What precautions should be taken when using supplemental oxygen during surgery for someone with Duchenne muscular dystrophy?

Surgery & Anesthesia
When a patient with Duchenne muscular dystrophy has general anesthesia, a number of issues should be considered, including cardiac and pulmonary function, anesthesia, and the potential for blood loss.
Considerations for Surgery & Anesthesia
If you require surgery or a medical procedure, go to a medical center with expertise in the anesthetic management of people living with Duchenne if possible. Your anesthesiologist should be aware that you have Duchenne. It is important to discuss the anesthesia plan with your anesthesiologist before any surgery or procedure that involves anesthesia.
Additionally, your neuromuscular team should always be made aware if you are undergoing surgery or a medical procedure. Additionally, you should have evaluations by your cardiologist and pulmonologist before undergoing any type of surgery or medical procedure. Any cardiac and/or respiratory abnormalities should be identified and optimally treated before any surgery or procedure involving anesthesia.
These recommendations have been reviewed and approved by the Professional Advisory Council of the Malignant Hyperthermia Association of the U.S. (MHAUS). Discuss risks and benefits of planned anesthetic medications (agents) with your anesthesiologist.
Anesthesia agents requiring caution in Duchenne
People with Duchenne should NOT receive succinylcholine.
The drug succinylcholine (suxamethonium) is a depolarizing muscle relaxant. It is sometimes used in emergencies to relieve breathing difficulties in anesthetized patients. However, when succinylcholine is administered to patients with any kind of ongoing muscle atrophy, no matter the underlying cause, succinylcholine can cause severe, life-threatening (and sometimes fatal) increases in blood potassium.
Instead of succinylcholine there are other commonly available muscle relaxants (e.g., any non-depolarizing neuromuscular blocker) that can be used in emergency situations if necessary (see the “Safe” list section below). It is possible, however, that there exists a rare situation (such as life-threatening airway obstruction that requires immediate treatment) where an anesthesiologist may be justified in administering succinylcholine to a patient with Duchenne whose life is in imminent danger.
Avoid inhaled anesthetic agents if possible.
Commonly used inhaled anesthetic agents include Desflurane, Enflurane, Halothane, Isoflurane, and Sevoflurane.

People with Duchenne are at risk of developing rhabdomyolysis (the breakdown of skeletal muscle tissue that may cause the release of myoglobin that can damage the kidneys) and hyperkalemia (the release of too much potassium into the bloodstream), which can result in life-threatening heart rhythms.
There are known cases of serious (and sometimes fatal) muscle breakdown (rhabdomyolysis) in Duchenne patients when exposed to inhalation anesthetic gases even when succinylcholine was avoided. Therefore, we recommend that when possible, inhalational anesthetic gases should be avoided or used sparingly in people with Duchenne. However, there are certain circumstances when the benefit/risk ratio favors the use of these inhaled agents. The administration of inhaled anesthetic agents may be suggested for the following reasons:
- Prior to IV catheter insertion
The only other type of anesthetic agents are given intravenously (through an IV catheter). Inserting IV catheter can be painful, and people with Duchenne may require multiple sticks due to difficulty finding veins in people with decreased muscle mass. Giving inhaled anesthetic before the nurse attempts an IV stick can reduce the pain and make it easier to obtain IV access.
- Propofol administration
The drug Propofol is a commonly used IV anesthetic agent for procedures. However, it can be very painful when it starts infusing through an IV. Sometimes inhaled anesthetic agents will be given before Propofol is started to avoid the pain of the infusion.
- IV anesthesia is not available
There may be rare situations where IV anesthesia is not available, or is considered an inferior anesthetic choice based on the patient’s specific clinical situation.
Am I at risk for “malignant hyperthermia?”
Among anesthesiologists, it is established knowledge that patients with Duchenne muscular dystrophy may develop unique complications when undergoing medical or surgical procedures that require certain anesthetic agents (discussed above). The complications including rhabdomyolysis and hyperkalemia are nearly indistinguishable from those seen when a patient develops a rare anesthetic-related complication called malignant hyperthermia (MH).
Although clinically similar in appearance to the complications that may occur in Duchenne patients, they are actually two separate entities. MH is typically an inherited genetic condition that has nothing to do with the dystrophin gene.

Norcuron (Vecuronium), Pavulon (Pancuronium), Tracrium (Atracurium), Zemuron (Rocuronium)
Gabapentin (Neurontin), Topiramate (Topamax)
- Anxiety Relieving Medications
Ativan (Lorazepam), Centrax, Dalmane (Flurazepam), Halcion (Triazolam), Klonopin, Librax, Librium (Chlordiazepoxide), Midazolam (Versed), Paxipam (Halazepam), Restoril (Temazepam), Serax (Oxazepam), Tranxene (Clorazepate), Valium (Diazepam)
Because people with with Duchenne have weak respiratory muscles, their diaphragms do not move up and down well and their intercostal muscles (the muscles that move the chest walls) do not expand the ribs well. This causes shallow breathing, but people with Duchenne compensate for this over time, and can provide the body with adequate oxygen supply and adequate removal of carbon dioxide. During surgery or procedures, certain anesthetics may lead to increasingly shallow breathing. Too shallow of breathing (hypoventilation) may lead to low oxygen levels and high carbon dioxide levels.
Your anesthesiologist may decide you will need supplemental oxygen during your procedure, but they must use caution. When extra or supplemental oxygen is given, this delicate balance is disturbed. The respiratory center may get the false impression that the body has enough oxygen and no longer needs to breathe. Without breathing, carbon dioxide can build to dangerous levels (called hypercapnia). If oxygen is required during surgery or medical procedures, the anesthesiologist must use caution and monitor you closely. They may also use non-invasive ventilation (i.e. BiPAP machine) during the procedure to ensure you are breathing adequately.
During surgery, it is sometimes necessary to support your breathing due to anesthesia or muscle relaxants given during the procedure. Intubation involves putting a breathing tube (also known as an endotracheal tube) into your airway. This breathing tube is then connected to a breathing machine (respirator or ventilator). This machine will then either assist with your breathing or actually breath for you, depending on your pulmonary function, the length of the surgery, or the type of surgery.

