of systems. 1. Usually negative except for cold hands/feet. 2. Seasonal allergies. Physical Examination A. Dry erythematous patches. B. Lichenification of older lesions. C. Crusting and oozing may happen with and without infec-tion (may be impetiginized). D. Excoriations (scratched areas). E. Locations tend to be on face and flexural folds of neck, arms, trunk, legs, wrists, and ankles (see Figure 15. 1A and 15. 1B). Diagnostic Tests A. Potassium hydroxide (KOH) preparation should be negative. B. Skin biopsy: New lesions are preferred over older lesions that have either been lichenified or “burnt out”; hyperpig-mented macules and patches may represent postinflamma-tory hyperpigmentation and not active rash. Differential Diagnosis A. Tinea (corporis, gruris, versicolor, manis, pedis). B. Seborrheic dermatitis. C. Stasis dermatitis. D. Scabies. E. Psoriasis. F. Contact dermatitis. G. Molluscum contagiosum. H. Mycosis fungoides/cutaneous T cell lymphoma. Evaluation and Management Plan A. General plan. 1. Avoid triggers. 2. Avoid exacerbations (dry heat, excessive washing/ bathing, contact with irritants, or use of irritants). Atopic Dermatitis	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
328 A B FIGURE 15. 1 Examplesof AD on the (A) face and (B) arms/trunk. AD, atopic dermatitis. Sources: (A) Lyons,F.,& Ousley,L. (2015). Dermatology for the advanced practice nurse. New York,NY:Springer Publishing Company; (B) Courtesy of Centers for Disease Controland Prevention. 3. Maintain skin integrity through moisturization and decreasing inflammation. B. Patient/family teaching points. 1. Practice gentle skin care. a. Limit bathing to 5 minutes once daily at the most. b. Limit soap use. c. Use gentle nonsoap cleansers only. d. Do not use loofah or washcloth, only use hands to wash body. e. Only wash “dirty” areas: Face, axilla, genitalia, groin, hands, and feet. f. When drying after bathing pat skin dry gently; do not rub. g. For flares, apply topical medications within 5 min-utes of leaving shower/bath. h. For nonflared areas and daily maintenance, apply moisturizer within 5 minutes of leaving shower/bath. i. Avoid wool clothing. j. Use hypoallergenic laundry detergents, hand soaps, body soaps, facial cleansers, and moisturizers. k. Use humidifier. 2. Decrease stress. 3. Avoid scratching. 4. Treat early to help limit amount of topical/oral steroids needed. C. Pharmacotherapy. 1. Topical cream. a. Moisturizers. i. Lotions: Tend to not hold moisture in skin despite containing more water than creams and ointments. ii. Creams: Help lock in moisture better than lotions. Examples: Aveeno cream, Cetaphil cream, Cera Ve cream, Eucerin cream, Lubriderm cream, Vanicream. iii. Ointments: Help lock in moisture better than creams. Examples: Vaseline, petroleum jelly. iv. Barrier creams: Zinc oxide. 2. Topical steroid, typically twice daily for two consecu-tive weeks. 15. Dermatology Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
329 a. Low potency for face, neck, groin, inner thighs, and buttocks. b. Medium potency for other areas. c. High potency for hands and feet. 3. Oral steroid: Prednisone. 4. Antihistamines. a. Low to medium strength: Claritin, Zyrtec, Benadryl. b. Medium to high strength: Hydroxyzine. 5. Phototherapy: Refer to dermatology. 6. Treat any secondary infections with oral therapy (viral, bacterial). D. Discharge instructions (if standard accepted guidelines exist please use discharge template): If develops systemic signs of toxicity return to emergency department (ED). Follow-Up A. Primary care provider in 1 week. B. Dermatology in 1 to 3 months depending on severity. Consultation/Referral A. If persists or worsens despite treatment, consult or refer to dermatology. B. If diffuse, always refer to dermatology to rule out cutaneous lymphoma or another erythroderma. Cutaneous lymphoma is difficult to diagnosis and may take several skin biopsies before diagnosis is made. Special/Geriatric Considerations A. Controlling other allergies is essential. B. Poor compliance and poor education will likely lead to longer duration of flares and worsening of them; consistent early treatment is best. C. Elderly patients all develop drier and thinner skin with age, making it harder to clear and prevent flares. Bibliography Buttaro, T., Trybulski, J., Polgar Bailey, P., & Sandberg-Cook, J. (2013). Primary care—E-book (4th ed. ). St. Louis, MO: Elsevier. Fitzpatrick, J., & Morelli, J. (Eds. ). (2011). Dermatology secrets plus (4th ed. ) Philadelphia, PA: Elsevier. Habif, T., Campbell, J. L., Jr., Chapman, M. S., Dinulos, J. G. H., & Zug, K. A. (2011). Skin disease (3rd ed. ). Edinburgh, Scotland: Saunders/ Elsevier. Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse. New York, NY: Springer Publishing Company. Nutten, S. (2015). Atopic dermatitis: Global epidemiology and risk factors. Annals of Nutrition and Metabolism, 66 (Suppl. 1), 8-16. doi:10. 1159/ 000370220 Cellulitis Amber Tran Definition A. Soft tissue infection primarily involving the skin that spreads and is frequently characterized by redness, warmth, swelling, and pain. B. Cellulitis commonly occurs when there is a break in the skin. C. An abscess may or may not be involved. Incidence A. May occur at any age. B. More common in males. C. May occur after an abrasion or surgical incision. D. Typically in extremities, especially lower extremities. E. Highly seasonal, more likely to occur during warmer summer months. F. Costs $3. 74 billion annually; 30% of patients diagnosed with cellulitis are misdiagnosed, leading to unnecessary hos-pitalization and antibiotic use. Pathogenesis A. Most commonly caused by Group A beta-hemolytic streptococcus or methicillin-susceptible Staphylococcus aureus (MSSA). B. Other less common causes. 1. Other beta-hemolytic streptococcus. 2. Methicillin-resistant Staphylococcus aureus (MRSA). 3. Streptococcus pyogenes (presents with lymphangitis). 4. Pseudomonas aeruginosa. 5. Erysipelothrix rhusiopathiae from contact with raw meat (poultry, fish, other meat) typically seen in butchers or other handlers. 6. Vibrio species from saltwater swimming, sea urchin impalement, or contact with raw seafood. 7. Aeromonas hydrophilia from fresh water swimming. 8. Pasteurella multocida from animal bite or injury. Predisposing Factors A. Injury or cut in affected area (abrasion, surgical incision, intravenous (IV) drug abuse, insect/animal bites, etc. ). B. Previous cellulitis. C. Decreased mobility. D. Impairment of vascular-lymphatic system. 1. Venous insufficiency. 2. Lymphedema due to impaired lymphatic drainage. 3. Lymph node resection. 4. Prior radiation treatments to affected area. E. Chronic comorbidity conditions. 1. Malnourishment, obesity, diabetes, chronic kidney disease, chronic liver disease, alcohol abuse. 2. Immunosuppression (HIV, cancer, taking immuno-suppressive agents). 3. Tinea pedis or other dermatitis-affected skin integrity. Subjective Data A. Common complaints/symptoms. 1. Elicit onset and duration of symptoms. 2. Edema. 3. Erythema. 4. Tenderness or pain. B. Common/typical scenario. 1. Expanding sore erythematous edematous patch on lower extremity for 1 to 2 days, possibly near recent wound or injury. C. Family and social history. 1. Alcohol abuse. 2. IV drug abuse. 3. Any trauma to affected areas. D. Review of systems. 1. May have malaise. 2. Fevers. 3. Chills. 4. Regional lymphadenopathy. 5. Decreased mobility due to pain or swelling. Physical Examination A. One extremity (if bilateral it is very unlikely to be celluli-tis. Stasis dermatitis is often bilateral and frequently misdiag-nosed as cellulitis). Cellulitis	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
330 B. Usually a somewhat well-demarcated erythematous patch (a sharply demarcated indurated border increases likelihood of erysipelas; see Figure 15. 2). C. Tender. D. Mild to moderate swelling. E. Sometimes regional lymphadenitis (tender or enlarged) or lymphangitis. F. Rarely blisters, necrosis. G. If palpate warmth, need to rule out deep vein thrombosis (DVT). H. If exquisite tenderness and rapid progression occurs, rule out necrotizing fasciitis. I. Systemic signs of toxicity: Fever, hypotension, tachycar-dia. Diagnostic Tests A. Culture—when purulent discharge is present. Majority cannot be cultured unless abscess present for incision and drainage. B. Biopsy—poor healing and low diagnostic yield. C. Lab—elevated sedimentation rate and leukocytosis. Differential Diagnosis A. Stasis dermatitis. B. Lipodermatosclerosis. C. DVT. D. Folliculitis. E. Insect bite reaction. F. Contact dermatitis. G. Erysipelas. H. Necrotizing fasciitis. Evaluation and Management Plan A. General plan. 1. Antibiotics coverage for either gram-positive (most common), MRSA, or gram-negative (rare). 2. Keep affected extremity raised. A B FIGURE 15. 2 (A)An example of cellulitis. (B) Cellulitis resultingfroma vaccination for varicella. Source:Lyons,F.,& Ousley,L. (2015). Dermatology for the advanced practice nurse. New York,NY:Springer Publishing Company. 15. Dermatology Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
331 3. Draw line on borders to monitor improvement or worsening. 4. If drainable abscess, incise and drain affected lesion. 5. If systemic symptoms present, check blood cultures first then initiate IV antibiotics. 6. Point of care ultrasound to differentiate abscess from cellulitis (which usually has cobblestone appear-ance). B. Patient/family teaching points. 1. Keep affected extremity elevated. 2. Bathe once daily and clean area once daily with gentle soap and water. 3. Do not squeeze or irritate area. 4. If pain or rash is worsening, notify provider. C. Pharmacotherapy. 1. Antibiotics for staphylococcus and streptococcus cov-erage: Dicloxacillin, azithromycin, clarithromycin, cel-phalexin, or cefazolin for 5 days. 2. Antibiotics for MRSA coverage: Clindamycin, trimethoprim-sulfamethoxazole, doxycycline, minocy-cline, linezolid, or tedizolid for 5 to 10 days. 3. Antibiotics for those with systemic signs of toxicity or who have extensive skin involvement, close proximity to indwelling medical device, inability to tolerate oral ther-apy, prior episode of MRSA or known colonization, or lack of response to antibiotic regimen that does not cover for MRSA. a. Empiric IV therapy for MRSA: Vancomycin or daptomycin. b. Once signs of infection are resolving, switch to oral regimen with coverage for MRSA and strepto-coccus. 4. Antibiotics for those with systemic signs of toxicity or who have extensive skin involvement with at least one of the following: Perioral/perirectal abscess, possible con-nection to pressure ulcer, or skin necrosis. a. Empiric IV therapy for MRSA. b. Start vancomycin or daptomycin with another antibiotic(s) to cover for gram-positive, gram-negative, and anaerobes. D. Discharge instructions. 1. Complete course of antibiotics as directed by the provider. 2. Review with patient the common side effects of given antibiotic treatment (nausea, diarrhea, rash, and thrush/yeast infections). 3. Keep affected extremity elevated. 4. Warm compresses to affected area. 5. Avoid Neosporin to area as this can cause an allergic contact dermatitis. 6. If condition worsens, return to office. Follow-Up A. PCP in 1 to 2 days. B. Dermatologist in 3 days. C. If worsening or develops signs of systemic toxicity, patient should return to ED. Consultation/Referral A. If periorbital or orbital cellulitis, consult physician or infectious disease. B. If no improvement within 24 to 48 hours of starting antibiotic therapy, consult infectious disease or dermatology. C. If recurrent, consult/refer to dermatology and infectious disease. Special/Geriatric Considerations A. See section “Predisposing Factors. ” Many patients with cellulitis have comorbidities. B. Immunosuppressed individuals have higher risk for com-plications such as necrotizing fasciitis, lymphangitis, gan-grene, and severe sepsis. C. Use extra caution with patients who have prosthetic joints or recent surgeries. D. If patient has history of another known skin rash such as psoriasis, atopic dermatitis, or other, may be best to consult dermatology. Bibliography Cranendonk, D., van Vught, L., Wiewel, M., Cremer, O., Horn, J., Bonten, M., & Wiersinga, W. (2017). Clinical characteristics and outcomes of patients with cellulitis requiring intensive care. Journal of the American Medical Association Dermatology, 153 (6), 578-582. doi:10. 1001/jamadermatol. 2017. 0159 Dalal, A., Eskin-Schwartz, M., Mimouni, D., Ray, S., Days, W., Hodak, E.,... Paul, M. (2017). Interventions for cellulitis and erysipelas: A sum-marised Cochrane review. Cochrane Database System Review, 2017 (6), 227-228. doi:10. 1002/14651858. CD009758. pub2 Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse. New York, NY: Springer Publishing Company. Marcelin, J., Challener, D., Tan, E., Lahr, B., & Baddour, L. (2017). Incidence and effects of seasonality on nonpurulent lower extremity cellulitis after the emergence of community-acquired methicillin-resistant Staphylococcus aureus. Mayo Clinic Proceedings, 92 (8), 1227-1233. doi:10. 1016/j. mayocp. 2017. 04. 008 Mc Creary, E., Heim, M., Schulz, L., Hoffman, R., Pothof, J., & Fox, B. (2017). Top 10 myths regarding the diagnosis and treat-ment of cellulitis. The Journal of Emergency Medicine, 53, 485-492. doi:10. 1016/j. jemermed. 2017. 05. 007 Murphy-Lavoie, H., & Le Gros, T. L. (2010). Emergent diagno-sis of the unknown rash: An algorithmic approach. Emergency Medicine, 42 (3), 6-17. Retrieved from https://www. mdedge. com /emergencymedicine/article/71662/dermatology/emergent-diagnosis-of-the-unknown-rash-algorithmic-approach Peterson, R., Polgreen, L., Cavanaugh, J., & Polgreen, P. (2017). Increas-ing incidence, cost, and seasonality in patients hospitalized for cellulitis. Open Forum Infectious Diseases, 4 (1), ofx008. doi:10. 1093/ofid/ofx008 Santistevan, J., Long, B., & Koyfman, A. (2017). Rash decisions: An approach to dangerous rashes based on morphology. The Journal of Emer-gency Medicine, 52 (4), 457-471. doi:10. 1016/j. jemermed. 2016. 10. 027 Spelman, D., & Baddour, L. (2017). Cellulitis and skin abscess in adults: Treatment. In E. L. Baron (Ed. ), Up To Date. Retrieved from https: //www. uptodate. com/contents/cellulitis-and-skin-abscess-in-adults-treatment Weng, Q., Raff, A., Cohen, J., Gunasekera, N., Okhovat, J. P., Vedak, P., & Mostaghimi, A. (2017). Costs and consequences associated with mis-diagnosed lower extremity cellulitis. JAMA Dermatology, 153 (2), 141-146. doi:10. 1001/jamadermatol. 2016. 3816 Seborrheic Dermatitis Amber Tran Definition A. Chronic inflammatory superficial disease that mainly affects body oil baring surfaces such as scalp, brows, nasolabial folds, ears, chest, and groin. Incidence A. 3% to 5% of general population. B. 40% to 80% of HIV population. Pathogenesis A. Caused by Malassezia furfur, lipophilic yeast that can overgrow in oily areas of the body. Seborrheic Dermatitis	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
332 Predisposing Factors A. Stress. B. Neurological disease (Parkinson's disease, stroke). C. Rosacea or other oily skin. D. Hormonal imbalance (diabetes, polycystic ovarian syn-drome [PCOS]). E. Immunosuppression (HIV common in diffuse and treatment-resistant forms). Subjective Data A. Common complaints/symptoms. 1. Itch. 2. Scale/flakes. 3. Greasy hair. B. Common/typical scenario. 1. Chronic itchy flaky scalp for years. 2. Better with more frequent hair washing. 3. Worse in summer. C. Family and social history. 1. Typically negative. 2. May have other family members with seborrheic der-matitis. D. Review of systems. 1. Typically negative. Physical Examination A. Yellow greasy scale on erythematous plaques; can be annular or polycyclic. B. Mostly found on scalp (see Figure 15. 3), brows, nasolabial folds, nasal alae, conchal bowls, and postauricular, sometimes on neck, chest, axillae, or groin folds. Diagnostic Tests A. KOH preparation should demonstrate hyphae. B. Fungal culture —especially if suspicion for tinea is in dif-ferential diagnosis. C. Skin biopsy —helpful for odd presentations that overlap with other dermatoses. Differential Diagnosis A. Tinea (capitis, corporis, cruris, versicolor). B. Pityriasis rosacea. C. Psoriasis. D. Contact dermatitis. E. Drug eruption. F. Lupus erythematous. Evaluation and Management Plan A. General plan. 1. Decrease oils on scalp and other affected areas. 2. Decrease scale and itch. B. Patient/family teaching points: Wash scalp more fre-quently, focus on scalp more than hair. C. Pharmacotherapy. 1. Topical antifungals. a. For face and body. i. Ketoconazole 2% cream once daily to affected areas for 2 weeks. ii. Ciclopirox 0. 77% cream twice daily to affected areas for 2 to 4 weeks. b. For scalp. i. Ketoconazole 1% to 2% shampoo twice weekly; leave on damp scalp for 5 minutes, then rinse; repeat for 4 to 8 weeks. ii. Ciclopirox 1% shampoo twice weekly; leave on scalp damp for 5 minutes, then rinse; repeat for 2 to 4 weeks. iii. Selenium sulfide 1% to 2. 5% shampoo or lotion twice weekly; leave on damp scalp for 5 minutes, then rinse; repeat for 2 to 4 weeks. 2. Topical steroids for itch and irritation only. a. For face: Hydrocortisone 1% to 2. 5% cream twice daily for 5 days. b. For scalp: Mometasone 0. 1% solution nightly on affected areas of scalp after showers for 3 weeks. D. Discharge instructions. FIGURE 15. 3 Seborrheicdermatitis. Source:Lyons,F.,& Ousley,L. (2015). Dermatology for the advanced practice nurse. New York,NY:Springer Publishing Company. 15. Dermatology Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
333 1. Discuss risks of prolonged topical steroid use: Atrophy of skin, hypopigmentation of skin, risk for glaucoma if use is near eyes or hands are not washed after use. 2. May take a few weeks to improve. Follow-Up A. Dermatology in next 1 to 3 months. Consultation/Referral A. If persists or worsens, consult/refer to dermatology. Special/Geriatric Considerations A. Nursing home patients may have a hard time adhering to washing regimen. Bibliography Buttaro, T., Trybulski, J., Polgar-Bailey, P., & Sandberg-Cook, J. (2013). Primary care—E-book (4th ed. ). St. Louis, MO: Elsevier. Fitzpatrick, J., & Morelli, J. (2011). Dermatology secrets plus (4th ed. ). Philadelphia, PA: Elsevier. Habif, T. (2011). Skin disease. Edinburgh, Scotland: Saunders/Elsevier. Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse. New York, NY: Springer Publishing Company. Mameri, A., Carneiro, S., Mameri, L., Telles da Cunha, J., & Ramos-E-Silva, M. (2017). History of seborrheic dermatitis: Conceptual and clinico-pathologic evolution. Skinmed, 15 (3 ), 187-194. Yalçin, B., Tamer, E., Toy, G. G., Oztaş, P., Hayran, M., & Alli, N. (2006). The prevalence of skin diseases in the elderly: Analysis of 4099 geri-atric patients. International Journal of Dermatology, 45 (6), 672-676. doi:10. 1111/j. 1365-4632. 2005. 02607. x Stasis Dermatitis Amber Tran Definition A. Eczema-like inflammation of the lower extremities asso-ciated with impairment of the vascular-lymphatic system. Incidence A. Happens to 6. 2% of people equal to or older than 65 years old. Pathogenesis A. Caused by back flow of veins with leaking hemosiderin from congested blood vessels. Predisposing Factors A. Decreased mobility. B. Impairment of vascular-lymphatic system. 1. Venous insufficiency. 2. Lymphedema due to impaired lymphatic drainage. 3. Lymph node resection. 4. Prior radiation treatments to affected area. C. Chronic comorbidity conditions. 1. Malnourishment, obesity, diabetes, chronic kidney disease, chronic liver disease, alcohol abuse. 2. Immunosuppression (HIV, cancer, taking immuno-suppressive agents). 3. Tinea pedis or other dermatitis-affected skin integrity. Subjective Data A. Common complaints/symptoms. 1. Itch, erythema. 2. Dark patches. 3. Dry skin. 4. Sometimes swelling. B. Common/typical scenario. 1. Chronic rash that started on one lower leg at ankle and now is on both. 2. Sometimes itchy. 3. Happened over several weeks to months. C. Family and social history. 1. Smoker. D. Review of systems. 1. Usually negative. FIGURE 15. 4 Exampleof stasis dermatitis. Source:Lyons,F.,& Ousley,L. (2015). Dermatology for the advanced practice nurse. New York,NY:Springer Publishing Company. Stasis Dermatitis	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
334 Physical Examination A. Bronze to erythematous dry patch of skin with or without scale. B. On bilateral extremities, worst on ankles (see Figure 15. 4). C. Mild to moderate swelling. D. Rarely blisters, necrosis. E. If palpate warmth, need to rule out deep vein thrombosis (DVT). F. If exquisite tenderness and rapid progression occurs, rule out necrotizing fasciitis. Diagnostic Tests A. Culture: Usually negative, but can have secondary infec-tion when purulent discharge is present. Majority cannot be cultured unless abscess present for incision and drainage. B. Biopsy: Poor healing and low diagnostic yield. C. Doppler ultrasound (if suspect DVT). Differential Diagnosis A. Cellulitis. B. Lipodermatosclerosis. C. DVT. D. Venous ulcer. E. Insect bite reaction. F. Contact dermatitis. G. Skin cancer (squamous cell carcinoma). H. Erysipelas. I. Necrotizing fasciitis. Evaluation and Management Plan A. General plan. 1. Maintenance skin integrity. 2. Increase venous return. B. Patient/family teaching points. 1. Elevate legs daily for 30 minutes four to five times daily. 2. Compression stockings during daytime activities. C. Pharmacotherapy. 1. Topical steroids: Triamcinolone 0. 05% cream/ ointment twice daily for 2 weeks. D. Discharge instructions (if standard accepted guidelines exist please use discharge template). Follow-Up A. Dermatology. B. Follow-up in 1 to 3 months. Consultation/Referral A. If persists or worsens, consult/refer to dermatology. Special/Geriatric Considerations A. Elderly populations will have more difficulty with stay-ing active to prevent blood and fluid from pooling in lower extremities. Bibliography Buttaro, T., Trybulski, J., Polgar-Bailey, P., & Sandberg-Cook, J. (2013). Primary care—E-book (4th ed. ). St. Louis, MO: Elsevier. Fitzpatrick, J., & Morelli, J. (2011). Dermatology secrets plus (4th ed. ). Philadelphia, PA: Elsevier. Habif, T. (2011). Skin disease (pp. 160-163). Edinburgh, Scotland: Saun-ders/Elsevier. Lyons, F., & Ousley, L. (2015). Dermatology for the advanced practice nurse. New York, NY: Springer Publishing Company. Yalçin, B., Tamer, E., Toy, G. G., Oztaş, P., Hayran, M., & Alli, N. (2006). The prevalence of skin diseases in the elderly: Analysis of 4099 geri-atric patients. International Journal of Dermatology, 45 (6), 672-676. doi:10. 1111/j. 1365-4632. 2005. 02607. x15. Dermatology Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
16 Geriatric Guidelines Delirium Karen Sheffield O'Brien Definition A. Delirium includes five key characteristics as described in the Diagnostic and Statistical Manual of Mental Disorders (5th ed. ;DSM-5 ; American Psychiatric Publishing; needed for diagnosis). 1. Lack of attention and awareness. 2. Developed over hours to days with a change in base-line functioning. May fluctuate with the time of day. 3. Changes in cognition. 4. Not influenced by an existing neurocognitive disorder or state of arousal (e. g., coma). 5. Reasonable suspicion the change is caused by a medi-cal condition, substance addiction or withdrawal, or med-ication side effect. B. Additional features. 1. Hyper-or hypoactivity with alterations in sleep. 2. Emotional disturbance, some seeming psychotic, such as fear, euphoria, confusion, or depression. 3. Extremes of mood including agitation. 4. Sensory disturbances such as hallucinations. 5. Motor alterations including tremors. C. The terms acute confusional state,delirium, and encephalopathy are often used interchangeably. Incidence A. Age: More common in the aged, but can occur with any illness. B. Incidence. 1. Up to 50% of older surgical patients can experience delirium. 2. Highest rates found among ICU patients, followed by ED and hospice. C. Frequency: While once considered only a temporary con-dition common in ill patients, delirium is now associated with increased length of stay, rate of complications, and cost of hospitalization and, more importantly, in hospital mortal-ity rates. Pathogenesis A. Multifactorial. 1. Difficult to study in already ill patients. 2. Affects arousal and attention. a. Arousal and attention are affected by the reticular activation system (RAS). b. The nondominant parietal and frontal lobes govern attention. c. Cortical functions are needed for insight and judgment. 3. May be related to drug toxicity, inflammation from trauma, sepsis, surgery, neuronal injury, and environ-mental factors. Predisposing Factors A. Increase baseline vulnerability. 1. Underlying brain disease. 2. Advanced age. 3. Sensory impairment. 4. Use of restraints. B. Precipitate the disturbance. 1. Polypharmacy. 2. Infection. 3. Dehydration. 4. Immobility. 5. Malnutrition. 6. Bladder catheters. Subjective Data A. Common complaints/symptoms. 1. Feeling confused. 2. Hallucinations. 3. Difficulty maintaining attention. B. Common/typical scenario. 1. Patient with delirium is not able to give information or accurate details. 2. Family or caregivers will often seek medical attention for the patient or the patient is brought in through emer-gency services. C. Family and social history. 1. Inquire if the patient uses drugs or drinks alcohol. 2. Inquire about medications and recent travel. D. Review of systems. 1. Inquire about disturbances of consciousness. a. Change in level of awareness. b. Inability to focus. c. Loss of mental clarity. d. Family member may report “not acting like herself” or “not acting right. ” e. Distractible, usually noted in conversation. f. May have decreased level of consciousness (typical) or be hypervigilant (some situations like withdrawal). g. Day/night reversal. 2. Inquire about altered cognition. a. Memory loss. b. Disorientation. c. Difficulty with language and speech. d. Perceptual disturbances. i. Delusions. Delirium Frances M. Stokes and Karen Sheffield O'Brien335	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
ii. Hallucinations: Visual, auditory, or somatosensory. iii. Lack of insight. 3. Medications. a. Changes in medications, particularly any new medications, dose changes, or brand changes. 4. Changes in health status. 5. Note time of acute onset, fluctuation of symptoms, changes in consciousness, and decline. 6. Identify modifiable risk factors. a. Sensory impairment. b. Immobilization. c. Concurrent disease or illness. d. Metabolic derangements. e. Environment. f. Pain. g. Sleep deprivation. 7. Identify nonmodifiable risk factors. a. Dementia. b. Age older than 65. c. Multiple comorbidities. d. Renal or hepatic disease. Physical Examination A. Sometimes difficult with the delusional patient. B. Be alert for signs that may point to a cause of the delirium. 1. Diaphoresis may be postfebrile, indicating some type of infection. 2. Jaundice indicating hepatic failure. 3. Stigmata of drug use. 4. Smell of alcohol. 5. Indication of postictal state. 6. Indication of sepsis. C. Neurological examination is typically very difficult and can be misleading. Should assess : 1. Attention. 2. Arousal. 3. Motor function. 4. Senses. 5. Deep tendon reflexes. 6. Higher cognitive functioning. 7. Thought cohesiveness. Diagnostic Tests A. Confusion Assessment Method (CAM; see Exhibit 16. 1). 1. Standard screen for delirium. 2. Takes 5 minutes. 3. Has a method especially for ICU patients, including vented patients, called the CAM-ICU. B. Intensive care delirium screening checklist (ICDSC) is also used in the ICU setting (see Exhibit 16. 2). C. Mini Mental is not useful for this population. D. Use the history and physical examination to guide addi-tional diagnostic testing. 1. Labs for fluid/electrolyte disturbances, infections, tox-icities, metabolic disorders, shock states, and postopera-tive status. 2. Arterial blood gas (ABGs). 3. Liver function test (LFT), thyroid, and B12as with dementia. 4. EKG. E. Medication review is very important as toxicities are cul-prits in 30% of all cases of delirium. F. If no cause is found, further diagnostics are necessary. 1. CT/MRI head. 2. EEG. 3. Lumbar puncture. Differential Diagnosis A. Medical issues; determine if patient has a masked baseline dementia. B. T reat sundowning as delirium until all medical issues are ruled out. C. Wernicke's aphasia, bitemporal dysfunction, Anton's syn-drome, tumors, or trauma in the frontal region. D. Subacute brain lesions, stroke, or inflammation. Head injuries. E. Nonconvulsive status epilepticus. F. Dementia or primary psychiatric illness. Evaluation and Management Plan A. General plan. 1. T reat the underlying cause. 2. Supportive care. B. Patient/family teaching points. 1. T reat pain issues. 2. Encourage movement. 3. Avoid overstimulation. 4. Manage behaviors. 5. Family might need a sitter to assist with care. C. Pharmacotherapy. 1. Pharmacological treatment of delirium depends on cause. a. Removing medications may be the treatment. b. All medications should be evaluated for polyphar-macy interactions. 2. Use BEERS criteria for prescribing medications for the elderly. a. Behavioral control. i. Haloperidol. ii. Risperidol. iii. Quetiapine. b. Agitation. i. Haloperidol (first line). ii. Olanzapine (oral only). iii. Risperidone. c. Anxiolytics-benzodiazepine, such as lorazepam. d. Cholinesterase inhibitor, such as donepezil. D. Discharge instructions. 1. Behavioral management. a. Reorient patient frequently. b. Use large, visible clocks. c. An outside-facing window is preferable. d. Keep nighttime noise to a minimum. e. T ry to provide uninterrupted sleep overnight. f. Limit napping during the day. g. T ry to make the hospital room more like home. h. Allow family visits and support. 2. Safety. a. Consider a sitter to stay with the patient. Follow-Up A. Delirium usually subsides as the acute illness resolves. B. If delirium persists, additional diagnostics should be considered. Consultation/Referral A. Geriatric psychiatry may be consulted if the patient has behavioral issues or is unusually aggressive. B. Consult case management if placement outside the home will be required. C. Consult social work if there is any concern for drugs or alcohol or evidence of abuse or neglect. 16. Geriatric Guidelines336	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Special/Geriatric Considerations A. It may take geriatric patients 6 to 8 weeks to fully recover from a delirious event and they are at high risk of persistent delirium even if the cause is eliminated or treated. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Publish-ing. Bergeron, N., Dubois, M. J., Dumont, M., Dial, S., & Skrobik, Y. (2001). Intensive care delirium screening checklist: Evaluation of a new screening tool. Intensive Care Medicine, 27, 859-864. Folstein, M. F., Folstein, S. E., & Mc Hugh, P. R. (1975). “Mini-Mental state. ” A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12 (3), 189. Francis, J., Jr., & Young, G. B. (2014, August 22). Diagnosis of delirium and confusional states. In J. L. Wilterdink (Ed. ), Up To-Date. Retrieved from http://www. uptodate. com/contents/diagnosis-of-delirium-and-confusional-states Ouimet, S., Riker, R., Bergeron, N., Cossette, M., Kavanagh, B., & Skrobik, Y. (2007). Subsyndromal delirium in the ICU: Evidence for a disease spectrum. Intensive Care Medicine, 33, 1007-1013. Delirium EXHIBIT 16. 1 Confusion Assessment Method for the ICU (CAM-ICU) Worksheet Instructions : Toevaluate for the presenceof delirium in your patient, complete this clinical assessment everyshift (8-12 hours). CAM-ICUisavalidandreliabledeliriumassessmenttoolrecommendedbythe Societyof Critical Care Medicine(SCCM)inits2013Pain, Agitation, and Delirium (PAD)guidelines. Confusion Assessment Method CAM-ICU Criteria ✓Present FEATURE 1: Alteration/Fluctuation in Mental Status ■Is the patient'smental status differentthan his/her baseline? OR ■Has the patient had any fluctuation in mental status in the past 24 hours as evidenced by fluctuation on a sedation scale (e. g., RASS, GCS), or previous delirium assessment?If Yesfor either question ▸ FEATURE 2: Inattention 1: Alteration/Fluctuation in Mental Status Letters Attention Test: Tellthe patient “I am going to read to you a series of 10 letters. Whenever you hear the letter 'A,' squeeze my hand. ”If number of errors >2▸ SAVEAHAART Counterrors(each time patient fails to squeeze on the letter “A” and squeezes on a letterother than “A”). FEATURE 3: Altered LOC ■Presentif the RASS scoreis anything otherthan Alert and Calm (zero)OR ■If SAS is anything otherthan Calm (4). If RASS ≠0OR SAS≠4▸ FEATURE 4: Disorganized Thinking Yes/No Questions: Ask the patient to respond: 1. Willa stone float on water? 2. Aretherefish in the sea? 3. Does1 pound weigh morethan 2 pounds? 4. Canyou use a hammer to pound a nail? Counterrors(each time patient answers incorrectly). Commands: Ask the patient to follow your instructions: a. “Hold up this many fingers. ” (Holdtwo fingers up in frontof the patient. ) b. “Now do the same thing with the other hand. ” (Donotdemonstratethenumberof fingersthis time. ) ■If unable to move both arms, for part “b” of command ask patient to “Hold up one morefinger. ” Count errors if patient is unable to complete the entire command. If combined number of errors >1▸ If Features 1 and 2 are both present and either Features 3 or 4 are present: Delirium present CAM-ICU is positive, delirium is present. Delirium absent Copyright 2002, E. Wesley Ely,MD, MPH, and Vanderbilt University,all rights reserved. Adapted with permission. CAM-ICU, confusion assessment method for the ICU; GCS; Glasgow Coma Scale; LOC, level of consciousness. T ullmann, D. F., Mion, L. C., Fletcher, K., & Foreman, M. D. (2012). Delir-ium. In M. Boltz, E. Capezuti, T. Fulmer, & D. Zwicker (Eds. ), Evidence-based geriatric nursing protocols for best practice (4th ed., pp. 186-199). New York, NY: Springer Publishing Company. 337	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
EXHIBIT 16. 2 Intensive Care Delirium Checklist for Screening Intensive Care Delirium Screening Checklist (ICDSC) Worksheet ■Scoreyour patient over the entireshift. Components don'tall need to be presentat the same time. ■Components #1 through #4 require a focused bedside patient assessment. This cannot be completed when the patient is deeply sedatedor comatose (i. e., SAS =1or 2; RASS =-4 or-5). ■Components#5through#8arebasedonobservationsthroughouttheentireshift. Informationfromtheprior24hr(i. e.,fromprior1-2 nursingshifts) should be obtained for components #7 and #8. 1. Altered Level of Consciousness NO 0 1 Yes Deepsedation/coma over entireshift [SAS =1,2; RASS =-4,-5]=Notassessable Agitation[SAS =5,6,or7;RASS =1-4]atanypoint =1point Normalwakefulness [SAS =4; RASS =0] over the entireshift=0points Lightsedation [SAS =3; RASS =-1,-2,-3] =1point (if no recentsedatives) =0points (if recentsedatives) 2. Inattention NO 0 1 Yes Difficultyfollowinginstructionsorconversation;patienteasilydistractedbyexternalstimuli. Will notreliablysqueeze hands to spoken letter A: SAVEAHAART 3. Disorientation NO 0 1 Yes In addition to name, place, and date, does the patient recognize ICU caregivers? Does patient knowwhat kind of place he or she is in (list examples: Dentist'soffice,home, work, hospital)? 4. Hallucination, delusion, or psychosis NO0 1 Yes Ask the patient if he or she is having hallucinations or delusions (e. g., trying to catch an object thatisn'tthere). Is the patient afraid of the people or things aroundhim or her? 5. Psychomotor agitation or retardation NO0 1 Yes Either:(a)Hyperactivityrequiringtheuseofsedativedrugsorrestraintsinordertocontrolpoten-tiallydangerousbehavior(e. g.,pulling IVlinesoutorhittingstaff)OR(b)Hypoactiveorclinically noticeablepsychomotor slowing or retardation 6. Inappropriate speech or mood NO0 1 Yes Patient displays: Inappropriate emotion; disorganized or incoherent speech; sexual or inappro-priateinteractions; is either apathetic or overly demanding 7. Sleep-wake cycle disturbance NO0 1 Yes Either:Frequentawakening/ <4 hr sleep at night OR sleeping during much of the day 8. Symptom fluctuation NO0 1 Yes Fluctuationof any of the previoussymptoms over a 24 hr period. TOTAL SHIFT SCORE: (0-8) Score Classification 0 Normal 1-3 Subsyndromaldelirium 4-8 Delirium Source:Adapted from Bergeron,N., Dubois, M. J., Dumont, M., Dial, S., & Skrobik,Y. (2001). Intensive caredelirium screeningchecklist: Evaluation of a new screeningtool. Intensive Care Medicine, 27, 859-864; Ouimet, S., Riker,R., Bergeron,N., Cossette, M., Kavanagh, B., & Skrobik,Y. (2007). doi:10. 1007/s001340100909 Subsyndromaldelirium in the ICU: Evidence for a disease spectrum. Intensive Care Medicine, 33,1007-1013. doi:10. 1007/s00134-007-0618-y Dementia Karen Sheffield O'Brien Definition A. A major neurocognitive disorder in which the patient exhibits a significant cognitive decline in one or more of the areas described in the Diagnostic and Statistical Manual of Mental Disorders (5th ed. ; DSM-5 ). 1. Complex attention. 2. Executive function. 3. Language. 4. Learning and memory. 5. Perceptual-motor function. 6. Social cognition. B. The DSM-5 also states the impairment should be acquired and a decline from the patient's normal functioning, inhibit independence and activities of daily living (ADLs), and not be occurring during bouts of delirium or as a function of another mental condition (e. g., depression or schizophrenia). C. Alzheimer's disease (AD) accounts for most cases of dementia. While the term is often used interchangeably with dementia, AD only represents a single subtype of neurodegen-erative dementia. Neurodegenerative dementias are progres-sive and exhibit an insidious onset. Incidence A. Age: Typically over the age of 65; however, early onset dementia accounts for 40 to 100 cases per 100,000 people in the developed world. 16. Geriatric Guidelines338	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
B. Incidence: Alzheimer's dementia affects more than 5 mil-lion individuals over the age of 65, accounting for 80% of dementia cases, with vascular dementia second. Pathogenesis A. Dementia can be influenced by multiple pathologies and is disease specific. B. Types of dementia and selected pathophysiology. 1. Neurodegenerative (Alzheimer's, dementia with Lewy bodies, Parkinson's disease). 2. Vascular diseases (vascular, cerebral amyloid angiopa-thy, and angitis). 3. Infectious diseases (prion disease such as Creutzfeldt-Jakob disease [CJD; mad cow], herpes encephalitis, neurosyphilis). 4. Inflammatory and autoimmune (multiple sclerosis, para-and nonparaneoplastic, autoimmune diseases). 5. Neurometabolic disorders. 6. Other (traumatic encephalopathy, alcohol abuse, Wilson and Huntington diseases). a. Genetic. b. Malnutrition. Predisposing Factors A. Age (frequency increases with age). B. Positive family history. C. Female (could be related to life span). D. History of head trauma or cerebrovascular accident (CVA). E. Low education level. F. Environmental factors: Aluminum, mercury, and viruses. G. Physical condition and other medical factors (e. g., dia-betes, hypertension, and hypercholesterolemia). Subjective Data A. Common complaints/symptoms. 1. While memory is a problem, it is usually not men-tioned by the patient, but by the significant other or fam-ily. 2. Frequently cannot pinpoint the condition's onset; years may have passed with problems, but until a major change happens, such as needing to stop driving or a hos-pital admission, the patient may be mostly functional in his or her familiar environment. 3. Signs and symptoms. a. Difficulty maintaining new information or task. b. Inability to manage complex task like balancing a checkbook. c. Lapses in reasoning. d. Becoming lost in familiar places. e. Word finding issues. f. Changes in behavior. B. Common/typical scenario. 1. Patients typically start with subtle short-term memory changes, frequent forgetfulness, difficulty finding the right words, or difficulty completing tasks. 2. The patient may progress over months and years before coming to a provider. C. Family and social history. 1. Family history and first degree relatives may be impor-tant in AD. 2. Obesity and chronic sedentary lifestyle may increase risk. 3. Smoking, alcohol, and drug abuse increase risk of dementia. D. Review of systems. 1. Neurological: Ask about memory and any confusion or deficits in calculation and abstraction. 2. Psychological: Ask about depressed mood, hopeless-ness, or suicide tendencies or changes in personality. 3. Inquire about rate of onset of changes. 4. History from a reliable source including medications. Physical Examination A. Assessment and physical examination change with the type of dementia present. Motor, somatosensory, and visual functions may remain intact until later in the disease process. 1. Disorder of motion. 2. Eye movement. 3. Primary memory. 4. Performance on cognitive assessments. Diagnostic Tests A. Cognitive function. 1. Mini-Mental state examination (max score 30; less than 24 indicates possible dementia). a. Concentration. b. Language. c. Orientation. d. Memory. e. Attention. 2. Montreal cognitive assessment (max score 30; lower than 25 indicates possible dementia). 3. Clinical dementia rating (includes a caregiver). 4. Mini-Cog (clock draw and recall test). 5. Informant interview to ask caregivers about the patient's functioning. a. Issues with judgment. b. Lack of interest in usual activities. c. Repetition of questions, statements, stories. d. Difficulty learning new tools or household appliances. e. Inability to remember the month or year. f. Loss of ability to manage finances. g. Missing appointments. h. Persistent issues with thinking or memory. B. Physical examination. 1. Full neurological examination. 2. General physical examination to identify any medical illness that could account for deficits. 3. Motor examination to identify prior stroke or evidence of Parkinson disease or autoimmune issues. 4. Evaluation of sleeping habits. C. Lab studies (as recommended by the American Academy of Neurology). 1. Screen for B12deficiency. 2. Hypothyroidism. 3. Rapid plasma reagin (RPR) screening. 4. Complete blood count (CBC). 5. C omprehensive metabolic panel (CMP). 6. LFT. 7. Immune/autoimmune workup. 8. C erebrospinal fluid (CSF) analysis if infective cause is suspected. D. Imaging: Neuroimaging (as recommended by the Ameri-can Academy of Neurology) including CT or MRI and possi-bly electrophysiologic testing. E. Brain biopsy not recommended unless in vasculitis, cancers, or infection. F. Genetic testing is not recommended except for specific diseases in family history (e. g., Huntington disease). Dementia339	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Differential Diagnosis A. T reatable: Thyroid, vitamin deficiencies, tumor, drug and medication intoxication, chronic infection, and severe depres-sion. Once these are ruled out, the differential is among the types of dementia. B. Structural: Cortical and hippocampus atrophy leads to AD. C. Psychiatric history with pharmacological treatment may be drug related. D. Associated: Gait disturbances could be vascular or Lewy body, including Parkinson, which may be based on time of onset. E. Rapid onset could be CJD or frontotemporal dementia. F. For early onset (under the age of 65): There is a much broader list of differentials and requires more extensive testing. Evaluation and Management Plan A. General plan. 1. Includes finding and correcting any reversible causes. a. Vitamin or thyroid replacements. b. Stopping contributing medications or starting medications for contributing conditions such as depression. c. T reating any structural dysfunction such as neo-plasms or increased intracranial pressure. d. T reating any infections contributing to mental status. 2. When no correctable cause is found, supportive care for the patient and the caregiver is warranted. 3. Diet. a. Patients with dementia often have decreased appetite for a variety of reasons. b. When possible, provide food to support adequate nutrition. c. Supplement any deficiencies. d. Adequate overall intake may be preferred over fol-lowing a strict low cholesterol/glucose/fat/sodium diet. 4. Other therapies/considerations. a. Provide utmost safety for the patient and caregivers while maintaining some form of independence for the patient. b. Modify environment. c. Maintain a routine. d. T reat occult conditions that could contribute to behavioral problems (like toothache or constipation). e. Provide simple physical activities. f. Provide caregiver respite as needed. B. Patient/family teaching points. 