Because of the similar symptoms of these two complications, there was a time when many clinicians believed that the anesthesia complications in Duchenne patients were, in fact, MH. However, after studying this over the years, we now know that this isn’t true. MH occurs in patients who have inherited MH-causing mutations, which people with Duchenne are not at a higher risk for than the general population.
Duchenne patients are not at an increased risk of developing MH, but may continue to be at increased risk of rhabdomyolysis when administered inhaled anesthetic gases. These guidelines have been reviewed and approved by the Professional Advisory Council of the Malignant Hyperthermia Association of the U.S. (MHAUS).
All intravenous (IV) anesthetic agents are considered to be safe to give to people with Duchenne with close monitoring.
- Barbiturates/Intravenous Anesthetics
Diazepam (valium), Etomidate (Amidate), Ketamine (Ketalar), Methohexital (Brevital), Midazolam (Versed), Propofol (Diprivan), Thiopental (Pentothal)
- Inhaled Non-Volatile General Anesthetic
Nitrous Oxide (“laughing gas”)
- Local Anesthetics
Amethocaine, Articaine, Bupivicaine, Etidocaine, Lidocaine (Xylocaine), Levobupivacaine, Mepivicaine (Carbocaine), Procaine (Novocain), Prilocaine (Citanest), Ropivacaine, Benzocaine (caution re: methemoglobinemia risk), Ropivacaine
- Narcotics (opiods)
Alfentanil (Alfenta), Codeine (Methyl Morphine), Fentanyl (Sublimaze), Hydromorphone (Dilaudid), Meperidine (Demerol), Methadone, Morphine, Naloxone, Oxycodone, Remifentanil, Sufentanil (Sufenta)
- Muscle Relaxants
Arduan (Pipecuronium), Curare (The active ingredient is d-Tubocurarine), Metocurine, Mivacron (Mivacurium), Neuromax (Doxacurium), Nimbex (Cisatracurium),

Pulmonary function tests and blood-gases are recommended in the case of significant respiratory embarrassment.  As diminution of respiratory muscle strength cannot be ruled out even without symptoms vigilance during postoperative period is essential. ,
Perioperative steroid supplementation to avoid adrenal suppression has been advocated in patients with recent steroid usage  and we used I.V. hydrocortisone 100 mg just before induction as our patient had received steroids recently.
Our patient requested for G.A and induction with propofol-fentanyl provided smooth intubation in spite of 65-70% TOF ratio by ED90 dose of atracurium indicating resistance. Intraoperatively TOF ratio-guided top-ups of atracurium provided adequate NM block required for the orthopaedic procedure. Maintenance of O.T temperature to 22°C helped in maintaining normal core temperature. Postoperatively we treated rise of 1°C of body temperature promptly and no relapses occurred in our patient. The postoperative respiratory distress was successfully treated with oxygen therapy by ventimask.
The perioperative period was thus uneventful. To summarize, the optimal anaesthetic management of MS requires careful preoperative assessment, awareness towards perioperative care and postoperative exacerbations of MS. The latter invites special attention and recovery room care with appropriate monitors, oxygen therapy/mechanical ventilation is necessary.
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Oxygen therapy, a lifeline for many critically ill patients, can be delivered in nonintubated patients via several devices. Unlike patients with chronic hypoxemia, the long-term comfort or cosmetics of the patient are not a concern of intensivists; instead, the goal is to ensure adequate oxygen delivery to prevent hypoxemia. Although hypoxemia is often corrected with oxygen therapy, care should be taken to understand the pathophysiology leading to hypoxemia. The appropriate management of hypoxemia should include treatment of the underlying pathology to prevent any complication and progression of the disease. For example, many patients with postoperative atelectasis develop hypoxemia responsive to oxygen therapy. Treatment of postoperative hypoxemia with oxygen supplementation alone without initiating lung reexpansion measures to treat atelectasis is insufficient. This chapter covers noninvasive modes of supplying oxygen and does not discuss other means of correcting hypoxemia.
KeywordsChronic Obstructive Pulmonary Disease Obstructive Sleep Apnea Continuous Positive Airway Pressure Oxygen Therapy Oxygen Supplementation
Unable to display preview. Download preview PDF.
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Intubation is usually done after you have received anesthesia and are asleep. The anesthesiologist will monitor you closely and control the ventilator. The tube will usually remain in and connected to the machine until the surgery is completed.
After the surgery, the breathing tube must be removed. The process of removing the breathing tube is called extubation. Because breathing tubes were sometimes, in the past, left in place too long or were removed incorrectly, a protocol for extubation was developed by Drs. Mary Schroth and John Bach. When you meet with your anesthesiologist before surgery, be sure you discuss the intubation/extubation and show them the protocol.
Dentistry generally can, and should, be performed with the minimal amount of anesthesia possible while providing the patient maximal physical and emotional comfort. Local anesthetics, nitrous oxide, and an oxygen “wash out” are safe for most patients with Duchenne, especially patients who are ambulatory with normal pulmonary function (normal breathing).
Patients with Duchenne who have pulmonary dysfunction (abnormal breathing) should consider receiving dental care requiring general anesthesia in a hospital or surgery center staffed with an anesthesiologist, and equipped to monitor intra-operative respiratory functioning and to manage potential respiratory and cardiac emergencies. Visit this page for more information concerning dental procedures.

Evaluate pulmonary function
(clinical, chest radiographs, CT, pulmonary function test, arterial blood
gas analysis). Echocardiography should be performed if cor pulmonale and
pulmonary hypertension are suspected. Assess the airway for difficult airway
management. Evaluate neurologic function (clinical, full history,
electroencephalogram, CT, MRI). Postoperative ventilatory support may be
necessary and should be arranged beforehand.
No literature is available.
Potentially difficult airway management in view of facial abnormalities.
Spontaneous ventilation should be maintained until the airway is secured.
Patients may not tolerate general anesthesia if respiratory function is
Because of increased sensitivity to
muscle relaxants, avoid depolarizing muscle relaxants and use
nondepolarizing agents cautiously under the control of a peripheral nerve
stimulator. Consider interaction between anesthetic drugs and antiepileptic
Numerous syndromes are
associated with agenesis of the corpus callosum. The following list is not
Aicardi Syndrome: Combination of myoclonic seizures with
characteristic EEG pattern, lacunar chorioretinopathy, and (complete or
partial) agenesis of the corpus callosum is characteristic of this X-linked
dominant inherited syndrome.

We excluded patients with a history of fever or infection within 24 hours of surgery, a history of susceptibility to malignant hyperthermia, or with current heart and lung disease.
Patients were premedicated with 2 to 3 mg midazolam in the preoperative holding area or just before anesthetic induction. Anesthesia was induced with IV propofol and maintained with a volatile anesthetic that was adjusted to keep mean arterial blood pressure near 90% of the preinduction value. An inspired oxygen fraction of 1.0 was used at induction of anesthesia until tracheal intubation and during extubation. All patients were standardized to receive 80% inspired oxygen during the intraoperative period. Patients’ lungs were mechanically ventilated with a tidal volume of 6 to 8 mL/kg of ideal body weight at a rate sufficient to maintain end-tidal PCO2 near 40 mm Hg; a positive end-expiratory pressure of 5 to 10 cm H2O was applied.
Patients were given approximately 10 mL/kg/h of crystalloid throughout surgery, normalized to ideal body weight. Fluids were standardized at a rate of 3.5 mL/kg/h for the first 24 postoperative hours and at a rate of 2 mL/kg/h for the subsequent 24 hours, again normalized to ideal body weight. Intraoperative core temperature was maintained near 36°C using forced-air warming and heated IV fluids.33,34 Patients were given 100% inspired oxygen before tracheal extubation. Intraoperative analgesia was provided with IV fentanyl titrated at the discretion of individual anesthesiologists. Each morbidly obese patient may have had different requirements of opioids, so the protocol was not strict. Postoperative analgesia was provided by patient-controlled morphine or hydromorphone.
Patients were assigned 1:1 to routine or supplemental postoperative oxygen. Randomization was based on reproducible computer-generated codes that were maintained in sequentially numbered opaque envelopes until the end of surgery. Randomization was stratified by study site. The 2 groups are listed below:
1. Routine oxygen administration: Extubated patients were given 2 L/min oxygen via a nasal cannula until the first postoperative morning.