1. Patient teaching is more geared toward the caregiver. 2. Many changes must be made in the patient's life, including relinquishing some independence for the sake of safety. 3. When considering activities such as driving, safety for both the patient and public should be considered. C. Pharmacotherapy. 1. Food and Drug Administration (FDA) approved for AD: Cholinesterase inhibitors. a. Donepezil. b. Rivastigmine. c. Galantamine. 2. FDA approved for AD: N-methyl-D-aspartate (NMDA) receptor antagonist. a. Memantine. 3. Pharmaceutical therapy for symptom control. a. Phenothiazine. b. Benzodiazepines. c. Second-generation antipsychotics: Risperidone, quetiapine, olanzapine. d. Anticholinergics or sedatives. e. Antidepressants, especially selective serotonin reup-take inhibitors (SSRIs). Follow-Up A. Patient should be seen at regularly scheduled appoint-ments dependent on several factors. 1. Physical needs of the patient. 2. Mental status and rate of decline. 3. Emotional status. 4. Ability of caregiver to maintain the safety and health of the patient. B. Follow-up assessments include efficacy of medication, with changes, additions, and discontinuance as needed. C. Monitor for correctable physical factors that may con-tribute to behavioral issues, both becoming withdrawn and outburst. D. Assess for additional resources needed by the patient and caregiver, including ability of the patient to function with safety as the determining factor when discussing activity limitations. Consultation/Referral A. Neuropsychologist. B. Social workers. C. Cognitive rehab can help maintain memory and cognitive functioning while also providing some respite to caregiver. D. Exercise programs. E. Occupational therapy. Special/Geriatric Considerations A. Comorbid conditions. B. Family support. C. Daily care. D. End of life plans. Bibliography Alzheimer's Association (n. d. ). Know what to expect. Retrieved from https: //www. alz. org/help-support/i-have-alz/know-what-to-expect American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5) (5th ed. ) Arlington, TX: Author. Brosch, J. R., & Farlow, M. R. (2018, June 8). Early-onset dementia in adults. In J. L. Wilterdink (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/early-onset-dementia-in-adults Cordell, C. B., Borson, S., Boustani, M., Chodosh, J., Reuben, D., Verghese, J.,... Fried, L. B. (2013). Medicare detection of cognitive impairment workgroup. Alzheimer's Association recommendations for operationaliz-ing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dementia, 9 (2), 141-150. doi:10. 1016/j. jalz. 2012. 09. 011 Folstein, M. F., Folstein, S. E., & Mc Hugh, P. R. (1975). “Mini-Mental state. ” A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12 (3), 189-198. Galvin, J. E., Roe, C. M., Xiong, C., & Morris, J. C. (2006). Validity and reli-ability of the AD8 Informant interview in dementia. Neurology, 67 (11), 1942-1948. Falls Frances M. Stokes Definition A. The clinician definition of a fall describes it as an inadver-tent change in position and coming to rest on the ground, floor, or other lower level. This may include injury or16. Geriatric Guidelines340	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
noninjury as a result. There are a multitude of billing codes for falls within the ICD-10 coding system. These include falls on the same level, from an upper level, and other unspecified types of falls. This definition excludes an intentional change of position. B. Categories. 1. Accidental: This category is for the low risk patient. These patients fall for numbers of unplanned reasons: T ripping over an intravenous (IV) line or falling or sliding out of bed while reaching for something or another type of encounter with an environmental hazard, like a slippery floor, or other hazard such as the garbage can. 2. Anticipated physiological: Patients with risk factors identified on admission or in advance secondary to a pro-cedure or surgery such as an unsteady gait; use of walkers, canes, or medications; vision issues; urinary or fecal incon-tinence; delirium,; or dementia. 3. Unanticipated physiological: Patients who are low risk who develop an event such as a seizure, stroke, arrhythmia, or syncopal episode. Falls that occur are unpredictable. 4. Behavioral or intentional: Patients who purposely act out. Incidence A. Inpatient falls. 1. In the United States, 700,000 to 1,000,000 patients fall yearly; two-thirds are elderly with 30% to 50% incur-ring injury overall. 2. Length of stay may increase to as many as 6. 7 addi-tional inpatient hospital days. 3. In the United States the cost of falls can exceed $34 billion annually. 4. Elderly patients 65 years and older account for two-thirds of the total expenditures. 5. Medical and surgical costs for a fall with injury can reach $14,000 per case. 6. Costs incurred should also include postacute hospital needs, discharge to rehabilitation hospitals, and skilled nursing facilities. B. Morbidity. 1. Women are more likely to fall and sustain non-life-threatening injuries than men. 2. Women are also 1. 8% to 2. 3% more likely to end up hospitalized and 2. 2 times more likely to sustain a fracture after a fall than men. 3. Falls are a contributing factor to admissions to reha-bilitation centers, skilled nursing facilities, and ultimately nursing homes. C. Mortality. 1. Falls are the number one cause of death from unin-tentional injuries for those adults 65 years or older in the United States. 2. Falls can also be associated with an indirect cause of death. Pathogenesis A. Intrinsic factors. 1. Age-related decline. 2. Chronic disease. 3. Medications. 4. Vitamin D. B. Challenges to postural control. 1. Environment. 2. Changing positions. 3. Normal activity. C. Mediating factors. 1. Risk-taking behaviors. 2. Situational hazards. Predisposing Factors A. Medications. 1. Anticholinergics. 2. Antiarrhythmics. 3. Antihypertensive medications. 4. Narcotics. 5. Muscle relaxants. 6. Alcohol. B. Incontinence: Urine and fecal incontinence. C. Health conditions. 1. Alzheimer's disease: Have two times the probability of falling than those of the same age without the disease. 2. Parkinson disease: 38% to 68% of Parkinson disease fall due to gait disturbances. 3. Diabetes: Women with diabetes are 1. 6 times more likely to fall, and two times more likely to suffer fall-related injuries than women without diabetes. 4. Depression: There is a 2. 2-fold increase in the risk of falls in this population of elderly patients. D. Physical impairments. E. Past medical history. 1. Previous falls. 2. Diabetes. 3. Chronic obstructive pulmonary disease (COPD). 4. C oronary artery disease (CAD). 5. Arrhythmias. 6. Dementia-related diseases, Alzheimer's disease, vascu-lar dementia (includes cerebrovascular accident [CVA]), Parkinson's dementia, and so forth. 7. Osteoarthritis. 8. Joint replacements (knee surgeries especially suscep-tible). 9. Chronic pain. 10. Blindness. 11. Macular degeneration. 12. Glaucoma. 13. Chronic kidney disease. 14. Vestibular disease. Subjective Data A. Common complaints/symptoms. 1. Dizziness when bending over. 2. Unsteady gait/balance. 3. Poor vision. 4. Fatigue, weakness. 5. Other signs and symptoms. a. The need to use assistive equipment to ambulate. b. Walks along walls and uses furniture to maintain balance. c. Assistive devices or medications for visual or hear-ing impairments related to aging and other geriatric syndromes. B. Family and social history. 1. Noncontributory in most cases. C. Review of systems. 1. Review all medications. 2. Use STRATIFY risk assessment tool to inquire abou t: a. History of falls. b. Mental status. c. Vision. d. Toileting. Falls341	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
e. T ransfer and mobility. f. Head, ear, eyes, nose, and throat (HEENT). i. Dizziness. ii. Poor vision. iii. Loss of peripheral vision. iv. Depth perception. g. Musculoskeletal. i. Unsteady gait. ii. Uses walls to maintain balance. h. Neurological. i. Neuropathy. i. General. i. Overall hazards in the home (rugs). Physical Examination A. Perform a head-to-toe physical examination. 1. Neurological examination. a. Glasgow Coma Scale. b. National Institute of Health (NIH) stroke scale. c. Detailed neurological examination if indicated, cra-nial nerves, gait, and balance testing. 2. Mentation status. a. Mini-Mental status examination. b. Confusion assessment method or other delirium screening tool. c. Thorough review of medications for offending medications. 3. Cardiovascular examination. a. Murmurs/arrhythmias. b. Carotid bruits. c. Pulses weak/thready. d. Evaluate for edema. 4. Orthostatic readings/pulmonary examination. a. Sp O2. b. Breath sounds. c. Accessory muscle use. 5. Integumentary. a. Bruising, scrapes, and lacerations over knees, shoul-ders, forearms, shins, ankles, and toes. This indi-cates the patient is bumping into furniture or walls, which may indicate unaddressed balance issues or are defensive in nature. b. Excoriation in perianal area: This may indicate urinary (female) or fecal incontinence (male/female) related to diet, medications, or infection. 6. Gastrointestinal. a. Abdominal bruits. b. Pain. c. Nodules or skin changes. d. Look for ecchymosis and signs of bleeding. 7. Genitourinary. a. Incontinence, urgency, frequency. Diagnostic Tests A. Chiefly depends upon the etiology of the fall, past medical history, medications, and findings of physical examination. B. CT of the head to rule out bleeding either from a stroke or as a result of the fall or a subdural or subarachnoid hemor-rhage. Some cranial bleeds that are not related to a CVA can be spontaneous if a patient is on anticoagulation therapy or American Society of Anesthesiologists (ASA). CT Angiogra-phy (CTA) or MRI/m agnetic resonance angiography (MRA) may be indicated. C. X-rays of spinal column, ribs, long bones, and so forth, to rule out fractures in suspicious areas where there is evidence of impact from the fall. D. Other diagnostics should be dependent upon patient his-tory of present illness, past medical history, and physical examination. 1. Basic chemistry with glucose. 2. Carotid Doppler study. 3. C omplete blood count (CBC) w/differential. 4. EKG. 5. Echocardiogram (heart murmurs). 6. Evaluate for vitamin deficiencies, B12, Thiamine. 7. Guaiac stools if indicated. 8. MRA (suspect thrombus, hemorrhage). 9. MRI (gait disturbances or neurological deficits). 10. Serum 25-hydroxyvitamin D level. 11. Tilt table test. 12. Urinalysis to rule out infection. E. Review diagnostic test results. 1. Laboratory findings. 2. Radiological examinations. Differential Diagnosis A. Anemia. B. Arrhythmia. C. Arthritis. D. Carotid stenosis. E. Dehydration. F. Dementia. G. Depression. H. Electrolyte deficiencies (severe hyponatremia) and vitamin deficiencies. I. Frailty. J. Hypoglycemia/hyperglycemia. K. Infection/sepsis. L. Labyrinthitis. M. Malnutrition. N. Orthostatic/postural hypotension. O. Peripheral neuropathy. P. Peripheral vascular disease. Q. Neurological disorders such as stroke, seizure, Parkinson disease, or vertigo. R. Uncorrected farsightedness/nearsightedness or poor vision from macular degeneration, glaucoma, underlying infection, or diabetic retinopathy. S. Medications can create a delirious state. 1. Alcohol. 2. Antiarrhythmics. 3. Antidepressants. 4. Antihypertensives. 5. Antipsychotics. 6. Diuretics. 7. Hypnotics. 8. Neuroleptics. 9. Sedatives. Evaluation and Management Plan A. General plan. 1. Perform a full medication review and use the BEERS criteria to determine medications that are contraindicated for older adults. 2. Perform multidisciplinary rounds for patients at mod-erate and higher fall risk, all patients over 75 years of age, and those who are frail. 3. Evaluate nutritional status, and order nutritional con-sult if indicated. 4. Evaluate for safe discharge on admission utilizing case management and a social worker to collaborate with family and caregivers. Include nurses, advanced practice16. Geriatric Guidelines342	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
nurses (APNs), prothrombin time (PT)/OT, a dietician, a pharmacist, and physicians. 5. Request fall risk alerts for patient safety to include an order for bed and chair alarms. 6. Correct underlying medical etiology or physical deficit if possible, which may include medication revisions, cor-rection of vision/hearing with assist devices, and use of ambulatory devices to aid with balance. 7. Place on telemetry. B. Patient/family teaching points. 1. Discuss with patient/caregiver. a. Signs and symptoms to monitor. b. Common occurrences. c. Readmission concerns. C. Discharge instructions. 1. Evaluate for safe transfer of care from initiated unit, that is, ICU to floor, floor to home, or other institution. 2. Accurate discharge summary of events including chief complaint and events leading up to admission and during hospitalization. 3. Copy of discharge summary to the family or caregivers, primary care provider, and specialists to ensure commu-nication and history of recent events are transferred to community providers. Inpatient providers should state patient's condition upon discharge and the patient's ability to transfer to the next level of care. 4. Thorough medication reconciliation; ensure obsolete medications are removed from medication list. 5. Separate education for medication reconciliation regarding discontinued medications, new medications, and administration. 6. Education for signs and symptoms of worsening con-dition, what is expected to happen, and readmission concerns. 7. Discharge education regarding physician follow-up; medications and instructions on medications; any medical treatments that require an explanation, includ-ing physical therapy or wound care therapy; and breathing treatment or injections, to name but a few. 8. Use of any new assistive devices, walkers, canes, or braces. 9. Education on making the patient's home safe from falls, such as removing scatter rugs and keeping lights on. Follow-Up A. Follow-up depends on the cause of the fall and the conse-quences of it. B. For falls caused by cardiac disease, the patient should follow-up with cardiology. C. If a patient has an injury due to the fall, the patient should follow-up with the appropriate services such as orthopedics for fractured bones or neurosurgery for head injury. Consultation/Referral A. Case management and social workers ensure safe discharge to appropriate level of care. B. Arrange for delivery of any durable medical equipment to the patient's assisted living, adult living, group home, or home. C. Considerations of insurance coverage and deductible amounts are important for elders on fixed budgets. D. Financial resources and availability of social support through appropriate government resources are important for safe transition, especially to independent living and home. 1. Medications: Ensure insurance is available for medi-cations and durable medical equipment necessary for safe patient discharge. 2. If possible, arrange for first follow-up medical appoint-ments with appropriate physicians and/or specialists. 3. If home therapy is utilized for wound or physical/oc-cupational therapy, ensure set-up and appointments for home visits are arranged. 4. If indicated, a home health visit can be set up to provide support and help arrange first appointments. Special/Geriatric Considerations A. Up to 50% of geriatric patients may not report his-tory of falls to anyone for fear of being removed from the home. Bibliography Fauci, A. S. (2008). Nervous system dysfunction. In A. S. Fauci, E. Braun-wald, D. L. Kasper, S. L. Hauser, D. L. Longo, J. L. Jameson, & J. Loscalzo (Eds. ), Harrison's principles of i nternal medicine (pp. 139-180). New York, NY: Mc Graw-Hill Professional. Fletcher, K. (2012). Dementia. In M. Boltz, E. Capezuti, T. Fulmer, & D. Zwicker (Eds. ), Evidence-based geriatric nursing protocols for best practice (4thed.,pp. 163-185). New York,NY:Springer Publishing. Fulmer, T., & Zwicker, D. (2012). Evidence-based geriatric nursing proto-cols for best practice (4th ed., pp. 186-199). New York, NY: Springer Publishing Company. Stevens, J., Ballesteros, M., Mack, K., Rudd, R., De Caro, E., & Adler, G. (2012). Gender differences in seeking care for falls in the aged Medicare population. American Journal of Preventive Medicine, 43 (1), 59-62. Urinary Incontinence Frances M. Stokes Definition A. Urinary incontinence in men and women is defined as an involuntary leakage of urine. Incontinence is further broken down into types of urinary leakage as follows. 1. Urgency is associated with a sense of an urgency to void. This may present suddenly. Precipitating factors include cold, the sound of running water, or washing hands, that is, putting hands in water. 2. Stress incontinence occurs with strain, exertion, sneezing, or coughing. 3. Mixed incontinence is the most common type of urinary incontinence for women. There is an urgency and exertion associated with it. 4. Post void incontinence is associated with post void residual urine in the urethra which leaks out after voiding. 5. Overactive bladder is associated with frequency, urgency, and nocturia. This may or may not have incon-tinence associated with it. 6. Incomplete urinary emptying (overflow) incontinence relates to incomplete emptying of the bladder due to an impaired detrusor contractility or a bladder outlet obstruction. 7. Functional/transient incontinence is usually self-limiting, transient, and potentially reversible due to treatable causes. 8. Inability to reach bathroom secondary to functional ability. 9. Reflex incontinence etiology is related to neurological dysfunction of the central nervous system. Urinary Incontinence Company 343	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Incidence A. Globally, incidence affects 200 million people worldwide; in the United States, the number is 10 to 13 million. 1. The percentage of elderly patients who reside in long-term care facilities is between 50% and 84%. B. Prevalence in men increases with age. C. Prevalence in females. 1. 60 to 79 years is 23. 3%. 2. Over 80 years increases to 31. 7%. 3. Of the types of incontinence, stress is most commonly seen in women who are younger than 65 years old. How-ever, urge incontinence and mixed are more common among women older than 65 years. Stress incontinence affects both young and older women at a rate of 15% to 60%; of these, 25% are nulliparous young college athletes. Pathogenesis A. Urgency can be related to an uninhibited detrusor activity. This is most common in men. B. Stress incontinence is generally due to pressure on the bladder, which can happen with coughing, sneezing, laugh-ing, heavy lifting, and so forth. 1. Radical prostatectomy surgery is the most common cause in men due to damage to the prostatic apex. T ransurethral resection of the bladder has less incidence of damage to the external sphincter and has a degree of less than 1%. 2. In women, stress incontinence is due to lax perineal muscles. C. Overflow incontinence is the least common cause of incontinence due to impaired detrusor contractility and/or a bladder outlet obstruction. Impaired detrusor contractil-ity is usually related to neurogenic etiologies. These include neuropathies such as mitral stenosis (MS), diabetes mel-litus, meningomyelocele, lumbosacral nerve disease from tumors, prolapsed intravertebral discs, and higher spinal cord injuries. D. Mixed incontinence is a combination incontinence of stress and urge; this is most common in women. The blad-der outlet is weak and the detrusor is overactive. This may also include urethral hypermobility coupled with detrusor instability. E. T ransient incontinence refers to a temporary loss of urine due to causes that could be reversible such as delirium, infection, atrophic vaginitis or urethritis, pharmaceuti-cals, or a psychological etiology related to excess fluid intake. Impaired mobility, endocrine disorders, medications, fecal impaction, atrophic urethritis or vaginitis, infections, and delirium are also included in etiologies of transient incontinence. F. Reflex incontinence for specific neurological disease pro-cesses include, but are not limited to, MS and demyelinating plaques of the frontal lobe or lateral columns. Cerebrovascular accident (CVA) or vascular compromise of particular areas of the brain may result in lower urinary tract dysfunction. Predisposing Factors A. Advanced age. B. Aging process. 1. Atrophic vaginitis or urethritis. 2. Enlarged prostate (urge/stress). C. Problems with gastrointestinal system. 1. Constipation. 2. Fecal impaction. D. Cancer. 1. Pelvic organs. 2. Pelvic radiation within 6 months. 3. Prostate cancer (tumor status; urge/stress). 4. Prostate surgery or radiation. E. Central nervous system (CNS) or spinal cord disorders. 1. Delirium or dementia. 2. Normal pressure hydrocephalus. 3. Neuropathies. F. Connective tissue disorders. G. Depression medications. H. Obesity. I. Pelvic organ prolapse (uterus/bladder). J. Chronic obstructive pulmonary disease (COPD). K. Mobility. L. Sleep apnea. M. Urinary tract stones or urinary tract infection (UTI), more than two episodes a year. Subjective Data A. Common complaints/symptoms. 1. Sudden onset of the need to urinate. 2. Urine leakage after emptying bladder. 3. Unable to make it to the bathroom with the urge to urinate. 4. Feeling of incomplete emptying of the bladder with urination. 5. Burning with urination. 6. Flu-like symptoms. 7. Morbidity related to incontinence. 8. Psychological morbidity related to incontinence. a. Depression. b. Poor self-esteem. c. Sexual dysfunction. d. Social withdrawal. 9. Urine leakage. 10. May complain of hygiene issues. B. Common/typical scenario. 1. Patients do not typically like to discuss incontinence, but will report varying degrees of urine urgency, frequency, or pain when urinating that may be minor, situational, or even debilitating. C. Family and social history. 1. Family and social history is noncontributory. D. Review of systems. 1. Dermatological: Ask about skin infections, itchiness, redness, and pressure sores. 2. Psychological: Ask about social involvement, sexual functioning, mood, and sleep habits. 3. Genitourinary: Ask about moisture felt in under-wear, leakage issues, itching, burning during urination, frequency, urinating at night, perineal irritation. 4. Gastrointestinal: What is the typical bowel pattern? Any there complaints of constipation or impaction? Physical Examination A. General. 1. Appearance. 2. Signs of depression. 3. Any distress. 4. Anxiety. 16. Geriatric Guidelines a. Cellulitis. b. Constant skin irritation and sores. c. Falls and subsequent fractures. d. Perineal candida infections. e. Pressure sores. f. Sleep deprivation. 344	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
B. Gastrointestinal: Abdominal distention. C. Musculoskeletal. 1. Joint stiffness. 2. Mobility. 3. R ange of motion (ROM). 4. Use of assistive devices. D. Neurological with emphasis on cognition, functional status, and pyramidal and extra-pyramidal symptoms. Integrity of sacral roots S2, S3, and S4; resting and folli-tional anal tone; and anal wink reflex. Evaluate for peripheral neuropathy. E. Male. 1. Visual examination of the penis, enlarged prostate, and scrotum. 2. Review past medical history (PMH) for prostate issues. F. Female. 1. Review PMH for prolapse of pelvic organs and perineal irritation. Diagnostic Tests A. Laboratory. 1. Chemistries with renal function and complete blood count (CBC). 2. Prostate specific antigen (PSA) level. 3. Urine analysis with cytology and microscopy. B. Radiology. 1. Post residual bladder scan. 2. Renal ultrasound (US) if indicated by abnormal renal laboratory studies. 3. CT of brain if hydrocephalus is suspected. Differential Diagnosis A. CNS or spinal cord disorders. B. Connective tissue disorders. C. Constipation or fecal impaction. D. Medication induced. E. Normal pressure hydrocephalus. F. Neuropathy, diabetic neuropathy. G. Obesity. H. Pelvic organ prolapse (uterus/bladder). I. Sleep apnea. J. Urinary tract stones. K. UTI. Evaluation and Management Plan A. General plan. 1. Perform a full medication review and reconciliation. 2. Perform multidisciplinary rounds for geriatric patients and include continence strategies for those who are incon-tinent, all patients over 75 years of age, and those who are frail. Include pharmacist, dietician, radiation ther-apy (RT), prothrombin time (PT)/OT, advanced practice provider, case management, social worker, and caregivers when indicated. 3. Evaluate nutritional status; order nutritional consult if indicated. 4. Patient safety. a. Modify inpatient environment; include toileting into hourly rounds, place call light within reach, use lights at night, and clear the walkway to bath-room/bedside commode. b. Patient/family caregiver education on use of the call light for assistance. c. Evaluate for safe discharge on admission utilizing case management and social worker to collaborate withfamily and caregivers. Include nurses, APNs, PT/OT, dietician, pharmacist, and physicians. d. Request toileting rounds for patient safety to include an order for bed and chair alarms for those elderly patients with urgency and frequency. e. Urinals at bedside for male patients, bedpans for those unable to ambulate or get up to use a commode. 5. Correct underlying medical etiology or physical deficit if possible, which may include medication revisions, cor-rection of vision/hearing with assistive devices, and use of ambulatory devices. B. Patient/family teaching points. 1. Pelvic floor exercises. 2. How to use absorbent products. 3. Approaches to dealing with incontinence. 4. Modifications to diet and lifestyle may help patient control incontinence to a certain degree. C. Pharmacotherapy. 1. Medications depend upon the type of urinary inconti-nence being treated. 2. Medications may not be effective in stress inconti-nence. 3. Anticholinergics (antimuscarinics) block cholinergic receptors of the bladder and decrease contractility. 4. All antimuscarinics are contraindicated in narrow angle glaucoma, gastric retention, and if post void resid-ual (PVR) is greater than 150 L. Educate for side effects. Costs vary. 5. Benign prostatic hypertrophy (BPH)-related incon-tinence: Alpha blockers have extensive precautions for administration. Orthostatic hypotension, hypotension, bradycardia, vertigo, priapism, cautious administration, and lab surveillance in patients with hepatic impairment should be considered. 6. UTI: Antibiotic-focused therapy, either oral or intra-venous (IV), depending upon the severity and hemody-namic status of the patient. 7. Other treatments. a. Barrier creams. b. Oral multivitamins with zinc. c. Absorbent undergarments. d. Pelvic floor exercises. e. T ransient incontinence; treat the underlying cause, that is, infection, outlet obstruction, and so forth. f. Surgical interventions. D. Discharge instructions. 1. Evaluate for safe transfer of care from initiated unit, that is, ICU to floor, floor to home, or other institution. 2. Doctor to doctor report or APN to doctor/APN report. 3. Accurate discharge summary of events including chief complaint and events leading up to admission and medical nursing care during hospitalization. 4. Copy of discharge summary to the family or care-givers, primary care provider, and specialists to ensure communication and history of recent events are trans-ferred to community providers. Inpatient providers should state patient's condition upon discharge and the patient's ability to transfer to the next level of care. 5. Thorough medication reconciliation; ensure obsolete medications are removed from medical admissions record (MAR) and home medication list. 6. Separate education for medication reconciliation regarding discontinued medications, new medications, and administration. Urinary Incontinence345	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
7. Education for signs and symptoms of worsening condition, what is expected to happen, and readmission concerns. 8. Discharge education regarding physician follow-up; medications and instructions on medications; any medical treatments that require an explanation, includ-ing physical therapy or wound care therapy; and breathing treatment or injections, to name but a few. 9. Use of any new assistive devices, walkers, canes, braces, or hearing devices. 10. Education on making the incontinent patient's home safe from falls, such as removing scatter rugs and keeping lights on. Follow-Up A. Patient should follow-up with the provider in 2 weeks to assess progress in treatment plan. Consultation/Referral A. Urology. B. Primary care provider/gerontologist. C. Wound care if indicated. D. Physiotherapist: Pelvic floor exercises, bladder training, and strategies to maintain continence. Special/Geriatric Considerations A. Case management and social worker are utilized to ensure safe discharge to appropriate level of care. B. Arrange for delivery of any durable medical equipment to the patient's assisted living, adult living, group home, or home. Considerations of insurance coverage and deductibleamounts are important for elders on fixed budgets. Financial resources and availability of social support through appropri-ate government resources is important for safe transition, espe-cially to independent living and home. 1. Medications: Ensure insurance is available for medi-cations and durable medical equipment necessary for safe patient discharge, such as bedside commode, and so forth. 2. If possible, arrange first follow-up medical appoint-ments with appropriate physicians, and/or specialists (urologist). 3. If home therapy is needed for wound therapy, ensure appointments for home visits are set up. C. If indicated, set up home health visit to provide appropri-ate support in arranging first appointments. D. Discuss with patient, caregiver, and/or family. 1. Signs and symptoms to monitor. 2. Common occurrences. 3. Readmission concerns. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5) (5th ed. ). Arlington, VA: American Psychiatric Association. Fauci, A. S. (2008). Nervous system dysfunction. In A. S. Fauci, E. Braun-wald, D. L. Kasper, S. L. Hauser, D. L. Longo, J. L. Jameson, & J. Loscalzo (Eds. ), Harrison's principles of internal medicine (17th ed., pp. 139-180). New York, NY: Mc Graw-Hill Professional. Fletcher, K. (2012). Dementia. In M. Boltz, E. Capezuti, T. Fulmer, & D. Zwicker (Eds. ), Evidence-based geriatric nursing protocols for best practice (4thed.,pp. 163-185). New York,NY:Springer Publishing. Fulmer, T., & Zwicker, D. (2012). Evidence-based geriatric nursing protocols for bestpractice(4thed.,pp. 186-199). New York,NY:Springer Publishing. 16. Geriatric Guidelines Company Company346	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2019/9/19 5:07 Page 347 #1 347 17 Trauma Guidelines Susan F. Galiczynski Chest Trauma Susan F. Galiczynski Definition A. Any mechanism that causes injury to the bony or soft tissue in the thorax. B. Any of these injuries alone or in combination can be dev-astating and life-threatening to the patient, in a very short period of time. Incidence A. Account for up to 25% of all trauma-related deaths. B. Approximately 80% to 85% of patients with chest trauma will experience at least one rib fracture. C. Gunshot wounds to the chest tend to be more fatal. D. Approximately 5% to 10% of chest trauma will involve sternal fractures. Pathogenesis A. Related to mechanism of injury. B. Common mechanisms: Blunt chest trauma, penetrat-ing trauma (gunshot wounds, stab wounds, impalements, acceleration-deceleration shearing forces, and compressive forces). Predisposing Factors A. Chest trauma can occur in anyone, but there is a higher incidence in younger males who may engage in high risk behaviors. Subjective Data A. Common complaints/symptoms. 1. Chest wall and back pain, worse with movement, coughing, breathing. 2. Shortness of breath. 3. Increased pain with palpation. B. Common/typical scenario. 1. Other signs and symptoms. a. Crepitus in the presence of fractures. b. Splinting or shallow breathing. c. Decreased breath sounds on the affected side (pneumothorax). d. Beck's triad: Muffled, distant heart sounds (cardiac tamponade), jugular venous distention, and narrowed pulse pressures. C. Subjective data/review of systems. 1. Ask the patient about the events surrounding the injury. With falls, ask if the patient tripped or passed out. Determine if syncope needs to be ruled out. 2. If motor vehicle collisions (MVC) occur, ask the patient about restraints. Was there a steering wheel defor-mity? 3. Assess for chest pain. Location? Characteristics? Reproducible? Physical Examination A. Aimed at identifying the most life-threatening injury first. B. Advanced trauma life support (ATLS) guidelines provide a quick but thorough approach to patient assessment. Diagnostic Tests A. FAST examination: May show cardiac tamponade and can be used to determine the presence of a pneumothorax without the use of chest x-ray. B. Plain radiograph of the chest to identify fractures, atelec-tasis, pneumothorax, or widened mediastinum (possible aorta injury). C. CT and CT angiogram help to identify specific bony, organ, and vascular injuries. D. ECG. E. Arterial blood gas: May show respiratory acidosis related to hypoventilation as a result of pain and splinting. F. Cardiac enzymes. Differential Diagnosis A. Common traumatic chest injuries. 1. Bony injuries. a. Rib fractures. i. Definition: Fractures of one or more ribs. Can be located bilaterally, or may be displaced and can stand alone or result in injury to underlying structures such as the lungs, subclavian vessels, or organs such as the spleen and liver. 1)Flail chest: Occurs when at least two adja-cent ribs are broken in multiple places, cre-ating a free moving segment allowing that segment of the chest wall to move indepen-dently. If fractures are near the sternum, there can be a free-floating segment of the sternum, as well as rib. This can be a life-threatening condition. b. Sternal fractures. i. Definition: Fractures of the manubrium or sternal body. Persons older than 65 years will have increased risk of death (10%-12%) with one rib Chest Trauma	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
348 fracture. The rate increases by 5% with each addi-tional rib fracture. ii. Management. 1)Rule out underlying injury to other tissues or organs. 2)Cardiac echo will determine if there is a cardiac contusion or other heart-related injury. 3)Pain management. 4)Aggressive pulmonary hygiene. Encour-age incentive spirometer. 5)Supplemental oxygen. 6)Displaced rib fractures or flail segments may require operative intervention for stabi-lization. 2. Lung injuries. a. Pulmonary contusion. i. Definition. 1)Bruising to the lung parenchyma. 2)Clinical course: Tend to worsen in the first 24 to 48 hours. Can lead to atelectasis, infil-trate, effusions, or empyema. 3)Frequently associated with rib fractures. ii. Management. 1)Supplemental oxygen. 2)May require intubation and supported ventilation. 3)Analgesia. 4)Chest physiotherapy. b. Pneumothorax. i. Definition. 1)Accumulation of air in the pleural space, resulting in partial or complete collapse of the lung. 2)Tension pneumothorax: Life-threatening condition. As air accumulates in the pleural space, it exerts an increased pressure on the heart; mediastinal shift to the unaffected side can lead to circulatory collapse. c. Hemothorax. i. Definition. 1)Blood accumulates in the pleural space. 2)Considered “massive hemothorax” when drainage exceeds 1. 5 L in less than 2 hours after injury, necessitating emergent thoraco-tomy. ii. Physical examination findings of pneumotho-rax or hemothorax. 1)Decreased breath sounds on the affected side. 2)Deviated trachea is a late sign. 3)Respiratory distress, hypoxia, tachycardia, or hypotension may be present. iii. Other physical findings. 1)Cyanosis. 2)Diaphoresis. 3)Chest pain. 4)Altered mental status. iv. Management. 1)Small pneumothorax or hemothorax can be managed conservatively by observation and repeat chest x-ray (CXR). 2)Pneumothorax greater than 20% requires thoracostomy tube (chest tube) insertion. 3)Massive hemothorax with drainage of more than 1. 5 L in 2 hours may require thoracotomy and repair of lung injury. d. Cardiac tamponade. i. Definition: Accumulation of blood or fluid in the pericardial sac, causing a compression of the heart muscles. This leads to decreased cardiac output, which is life-threatening. ii. Physical examination findings. 1)Beck's triad: A constellation of findings suggestive of tamponade. a)Jugular vein distention. b)Hypotension with narrowing pulse pressures. c)Distant or muffled heart sounds. iii. Other physical findings. 1)Tachycardia. 2)Pulsus paradoxus. 3)Altered mentation. 4)Oliguria. 5)Signs of impending shock. iv. Management. 1)Pericardiocentesis. 2)Management of shock. e. Great vessel injuries. i. Definition. 1)Interruption of the wall of any of the great vessels is a life-threatening event. Injuries to the aorta, internal vena cava, or subclavian ves-sels can be the result of laceration from bony segments or shearing or compressive forces. These require operative intervention. 2)Physical findings. a)Chest or back pain, shortness of breath, weakness. b)Hypotension. c)Variations in blood p ressure (BP) in both upper extremities. d)Shock. 3)Management. a)Thoracotomy with repair to affected vessels; may require cardiopulmonary bypass. b)Mechanical ventilation. c)Replacement of blood volume with transfusion, may require massive transfu-sion protocols. d)May require hemodynamic support with vasopressors and volume resuscita-tion. Evaluation and Management Plan A. General plan. 1. Identify specific injuries and treat accordingly. 2. Primary goals of therapy. a. Pain management. b. Prevention of atelectasis and pneumonia. c. Supplemental oxygen. 3. Explain expectant course with patient and family. 4. Consider adding cardiac enzymes to workup to rule out underlying stress to heart. 5. May require multiple radiographs to evaluate course of healing. 6. For patients with chest tubes, document the output and consistency of drainage and whether or not an air leak is present. B. Patient/family teaching points. 1. Cough and deep breathing exercises. 17. Trauma Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2019/9/19 5:07 Page 349 #3 349 2. Incentive spirometry or other airway clearance devices. 3. Incisional wound care. C. Pharmacotherapy. 1. When indicated, vasopressors to support hemody-namics. 2. Multimodal pain management using opioids only when indicated. a. Nonsteroidal anti-inflammatory drugs (NSAIDs) and Tylenol, mild pain. b. Lidocaine patch for localized pain. c. I ntravenous (IV) Toradol and Tylenol with sup-plemental opioid for moderate pain. d. For severe pain, consider: i. Epidural pain medication. ii. Intercostal nerve block. iii. Patient-controlled analgesia (PCA) pain man-agement. 3. Bronchodilator treatments when indicated. Follow-Up A. Follow-up should be dictated by the level of injury and hospital course. B. For minor injuries, patients may follow-up with the pri-mary care provider in 1 to 2 weeks. C. Postsurgical follow-up may be indicated in a 7-to 14-day period for wound checks, repeat imaging, or suture/staple removal. Consultation/Referral A. Patients with severe injury should always be referred to a high level of care if the institution does not have the resources to treat the patient. B. Refer any additional injuries requiring specialist consul-tation. Special/Geriatric Considerations A. Morbidity associated with rib fractures increases with age and is the highest in elderly patients. Bibliography Alisha, C., Gajanan, G., & Jyothi, H. (2015). Risk factors affecting the prognosis in patients with pulmonary contusion following chest trauma. Journal of Clinical Diagnostic Research, 9 (8), OC17-OC19. doi:10. 7860/JCDR/2015/13285. 6375 Sawa, J., Green, R., Thoma, B., Erdogan, M., & Davis, P. (2017, August 11). Risk factors for adverse outcomes in older adults with blunt chest trauma: A systematic review. Canadian Journal of Emergency Medicine, 20(4), 1-9. doi:10. 1017/cem. 2017. 377 Senn-Reeves, J. N., & Stafileno, B. A. (2013). Long term outcomes after blunt injury to the boney thorax. Journal of Trauma Nursing, 20 (1), 56-64. doi:10. 1097/JTN. 0b013e318286629b Stewart, D. J. (2014). Blunt chest trauma. Journal of Trauma Nursing, 21 (6), 282-286. doi:10. 1097/JTN. 0000000000000079 Penetrating Chest Injuries Susan F. Galiczynski Definition A. A penetrating chest injury is one in which the projectile enters the thorax in any area below the level of the clavicle to the diaphragm. B. Organs at risk for injury include: Chest wall, ribs, lungs and pleura, esophagus, trachea, diaphragm, thoracic blood vessels, the heart, and mediastinal structures. C. As stated previously, gunshot wounds carry a higher mor-tality than blunt trauma. Incidence A. Thoracic injuries account for approximately 20% to 25% of all traumatic deaths. B. Approximately 16,000 deaths annually in the United States can be attributed to thoracic injury. C. Increase in number with the increase in the number of violent crimes. D. Much of the research in thoracic trauma comes from mil-itary experiences. Pathogenesis A. A bullet or projectile object can enter the body at any location but if it travels into the thoracic cavity, any of the structures there are at risk for injury. Predisposing Factors A. Males are more prone than females. B. Males older than 65 years of age. C. Single people are more prone than married people. D. Inner city resident. E. Lower income individuals. F. Members of ethnic minority groups. G. Drug and alcohol use. H. History of depression. I. History of previous suicide attempts. Subjective Data A. Common complaints/symptoms. 1. Most patients with penetrating chest wounds will be brought into the ED via emergency medical services. 2. These patients complain of chest pain and shortness of breath. If the patient is in a state of shock, he or she may be minimally responsive to answering questions. B. Common/typical scenario. 1. Common scenario occurs from low velocity injuries such as an impalement by a structure like a knife, medium velocity injuries from hand guns, or high velocity injuries from rifles and military weapons. C. Family and social history. 1. Family history is noncontributory. Penetrating chest injuries occur more frequently in violent areas, large metropolitan areas, and areas of conflict. D. Review of systems. 1. Neuro: Ask about dizziness, lightheadedness. 2. Cardiac: Heart racing, palpitations, lightheadedness. 3. Respiratory: Shortness of breath, breathing difficul-ties, airway obstructions. 4. Dermatology: Areas of bleeding or bruising. Physical Examination A. Assess chest, back, and abdomen for additional wounds. B. Dermatology—The physical examination requires a thor-ough investigation of the skin for breaks in the skin, redness, or discoloration with particular attention to the chest, back, and abdomen. C. Neurology—Assess cognition and responsiveness. D. Cardiology—Monitor blood pressure (BP) and heart rate (HR). E. Respiratory—Assess quality of breath sounds and respi-ratory rate. Penetrating Chest Injuries	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2019/9/19 5:07 Page 350 #4 350 Diagnostic Tests A. CT. B. Supine chest film can help to identify foreign bodies, that is, bullets and pneumothorax. Differential Diagnosis A. There is typically no need for a differential diagnosis. An inspection will provide the diagnosis in this case. Evaluation and Management Plan A. General plan. 1. The primary approach to penetrating trauma to the thorax is to answer the question of whether or not the patient needs operative intervention. 2. Criteria for operative intervention. a. Hemodynamic instability: BP less than 90 or HR greater than 120. b. Hypotension despite fluid resuscitation. c. Altered mental status without obvious head injury. d. Metabolic acidosis. e. Significant findings on diagnostic studies. 3. Goals of treatment are aimed at controlling hem-orrhage and maintaining perfusion, promptly address-ing airway compromise, and maintaining adequate perfusion. B. Patient/family teaching points. 