Induction of anesthesia was achieved with 1–2 mg/kg of propofol, 2–3 µg/kg of fentanyl, and 0.1 mg/kg of vecuronium. A double-lumen endobronchial tube was placed for lung isolation. Maintenance of anesthesia consisted of oxygen, sevoflurane, and intermittent intravenous bolus doses of fentanyl 0.5 µg/kg. Dose adjustments of sevoflurane and fentanyl were based on standard clinical signs and hemodynamic measurements. Signs of inadequate analgesia were defined as an increase in heart rate (HR) and mean arterial pressure (MAP) of more than 20% from baseline. Hypotension was defined as a MAP of less than 20% from baseline. Supplemental vecuronium was administered if indicated by monitoring muscle relaxation with a nerve stimulator (model NS242; Fisher Paykel, Auckland, New Zealand. +6495740100). During the perioperative period, both groups received intravenous fluid (lactated Ringer solution) at 5 ml/kg/h.
Pressure-controlled ventilation was applied with FiO2 of 0.5 in air. During one-lung ventilation, FiO2 was increased to 0.8. At the end of surgery, residual neuromuscular block was reversed with neostigmine (0.04 mg/kg) and atropine (0.01 mg/kg), and the endotracheal tube was removed when the patient met criteria for extubation. Patients were transferred to the postanesthesia care unit (PACU) at the end of surgery. The final fentanyl dose was given ∼20 min before the end of surgery. After extubation, patients received 0.45–0.5% nebulized oxygen by facemask. Patients were monitored in the PACU for 2 h, and the need for reintubation in the postoperative period was recorded. Patients were then transferred to the high dependency unit for the rest of the 24 h follow-up. Patients who completed the 24 h follow-up were transferred to the ward. All the operations were performed by the same surgical team. The anesthetic technique for surgery was performed similarly for all patients by the same anesthetic team.

All patients were premedicated with oral alprazolam 0.25 mg the night before surgery. On the day of surgery, they received premedication of glycopyrrolate 0.2 mg intramuscularly 30 min prior to induction of anesthesia. On arrival to operation room, routine, hemodynamic monitoring was performed by automatic blood pressure measurements, five-lead ECG monitor, and finger pulse oximetry. An intravenous infusion of ringer lactate was started, followed by intravenous metoclopramide 10 mg and midazolam 2 mg. Group D patients (n0 = 30) were given intravenous dexmedetomidine 1μg/kg and Group F patients (n = 30) were given fentanyl 2 μg/kg, over a 10-min period before induction of general anesthesia.
After preoxygenation for 3 min, the anesthesia was induced with propofol (2 mg/kg) and tracheal intubation was facilitated by vecuronium 0.1 mg/kg. Anesthesia was maintained with isoflurane 1-1.5% and 60% nitrous oxide in oxygen with supplementary fentanyl (50-100 μg) to maintain the heart rate and mean arterial pressure within 20% of preinduction values and/or heart rate <85 beats/min during surgical stimulation. The patient's lungs were initially mechanically ventilated with a tidal volume of 8 ml/kg, a respiratory rate of 12 breaths/min, and an I:E ratio of 1:2 in volume-controlled mode. Five minutes after securing the airway and abdominal insufflation by carbon dioxide, the lung mechanics were adjusted to maintain normocapnia (an end-tidal carbon dioxide value of 35-40 mm Hg) and intra-abdominal pressure was maintained between 12 and 15 mm Hg. The degree of muscle relaxation was maintained using the train-of-four ratio of <25% with supplemental doses of vecuronium bromide (0.05 mg). All patients were covered to maintain normothermia.

If respiratory muscles become weakened, using a ventilator may become necessary.
To release the contractures that may develop and that can position joints in painful ways, doctors can perform a tendon release surgery. This may be done to relieve tendons of your hip and knee and on the Achilles tendon at the back of your foot. Surgery may also be needed to correct curvature of the spine.
Because respiratory infections may become a problem in later stages of muscular dystrophy, it's important to be vaccinated for pneumonia and to keep up to date with influenza shots.

Neuromuscular monitoring is suggested in these patients due to lack of standard recommendations regarding to the application of nondepolarizing muscle relaxants. , Succinylcholine should be avoided as it might trigger hyperthermia and may lead to hyperkalemia.
We used regional anesthesia considering all these implications of general anesthesia and wish to highlight that regional anesthesia should be used in these patients, whenever possible.
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Gunusen I, Karaman S, Nemli S, Firat V. Anesthetic management for cesarean delivery in a pregnant woman with polymyositis: A case report and review of literature. Cases J 2009;2:9107.
Shrestha GS, Aryal D. Anaesthetic management of a patient with dermatomyositis and valvular heart disease. Kathmandu Univ Med J (KUMJ) 2012;10:100-2.
Röckelein S, Gebert M, Baar H, Endsberger G. Neuromuscular blockade with atracurium in dermatomyositis. Anaesthesist 1995;44:442-4.
Ganta R, Campbell IT, Mostafa SM. Anesthesia and acute dermatomyositis/polymyositis. Br J Anaesth 1988;60:854-8.
Johns RA, Finholt DA, Stirt JA. Anaesthetic management of a child with dermatomyositis. Can Anaesth Soc J 1986;33:71-4.
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Anaesthesia was maintained with dexmedetomidine and desflurane titrated to a minimum alveolar concentration of 1 to 1.2 via an 8 mm ID endotracheal tube. Surgery lasted 6 h with a console time of 3 h. Pelvic lymphadenopathy could not be done because of gross fatty deposition in the pelvis. Blood gases done after undocking showed acceptable values of oxygenation, pH, and normocarbia. Considering the short console time, lesser than planned extent of surgery and high chances of pulmonary complications with prolonged ventilation, tracheal extubation was planned. However, as the patient was not conscious even 1 h after reversal of neuromuscular blockade and return of acceptable spontaneous minute volumes, she had to be ventilated postoperatively. The ONSD at this time point was elevated at 5.1 cm. She was extubated after 12 h of elective ventilation.
A 57-year-old diabetic patient of carcinoma endometrium was planned for robot-assisted radical hysterectomy with lymph node exenteration. Her body weight was 137 kg with a BMI of 55.5 kg/m2. She had a history of sleep apnoea. Pulmonary function tests showed mild restriction with an FVC of 79% of predicted and an FEV1:FVC ratio of 108% of predicted.
Baseline ONSD was 3.5 cm. Anaesthesia was maintained via an 8-mm ID endotracheal tube on pressure controlled ventilation with desflurane titrated to a bispectral index of 40–50, and dexmedetomidine. Surgery lasted 7.5 h. The ONSD was 4.4 cm at 30 min after undocking. The pre extubation values of bispectral index and blood gases were acceptable. She was extubated uneventfully on the operating table after complete awakening.
A 70-year-old hypertensive and diabetic male patient of carcinoma rectum was planned for robotic abdominoperineal resection. He was a known asthmatic with poor effort tolerance. He weighed 117 kg with a BMI of 39.44 kg/m2. Pulmonary function test showed an FVC of 70% of predicted and moderate reversibility with bronchodialators.