1. Patient and family education should be geared toward anticipated patient needs as discharge nears. 2. Some examples include wound care, tracheotomy care, physical medicine, and rehab goals. C. Pharmacotherapy. 1. In the acute phase of care, interventions may include: a. Hemodynamic support: Blood transfusions and vasopressors may be necessary to reduce risks of hypotension related to hypovolemia and shock states. b. Sedation and pain management with continuous infusions to keep the patient comfortable. c. Prophylactic antibiotic treatment for operative care and for any ICU-related infections. Follow-Up A. Many of these patients have a long critical care and hospital course and will become deconditioned. Preparing the patient and family for potential rehabilitation needs is key. B. If the patient has multiple injuries not related to just one organ system, education about follow-up with those injury-specific specialty groups is recommended. C. Physical medicine and rehab may have a very active role in postdischarge care. Consultation/Referral A. T rauma. B. Cardiothoracic surgery. C. Other necessary consultants, based on injury. D. Physical medicine and rehab services. E. Psychiatry for self-inflicted wounds/suicide attempts. Special/Geriatric Considerations A. Indicators of poor outcomes/higher mortality include : 1. Lower Glasgow Coma Score (GCS) on arrival. 2. Increased age. 3. Suicide attempt (self-inflicted). 4. Coagulopathy. Bibliography Berg, R. J., Karamanos, E., Inaba, K., Okoye, O., Teixeira, P. G., & Deme-triades, D. (2014, February). The persistent diagnostic challenge of tho-racoabdominal stab wounds. Journal of Trauma and Acute Care Surgery, 76(2), 418-423. doi:10. 1097/TA. 0000000000000120 Davis, J. S., Satahoo, S. S., Butler, F. K., Dermer, H., Naranjo, D., Julien, K.,... Schulman, C. I. (2014, August). An analysis of prehospital deaths: Who can we save? Journal of Trauma and Acute Care Surgery, 77 (2), 213-218. doi:10. 1097/TA. 0000000000000292 Kamarova, M., & Kendall, R. (2017, December). 13 Prophylactic antibi-otics for penetrating injury: A review of practice at a major trauma cen-tre, literature review and recommendations. Emergency Medicine Journal, 34(12), A869. doi:10. 1136/emermed-2017-207308. 13 Madden, B. P. (2017, January). Evolutional trends in the management of tracheal and bronchial injuries. Journal of Thoracic Disease, 9 (1), E67-E70. doi:10. 21037/jtd. 2017. 01. 43 Mollberg, N. M., Tabachnik, D., Farjah, F., Lin, F. J., Vafa, A., Abdelhady, K.,... Massad, M. G. (2013, August). Utilization of cardiothoracic surgeons for operative penetrating thoracic trauma and its impact on clinical outcomes. Annals of Thoracic Surgery, 96 (2), 445-450. doi:10. 1016/j. athoracsur. 2013. 04. 033 Seamon, M. J., Haut, E. R., Van Arendonk, K., Barbosa, R. R., Chiu, W. C., Dente, C. J.,... Rhee, P. (2015, July). An evidence-based approach to patient selection for emergency department thoracotomy: A practice management guideline from the Eastern Association for the Surgery of T rauma. Journal of Trauma and Acute Care Surgery, 79 (1), 159-173. doi:10. 1097/TA. 0000000000000648 Penetrating Intracranial Injuries Susan F. Galiczynski Definition A. A penetrating intracranial injury is one in which the pro-jectile enters the cranium. B. Penetrating injuries, more specifically gunshot wounds (GSW), are high energy, high velocity injuries that can cause extensive damage as the object enters the body. C. Gunshot wounds carry a higher mortality than other pen-etrating wounds. They are almost always fatal if the bullet crosses the mid-line, crosses both hemispheres, or lodges in the brain. D. The blast energy of a bullet can be as high as 30 to 40 times the diameter of the bullet and can cause increased tissue damage as the bullet travels and displaces surrounding tissue. In contrast, stab wounds are considered low impact and the focus is more on the immediate tissue injury. Incidence A. Death rates have increased over the past 20 years. B. Affects almost 2 million people annually. C. Stab wounds are considered low velocity and are localized to the area of impact. Pathogenesis A. A bullet or projectile object crosses the skull barrier and enters the brain parenchyma. Predisposing Factors A. Males are more prone than females. B. Males older than 65 years of age. C. Single people are more prone than married people. D. Inner city resident. E. Lower income individuals. F. Members of ethnic minority groups. G. Drug and alcohol use. H. History of depression. I. History of previous suicide attempts. 17. Trauma Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
351 Subjective Data A. Common complaints/symptoms. 1. Patients will typically come in via emergency ser-vices, but will occasionally walk in or be driven by friends or family with a foreign object that has penetrated the skull. B. Family and social history (pertinent findings— positive/negative). 1. Family history is noncontributory. Penetrating head injuries occur more frequently in violent areas, large metropolitan areas, and areas of conflict. C. Review of systems (pertinent findings—positive/ negative). 1. Neuro—ask about headaches, dizziness, vertigo. 2. Head, ear, eyes, nose, and throat (HEENT)—blurry vision, double vision, loss of vision, changes in smell, bleeding from anywhere on the head. 3. Musculoskeletal—any weakness in the arms or legs or numbness/tingling. Physical Examination A. Perform a Glasgow Coma Score (GCS; see Table 17. 1). The score ranges from 3 to 15. If the patient is intubated, that is notated by the use of the letter “T” after the num-ber, such as 8T to indicate GCS of 8 in an intubated patient. B. Assess for signs of other injuries by completely undress-ing the patient. Axillae and groin are areas that require inspection—as stab wounds and GSW wounds are often found in those locations. C. Assess the head, scalp, and face for contusions, lacera-tions, or hematoma. D. A detailed neuro examination is performed when possible to determine baseline neurological function. Diagnostic Tests A. CT—noncontrast of head and cervical spine as indicated. B. Flat plate of skull can be done to identify foreign bodies (i. e., bullets). TABLE 17. 1 Glasgow Coma Score (GCS) Eye Opening (E) Spontaneous4 Tovoice 3 Topain 2 Noresponse1 Verbal Response (V) Orientedconversation 5 Confused/disoriented4 Incomprehensiblewords3 Incomprehensiblesounds 2 Noresponse1 Motor Response (M) Movesall extremities6 Localizesto pain 5 Withdrawsto pain 4 Decorticateposture3 Decerebrateposture2 Noresponse1 Total GCS =E+V+M GCS, Glasgow Coma Score. Differential Diagnosis A. There is typically no need for a differential diagnosis. An inspection will provide the diagnosis in this case. Evaluation and Management Plan A. General plan. 1. These patients are often critically ill and have a higher mortality. 2. Goals of treatment are geared toward preventing secondary brain injury by maintaining adequate perfu-sion and oxygenation to the brain. B. Patient/family teaching points. 1. Patient and family education should be geared toward anticipated patient needs as discharge nears. 2. Some examples include wound care, tracheotomy care, physical medicine, and rehab goals. C. Pharmacotherapy. 1. In the acute phase of care, interventions may include: a. Hemodynamic support: Blood transfusions and vasopressors may be necessary to reduce risks of hypotension related to hypovolemia and shock states. b. Seizure prophylaxis is indicated for severe brain injury and may include Keppra, Dilantin, or fos-phenytoin. c. Sedation and pain management with continuous infusions are used to keep the patient comfortable and avoid elevations in increased intracranial pressure (ICP). d. Antibiotic treatments that cross the blood-brain barrier such as ceftriaxone are warranted for open frac-tures and for any ICU-related infections. e. Osmotic diuretics such as mannitol and hyper-tonic saline help to reduce ICP. Follow-Up A. If the patient survives, follow-up with neurosurgeon in 10 to 14 days post discharge is recommended. B. If the patient had any additional injuries (multiple GSW often do), follow-up with those injury-specific specialty groups is recommended. C. Physical medicine and rehab may have a very active role in postdischarge care. Most head trauma will require reha-bilitative care and potentially neurological cognitive testing, evaluation, and management. Consultation/Referral A. T rauma is consulted on all trauma cases. B. Neurosurgery will be consulted on penetrating injuries to the brain. C. Other necessary consultants are selected based on the type and extent of injury. D. Physical medicine and rehab services are needed. E. Refer to psychiatry for self-inflicted wounds/suicide attempts. Special/Geriatric Considerations A. Indicators of poor outcomes/higher mortality include: 1. Lower GCS on arrival. 2. Increased age. 3. Suicide attempt (self-inflicted). 4. T ranscranial injury. 5. Perforated brain injury (entrance and exit wounds). 6. Coagulopathy. 7. Any episode of hypoxia prehospital or during hospi-talization. Penetrating Intracranial Injuries	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
352 Bibliography Aarabi, B., Tofighi, B., Kufera, J. A., Hadley, J., Ahn, E. S., Cooper, C.,... Uscinski, R. H. (2014, May). Predictors of outcome in civilian gunshot wounds to the head. Journal of Neurosurgery, 120 (5), 1138-1146. doi:10. 3171/2014. 1. JNS131869 Burgess, P., Sullivent, E., Sasser, S., Wald, M., Ossmann, E., & Kapil, V. (2010). Managing traumatic brain injury secondary to explosions. Journal of Emergencies, Trauma and Shock, 3 (2), 164-172. doi:10. 4103/ 0974-2700. 62120 Folio, L., Solomon, J., Biassou, N., Fischer, T., Dworzak, J., Raymont, V.,... Grafman, J. (2013, March). Semi-automated trajectory analysis of deep ballistic penetrating brain injury. Military Medicine, 178 (3), 338-345. doi:10. 7205/MILMED-D-12-00353 Mac Donald, C. L., Johnson, A. M., Cooper, D., Nelson, E. C., Werner, N. J., Shimony, J. S.,... Brody, D. L. (2011, June 2). Detection of blast-related traumatic brain injury in U. S. military personnel. The New England Journal of Medicine, 364 (22), 2091-2100. doi:10. 1056/ NEJMoa1008069 Paiva, W. S., de Andrade, A. F., Amorim, R. L., Figueiredo, E. G., & Teixeira, M. J. (2012, October). Brainstem injury by penetrating head trauma with a knife. British Journal of Neurosurgery, 26 (5), 779-781. doi:10. 3109/02688697. 2012. 655809 Saito, N., Hito, R., Burke, P. A., & Sakai, O. (2014). Imaging of penetrating injuries of the head and neck: Current practice at a level I trauma center in the United States. The Keio Journal of Medicine, 63 (2), 23-33. doi:10. 2302/kjm. 2013-0009-RE Shock Definition A. Impaired tissue oxygenation or inadequate cell utilization of oxygen. B. Shock is a condition that occurs due to inadequate oxygen delivery for aerobic cellular respiration, therefore leading to inadequate perfusion of tissue, irreversible cellular damage, and subsequently leading to death. C. Shock is not defined as hypotension; however, hypoten-sion can be a clinical indicator. D. Types of shock (see Table 17. 2). 1. Hypovolemic: Intravascular volume depletion. 2. Cardiogenic: Pump failure. 3. Distributive: Loss of peripheral vascular tone. 4. Obstructive: Impedance of adequate cardiac filling. Incidence A. 16% of shock states are hypovolemic. B. 16% of shock states are cardiogenic. C. Incidence—62% of shock states are distributive in nature and due to sepsis and 4% are distributive in nature from causes other than sepsis (Angus & van der Poll, 2013). D. Incidence—2% of shock states are obstructive (NEJM, 2013). Pathogenesis A. Inadequate oxygen delivery changes cell metabolism from aerobic to anaerobic. B. This leads to inadequate energy production and metabolic failure. C. Anaerobic metabolism leads to lactic acid production, causing the cell to cease function and swell. Once the cell swells, the membrane becomes permeable, allowing elec-trolytes and fluids to seep in. This causes the sodium and potassium pumps to fail, leading to mitochondrial damage and cell death. Predisposing Factors A. Hemodynamic. 1. Hemorrhage. 2. Vomiting. 3. Diarrhea. 4. Poor oral intake. B. Cardiogenic. 1. Myopathic: Myocardial ischemia. 2. Valvular/mechanical failure. 3. Drug overdose. C. Distributive. 1. Sepsis. 2. Anaphylaxis. 3. Adrenal insufficiency. 4. Neurogenic. 5. Liver failure. D. Obstructive. 1. Cardiac tamponade. 2. Pulmonary embolism. 3. Tension pneumothorax. 4. Constrictive pericarditis. Subjective Data A. Common complaints/symptoms. 1. Blood pressure. a. Systolic blood pressure (SBP) less than 90 mm Hg. b. Mean arterial pressure (MAP) less than 60 mm Hg. c. Change is SBP greater than 40 mm Hg. 2. Altered mental status. 3. Oliguria. 4. Lactic acidosis (anion gap acidosis). B. Common/typical scenario. 1. Noted hypotension. a. Chronic—absence of tissue hypoperfusion. b. Acute—presence of tissue hypoperfusion ( ↓urine output [UOP], altered mental status [AMS]). i. Start workup to determine type of shock while treating patient so as to not to allow circulatory collapse to occur. TABLE 17. 2 Hemodynamic Profile of Shock Types of Shock HR CO Ventricular Filling Pressure SVR Pulse Pressure SVO2 Cardiogenic ↑ ↓ ↑ ↑ ↓ ↓ Hypovolemic ↑ ↓ ↓ ↑ ↓ ↓ Distributive ↑ ↑or↓ ↓ ↓ ↑ ↑ Obstructive ↑ ↓ ↑or normal ↑ ↓ ↓ CO, cardiacoutput; HR, heart rate; SVO2, Mixed venous oxygen saturation; SVR, systemic vascular resistance. Source:Information was taken from Bergeron,N., Dubois, M. J., Dumont, M., Dial, S., Skrobik,Y. (2001). Intensive caredelirium screeningchecklist: evaluation of a new screeningtool. Intensive Care Medicine, 27, pp. 859-864. doi:10. 1007/s00134010090917. Trauma Guidelines Heather H. Meissen and Alison M. Kelley	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
353 C. Family/social history. 1. Further history needs to be obtained as well as a more thorough assessment. 2. Does the patient have a history that is significant for cardiac problems? 3. Does the patient have a history that is significant for exposure to infectious sources? Physical Examination A. Does the patient's skin feel cool and clammy, warm, or normal? B. If the patient has cool and clammy skin, significant car-diac history, or new chest pain, avoid fluids and start workup by obtaining a stat ECHO. C. Is skin warm or normal to touch? 62% of patients in shock will be distributive/septic in nature. Start treatment for presumed sepsis until otherwise noted. 1. Fluid bolus of 30 m L/kg of isotonic fluids within the first 3 hours. Diagnostic Tests A. For all forms of shock, obtain labwork and additional data points as quickly as possible. B. Complete b lood c ount (CBC). C. Arterial blood gas (ABG). D. Lactate. E. Comprehensive metabolic panel (CMP). F. Sc VO2 (if central access is in place). G. Central venous pressure (CVP) can be monitored with minimally invasive monitoring through the arterial line. H. Obtaining additional parameters such as passive leg raise, fluid challenges against stroke volume measurements, or vari-ations in systolic pressures, pulse pressure, or stroke volume changes while on mechanical ventilation should be consid-ered when applicable. I. Start vasopressors if patient is unresponsive to fluid for all forms of shock. 1. If patient is unresponsive to vasopressor support and history is suggestive, consider obstructive shock and implement treatment quickly. This is often referred to as pressor refractory shock. J. Once data points are back—identify correct diagnosis and treat appropriately (see Table 17. 2). Differential Diagnosis A. Myocardial infarction. B. Thyroid storm. C. Acute pancreatitis. D. Pulmonary embolism. E. Sepsis. F. Toxic/metabolic syndrome. G. Coagulopathy. H. Poisoning. Evaluation and Management Plan A. General plan. 1. Correct underlying process. 2. Fluids. a. Bolus. i. 10 to 30 m L/kg depending on the type of shock encountered. ii. The Surviving Sepsis Campaign recommends 30 m L/kg intravenous (IV) fluids within the first 3 hours of diagnosis of septic shock. b. Types of fluids. i. Isotonic fluids. 1)Lactated Ringers. 2)Normal saline. 3)Plasma-lyte A. ii. Blood products: Replacement of blood prod-ucts should be based on the individual patient's laboratory values. Advanced trauma life support guidelines recommend massive transfusion pro-tocol with universal red blood cells (RBCs) and plasma platelet pool for each six units of RBCs. 3. Vasopressor support. a. Terminology. i. Chronotropic: To change heart rate. ii. Inotropic: To change the force of the heart contraction. Positive inotropes increase the force of the contraction and negative inotropes weaken the force of contraction—otherwise known as squeeze. b. Norepinephrine. i. Endogenous catecholamine. ii. Acts as an excitatory neurotransmitter. iii. Alpha receptor-mediated peripheral vasocon-striction. iv. Weak 𝛽₁ receptor agonist. v. Dose: 0. 01 to 1 mcq/kg/min and titrate to effect. vi. Side effects: Local tissue necrosis. vii. First line pressor for septic shock. c. Epinephrine. i. Endogenous catecholamine. ii. Most potent 𝛽₁ agonist. iii. Both alpha and beta properties. iv. Potent inotropic and chronotropic. v. Dose: 0. 01 to 1 mcq/kg/min. vi. Second pressor choice in septic shock. d. Phenylephrine. i. Pure alpha receptor agonist. ii. Produces widespread vasoconstriction. iii. Dose: 0. 1 to 5 mcq/kg/min. iv. Side effects. 1)Bradycardia. 2)Low cardiac output. 3)Hypoperfusion to kidneys and bowel. v. Not recommended in septic shock. e. Vasopressin. i. Antidiuretic hormone (ADH)/osmoregulatory hormone. ii. Acts through v1 receptors to produce vasocon-striction. iii. Dose: 0. 03 units/min. iv. Typically not titratable. v. Not recommended as single agent. vi. Use with norepinephrine to decrease dose or to improve perfusion by increasing mean arterial pressure (MAP). B. T reatment of specific shock states. 1. Hypovolemic. a. Fluids. b. Vasopressor support. c. Control cause of fluid loss. i. Stop ongoing bleeding. ii. Stop ongoing emesis or diarrhea. 2. Cardiogenic. a. Improve myocardial function—percutaneous coronary intervention (PCI). b. T reat arrhythmias. c. Vasopressors plus inotropes. Shock	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2019/9/19 5:07 Page 354 #8 354 3. Obstructive. a. Relief of obstruction. 4. Distributive. a. Fluids. b. Vasopressors. c. T reatment of cause. i. Antibiotics. ii. Removal of source of infection. Follow-Up A. Resolution of hypotension. B. Increased urine output. C. Decreased heart rate. D. Lactic acid—trend until the level falls below 2. Consultation/Referral A. Consult critical care team for management of shock. B. Consult appropriate service for type of shock. 1. Cardiac surgery for cardiogenic shock or interven-tional radiology for obstructive shock, that is, pulmonary embolism or infectious diseases when sepsis is the cause of shock. 2. General surgery may need to be consulted if an abdominal source of sepsis is suspected. Special/Geriatric Considerations A. Consider age-related changes in geriatric patients. B. Response to treatment may occur much more slowly than in younger patients. C. Signs of shock may go unrecognized early on in geriatric patients due to loss of compensatory mechanisms that are common with aging. D. Also medications such as beta-blockers may diminish the body's ability to compensate. Bibliography Angus, D., & van der Poll, T. (2013). Severe sepsis and septic shock. The New England Journal of Medicine, 369, 840-851. doi:10. 1056/ NEJMra1208623 Beck, V., Chateau, D., & Bryson, G. L. (2014). Timing of vasopressor initi-ation and mortality in septic shock: A cohort study. Critical Care, 18 (3), R97. doi:10. 1186/cc13868 Bisschop, M., & Bellou, A. (2012). Anaphylaxis. Current Opinion in Critical Care, 18, 308-317. doi: 10. 1097/MCC. 0b013e3283557a63 Dalton, T., Rushing, M., Escott, M., & Monroe, B. (2015, November 2). Complexities of geriatric trauma patients. Journal of Emergency Medical Services, 40. Retrieved from http://www. jems. com/articles/ print/volume-40/issue-11/features/complexities-of-geriatric-trauma-patients. html?c =1 Dellinger, R., Levy, M., Rhodes, A., Annane, D., Gerlach, H., Opal, S.,... Moreno, R. (2013). Surviving Sepsis Campaign: International guide-lines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41 (2), 580-637. doi:10. 1097/CCM. 0b013e31827e83af Gutierrez, G., Reines, H., & Wulf-Gutierrez, M. (2004). Clinical review: Hemorrhagic stroke. Critical Care, 8, 373-381. doi:10. 1186/cc2851 Kadri, S., Rhee, C., Strich, J., Morales, M., Hohmann, S., Menchaca, J.,... Klompas, M. (2017). Estimating ten year trends in septic shock inci-dence and mortality in United States Academic Medical Centers using clinical data. Chest, 151 (2), 278-285. doi:10. 1016/j. chest. 2016. 07. 010 Klein, T., & Ramani, G. (2012). Assessment and management of cardiogenic shock in the emergency department. Cardiology Clinics, 30, 651-664. doi:10. 1016/j. ccl. 2012. 07. 004 Maier, R. V. (2001). Approach to the patient with shock. In J. Jameson, A. S. Fauci, D. L. Kasper, S. L. Hauser, D. L. Longo, & J. Loscalzo (Eds. ), Harrison's principles of internal medicine (20th ed. ). New York, NY: Mc Graw-Hill. Moranville, M., Mieure, K., & Santayana, E. (2011). Evaluation and management of shock states: Hypovolemic, distributive and car-diogenic. Journal of Pharmacy Practice, 24 (1), 44-60. doi:10. 1177/ 0897190010388150 Pandit, V., Rhee, P., Hashmi, A., Kulvatunyou, N., Tang, A., Khalil, M.,... Joseph, B. (2014). Shock index predicts mortality in geriatrictrauma patients: An analysis of the National T rauma Data Bank. Journal of Trauma and Acute Care Surgery, 76 (4), 1111-1115. doi:10. 1097/TA. 0000000000000160 Pauler, P., Newell, M., Hildebrandt, D., & Kirkland, L. (2017). Incidence, etiology and implications of shock in therapeutic hypothermia. Journal of the Minneapolis Heart Institute Foundation, 1, 19-23. doi:10. 21925/ 2475-0204-1. 1. 19 Reynolds, H., & Hochman, J. (2008). Cardiogenic shock: Current con-cepts and improving outcomes. Circulation, 117, 686-697. doi:10. 1161/CIRCULATIONAHA. 106. 613596 Rhee, C., Murphy, M. V., & Li, L. (2015). Lactate testing in suspected sepsis: T rends and predictors of failure to measure levels. Critical Care Medicine, 43(8), 1669-1676. doi:10. 1097/CCM. 0000000000001087 Richards, J., & Wilcox, S. (2014). Diagnosis and management of shock in the emergency department. Emergency Medicine Practice, 16 (3), 1-22. Silva, J., Concalves, L., & Sousa, P. (2018). Fluid therapy and shock: An integrative review. British Journal of Nursing, 27 (8), 449-454. doi:10. 12968/bjon. 2018. 27. 8. 449 Spinal Cord Injuries Susan F. Galiczynski Definition A. Spinal cord injury (SCI) is any damage to the spinal cord that causes temporary or permanent changes that disrupt normal function. This includes changes to motor, sensory, or autonomic function in the body below the level of the SCI. B. It is a challenging medical condition due to the limited therapeutic options available to treating physicians. There is a significant economic and social burden of SCI patients as well as society. Incidence A. Can affect up to 750 per million annually. B. In the United States, there are approximately 10,000 to 12,000 new traumatic SCIs per year. C. Approximately 280,000 people are presently living with SCI in North America. D. Up to 60% of injuries include the cervical spine. E. For the geriatric population, a majority of injuries are incomplete. F. For the geriatric patient, mortality and morbidity are significantly higher. G. Higher incidence of central cord injuries occurs in the geriatric population. Pathogenesis A. Spinal cord injuries are considered high impact injuries, often resulting from high speed motor vehicle crashes or falls from significant height. B. Other mechanisms may include: 1. Hyperextension injury with or without longitudinal ligament tear. 2. Vertical column loading (axial load) compression. 3. Distraction injuries (seen with hangings). 4. Penetrating injuries. 5. Pathological fractures (seen more commonly in the elderly). Predisposing Factors A. Male. B. Persons between 15 and 24 years of age. C. Increasing occurrence in elderly. Subjective Data A. Common complaints/symptoms. 17. Trauma Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