Doctors know that giving patients too many fluids or too big breaths during anesthesia can cause pulmonary problems afterwards.
Fernandez-Bustamante said that paying more attention to preventing atelectasis, for example, before, during and after surgery, could reduce some of them, improve oxygenation and prevent the need of oxygen therapy and hospital stay.
She noted that physicians must also optimize fluids and pain control, and minimize blood loss during operations to prevent PPCs. Doing all of this, she said, could improve patient outcomes and result in shorter hospital stays.
"Surgeons, anesthesiologists, nurses, respiratory therapists, and others, must collaborate better to make this successful. And of course patients need to know they play a critical role in their own recovery. We must work with them closely before, during and after surgery," Fernandez-Bustamante said. "If we want patients to have less pulmonary complications, we need a truly comprehensive approach to this problem."
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We therefore intentionally delayed our formal evaluation of lung function to the first postoperative day. We tested 80% oxygen because this concentration provides many of the benefits of 100% oxygen but with less direct pulmonary toxicity. It therefore remains possible that administration of 100% perioperative oxygen is associated with clinically important atelectasis.
In summary, lung volumes, the incidence and severity of atelectasis, as well as alveolar gas exchange were comparable in patients given 30% and 80% oxygen during and for 2 h after colon resection. We conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.
The authors gratefully acknowledge the support and generous assistance of the CT technicians, Marlene Thiem, R.T.A., and Slyvia Kiss, R.T.A., and the generous contributions of Alois Werba, M.D., Cem F. Arkiliç, M.D., and Folke Seibt, M.D.
1. Lindberg P, Gunnarsson L, Tokics L, Secher E, Lundquist H, Brismar B, Hedenstierna G: Atelectasis and lung function in the postoperative period. Acta Anaesthesiol Scand 1992; 36: 546–53
2. Joyce CJ, Baker AB: Effects of inspired gas composition during anaesthesia for abdominal hysterectomy on postoperative lung volumes. Br J Anaesth 1993; 75: 417–21
3. Schwieger I, Gamulin Z, Suter PM: Lung function during anesthesia and respiratory insufficiency in the postoperative period: Pysiological and clinical implications. Acta Anaesthesiol Scand 1989; 33: 527–34
4. Bergman NA: Distribution of inspired gas during anesthesia and artificial ventilation. J Appl Physiol 1963; 18: 1085–9
5. Bendixen HH, Hedley-Ehyte J, Laver MB: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation: A concept of atelectasis. N Engl J Med 1963; 269: 991–6
6.

Supplemental oxygen also improves tissue oxygenation adjacent to abdominal wounds: 75 vs 52 mm Hg, P = 0.005.37
We were thus unsurprised that supplemental postoperative oxygen almost halved the risk of infection-related complications in our preliminary study of morbidly obese patients having open Roux-en-Y gastric bypass (n = 96).48 There was, nonetheless, no statistically significant difference in the risk of surgical site infections or associated complications in the 400 patients we randomized to supplemental (approximately 80%) or nasal cannula (approximately 30%) oxygen for 12 to 16 postoperative hours. Major complications were chosen to be serious and plausibly related to infection or wound healing, both of which were likely to be improved by supplemental oxygen. Use of a composite outcome was intuitive for this study because we expected supplemental oxygen to reduce the risk of various complications; a single outcome, such as surgical site infection, was unlikely to capture the anticipated treatment benefit so well.
The most obvious difference between the preliminary study and full trial was that a laparoscopic approach was used in 91% of the patients in the full trial, whereas all the preliminary cases were open. Although there was a nonsignificant trend toward a benefit from supplemental oxygen in open procedures in the full trial (n = 37, relative risk 0.67 [95% CI: 0.2–2.3]), there was no overall benefit when open and laparoscopic cases were combined. Since the current surgical trend is toward laparoscopic procedures even in the most morbidly obese patients, it is the results in all patients (mostly laparoscopic) that are most relevant to current practice.
The overall rate of surgical site infections and complications (13%) was lower in both groups than the 25% we expected based on previous studies25,50,51 and our preliminary data.48 However, as more Roux-en-Y gastric bypasses are done laparoscopically and surgical technique improves, the incidence of complications has decreased even in the largest patients.52,53 Neither the futility nor efficacy boundaries were crossed after recruitment of the initial quarter of the patients. However, the futility boundary was crossed at the final analysis of 400 patients (P = 0.80 > the futility boundary of 0.2757). The Executive Committee thus stopped the trial since the probability of identifying a significant difference was low even if the trial continued to completion.

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BACKGROUND: Morbidly obese patients are at high risk for perioperative complications, including surgical site infections. Baseline arterial oxygenation is low in the morbidly obese, leading to low tissue oxygenation, which in turn is a primary determinant of infection risk. We therefore tested the hypothesis that extending intraoperative supplemental oxygen 12 to 16 hours into the postoperative period reduces the risk of surgical site infection and healing-related complications.
METHODS: Morbidly obese patients having open or laparoscopic bariatric surgery were given 80% inspired oxygen intraoperatively. Postoperatively, patients were randomly assigned to either 2 L/min of oxygen via nasal cannula or approximately 80% supplemental inspired oxygen after tracheal extubation until the first postoperative morning. The risks of surgical site infection and of major healing-related complications were evaluated 60 days after surgery.
RESULTS: In a preplanned interim analysis based on the initial 400 patients, the overall observed incidence of the collapsed composite of major complications was 13.3%; the observed incidence of components of the composite outcome ranged from 0% (peritonitis) to 8.5% (surgical wound infection). The estimated relative risk of any ≥1 major complications occurring within the first 60 days after surgery, adjusting for study site, was 0.94 (95% confidence interval, 0.52–1.68) (P = 0.80, Cochran–Mantel–Haenszel). The Executive Committee thus stopped the trial for futility.
CONCLUSIONS: Supplemental postoperative oxygen does not reduce the risk of surgical site infection rate and healing-related postoperative complications in patients having gastric bypass surgery.
From the *Department of Anesthesiology, University of Louisville, Louisville, Kentucky; †Department of Anesthesiology and General Intensive Care, Vienna General Hospital, University of Vienna, Vienna, Austria; and ‡Department of Outcomes Research, Cleveland Clinic, Cleveland, Ohio.
Anupama Wadhwa, MD, is currently affiliated with Department of Outcomes Research, Cleveland Clinic, Cleveland, Ohio.
Accepted for publication April 14, 2014.
Details of Supplemental Postoperative Oxygen Trial (SPOT) Investigators are provided in Appendix.
Funding: This study was funded from internal sources only. Viasys Healthcare, Inc. (Yorba Linda, CA) donated the Hi-Ox.
The authors declare no conflicts of interest.

When we started the trial, available evidence suggested that supplemental oxygen, continued to –6 hours postoperatively, almost halved infection risk.22 However, the extent to which supplemental oxygen might be protective for wound infection is now unclear after recent publications of the PROXI and ISO2 trials.25,54 Our current results do not directly address optimal intraoperative oxygen management since randomization was restricted to the postoperative period and all patients received supplemental oxygen in the intraoperative period. Nonetheless, our results seem inconsistent with the general theory that supplemental oxygen reduces wound infection risk.
Why supplemental oxygen does not further reduce surgical site infections and complications in the morbidly obese population remains unclear, especially given the overwhelming evidence that tissue oxygenation is a key determinant of oxidative killing and that oxidative killing is the primary defense against bacterial contamination.8,9 But it is possible that oxygen is no longer effective after the “decisive period” for infection has passed, which is determined to be within a few hours after contamination, which is the incision.
Aside from the timing and duration of supplemental oxygen administration, the major difference between previous trials of supplemental oxygen and our current results is that our patients were morbidly obese. The obese patient population was selected in this study for providing supplemental oxygen since perioperative tissue oxygenation is normally low in this population,22 and high inspired concentrations are required to return tissue partial pressures to the normal range.27 Tissue oxygenation is also impaired by frequent hypoxemic episodes during sleep by the presence of obstructive sleep apnea, which has a prevalence approaching 75% to 86% in this obese population.30–32
Consistent with their many risk factors, wound infections and infection-related complications are common in the obese. In 189 patients having colorectal procedures, for example, wound infection risk significantly correlated with the thickness of subcutaneous fat: 8% of those with <2 cm of subcutaneous fat developed a wound infection compared with 27% with >4.5-cm fat.

They discuss proper configuration of surgical drapes to avoid accumulation of oxygen and stress adequate drying time when alcohol-based skin preps are used. And sponges, gauze or other cottonoids used should be moistened when being used near an ignition source or near an oxygen-enriched area such as the airway. Scavenging the operating field with suction may help avoid buildup of oxygen (or nitrous oxide).
They discuss use of laser-resistant tracheal tubes (matching the tube type to the laser type) and note that the tracheal tube cuff should be filled with saline rather than air. The saline could also be tinted with methylene blue to help identify laser punctures. They also discuss the type of oxygen delivery system that should be used, based on the required depth of sedation and oxygen dependence.
Coordination between the anesthesiologist and surgeon are critical when it comes to using lasers, electrocautery tools, electrosurgical tools, or other potential sources of ignition. The surgeon should give adequate notice that he/she is about to use such a device and then adequate time should be allowed to elapse to allow the anesthesiologist to take steps to minimize the oxygen in the area.
Their discussion on management of an actual fire is a good one. They emphasize early recognition and that the early signs of a fire may not just be a flame or flash but might include unusual sounds (eg. “pop”, “snap”, or “foomp”), odors, smoke, heat, unexpected movement of the drapes or patient, or discoloration of the drapes or breathing apparatus. When a fire is determined, the fire should immediately be announced, the procedure halted, and fire management tasks should be begun. Each team member should do their assigned task as quickly as possible, not waiting if another team member has not been able to do their task in a predetermined order. The specific tasks are outlined in the document and depend on whether the fire is in the airway or breathing circuit or elsewhere on the patient. They discuss assessment and management of the patient after a fire and discuss more general fire responses as well.
The advisory is very well-referenced and levels of evidence are graded. They do provide a nice algorithm on operating room fires. It can be used as an educational tool and as part of the preoperative procedure, but it does not look like it would be of much use emergently during a fire.

NIMV has been well documented in COPD during periods of acute exacerbations, reducing the respiratory work and improving clinical results8,20, however its benefit during the anesthetic-surgical procedure remains undefined.
This case and the others reported in literature have proven the simple and easy applicability of NIMV at intraoperative period. NIMV appears to be a useful intraoperative ventilation support in situations of chronic disease, such as advanced COPD, as well as in worsened chronic and acute situations. Other groups of patients have been reported and may benefit. The anesthesiologist must become familiar with the noninvasive method and together with the clinical team, evaluate which patients will truly benefit from this type of support.
01. Mannino DM. COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest. 2002;121:(5 Suppl):121S-126S. Review. [ Links ]
02. Licker M, Schweizer A, Ellenberger C. Tschopp JM, Diaper J, Clergue F. Perioperative medical management of patients with COPD. Int J Chron Obstruct Pulmon Dis. 2007;2(4):493-515. [ Links ]
03. Wong DH, Weber EC, Schell MJ, Wong AB, Anderson CT, Barker SJ. Factors associated with postoperative pulmonary complications in patients with severe chronic obstructive pulmonary disease. Anesth Analg, 1995;80(2):276-84. [ Links ]
04. Menezes AM, Jardim JR, Perez-Padilla R, Camelier A, Rosa F, Nascimento O, et al. Prevalence of chronic obstructive pulmonary disease and associated factors: the PLATINO Study in Sao Paulo, Brazil. Cad Saude Publica. 2005;21(5):1565-73. [ Links ]
05. Mircea N, Constantinescu C, Jianu E, Busu G. Risk of pulmonary complications in surgical patients. Resuscitation. 1982;10(1):33-41. [ Links ]
06. Wightman JA. A prospective survey of the incidence of postoperative pulmonary complications. Br J Surg. 1968;55(2):85-91.