355 1. Neck or back pain. 2. Numbness. 3. Loss of limb function. 4. Paresthesia. B. Common/typical scenario. 1. Other signs and symptoms. a. Bowel and bladder dysfunction. b. Priapism. c. Hyperparesthesia/pain. C. Family and social history. 1. Emergency medical support (EMS) report may give you significant information regarding the scene and how the patient was found. 2. If possible, ask the patient about the history of events: Mechanism? Motor vehicle collisions (MVC)? Location in car? Restrained? Ejected? Mechanical fall or syncope? Fall from height? How far? 3. Blunt versus penetrating. 4. Distraction injury to spine? Hyperextension, hyper-flexion, hyperrotation? 5. Ask the patient about pain and the ability to move extremities after injury (see Figure 17. 1). 6. Assess for drug or alcohol use as this may impact your examination. Physical Examination A. Primary survey (advanced trauma life support [ATLS]) to assess for life-threatening injuries. B. Pay particular attention to respiratory status as level of injury can impact spontaneous breathing. 1. Injuries above C3 result in respiratory arrest. 2. Injuries at C5 to C6 spare the diaphragm and diaphragm breathing is seen. 3. Injuries below T1 to the level of L2 can affect the intercostals. C. Motor and sensory assessment to assess level of injury. D. Cardiovascular changes seen with SCI: SCI can impact the sympathetic pathways leading to alterations in blood pressure, heart rate, and temperature regulation. E. Gastrointestinal changes associated with SCI may include loss of bowel function, development of an ileus, or obstruc-tion. F. GU: urinary incontinence and retention. G. Always have a heightened suspicion for other injuries. Diagnostic Tests A. CT. B. MRI. C. Plain films (x-rays) can help identify fractures. Differential Diagnosis A. Central cord syndrome. B. Anterior cord syndrome. C. Posterior cord syndrome. D. Brown-Sequard syndrome (often seen with penetrating trauma). Evaluation and Management Plan A. General plan. 1. Interventions in SCI are aimed at preventing secondary injury. 2. Earlier surgical intervention, when indicated, has been shown to improve neurological recovery. 3. Maintain adequate airway and respirations. 4. Cervical spine immobilization. 5. Thoracic and lumbar bracing if necessary. 6. Maintain adequate circulation. 7. Ongoing neurological assessment. 8. Assess for signs of neurogenic shock and support hemodynamics. C2 C6 C3 C8C3 C4 C5(C4) T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 L1 L2 L3 L4 L5S3 S4S2T12(T2) C7 S2S1C6C5C4C3C2 L5L4L3L2L1T12T11T10T9T8C8C7 T7T6T5T4T3T2T1 S3 L1 L2 L3 L4 L4L5S4 S5C5 C8C1 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 S1 S2 S3 S4 S5L2 L3 L4 L5 FIGURE 17. 1 Dermatomemap. Spinal Cord Injuries	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
356 9. Aggressive bowel regimen to prevent constipation. 10. Monitor urine with either a Foley catheter or self-catheterization as needed. B. Patient/family teaching points. 1. Patients need to be taught how to monitor and assess their skin for any breakdown. 2. Depending on the level of the ACI, patients may have bowel, bladder, and sexual dysfunction. 3. Teach patients and caregivers to recognize a life-threatening condition called autonomic dysreflexia, which can be caused by bladder spasms, urinary tract infections, or even external factors such as too tight cloth-ing, belts, or shoes. 4. Physical and occupational therapy will be necessary for reducing muscle contractures and atrophy. C. Pharmacotherapy. 1. Use of glucocorticoids, specifically methylprednisone, after acute traumatic SCI has been a controversial con-cept. The recommendations were to use methylpred-nisone for either 24 or 48 hours, depending on whether it was started 3 or 8 hours after injury, respectively. a. Many studies are showing early surgical interven-tion with decompression is preferable to steroid use. 2. Other pharmacological agents used in human clinical trials include: Tirilazad, naloxone, GM ganglioside, and riluzole. Recent neuroprotection agents involved in clin-ical trial include BA-120 (Cethrin) and minocycline. 3. Antibiotics for penetrating injuries. 4. Gastrointestinal (GI) prophylaxis and bowel regimen. Follow-Up A. SCI patients have a long course of physical medicine and rehabilitation. B. Neurosurgery, orthopedics, and any other specialty group needed is involved in care. Consultation/Referral A. Neurosurgery/orthopedics (bony injuries) for manage-ment and possible fixation/fusion. B. Prompt transfer to a Level I trauma center needs to be prioritized. Special/Geriatric Considerations A. SCI is an ever-increasing challenge with annual incidence of 750 per million in the developed world and even higher incidence in the developing world. B. Pathophysiology of SCI involves primary and secondary injury mechanisms with future treatment strategies and emphasis on preventing or reversing secondary injury. C. Medical management of SCI patients is in accordance with Advanced T rauma Life Support guidelines. Surgery for acute SCI within 24 hours of injury as a treatment option is not associated with any increased risk of complications and may provide a neurological benefit. D. Patients with an unstable spinal column with incomplete SCI should be considered for acute stabilization as soon as possible after obtaining necessary imaging studies. Bibliography Bracken, M. B., Shepard, M. J., Collins, W. F., Jr., Holford, T. R., Baskin, D. S., Eisenberg, H. M.,... Marshall, L. F. (1992). Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the Second National Acute Spinal Cord Injury Study. Journal of Neurosurgery, 76 (1), 23-31. doi:10. 3171/jns. 1992. 76. 1. 0023 Bracken, M. B., Shepard, M. J., Collins, W. F., Holford, T. R., Young, W., Baskin, D. S.,... Maroon, J. (1990). A randomized, controlled trialof methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. The New England Journal of Medicine, 322 (20), 1405-1411. doi:10. 1056/NEJM199005173222001 Bracken, M. B., Shepard, M. J., Holford, T. R., Leo-Summers, L., Aldrich, E. F., Fazl, M., & Young, W. (1997). Administration of methylpred-nisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treat-ment of acute spinal cord injury: Results of the Third National Acute Spinal Cord Injury Randomized Controlled T rial. Journal of the Ameri-can Medical Association, 277 (20), 1597-1604. doi:10. 1001/jama. 1997. 03540440031029 Cengiz, S. L., Kalkan, E., Bayir, A., IIik, K., & Basefer, A. (2008). Timing of thoracolomber spine stabilization in trauma patients; impact on neuro-logical outcome and clinical course. A real prospective (rct) randomized controlled study. Archives of Orthopaedic and Trauma Surgery, 128 (9), 959-966. doi:10. 1007/s00402-007-0518-1 Cheung, V., Hoshide, R., Bansal, V., Kasper, E., & Chen, C. (2015). Methylprednisolone in the management of spinal cord injuries: Lessons from randomized, controlled trials. Surgical Neurology International, 6, 142. doi:10. 4103/2152-7806. 163452 Conrad, B. P., Horodyski, M., Wright, J., Ruetz, P., & Rechtine, G. R., 2nd. (2007). Log-rolling technique producing unacceptable motion during body position changes in patients with traumatic spinal cord injury. Journal of Neurosurgery Spine, 6 (6), 540-543. doi:10. 3171/spi. 2007. 6. 6. 4 De Vivo, M. J. (1997). Causes and costs of spinal cord injury in the United States. Spinal Cord, 35 (12), 809-813. doi:10. 1038/sj. sc. 3100501 Fassett, D. R., Harrop, J. S., Maltenfort, M., Jeyamohan, S. B., Ratliff, J. D., Anderson, D. G.,... Sharan, A. D. (2007). Mortality rates in geriatric patients with spinal cord injuries. Journal of Neurosurgery Spine, 7 (3), 277-281. doi:10. 3171/SPI-07/09/277 Fehlings, M. G., & Perrin, R. G. (2006). The timing of surgical inter-vention in the treatment of spinal cord injury: A systematic review of recent clinical evidence. Spine (Phila Pa 1976), 31 (11 Suppl. ), S28-S35. doi:10. 1371/journal. pone. 0032037 Fehlings, M. G., & Sekhon, L. (2000). Cellular, ionic, and biomolecular mechanisms of the injury process. In C. H. Tator & E. Benzel (Eds. ), Contemporary management of spinal cord injury: From impact to rehabili-tation (pp. 33-50). Chicago, IL: American Association of Neurological Surgeons. doi:10. 1097/01. brs. 0000217973. 11402. 7f Fehlings, M. G., Vaccaro, A., Wilson, J. R., Singh, A., Cadotte, W. D., Har-rop, J. S.,,... Rampersaud, R. (2012). Early versus delayed decom-pression for traumatic cervical spinal cord injury: Results of the surgical timing in acute spinal cord injury study (STASCIS). PLOS ONE, 7 (2), e32037. doi:10. 1371/journal. pone. 0032037 Hadley, M. N., Walters, B. C., Grabb, P. A., Oyesiku, N. M., Przybylski, G. J., Resnick, D. K., & Ryken, T. C. (2002a). Blood pressure manage-ment after acute spinal cord injury. Neurosurgery, 50 (Suppl. 3), S58-S62. doi:10. 1097/00006123-200203001-00012 Hadley, M. N., Walters, B. C., Grabb, P. A., Oyesiku, N. M., Przybylski, G. J., Resnick, D. K., & Ryken, T. C. (2002b). T reatment of sub-axial cervical spinal injuries. Neurosurgery, 50 (Suppl. 3), S156-S165. doi:10. 1097/00006123-200203001-00024 Hagen, S. (1999). CBO memorandum: Projections of expenditures for long-term care services for the elderly. Washington, DC: Congressional Budget Office. Hamamoto, Y., Ogata, T., Morino, T., Hino, M., & Yamamoto, H. (2007). Real-time direct measurement of spinal cord blood flow at the site of compression: Relationship between blood flow recovery and motor defi-ciency in spinal cord injury. Spine, 32 (18), 1955-1962. doi:10. 1097/ BRS. 0b013e3181316310 Katoh, S., el Masry, W. S., Jaffray, D., Mc Call, I. W., Eisenstein, S. M., Pringle, R. G., & Ikata, T. (1996). Neurologic outcome in conservatively treated patients with incomplete closed traumatic cer-vical spinal cord injuries. Spine, 21 (20), 2345-2351. doi:10. 1097/ 00007632-199610150-00008 La Rosa, G., Conti, A., Cardali, S., Cacciola, F., & Tomasello, F. (2004). Does early decompression improve neurological outcome of spinal cord injured patients? Appraisal of the literature using a meta-analytical approach. Spinal Cord, 42 (9), 503-512. doi:10. 1038/sj. sc. 3101627 Levi, L., Wolf, A., & Belzberg, H. (1993). Hemodynamic parameters in patients with acute cervical cord trauma: Description, intervention, and prediction of outcome. Neurosurgery, 33 (6), 1007-1016. doi:10. 1227/ 00006123-199312000-00008 Liverman, T. C., Altevogt, B. M., Joy, E. J., & Johnson, T. R. (Eds. ). (2005). Spinal cord injury: Progress, promise, and priorities. Washington, DC: National Academy of Sciences. Mc Kinley, W., Meade, M. A., Kirshblum, S., & Barnard, B. (2004). Out-comes of early surgical management versus late or no surgical inter-vention after acute spinal cord injury. Archives of Physical Medicine and Rehabilitation, 85 (11), 1818-1825. doi:10. 1016/j. apmr. 2004. 04. 03217. Trauma Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
2019/9/19 5:07 Page 357 #11 357 Oyinbo, C. A. (2011). Secondary injury mechanisms in traumatic spinal cord injury: A nugget of this multiply cascade. Acta Neurobiologiae Exper-imentalis, 71 (2), 281-299. Pointillart, V., Petitjean, M. E., Wiart, L., Vital, J. M., Lassi ́e, P., Thicoip ́e, M., & Dabadie, P. (2000). Pharmacological therapy of spinal cord injury during the acute phase. Spinal Cord, 38 (2), 71-76. doi:10. 1038/sj. sc. 3100962 Pollard, M. E., & Apple, D. F. (2003). Factors associated with improved neu-rologic outcomes in patients with incomplete tetraplegia. Spine, 28 (1), 33-39. doi:10. 1097/00007632-200301010-00009 Rahimi-Movaghar, V. (2005). Efficacy of surgical decompression in the set-ting of complete thoracic spinal cord injury. Journal of Spinal Cord Medicine, 28 (5), 415-420. doi:10. 1080/10790268. 2005. 11753841 Rowland, J. W., Hawryluk, G. W., Kwon, B., & Fehlings, M. G. (2008). Current status of acute spinal cord injury pathophysiology and emerg-ing therapies: Promise on the horizon. Neurosurgical Focus, 25 (5), E2. doi:10. 3171/FOC. 2008. 25. 11. E2 Sapkas, G. S., & Papadakis, S. A. (2007). Neurological outcome following early versus delayed lower cervical spine surgery. Journal of Orthopaedic Surgery, 15 (2), 183-186. doi:10. 1177/230949900701500212 Sekhon, L. H., & Fehlings, M. G. (2001). Epidemiology, demographics, and pathophysiology of acute spinal cord injury. Spine, 26 (24 Suppl. ), S2-S12. doi:10. 1097/00007632-200112151-00002 Tanhoffer, R. A., Yamazaki, R. K., Nunes, E. A., Pchevozniki, A. I., Pchevozniki, A. M., Nogata, C.,... Fernandes, L. C. (2007). Glutamine concentration and immune response of spinal cord-injured rats. Journal of Spinal Cord Medicine, 30 (2), 140-146. doi:10. 1080/10790268. 2007. 11753925 Tator, C. H., Duncan, E. G., Edmonds, V. E., Lapczak, L. I., & Andrews, D. F. (1987). Comparison of surgical and conservative management in 208 patients with acute spinal cord injury. The Canadian Journal of Neu-rological Sciences, 14 (1), 60-69. doi:10. 1017/S0317167100026858 Velmahos, G. C., Toutouzas, K., Chan, L., Tillou, A., Rhee, P., Murray, J., & Demetriades, D. (2003). Intubation after cervical spinal cord injury: To be done selectively or routinely? The American Surgeon, 69 (10), 891-894. Waters, R. L., Meyer, P. R., Jr., Adkins, R. H., & Felton, D. (1999). Emer-gency, acute, and surgical management of spine trauma. Archives of Physical Medicine and Rehabilitation, 80 (11), 1383-1390. doi:10. 1016/ S0003-9993(99)90248-4 Wyndaele, M., & Wyndaele, J. J. (2006). Incidence, prevalence and epidemi-ology of spinal cord injury: What learns a worldwide literature survey? Spinal Cord, 44 (9), 523-529. doi:10. 1038/sj. sc. 3101893 Xu, K., Chen, Q.-X., Li, F.-C., Chen, W.-S., Lin, M., & Wu, Q. (2009). Spinal cord decompression reduces rat neural cell apoptosis secondary to spinal cord injury. Journal of Zhejiang University Science B, 10 (3), 180-187. doi:10. 1631/jzus. B0820161 Traumatic Brain Injury Susan F. Galiczynski Definition A. T raumatic brain injury (TBI) is an insult to the brain caused by direct physical force causing a physical force that may produce a diminished or altered state of consciousness, which may result in an impairment of cognitive abilities or physical functioning. B. These impairments may be temporary or permanent, depending on the degree of injury. Incidence A. Leading cause of trauma-related death in persons under age 45. B. Often occurs during the most productive years. C. Represents approximately 200 cases per 100,000 injuries annually in the United States. D. Responsible for approximately 12% to 30% of all trau-matic deaths. E. Motor vehicle collisions (MVC) are the leading cause of TBI. F. Penetrating head trauma is the leading cause of brain injury deaths. Pathogenesis A. According to the Centers for Disease Control and Pre-vention, more than 130,000 unintentional deaths were doc-umented in 2013. Although there are many mechanisms that can result in traumatic injury, these injuries can be primar-ily divided into two categories: Blunt or penetrating injuries. Blunt injuries are those that result from a blunt force and do not break the skin. Injuries are usually localized to the area of impact. Mechanisms of injury described as blunt injury can be motor vehicle accidents, assaults, falls, and sports-related injuries. B. T wo main forces are associated with TBI. 1. Impact loading is the direct force against the skull, causing disruption of brain tissue, vascular, and nerve structures. 2. Impulsive loading is sudden movement without direct impact as seen with acceleration-deceleration injury. Predisposing Factors A. Males are more prone than femalea. B. Ages 15 to 25; over 65 years of age. C. Single people are more prone than married people. D. Inner city residents. E. Lower income individuals. F. Members of ethnic minority groups. G. Drug and alcohol use. H. History of previous TBI. Subjective Data A. Common complaints/symptoms. 1. ±loss of consciousness. 2. Nausea and/or vomiting. 3. Headache. 4. Amnesia to events surrounding trauma. B. Common/typical scenario. 1. Other signs and symptoms. a. Altered mentation. b. Increased lethargy. c. Slurred speech. d. Combative behavior. e. History of seizures. C. Family and social history. 1. Ask patient to describe events leading up to trauma. What is the last thing the patient remembers? What symptoms is he or she experiencing? Nausea? Vomiting? Headache? Dizziness? Photophobia? Does the patient have pain? Location? Characteristics? 2. Ask the patient about recent drug and alcohol use. 3. Ask the patient about past medical history. Seizures? Concussions? 4. Determine if the patient is on any anticoagulants or antiplatelet medications. Physical Examination A. The American College of Surgeons has developed the Advanced T rauma Life Support guidelines to provide a quick but systematic approach to assessment to help identify those injuries that can be life-threatening as soon as possible. Using the mnemonic A-B-C-D-E, the primary survey must be com-pleted before the secondary survey can be started and a plan of care established (see Table 17. 3). Traumatic Brain Injury	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
358 TABLE 17. 3 Primary Survey System Assessment Points A-Airway Is it patent? Is patient talking? Normal voice?Hoarse? Is airway occluded by debris?Blood?Vomit?Teeth?Couldthere bean airway injury given the mechanism? Isthe cervical spine immobilized? B-Breathing Is the patient breathing?Aretherebreath soundsbilaterally? Arelungs clear? C-Circulation Does the patient have pulses? Is there activehemorrhage? D-Disability What is the GCS? Is the patient awake and followingcommands? Is the patient confused?Is the patient conscious? E-Exposure Undressthe patient completely. Look for anyholes, lacerations, unusual bruising, ormarks. GCS, Glasgow Coma score. B. If any potentially life-threatening issue is identified during the primary survey, it needs to be addressed before moving onto the next assessment. For example, if the patient has decreased breath sounds (B) on the right side and has sus-tained chest trauma, a pneumothorax should be suspected. A chest tube should be placed before moving on with assess-ment to circulation (C). The secondary survey is a complete head-to-toe evaluation of the patient, looking for other potential injuries, once it is determined that the patient is stable at the end of the primary survey. C. Perform a Glasgow Coma Score (GCS; see Table 17. 1). D. Assess for signs of other injuries by completely undressing the patient. E. Assess head, scalp, and face for contusions, lacerations, or hematoma. Diagnostic Tests A. CT head, cervical spine, thoracic spine, lumbar spine, chest, abdomen, and pelvis. CT head and cervical, thoracic, and lumbar spine are noncontrast. CT chest, abdomen, and pelvis are with contrast. Differential Diagnosis A. Concussion. B. Cerebral contusion. C. Coup-contrecoup injuries. D. Epidural hematoma. E. Subdural hematoma. F. Subarachnoid hematoma. G. Mass lesion (may have prompted fall). Evaluation and Management Plan A. General plan. 1. For concussion, treatment is symptom based. 2. Consult neurosurgery for more severe injuries. 3. Prevent hypotension and hypoxemia. B. Patient/family teaching points. 1. Monitoring for postconcussive syndrome is impor-tant. 2. Follow-up with concussion clinic may be advised based on the degree of concussion and residual symp-toms. 3. Neuropsychology depending on severity of symptoms. C. Pharmacotherapy. 1. T ry to avoid opioids. 2. For more severe head injury, seizure prophylaxis may be indicated for up to 10 days. Length depends on whether the patient presents with a seizure or has any seizure activity during hospitalization. 3. For severe head injury, osmotic diuretics may be used to reduce edema. Follow-Up A. No contact sports for minimum of 6 weeks. B. Prothrombin time (PT)/OT/speech consults. C. Neurosurgical evaluation 10 to 14 days post discharge. May need repeat CT head. Consultation/Referral A. Inpatient referrals: T rauma and neurosurgery. B. May need rehab referral. C. Outpatient concussion follow-up for post concussive syndrome. Special/Geriatric Considerations A. For persons with repeated concussion, a discussion regarding cessation of sports is imperative. Repeated concus-sions have been shown to have a residual effect. B. For patient on anticoagulation or antiplatelet therapy, risk of injury and complications need to be discussed. C. If the GCS is less than 8, intubation should be considered as the patient may not be awake enough to maintain a patent airway. Bibliography Carney, N., Totten, A., O'Reilly, C., Ullman, J., Hawryluk, G., Bell, M., & Ghajar, J. (2016). Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery, 80, 1-10. doi:10. 1227/NEU. 0000000000001432 Esterov, D., & Greenwald, B. D. (2017, August 11). Autonomic dys-function after mild traumatic brain injury. Brain Sciences, 7 (8), e100. doi:10. 3390/brainsci7080100 Haring, R. S., Narang, K., Canner, J. K., Asemota, A. O., George, B. P., Selvarajah, S., & Schneider, E. B. (2015, January 15). T raumatic brain injury in the elderly: Morbidity and mortality trends and risk factors. The Journal of Surgical Research, 195, 1-9. doi:10. 1016/j. jss. 2015. 01. 017 Steyerberg, E. W., Mushkudiani, N., Perel, P., Butcher, I., Lu, J., Mc Hugh, G. S., & Maas, A. I. (2008, August 5). Predicting outcome after trau-matic brain injury: Development and international validation of prog-nostic scores based on admission characteristics. PLOS Medicine, 5 (8), e165. doi:10. 1371/journal. pmed. 0050165 Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired con-sciousness. Lancet, 2, 81-84. doi:10. 1016/S0140-6736(74)91639-0 Teasdale, G., & Jennett, B. (1976). Assessment and prognosis of coma after head injury. Acta Neurochirurgica, 34, 45-55. doi:10. 1007/ BF01405862 Thompson, D. O., Hurtado, T. R., Liao, M. M., Byyny, R. L., Gravitz, C., & Haukoos, J. S. (2011, November). Validation of the simplified motor score in the out-of-hospital setting for the prediction of outcomes after traumatic brain injury. Annals of Emergency Medicine, 58 (5), 417-425. doi:10. 1016/j. annemergmed. 2011. 05. 033 Tian, H. L., Geng, Z., Cui, Y. H., Hu, J., Xu, T., Cao, H. L., & Chen, H. (2008, August, 14). Risk factors for posttraumatic cerebral infarction in patients with moderate or severe head trauma. Neurosurgical Review, 31, 431-436. doi:10. 1007/s10143-008-0153-517. Trauma Guidelines	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