The ECRI recommends that anesthesiologist stop using 100 percent oxygen in the OR and deliver only what the surgical patient needs, perhaps by diluting the oxygen concentration with room air when surgical tools such as electronic scalpels and cauterizers are in use.
"What we've been advocating for years is that the open delivery of oxygen under the drapes essentially has to stop," Bruley says, with some exceptions such as cardiac pacemaker surgery or operations involving a neck artery.
It’s important for surgical professionals to be aware of the risks and what can be done to prevent fire in the OR because, while it’s rare, a surgical fire can be fatal to a patient.
Sources: The Associated Press; JointCommisson.org

Patients that have undergone emergency surgery to address respiratory distress are routinely supplemented with oxygen in the
early recovery period and are monitored for oxygenation status using physical parameters (respiratory rate, respiratory character,
and mucous membrane color), pulse oximetry (SpO2), and, when practical, arterial blood gases (PaO2). Clinical signs of hypoxia
(increased respiratory rate, abnormal respiratory character, and pale, cyanotic, or "muddy" mucous membranes), low SpO2 (less
than 96%), and low PaO2 (less than 80 mmHg) indicate continued use of supplemental oxygen. Oxygen therapy is continued if
normoxia cannot be achieved when the animal is breathing room air, and positive-pressure ventilation with positive end-expiratory
pressure may be necessary if normoxia cannot be achieved with administration of 100% inspired oxygen. Monitoring is not limited
to the above mentioned parameters. All critically ill respiratory patients are evaluated at periodic intervals by assessing
attitude, pulse rate and quality, and capillary refill time, and by performing thoracic auscultation. Invasive and/or noninvasive
arterial blood pressure is monitored in patients with potential (or existent) hemodynamic instability. Intakes (parenteral
fluid therapy and oral intake) and outputs (urine, emesis, and defecation) are monitored. Because of potential pulmonary compromise
in certain respiratory distress patients intravenous fluid therapy must be performed judiciously to prevent volume overload;
therefore, central venous pressure monitoring is employed.
Management Of Tracheostomy Tubes
Supplemental oxygen during recovery can be achieved through a small tube (8 french) placed into the lumen of the tracheostomy
tube. The oxygen flow rate should be nearly half of what is required with intranasal oxygen administration because oxygen
is delivered directly into the trachea, making the trachea an oxygen-rich reservoir. Upon recovery from anesthesia the need
for supplemental oxygen is based on the oxygenation parameters listed above.
Tracheostomy tube hygiene is extremely important because of the risk of iatrogenic respiratory infection and the possibility
of acute fatal obstruction due to accumulated respiratory tract secretions. Immediately after surgical placement and for the
first several hours tracheostomy tubes require constant vigilance and hourly removal of intraluminal secretions. Around-the-clock
observation and care are mandatory.

Comparable Postoperative Pulmonary Atelectasis in Patients Given 30% or 80% Oxygen during and 2 Hours after Colon Resection
Akça, Ozan M.D.*; Podolsky, Andrea M.D.†; Eisenhuber, Edith M.D.‡; Panzer, Oliver M.D.*; Hetz, Hubert M.D.§; Lampl, Karl M.D.§; Lackner, Franz X. M.D.∥; Wittmann, Karin M.D.#; Grabenwoeger, Florian M.D.**; Kurz, Andrea M.D.††; Schultz, Anette‐Marie M.D.§; Negishi, Chiharu M.D.‡‡; Sessler, Daniel I. M.D.§§
Background: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen.
Methods: Thirty patients aged 18–65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day.
Results: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar–arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%‐oxygen group and in 44% of those in the 80%‐oxygen group.

As previously mentioned, the safest place to manage the airway of a decompensating child is the operating room. A child will not cooperative with an awake intubation. In the OR, a slow, careful induction with inhalation agent can be done in a controlled setting.
However, if in your judgement the patient is in danger of immediate death, and you can’t wait for more specialized help, proceed with caution. Call for the tools to do cricothyroidotomy or tracheostomy just in case you need them.
Make sure you have the equipment you need to use after you secure an invasive airway. For example, if your choice is to do percutaneous cricothyrotomy with a large bore angiocath, you must be able to attach oxygen and ventilate through the angiocath. Make sure you have the jet ventilator hooked up and ready to go.
In the absence of a jet, have the correct adapters to hook up to an Ambu bag set up and ready to go. Don’t wait until you have a catheter in the cricothyroid membrane before you ask for something to attach it to. A previous article discussed use of percutaneous jet ventilation.
If a jet ventilator is unavailable, then there are several ways to connect the catheter to your ventilation system. The connector from a number 3 endotracheal tube fits snugly into the hub of any intravenous catheter. However, this tiny assembly is often difficult to hold while squeezing the bag. I prefer to place the connector from a number 7.5 endotracheal tube into the barrel of a 3 ml syringe.
The barrel of the syringe now mates to the hub of your catheter and gives you something more substantial to hold. You can also place an endotracheal tube within the barrel of a ten ml syringe and inflates the cuff to maintain the connection. You must ventilate vigorously to pass enough oxygen through the catheter.
Gas will escape through the mouth. You must allow the gas to escape and the patient to exhale, otherwise pneumothorax is a risk.
You can also attach the barrel from a tuberculin syringe to the catheter hub and connect this to oxygen tubing. If the oxygen tubing can then be connected to the fresh gas outflow from an anesthesia machine a “jet” can be jury rigged.

- Adequate analgesia
- Early mobilization
- Lung expansion maneuvers that increase positive end-expiratory pressure (PEEP)
- Treatment of underlying condition
The risk of atelectasis after surgery can be avoided by prescribing opioids in doses that are sufficient for pain relief, as well as encouraging the use of incentive spirometry. At the same time, opioids should be used with caution due to their suppression on coughing. Smoking should be avoided 6–8 weeks prior to surgery.
We list the most important complications. The selection is not exhaustive.

Until the child can walk, it is very important to go for a walk: walking is very useful not only for muscles, but also to support other functions of the body, particularly breathing. as the progression of the disease this feature may also have to maintain artificially. So, to prevent the stopping of breathing during sleep apply the ventilators.
Medication, unfortunately, can not slow the progression of the disease, but can help to alleviate the patient's condition, making symptoms less severe. Thus, corticosteroids help to replenish energy, β2-agonists supports muscle strength.
Otherwise, doctors recommend to maintain physical activity as much as possible time and condition of the patient. In addition to the walk, very useful lessons in the pool: while swimming reduces the load on muscles and joints, because water decreases body weight, improves blood circulation in the muscles. Therapeutic exercises should be combined with physiotherapy support procedures to extend the functionality of the muscles and joints, and progressive muscular dystrophy will be less apparent.
The Use of various orthopedic devices and accessories, from tires and couplers to wheelchairs and strollers, helps muscular dystrophy patients to provide some of their needs on their own and makes them more mobile. Bus are superimposed on the sleep time, to avoid unwanted joint mobility during this time. At the end of the disease for normal respiratory process require special tools, from respiratory masks to respirator.

The scapular is also called the shoulder blade and sits on the back. Often in FSHD progressive weakness in the muscles that hold the scapular against the back and attached to the arm, leads to winging and eventually an inability to lift arms. During the procedure the scapular is attached to the rib bones that lie underneath it. This can improve the function of the shoulder.
There are other surgical techniques that may provide some help. However, surgery does not always result in significant improvement and it’s important that you have considered all the risks and benefits with your health professional before deciding on a surgical treatment strategy.
Other muscular dystrophies are associated with breathing difficulties because eventually the progressive weakness spreads to the muscles that control breathing. This is not a common complication of FSHD. However regular monitoring of breathing function is recommended especially as you may not realise you have poor breathing function.
Difficulty breathing means there is not enough oxygen getting to your tissues. This can exacerbate the negative effect of FSHD on your muscles.
Breathing problems during sleep is also not a common complication of FSHD, but it can happen. Symptoms include disturbed sleep, morning headaches, daytime fatigue and sleepiness. It is relatively simple to diagnose and treat night time breathing problems. Some people may respond well to position therapy to help you sleep in a position that limits any obstruction to breathing. Non-invasive ventilation is also an option.
Orthotics, walkers, crutches and the chair
When many people think about muscular dystrophy they think about people confined to a wheelchair. While it is true that many people with FSHD do use a wheelchair for mobility the idea that they are confined to it is misleading. Some people may have lost the ability to walk and therefore need the chair to get from a to b. Others may use a chair for long distances to prevent fatigue. Some people may have significant foot drop and therefore use the chair because it allows them to get around while preventing falls and fractures that might seem them completely reliant of the chair.

Awake tracheostomy is reserved for patients with facial fractures or other, severe anomalies of airway anatomy that make safely securing the airway difficult and unsafe. Succinylcholine should be avoided in cases of neurogenic shock as it can increase the risk for extreme bradycardia. Atropine should be administered prior if succinylcholine must be used.
Breathing is best managed by mechanical ventilation, with ventilation for SPO2 > 95% and ETCO2 = 35 mmHg. Spinal cord injuries involving C4 and cranial result in interruption of the descending bulbospinal respiratory pathways, resulting in respiratory ...

Depending on the severity of the facial
a careful evaluation of the airway must be conducted (clinical, radiographic). Renal
function tests must include renal ultrasonography, intravenous pyelogram, routine
electrolytes, urea, and creatinine. Neurological test includes clinical, EEG, CT, and MRI.
Techniques should be tailored to the
cardiac defect present and the procedure planned. Measures to prevent air embolism must be
taken. Adequate intravascular hydration must be ensured. The presence of macroglossia and micrognathia may
contribute to difficult laryngoscopy and tracheal intubation. A laryngeal mask should
always be available. Positioning may be difficult if contracture occurred from hypertonia.
The risk of pressure necrosis must be considered.
May consider avoiding suxamethonium
if there is evidence of delayed myelination in CNS. Consider interaction
between antiepileptic medication and anesthetic drugs. Endocarditis
prophylaxis as indicated. Avoid muscle relaxants until airway is secured.
Fujimoto A, Wilson MG, Towner JW: Familial inversion of chromosome no. 8:
An affected child and a carrier fetus. Humangenetik
Gelb B, Towbin J, McCabe E, et al: San Luis Valley recombinant chromosome 8
and tetralogy of Fallot: A review of chromosome 8 anomalies and congenital
heart disease. Am J Med Genet 40:471, 1991....

The board-certified and fellowship-trained neurologists with Norton Children’s Neuroscience Institute, affiliated with the UofL School of Medicine, are the leading providers of care for children with neuromuscular disorders, including Duchenne muscular dystrophy (DMD), in Louisville, Kentucky, and Southern Indiana.
Norton Children’s Hospital is the pediatric teaching hospital for the University of Louisville School of Medicine. Our physicians are training the next generation of pediatric specialists.
We’ll determine the severity of your child’s DMD and create a treatment plan that minimizes risk, so your child can get back to being a kid.
Our multidisciplinary approach, in partnership with the Muscular Dystrophy Association (MDA), sees patients in a single clinic for multiple specialties, including neurology, pulmonology, orthopedics, physical therapy, occupational therapy and speech therapy.
What is DMD?
DMD is a genetic disorder that affects muscles and primarily occurs in boys. Symptoms typically start between age 3 and 5, with weakness that affects the hips and legs, and results in abnormal walking. As the disease progresses, the weakness affects the upper body as well. That weakness may also affect the heart and respiratory muscles.
If our team suspects DMD, we will order specific genetic testing through a blood test. Genetic testing will determine if there are abnormalities in a gene associated with a muscle protein called dystrophin. Dystrophin is a vital part of the muscle fiber. When it is abnormal, muscle cells are easily damaged.
Our physicians may prescribe medications known as corticosteroids, which have been shown to be effective in slowing the course of DMD. Depending on the specific mutation found in the genetic testing, your child may be eligible for specific gene therapies.
As a child’s muscles that aid in breathing become weaker, assistance with coughing and breathing may be necessary. Our team may prescribe noninvasive breathing devices, such as a CPAP (continuous positive airway pressure) or BiPAP (bilevel positive airway pressure) device. Additional support may include placement of a tracheostomy (a hole in the breathing tube) and use of a ventilator.
If tests show your child’s heart is affected, our team may prescribe medications that slow the course of cardiac muscle deterioration.
As children with DMD lose their mobility, they may need orthotics, braces, walking aids or wheelchairs.

During the procedure, the patient had one episode of bronchospasm that was promptly reverted pharmacologically with no complications in the postoperative period. The combination of less invasive anesthetic and ventilation techniques is easy to apply and may be useful in the perioperative management of patients with high anesthetic morbidity. Interaction between clinical, surgical and anesthetic teams for these cases is very important to reduce the mortality associated with extensive procedures in severe patients.
Keywords: Pulmonary disease, chronic obstructive; Arthroplasty, replacement, hip; Respiration, artificial; Positive pressure respiration Anesthesia, epidural; Human; Male; Aged; Case reports
Chronic obstructive pulmonary disease (COPD) is an increasingly prevalent condition in the overall population1 and is considered an independent risk factor for cardiopulmonary mortality and morbidity at postoperative period.2 While general anesthesia has been associated to a higher risk of complications during and after surgical procedure, regional anesthesia has the advantage of avoiding tracheal intubation and worsening of the postoperative pulmonary function.3 With improvement of anesthetic techniques, of drugs utilized and of intra- and postoperative cares, it became possible to reduce morbidity and mortality of patients, classically viewed as contraindicated for surgery. Interaction between the clinical, surgical and anesthetic teams becomes essential in the management of such patients.
The objective of this study was to present a case of application of noninvasive mechanical ventilation (NIMV) during hip arthroplasty of a patient with severe COPD, associated to regional anesthesia (spinal).
A male, 81 years old, 75 kg patient was admitted after a fall from his own height, presenting with pain, external rotation deformity and shortening of the lower right limb and was diagnosed as displaced femoral neck fracture Garden IV (Figure 1) with indication for partial hip arthroplasty. Bearer of severe COPD, presenting respiratory function test (RFT) with a forced expiratory volume in 1 second (FEV1) <20%, while using domestic oxygen therapy, corticoid therapy and presenting with dyspnea at minimal efforts.
Furthermore, the patient had undergone a coronary angioplasty with placement of a drug-eluting stent two years earlier.