II Perioperative Considerations 18. Preoperative Evaluation and Management 19. Perioperative and Intraoperative Management 20. Postoperative Evaluation and Management	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
361 18Preoperative Evaluation and Management Kristopher R. Maday Scope of Chapter The advanced practice provider (APP) frequently evaluates a patient prior to surgery. The APP must be aware of risk fac-tors, appropriate testing, and the American Society of Anes-thesiologists (ASA) classification of risk and medications in order to make an informed decision of a patient's readiness for surgery. This chapter explores what the APP needs to know to make these decisions. Considerations Kristopher R. Maday Risk Factors A. Age: There is a linear increase in surgical risk with age as a result of an increasing number of comorbidities. B. Exercise capacity. 1. Ability to perform four or more metabolic equivalents (METs) reduces the risk of cardiovascular complications associated with surgery. Examples include: a. Walking up a flight of stairs. b. Mowing the lawn. c. Walking at ground level at 4 miles per hour. d. Performing heavy work around the house. 2. Inability to perform four or more METs is associated with increased length of stay and perioperative complica-tions. a. Preoperative evaluation by physical therapy for prehabilitation, or cardiology for cardiac testing, can be beneficial in higher risk patients. C. Nutritional. 1. Obesity is a risk factor for pulmonary thromboem-bolism, and presents increased rate of wound infections, pneumonia, and others. 2. Malnutrition prior to surgery is associated with: a. Increased infection risk. b. Poor wound healing. c. Intestinal bacterial overgrowth. d. Increased hospital length of stay. It increases postoperative complications; for example, anastomotic leak can result in enterocutaneous fistula formation. D. Pulmonary. 1. Obstructive sleep apnea: Increases risk of postopera-tive hypoxemia, reintubation, and ICU admission. 2. Smoking: Increased risk of wound complications, infections, and ICU admissions. E. Alcohol: Screen for the possibility of developing with-drawal and/or delirium tremens in the postoperative period. F. Illicit drug use and prescription drug abuse: Screen for opioid narcotics, benzodiazepines, or amphetamines as peri-operative and postoperative pain control may prove to be dif-ficult. Withdrawal may also occur and needs to be assessed. G. Endocrine disorders: Diabetes increases risk of surgical site infection, as well as perioperative cardiac events. H. Medication use. 1. A full medication reconciliation should be obtained before surgery, including the use of over-the-counter medications, such as aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs ( NSAIDs), which are associated with an increased risk of perioperative bleed-ing. 2. Alternative, herbal, and natural supplement use should also be documented due to drug interactions and risk of bleeding. 3. Anticoagulants. I. Personal/family history of anesthetic complications such as malignant hypertension (HTN) or postoperative nausea and vomiting. Calculating Risk of Perioperative Complications A. American College of Surgeons Surgical Risk Calculator: riskcalculator. facs. org/Risk Calculator/. 1. Factors that can affect surgical risk. a. Age. b. Gender. c. Functional status. d. American Society of Anesthesiologists classifica-tion. e. Diabetes, HTN, and/or congestive heart failure (CHF). f. Smoking and/or history of chronic obstructive pulmonary disease (COPD). g. Renal disease and/or on dialysis. h. Steroid use for chronic conditions. i. Presence of ascites. j. Disseminated cancer. k. Emergency surgery. Bibliography Cohen, M. E., Liu, Y., Ko, C. Y., & Hall, B. L. (2017). An examination of American College of Surgeons NSQIP s urgical risk calculator a ccuracy. Journal of the American College of Surgeons, 224 (5), 787-795. doi:10. 1016/j. jamcollsurg. 2016. 12. 057 Dindo, D., Muller, M. K., Weber, M., & Clavien, P. A. (2003). Obesity in general elective surgery. Lancet, 361 (9374), 2032-2035. doi:10. 1016/ S0140-6736(03)13640-9 Considerations	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
362 Fleisher, L. A., Fleischmann, K. E., & Auerbach, A. D. (2014). 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiol-ogy, 64 (22), e77-e137. doi:10. 1016/j. jacc. 2014. 07. 945 Grønkjær, M., Eliasen, M., & Skov-Ettrup, L. S. (2014). Preoperative smoking status and postoperative complications: A systematic review and meta-analysis. Annals of Surgery, 259 (1), 52-71. doi:10. 1097/SLA. 0b013e3182911913 Kaw, R., Pasupuleti, V., Walker, E., Ramaswamy, A., & Foldvary-Schafer, N. (2012). Postoperative complications in patients with obstructive sleep apnea. Chest, 141 (2), 436-441. doi:10. 1378/chest. 11-0283 Kleinwächter, R., Kork, F., & Weiss-Gerlach, E. (2010). Improving the detection of illicit substance use in preoperative anesthesiological assess-ment. Minerva Anestesiologica, 76 (1), 29-37. Oresanya, L. B., Lyons, W. L., & Finlayson, E. (2014). Preoperative assess-ment of the older patient: A narrative review. Journal of the Ameri-can Medical Association, 311 (20), 2110-2120. doi:10. 1001/jama. 2014. 4573 Sidney, M. J. K., & Blumchen, G. (1990). Metabolic equivalents (METs) in exercise testing, exercise prescription, and evaluation of functional capac-ity. Clinical Cardiology, 13, 555-565. doi:10. 1002/clc. 4960130809 Tønnesen, H., Nielsen, P. R., Lauritzen, J. B., & Møller, A. M. (2009). Smoking and alcohol intervention before surgery: Evidence for best prac-tice. British Journal of Anaesthesia, 102 (3), 297-306. doi:10. 1093/bja/ aen401 Care Principles Kristopher R. Maday Testing in the Perioperative Setting A. The American Society of Anesthesiologists (ASA) recom-mends against routine preoperative laboratory testing in the absence of clinical indications. 1. Testing should occur depending on the patient's med-ical history, underlying disease, increased perioperative risk, or high risk surgery. Common testing includes: a. Complete blood count (CBC). i. Hemoglobin/hematocrit. 1)Cardiac surgery patients should have a hemoglobin greater than 7 g/d L to reduce cardiac complications as a result of surgery. Patients may require transfusion for hemoglobin of 7 or less. 2)Patients with anemia or thrombocytope-nia prior to major surgery may need to be seen and cleared by hematology. ii. Platelet count. 1)Greater than 50,000/ μL for most major surgery. 2)Greater than 100,00/ μL for neuro-surgery/ocular surgery. 3)Greater than 80,000/ μL for epidural anes-thesia. 4)20,000 to 50,000/ μL for endoscopy. b. Coagulation studies. i. Only perform if clinically indicated by history or physical examination. ii. Tests include prothrombin time (PT) or par-tial thromboplastin time (PTT). iii. International Ratio (INR) may be variable. If less than 2. 0, there is no indication that the patient will have more than normal tissue oozing. 1)If the patient is taking warfarin, the medi-cation should be stopped and the level should predictably drop to less than 1. 5 within 4 to 5 days. 2)In elderly patients, the reversal of warfarin may be longer and presents with increased riskof a thromboembolic event. Patients may need to be covered with therapeutic low molecular weight heparin or unfractionated heparin in these cases. c. Basic metabolic profile (BMP). i. It is recommended to obtain routine screening BMP. ii. Patients with type 2 diabetes mellitus taking oral antihypoglycemic agents should be converted to sliding scale insulin until oral medications can be resumed postoperatively. iii. Patients with a history of type 1 diabetes mellitus should have a perioperative insulin plan depending on the type of insulin they are using and the type of surgical procedure they are under-going. iv. Due to the risk of diabetic ketoacidosis, patients with type 1 diabetes mellitus must have basal insulin supplied at all times. v. Renal function: Obtain serum creatinine in patients over the age of 50 if undergoing inter-mediate or higher surgery. d. Urine pregnancy test for all women of childbearing years. e. EKG. i. Routine screening in asymptomatic patients undergoing low-risk surgery is not recommended. ii. Intermediate or high risk surgery, patients with known coronary disease, peripheral vascular disease, cerebrovascular disease, dysrhythmias, or other structural heart disease should have at least a preoperative 12-lead ECG performed. Consul-tation with anesthesiology or cardiology for fur-ther testing recommendations (such as cardiac stress testing or echocardiogram) may be needed depending on underlying cardiac conditions and the type of surgery the patient is undergoing. f. Chest radiography. i. Unless the type of surgery warrants preopera-tive radiograph, routine screening is not indicated. g. Pulmonary function testing. i. May be required for lung surgery, if patient has underlying history of chronic obstructive pul-monary disease (COPD), or if surgery is depen-dent on lung volume measurements. ii. Not indicated for routine screening. ASA Classifications A. Physical status classification system. 1. Simple classification system to predict preoperative risk of increased mortality and morbidity associated with anesthesia and surgery. 2. Six-tiered system. a. ASA 1: Healthy patient. b. ASA 2: Mild systemic disease. c. ASA 3: Severe systemic disease. d. ASA 4: Severe systemic disease that is a constant threat to life. e. ASA 5: Moribund patient who is not expected to survive without the operation. f. ASA 6: Declared brain-dead patient who is under-going organ procurement. B. Mallampati classification. 1. Used to predict ease of intubation. 2. May help predict obstructive sleep apnea. 3. Simple test done during physical examination. 18. Preoperative Evaluation and Management	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
363 a. Patient should sit upright with head in neutral position. b. Ask patient to open mouth and extend tongue without speaking or making noise. 4. Scoring. a. Class I—complete visualization of soft palate. b. Class II—complete visualization of uvula (see Figure 18. 1). c. Class III—visualization of base of uvula. d. Class IV—soft palate not visible at all. Nutrition and Fluids A. Preoperative nutritional considerations. 1. Preoperative nutritional assessment. a. Nutritional Risk Screening (NRS 2002) tool. i. This score is calculated from two variables. 1)Impaired nutritional status: Recent weight loss, decreased food intake, body mass index (BMI) ≤18. 5. 2)Severity of illness. ii. A score 3 or more would indicate need for nutritional supplementation/support prior to surgery. b. Protein status. i. Serum albumin, transferrin, and prealbumin have all been studied, but there is conflicting data on utility. ii. Only a serum albumin less than 2. 2 g/d L has shown to be the most predictive. c. Patient with severe preoperative malnutrition may benefit from nutritional support prior to surgery. i. Options include oral supplementation with high-protein shakes, tube feedings with indwelling feeding tube, and/or total parenteral nutrition (TPN). d. ASA fasting guidelines. i. Lowest risk for aspiration. ii. 2 hours after clear liquids. iii. 4 hours after breast milk. iv. 6 hours after light meal. v. 8 hours after regular meal. B. Fluid considerations. 1. Patients may be nil per os (NPO) for up to 12 hours before surgery. 2. Inpatient. a. Dextrose-containing fluids should be started when NPO to prevent lean muscle catabolism. 3. Outpatient. a. Fluid status should be assessed and intravenous fluid administered accordingly. Bibliography American Society of Anesthesiologists. (2014). ASA Physical Status Classifi-cation System. Retrieved from https://www. asahq. org/resources/clinical-information/asa-physical-status-classification-system American Society of Anesthesiologists Committee. (2011). Practice guide-lines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures: An updated report by the Ameri-can Society of Anesthesiologists Committee on Standards and Prac-tice Parameters. Anesthesiology, 114 (3), 495-511. doi:10. 1097/ALN. 0b013e3181fcbfd9 Apfelbaum, J. L., & Connis, R. T. (2012). Practice advisory for preanesthe-sia evaluation: An updated report by the American Society of Anesthesi-ologists Task Force on Preanesthesia Evaluation. Anesthesiology, 116 (3), 522-538. doi:10. 1097/ALN. 0b013e31823c1067 Chee, Y. L., Crawford, J. C., Watson, H. G., & Greaves, M. (2008). Guide-lines on the assessment of bleeding risk prior to surgery or invasive pro-cedures. British Committee for Standards in Haematology. British Jour-nal of Haematology, 140 (5), 496-504. doi:10. 1111/j. 1365-2141. 2007. 06968. x Fleisher, L. A., Fleischmann, K. E., & Auerbach, A. D. (2014). 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiol-ogy, 64 (22), e77-e137. doi:10. 1016/j. jacc. 2014. 07. 945 García-Miguel, F. J., Serrano-Aguilar, P. G., & López-Bastida, J. (2003). Preoperative assessment. Lancet, 362 (9397), 1749-1757. doi:10. 1016/ S0140-6736(03)14857-X Kaplan, E. B., Sheiner, L. B., & Boeckmann, A. J. (1985). The usefulness of preoperative laboratory screening. Journal of the American Medical Associ-ation, 253 (24), 3576-3581. doi:10. 1001/jama. 1985. 03350480084025 Kondrup, J., Rasmussen, H. H., Hamberg, O., & Stanga, Z. (2003). Nutri-tional risk screening (NRS 2002): A new method based on an anal-ysis of controlled clinical trials. Clinical Nutrition, 22 (3), 321-336. doi:10. 1016/S0261-5614(02)00214-5 Kumar, A., Mhaskar, R., & Grossman, B. J. (2015). Platelet transfusion: A systematic review of the clinical evidence. Transfusion, 55 (5), 1116-1127. doi:10. 1111/trf. 12943 Lawrence, V. A., Dhanda, R., Hilsenbeck, S. G., & Page, C. P. (1111). Risk of pulmonary complications after elective abdominal surgery. Chest, 110(3), 744-750. doi:10. 1378/chest. 110. 3. 744 Macpherson, D. S. (1993). Preoperative laboratory testing: Should any tests be “routine” before surgery? The Medical Clinics of North America, 77 (2), 289-308. doi:10. 1016/S0025-7125(16)30252-8 Mallampait, S. R. (1985). A clinical sign to predict difficult tracheal intuba-tion: A prospective study. Canadian Anaesthetists' Society Journal, 32 (4), 429-434. doi:10. 1007/BF03011357 Mc Clave, S. A., Kozar, R., Martindale, R. G., Heyland, D. K., Braga, M., Carli, F.,... Wischmeyer, P. E. (2013). Summary points and consensus recommendations from the North American Surgical Nutrition Sum-mit. Journal of Parenteral and Enteral Nutrition, 37 (5 Suppl. 1), 99S-105S. doi:10. 1177/0148607113495892 O'Neill, F., Carter, E., Pink, N., & Smith, I. (2016). Routine preoperative tests for elective surgery: Summary of updated NICE guidance. British Medical Journal, 354, i3292. doi:10. 1136/bmj. i3292 van Stijn, M. F., Korkic-Halilovic, I., Bakker, M. S., van der Ploeg, T., van Leeuwen, P. A., & Houdijk, A. P. (2013). Preoperative nutrition status and postoperative outcome in elderly general surgery patients: A system-atic review. Journal of Parenteral and Enteral Nutrition, 37 (1), 37-43. doi:10. 1177/0148607112445900 (a) Class 1 Class 2 Class 3 Class 4Soft palate Hard palate Uvula Pillars FIGURE 18. 1 Mallampati classification. Visualization used to predict ease of intubation. Care Principles	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
364Medication Management Kristopher R. Maday Preoperative Medication Management A. Anticoagulation. 1. Risk of bleeding versus risk of thromboembolism must be assessed when deciding to stop anticoagulation. a. Estimation of risk for a thromboembolic event. i. Atrial fibrillation 0. 2% to 1. 2% based on three major studies. 1)RE-LY. 2)Rocket AF. 3)ARISTOTLE. ii. Prosthetic heart valves—increase the risk of a thromboembolic event of anticoagulation by 3. 7-fold. iii. Recent thromboembolic event (venous or arterial) within last 3 months. 1)Elective surgery should be delayed if pos-sible. 2)Venous thromboembolism risk of antico-agulation. a)Within first month of occurrence is 50%. b)Between first month and third month of occurrence decreases to 8% to 10%. c)After 3 months, the risk decreases to 4% to 5%. 3)Arterial embolism risk of anticoagulation. a)0. 5% per day first month after occur-rence. b)Estimate risk of bleeding. iv. High bleeding risk 2% to 4%. 1)Coronary bypass surgery. 2)Procedures g reater than 45 minutes. 3)Procedures in compartments that can increase the severity of bleeding complications such as intracranial or pericardial. v. Low bleeding risk 0% to 2%. 1)Carpal tunnel surgery. 2)Hysterectomy. 2. Determine timing of anticoagulation cessation. a. Low bleeding risk surgeries may not require anti-coagulation cessation. i. Cutaneous procedures such as skin biopsy. ii. Cardiac implantable device. iii. Endovascular procedures. iv. Certain dental procedures. b. For surgeries with a moderate to high risk of bleed-ing, consider the following. i. Warfarin. 1)Stop 5 days prior to surgery. 2)Check the international r atio (INR) the day before. a)If greater than1. 5 administer 1 to 2 mg oral vitamin K. b)OK for surgery if 1. 4 or less. 3)Resume 12 to 24 hours after surgery due to prolonged action of onset. Full therapeutic effect may take up to 5 days. ii. Direct thrombin inhibitor—dabigatran. 1)Stop 2 to 3 days prior to surgery. 2)May need longer if:a)Patient has renal insufficiency. b)Surgery has high risk for bleeding. 3)Rapid onset of action. a)Delay restarting for 1 day after surgery with procedures that are low risk for bleeding. b)Delay restarting for 2 to 3 days after surgery with procedures that are high risk for bleeding. iii. Direct Factor Xa inhibitors—rivaroxaban, apixaban, edoxaban. 1)Stop 2 to 3 days prior to surgery. 2)May need longer if: a)Patient has renal insufficiency. b)Surgery has high risk for bleeding. 3)Rapid onset of action. a)Delay restarting for 1 day after surgery with procedures that are low risk for bleeding. b)Delay restarting for 2 to 3 days after surgery with procedures that are high risk for bleeding. 3. Determine if bridge needed. a. Used mainly in patients with high risk of throm-boembolic event due to atrial fibrillation, mechan-ical heart valve, or history of thromboembolic event. b. When to consider bridging (see Table 18. 1). c. Bridging preoperatively versus postoperatively or both. i. Use Thrombosis Canada Tool to determine if bridging is required preoperatively, postopera-tively, or both. 18. Preoperative Evaluation and Management TABLE 18. 1 Perioperative Bridging: When It Is Appropriate to Bridge in the Perioperative Period High Risk (consider bridging)Moderate Risk (case by case) Atrial fibrillation Recent ( <3 months) stroke/TIA CHADS25-6 Rheumatic heart Mechanical heart valve Ball or tilting disc valve Mitral valve Recent ( <3 month) stroke/TIA Venous thromboembolism Recent ( <3 months) VTE Severe thrombophilia Atrial fibrillation CHADS2=3-4 Mechanical heart valve Bileaflet aortic valve +risk factor Venous thromboembolism VTE 3-12 months prior cancer Low Risk (consider NOT bridging) Atrial fibrillation CHADS20-2 Mechanical heart valve Bileaflet aortic valve +risk factor Venous thromboembolism VTE>12 month ago TIA, transient ischemic attack; VTE, venous thromboembolism. Source: Data from Douketis, J. D., Spyropoulos, A. C., Spencer, F. A., Mayr, M., Jaffer, A. K., Eckman, M. H.,... Kunz, R. (2012). Perioperative management of antithrombotic therapy: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest, 141, e326. doi:10. 1378/chest. 11-2298.	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
365 ii. Url: thrombosiscanada. ca/tools/?calc =perioperative Anticoagulant Algorithm d. Inferior vena cava filter (IVC). i. Consider temporary IVC filter if patient is unable to restart anticoagulation for 3 to 4 weeks after surgery. 4. Case example: 74-year-old man, with nonvalvular atrial fibrillation and ischemic stroke, on warfarin who needs a total knee replacement. a. Stop warfarin 5 days before surgery. b. Preoperative bridging with low-molecular weight (LMW) heparin starting 3 days before surgery and stopped the day of surgery. c. Resume warfarin within 24 hours of surgery. d. Resume LMW heparin within 24 hours of surgery and continue until INR is therapeutic. B. Antiplatelet medications. 1. Common examples include: a. Aspirin: Can be continued through most surgeries. b. Clopidogrel and ticagrelor: Should be discontin-ued at least 5 days before surgery. c. Prasugrel: Should be discontinued at least 7 days before surgery. d. Ticlopidine: Should be discontinued at least 10 days before surgery. e. Cilostazol: Discontinued 3 to 5 days before surgery. 2. Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause decreased platelet function and should be discon-tinued 3 days before surgery. C. Diabetic medications. 1. Diabetes type 1. a. Patients with type 1 diabetes are prone to keto-sis and acidosis and extremes of blood glucose during surgery. b. Extreme caution in regulating fluid and electrolyte balance and blood sugar levels must be taken. c. Goal blood sugar is 110 to 180 mg/d L. d. Start dextrose containing solution during case at 75 to 125 cc/hr. e. Check blood sugar every hour. f. Short procedures less than 2 hours. i. Discontinue short or rapid acting insulin on the morning of surgery. ii. If patient takes two types of insulin only in the morning, give one-half to two-thirds of interme-diate or long acting insulin on day of surgery to prevent complications with ketosis. iii. If patients take insulin multiple times per day, give one-third to one-half total morning dose of intermediate or long acting insulin. g. Long procedures. i. Start intravenous (IV) insulin infusion. 2. Diabetes type 2. a. In patients who manage their diabetes with diet alone, no additional therapy is required. b. Oral hypoglycemics and non-insulin injectables. i. Should be held the morning of surgery. ii. Sliding scale insulin regimen can be used to manage postoperative hyperglycemia if needed. c. Insulin: Should give one-third to one-half the reg-ular morning dose on the day of surgery. Recommen-dations are to keep the same dose the night before. D. Glucocorticoid. 1. No need for perioperative stress dose corticosteroids if: a. Any dosing less than 3 weeks. b. Less than 5 mg daily, or less than 10 mg every other day. 2. Stress dose corticosteroids indicated if: a. Greater than 20 mg daily for more than 3 weeks. b. Cushingoid appearance. c. Adrenocorticotropic hormone (ACTH) stimula-tion testing should be performed for any patient with a question of hypothalamic-pituitary-adrenal (HPA) axis suppression. E. Cardiovascular medications. 1. Most commonly prescribed medications should be continued perioperatively and include: a. Beta blockers. b. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). c. Calcium channel blockers. d. Statins. Preoperative Checklist Bibliography De Lamar, L. M. (2005). Preparing your patient for surgery. Topics in Advanced Practice Nursing e Journal, 5 (1). Retrieved from https://www. medscape. com/viewarticle/500887_2 Douketis, J. D., Spyropoulos, A. C., Spencer, F. A., Mayr, M., Jaffer, A. K., Eckman, M. H., & Kunz, R. (2012). Perioperative management of antithrombotic therapy: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest, 141, e326. doi:10. 1378/chest. 11-2298 Douketis, J. D., Woods, K., Foster, G. A., & Crowther, M. A. (2005). Bridg-ing anticoagulation with low-molecular-weight heparin after interrup-tion of warfarin therapy is associated with a residual anticoagulant effect prior to surgery. Thrombosis and Haemostasis, 94, 528. doi:10. 1160/ TH05-01-0064 Dunn, A. S., Spyropoulos, A. C., & T urpie, A. G. (2007). Bridging ther-apy in patients on long-term oral anticoagulants who require surgery: The Prospective Peri-operative Enoxaparin Cohort T rial (PROSPECT). Journal of Thrombosis and Haemostasis, 5 (11), 2211-2218. doi:10. 1111/ j. 1538-7836. 2007. 02729. x Fleisher, L. A., Fleischmann, K. E., Auerbach, A. D., Barnason, S. A., Beckman, J. A., & Bozkurt, B. (2014). 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guide-lines. Circulation, 130, e278. doi:10. 1161/CIR. 0000000000000105 Medication Management Preoperative Checklist Risk factors 1. 2. 3. American College of Surgeons risk score(score) Preoperative testing 1. Test—Result 2. Test—Result ASA classification (class) Nutritional considerations(NRS2002 score). Nutritional support type Medications 1. Drug—why on—when to stop—plan 2. Drug—why on—when to stop—plan ASA, American Society of Anesthesiologists. Source: Data from De Lamar, L. M. (2005). Preparing your patient for surgery. Topics in Advanced Practice Nursing e Journal, 5 (1). Retrieved from https://www. medscape. com/viewarticle/500887_2	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
366 Garcia, D., Alexander, J. H., Wallentin, L., Wojdyla, D. M., Thomas, L., Hanna, M., & Lopes, R. D. (2014). Management and clinical outcomes in patients treated with apixaban vs warfarin undergoing procedures. Blood, 124 (25), 3692-3698. doi:10. 1182/blood-2014-08-595496 Healey, J. S., Eikelboom, J., Douketis, J., Wallentin, L., Oldgren, J., Yang, S.,... Ezekowitz, M. (2012). Periprocedural bleeding and throm-boembolic events with dabigatran compared with warfarin: Results from the Randomized Evaluation of Long-Term Anticoagulation Ther-apy (RE-LY) randomized trial. Circulation, 126 (3), 343. doi:10. 1161/ CIRCULATIONAHA. 111. 090464 Marik, P. E., & Varon, J. (2008). Requirement of perioperative stress doses of corticosteroids: A systematic review of the literature. Archives of Surgery, 143(12), 1222-1226. Sherwood, M. W., Douketis, J. D., Patel, M. R., Piccini, J. P., Hellkamp, A. S., Lokhnygina, Y.,... ROCKET AF. Investigators (2014). Out-comes of temporary interruption of rivaroxaban compared with warfarin in patients with nonvalvular atrial fibrillation: Results from the rivaroxa-ban once daily, oral, direct Factor Xa inhibition compared with vitamin K antagonism for prevention of stroke and embolism trial in atrial fibril-lation. Circulation, 129 (18), 1850. doi:10. 1161/CIRCULATIONAHA. 113. 005754 Thrombosis Canada (n. d. ). Retrieved from http://thrombosiscanada. ca/ tools/?calc =perioperative Anticoagulant Algorithm Umpierrez, G. E., Smiley, D., Jacobs, S., Peng, L., Temponi, A., Mulli-gan, P., & Rizzo, M. (2011). Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes undergoing general surgery (RABBIT 2 surgery). Diabetes Care, 34, 256. doi:10. 2337/dc10-1407 Van den Berghe, G., Wilmer, A., Hermans, G., Meersseman, W., Wouters, P. J., Milants, I.,... Bouillon, R. (2006). Intensive insulin therapy in the medical ICU. The New England Journal of Medicine, 354, 449-461. doi:10. 1056/NEJMoa052521 Van den Berghe, G., Wouters, P., Weekers, F., Verwaest, C., Bruyninckx, F., Schetz, M., & Bouillon, R. (2001). Intensive insulin therapy in criti-cally ill patients. The New England Journal of Medicine, 345, 1359-1367. doi:10. 1056/NEJMoa01130018. Preoperative Evaluation and Management	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
367 19Perioperative and Intraoperative Management Kristopher R. Maday Scope of Chapter Kristopher R. Maday This section is not meant to be exhaustive in teaching the advanced practice provider (APP) how to function in the intraoperative setting. Rather, this section is included to pro-vide an overview of the process that occurs to patients while they are in surgery, as well as to help the APP in the postop-erative period understand why certain complications occur. For instance, patient positioning may impact postoperative atelectasis or a difficult airway may delay extubation. By understanding the general concepts of anesthesia, the APP will be knowledgeable about how to optimize physiologic parameters. Considerations Kristopher R. Maday Goals of Anesthesia A. Primary. 1. Maintain homeostasis and optimize physiologic response to surgical insult. B. Secondary. 1. Amnesia and anxiolysis. a. Minimizing the memory of the operative and peri-operative experience. b. Data shows one patient per 14,560 will have recall of the surgical experience. c. Commonly used medications include: i. Benzodiazepines. ii. Propofol. iii. Ketamine. 2. Analgesia. a. Multimodal approach should be used to limit adverse effects of opioids and include: i. Opioid/narcotic medications. ii. Nonsteroidal anti-inflammatory drugs (such as Toradol). iii. Local anesthetics. iv. Regional blockade. 3. Monitored anesthesia care (MAC). a. Local anesthesia with sedation and analgesia. i. Patient-controlled sedation may be used. ii. Continuous intravenous (IV) infusion. iii. Target-controlled infusion. b. First choice in many types of surgery. i. Colonoscopy. ii. Bronchoscopy. iii. Outpatient procedures. c. Patients able to answer questions and protect airway. i. Use bispectral index (BIS) to monitor patient consciousness. d. Goal of MAC. i. Safe sedation. ii. Control of patient anxiety. iii. Pain control. e. Medications. i. Midazolam—short acting benzodiazepine without analgesic effect, can cause respiratory depression especially in conjunction with other sedatives or opioids. ii. Propofol—rapidly acting sedative without analgesic effects, can transition to general anesthe-sia if needed. iii. Opioids. 1)Fentanyl—short acting opioid. 2)Remifentanil—ultrashort acting opioid typically given as an infusion. iv. Dexmedetomidine—infusion with sedative, anxiolytic, and analgesic effects. Does not produce respiratory depression. v. Ketamine—heavy analgesic effect with mini-mal respiratory depression. Can reduce the need for opioids. 4. Neuromuscular blockade. a. Optimal operative conditions may require the patient to be still during surgery. b. Common medications include: i. Depolarizing agents. 1)Succinylcholine. a)Faster onset, shorter acting. b)Good for induction. c)Side effects include bradycardia, hyperkalemia, fasciculations, rhabdomy-olysis. ii. Nondepolarizing agents. 1)Longer acting, available in drip. 2)Good for surgical procedures or sustained blockade. 3)Examples. iii. Rocuronium. iv. Vecuronium. v. Cisatracurium. 1)Side effects include increased periph-eral vascular resistance, tachycardia, and hypertension. Considerations	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
368 5. Maintenance of hemodynamic stability and hemostasis. a. Fluids—goal of fluids during surgery is normov-olemia; avoid liberal or fixed volume approaches to fluid replacement. i. Crystalloid—such as Ringer's lactate or Plasma Lyte—used instead of normal saline. Goal is to maintain volume with balanced electrolytes. 1)Most commonly used. 2)Avoid large volume of fluid. 3)Typically 1 to 2 L balanced electrolyte solution is adequate hydration. ii. Colloid—such as human albumin or hydrox-yethyl starch (HES)—may expand microvascular volume without edema; it is not superior to use of crystalloids and should be reserved for unique situations. iii. Blood products—replace intraoperative blood loss. iv. Follow hemodynamic parameters and antic-ipated blood loss ( >500 m L) to guide fluid replacement. b. Vasopressors. i. Phenylephrine. ii. Norepinephrine. iii. Epinephrine. iv. Ephedrine. v. Dobutamine. c. Transfusions. i. Packed red blood cells (PRBCs)—transfusion should be considered at hemoglobin concentra-tions of 7 g/d L or less. ii. Fresh frozen or thawed plasma—given to cor-rect coagulopathy, reversal of warfarin, or correc-tion of known coagulation factor deficiencies. iii. Platelets—may be given if suspected platelet dysfunction such as in the presence of antiplatelet agents and bleeding. Indicated if platelet count falls below the accepted threshold of 50 ×109/L in the presence of excessive bleeding. iv. Cryoprecipitate—used when fibrinogen is less than 80 to 100 mg/d L in the presence of excessive bleeding, in the presence of fibrinolysis. v. Indications for autotransfusion—same as PRBC, but use patient's own supply. A person can donate his or her own blood weekly up to 5 days prior to surgery. Most hospitals can only hold autologous blood for a limited period of time such as 35 to 40 days. vi. Pharmacologic treatments. 1)Desmopressin—promotes platelet adhe-sion and aggregation. 2)Tranexamic acid—used as prophylaxis of excessive bleeding before and/or during a procedure. 3)Coagulation factor concentrates—can be beneficial in cardiac surgery for emergency reversal of novel oral anticoagulants (NOAC) therapy. Off label use for microvascular bleed-ing attributed to coagulation factor deficien-cies. Can increase risk of thromboembolic event. 4)Thrombin gel—used for hemostasis intra-operatively. 6. Antiemetics to prevent postoperative nausea and vom-iting (PONV). a. Highest risk in the 24 hours after surgery and also after laparoscopic gastrointestinal (GI) and GYN surgeries. b. Prevention. i. Scopolamine patch 2 hours prior to induction. ii. Dexamethasone 4 to 8 mg IV after induction. iii. Ondansetron 4 mg IV at the conclusion of surgery. c. Other alternative treatments. i. Promethazine 6. 25 to 12. 5 mg IV at induc-tion. ii. Prochlorperazine 5 to 10 mg IV at the conclu-sion of surgery. 7. Reversal agents. a. Most inhaled and IV anesthetics are turned off in advance of emergence at the end of the case. These volatile substances clear quite quickly from the system without the need for reversal. b. Neuromuscular blockade. i. Neostigmine. ii. Sugammadex. Anesthetic Considerations A. Local. 1. Indications: Used at incision site. 2. Most common medications used are as follows. a. Lidocaine (0. 5%, 1%, 2%). i. Onset: 2 to 5 minutes, but typically faster. ii. Duration: 30 to 120 minutes (180 minutes with epinephrine). iii. Maximum dose. 1)With epinephrine: 7 mg/kg. 2)Without epinephrine: 4 mg/kg. b. Bupivacaine (0. 125%, 0. 25%). i. Onset: 5 to 10 minutes. ii. Duration: Up to 6 hours. iii. Maximum dose. 1)With epinephrine: 3 mg/kg. 2)Without epinephrine: 2 mg/kg. 3. Complications. a. Toxicity. i. Cardiac. 1)Lidocaine is a Class I antiarrhythmic med-ication and can cause cardiac disturbances such as: a)Bradycardia. b)Decreased inotropy. c)Atrioventricular block. d)Vasodilation. e)Dysrhythmias. f)Cardiac arrest. ii. Central nervous system. 1)Seizures. 2)Paresthesias. 3)Tinnitus. 4)Neuraxial anesthesia. B. Regional blocks. 1. Types. a. Upper extremity. i. Brachial plexus. 1)Interscalene. 2)Supraclavicular. 3)Infraclavicular. 4)Axillary. 19. Perioperative and Intraoperative Management	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
369 b. Lower extremity. i. Sciatic. ii. Femoral. iii. Fascia iliaca. iv. Lumbar plexus. 2. Contraindications and complications. a. Body habitus may make regional blockade difficult due to equipment limitations. b. Active infection at the site of injection. c. Coagulopathy and noncompressive site of injection. d. Preexisting neural deficits in the distribution of the block. e. Hemidiaphragm paralysis. f. Laryngeal nerve paralysis. g. Horner's syndrome can be caused by upper extremity blocks. C. Spinal. 1. Indications. a. Lower extremity procedures (total hip/knee replacement, knee arthroscopy, etc. ) in patients with high risk for general anesthesia. b. Shorter, known duration of surgery. c. Patients who cannot withstand general anesthesia for a procedure. D. Epidural. 1. Indications. a. Longer surgical procedures. b. Unknown duration of surgery. c. Help with postoperative pain management. d. Extremity surgery in patients who are poor surgical candidates due to American Society of Anes-thesiologists (ASA) class or other comorbidities. 2. Contraindications and complications. a. Hypovolemia: May cause spinal shock. b. Coagulopathy: May cause spinal hematoma. c. Increased intracranial pressure. d. Abscess. 3. Procedure. a. Ultrasound has increased the safety and efficacy of regional blockade as the operator can identify the structures directly and inject at the site of the nerve. 4. Three phases of general anesthesia. a. Induction. i. Often achieved with a combination of IV and inhaled medications; however, may be done with either alone as well. ii. Rapid instillation ( <2 minutes) of medi-cations to prepare patient for intubation and surgery. iii. IV medications. 1)Propofol. 2)Etomidate. 3)Ketamine. 4)Midazolam. 5)Opioid narcotics: Fentanyl. 6)Neuromuscular blockade. iv. Inhalational medications. 1)Adult patients. a)Commonly used for quick induction. b)May have an unpleasant taste. c)May have increased postoperative nausea/vomiting. d)May be considered in higher risk patient who is spontaneously breathing. 2)Pediatric patients. a)May be preferred due to fear and pain of needle stick. b. Maintenance of general anesthesia. i. Inhalational. 1)Sevoflurane. 2)Desflurane. 3)Nitrous oxide. ii. IV. 1)Propofol. 2)Neuromuscular blockade. 3)Opioids. a)Fentanyl. b)Sufentanil. c)Remifentanil. c. Emergence. i. Returning the patient to a state of conscious-ness. ii. Many variables; depends on IV versus inhaled, type used, and patient physiology. The overall steps are to stop these and allow the patient to slowly metabolize and emerge. iii. Timing is critical and occurs in a stepwise approach. 1)Discontinue anesthetic agents. 2)Administer antiemetic. 3)Assess adequacy of analgesia: Elevations in blood pressure, heart rate, and respiratory rate indicate inadequate pain control. 4)Assess adequacy of tidal volume and minute ventilation of spontaneous respiration by arterial blood gas analysis. 5)Assess level of wakefulness. a)Patient following commands. b)Coughing with airway in place. 6)Extubation or removal of supraglottic airway. d. Complications of general anesthetics. i. Malignant hyperthermia. 1)Hallmark sign is temperature greater than 40ºC and muscle rigidity. ii. Laryngospasm/bronchospasm. 1)Hallmark sign is inspiratory stridor. iii. Nausea/vomiting. iv. Agitation/delirium. v. Urinary retention. Bibliography Berde, C. B. (1993). Toxicity of local anesthetics in infants and children. The Journal of Pediatrics, 122 (5 Pt. 2), S14-S20. doi:10. 1016/S0022-3476(11)80004-1 Borgeat, A., Ekatodramis, G., Kalberer, F., & Benz, C. (2001). Acute and nonacute complications associated with interscalene block and shoul-der surgery: A prospective study. Anesthesiology, 95 (4), 875-880. doi:10. 1097/00000542-200110000-00015 New York School of Regional Anesthesia. (n. d. ). Spinal anesthesia. Retrieved from http://www. nysora. com/techniques/neuraxial-and-perineuraxial-techniques/landmark-based/3423-spinal-anesthesia Pollard, R. J., Coyle, J. P., Gilbert, R. L., & Beck, J. E. (2007). Intraoperative awareness in a regional medical system: A review of 3 years' data. Anesthe-siology, 106 (2), 269-274. doi:10. 1097/00000542-200702000-00014 Thwaites, A., Edmends, S., & Smith, I. (1997). Inhalation induction with sevoflurane: A double-blind comparison with propofol. British Journal of Anaesthesia, 78 (4), 356-361. doi:10. 1093/bja/78. 4. 356 White, P. F., Kehlet, H., & Neal, J. M. (2007). The role of the anes-thesiologist in fast-track surgery: From multimodal analgesia to peri-operative medical care. Anesthesia and Analgesia, 104 (6), 1380-1396. doi:10. 1213/01. ane. 0000263034. 96885. e1 Considerations	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
370Care Principles Kristopher R. Maday Positioning A. Goals of proper patient positioning. 1. Maintain airway. 2. Provide adequate surgical exposure. 3. Allow for proper patient monitoring. 4. Prevent vascular compression and ischemia. 5. Prevent nerve damage. 6. Keep patient comfortable. B. Each surgical specialty has specific considerations for each surgery. C. Four basic positions. 1. Supine (see Figure 19. 1). 2. Prone. 3. Lateral. 4. Lithotomy (see Figure 19. 2). D. Special positions. 1. Trendelenburg (see Figure 19. 3). 2. Reverse Trendelenburg (see Figure 19. 4). 3. Fowler's (see Figure 19. 5). 4. Jackknife (see Figure 19. 6). E. Complications. 1. Compression nerve injuries: Specific nerve compres-sion is dependent on the position used and the adequacy of the padding. 2. Pressure sores: May start to occur in as little as 60 minutes if not positioned/padded appropriately. 3. Cerebral perfusion: Head positioning can cause decreased perfusion and can result in anoxic brain injuries if not properly monitored. Padded arm board Small pillow Pillow under knees Pad Heel Safety strap FIGURE 19. 1 Supineposition. Source:Goodman, T.,& Spry,C. (2017). Essentials of perioperative nursing (6th ed. ). Burlington, MA: Jones & Bartlett. Buttocks at edge of mattress FIGURE 19. 2 Lithotomyposition. Source:Goodman, T.,& Spry,C. (2017). Essentials of perioperative nursing (6th ed. ). Burlington, MA: Jones & Bartlett. 4. Upper airway edema: Particularly for patients in steep Trendelenburg. Principles of Aseptic Technique A. Surgical scrub. 1. Length. a. 3 to 5 minutes. b. Stroke count method. 2. Area: 5 cm above the elbow to the fingertips. 3. Procedure. a. Remove all jewelry from hands. b. Use nail file to clean under the nails. c. Always keep hands higher than elbow to prevent contamination. d. Lather entire area with soap. i. Commonly accepted soaps for scrub: Chlorhexidine or povidone-iodine-containing soaps. e. Use warm water. Hot water can destroy a healthy layer of protective skin. f. Start the scrub with fingertips and work to the elbows. i. Rinse from fingers to elbow in one direction only. ii. Scrub each side of the finger and back/front of the hand for 2 minutes. iii. Scrub from wrist to elbow on each arm for 1 minute. iv. Repeat the process on the other hand and arm. v. Rinse hands and arms by passing them through the water in one direction only. g. Proceed to the operating room with hands up and above the elbows. Pillow for head Padding for feet Arm wrap Safety strap Shoulder brace FIGURE 19. 3 Trendelenburgposition. Source:Goodman, T.,& Spry,C. (2017). Essentials of perioperative nursing (6th ed. ). Burlington, MA: Jones & Bartlett. Pillow Arm wrap Safety strap Heel padding Padded foot board Small soft roll FIGURE 19. 4 Reverse Trendelenburg. Source:Goodman, T.,& Spry,C. (2017). Essentials of perioperative nursing (6th ed. ). Burlington, MA: Jones & Bartlett. 19. Perioperative and Intraoperative Management	Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

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