Yet the risk factors associated to respiratory complications observed were: American Society of Anesthesiology (ASA) score > 4, Shapiro score > 5 and decrease of FEV1. The patient under study presented risk factors for the described complications, so much so that during the postoperative period he presented bronchospasm. If the ventilatory mode used during surgery of hip arthroplasty alters the intra- and postoperative complications of these patients is a fact that still remains unknown.
Due to the restricted number of patients with COPD submitted to hip arthroplasty and the large variation in the severity of this disease it is difficult to carry out a randomized study with a large population in order to evaluate the morbidity/mortality inherent to the ventilation mode.
Regional anesthesia is described as the preferential mode for patients with COPD and respiratory failure when compared to general anesthesia.2 Factors of general anesthesia such as atelectasia, cephalic displacement of the diaphragm and loss of respiratory stimulus are attributed to this worsening.8 Notwithstanding that regional anesthesia is also associated to a decrease of the respiratory function, occurrence of such an event is less frequent and intense when compared to general anesthesia.
General anesthesia, in addition to be considered a risk factor for mortality in hip surgery, is associated to complications and worsening in the ventilation pattern at intra- and postoperative of patients with COPD.9 Although regional anesthesia is suitable for hip surgery, factors related to its use, such as positioning, surgical stress, sedation and neuromuscular block may worsen the respiratory condition, therefore the need arises for adequate intraoperative support in patients with a previously poor pulmonary function, such as patients with COPD.10
The combination of regional anesthesia associated to NIMV during intraoperative of patients with COPD and respiratory failure was recently described in literature11-15, with few reports on hip arthroplasty.12-13
NIMV is a well-known method for decrease of mortality, improvement of respiratory distress and correction of blood gas disorders in exacerbation of COPD.16-17 During surgery, tracheal intubation may also be used as a support ventilatory mode in respiratory failure and in COPD.

At least 60% of surgical patients suffer from coexisting medical issues (Nierman & Zakrzewski 1999) Haematological, electrolyte and metabolic disturbance, respiratory support, analgesia, bowel and urinary management in particular, need to be addressed urgently prior to surgical treatment. Patients with a life expectancy of less than six weeks rarely gain benefit from major reconstructive surgery (BOA 2001). The burden of malignancy also increases the risk of thromboembolic events (deep vein thrombosis and pulmonary embolus) and therefore advice from haematologists should be sought or local guidelines strictly adhered to. A vena cava filter may also be required in patients with coexisting DVTs before to surgery.
Meticulous preoperative planning and a multidisciplinary approach are vital prior to proceeding with surgery. An alternative strategy must be made by the surgeon if the primary surgical plan fails. All surgical equipment must be sterilised, checked and be available prior to surgery (endoprostheses, cement, internal fixation instruments). In certain cases, the availability of general and vascular surgeon teams should be checked.
It is mandatory for the operating room to be well prepared (monitoring equipment, sterility) before surgery. Extra care must be given to patient positioning to prevent decubiti and nerve palsies. The use of extra padding is often helpful. Patient warming prevents risk of hypothermia in lengthy cases. Sequential compression devices, arterial and central venous lines, urethral catheters are all placed for monitoring and continuous blood sampling. End tidal Co2 is monitored during cementation as this can evoke a cardiopulmonary event. Spinal monitoring may also be required. Broad spectrum antibiotics are administered on induction of anaesthesia, followed by two postoperative doses in routine cases. Finally, the World Health Organisation (WHO) checklist should be performed in the operating room before surgery commences to minimise errors (Haynes et al 2009).
Postoperatively, patients are managed on the surgical unit. Unstable patients are transferred to the high dependency or intensive care unit, where closer monitoring and higher nurse to patient ratio is provided. Cardiopulmonary and haemodynamic monitoring provides a good indication of fluid balance, electrolyte and oxygenation.

Patients with OSA may have an increased sensitivity to anesthetics or opioids, greater upper airway collapsibility, and increased risk of postoperative complications. For surgical patients with OSA, supplemental oxygen may be more acceptable than CPAP therapy but three clinical concerns exist. First, hypoxemia may play a critical role in respiratory arousal in surgical patients with OSA. When supplemental oxygen abolishes hypoxemia, the apnea duration may increase, causing hypoventilation as evidenced by hypercarbia, leading to possible life-threatening respiratory depression. Second, postoperative opioids may depress respiration centrally and impair the arousal threshold causing arousal failure, possibly leading to sporadic case of death. The third concern is that supplemental oxygen may mask the ability of oximetry to detect abnormalities in the level of ventilation.
The authors set out to was to investigate the effect of postoperative supplemental oxygen on Sao2, sleep respiratory events, and CO2 level in patients with untreated OSA.
Postoperative supplemental oxygen improved oxygenation in surgical patients with OSA. Supplemental oxygen decreased AHI, hypopnea index, and central apnea index and shortened the longest apnea-hypopnea event duration. Although no overall difference was found between groups in PtcCO2 level, a significant increase of PtcCO2 was found in 11.4% of patients, especially those receiving oxygen on postoperative night 1. Postoperative supplemental oxygen could be used as an alternative therapy for patients with OSA not adherent to CPAP, newly diagnosed patients without adequate time to initiate CPAP therapy, or patients with suspected OSA. Additional monitoring of respiratory rate or PtcCO2, especially on postoperative night 1, is recommended. Further work is needed to identify OSA phenotypes which would benefit from postoperative supplemental oxygen and to identify which patients should be monitored for hypoventilation with respiratory rate or PtcCO2.
Sleep is integral to biologic function, and sleep disruption can result in both physiological and psychologic dysfunction including cognitive decline. The brain’s capacity to successfully respond to cognitive challenges through compensatory recruitment becomes overwhelmed if the patient is not presented with appropriate and continual sleep. Surgery activates the innate immune system, inducing neuroinflammatory changes that interfere with cognition.

Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean ± SD) did not differ significantly in the patients given 30% oxygen (2.5% ± 3.2%) or 80% oxygen (3.0% ± 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an α level of 0.05.
Conclusions: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.
THE major complication associated with brief periods of oxygen administration is pulmonary atelectasis. Concern about atelectasis is appropriate because it occurs in up to 85% of patients undergoing lower abdominal surgery and is thought to be an important cause of morbidity. 1–3
Two mechanisms contribute to perioperative atelectasis: compression and absorption. Compression results from cephalad displacement of diaphragm, decreased compliance, and reduced functional residual capacity. 4–6
To some extent, these factors are present with any anesthetic technique. In contrast, absorption is defined by uptake of oxygen from isolated alveoli and results from administration of high oxygen partial pressures. Administration of 100% oxygen, even for a few minutes, causes significant postoperative atelectasis via
this mechanism. 2,7,8
There is little doubt that high intraoperative oxygen concentrations produce atelectasis, at least in the immediate postoperative period. 7–10
However, the extent to which this atelectasis impairs pulmonary function and gas exchange remains controversial. 2,7–12
An additional complication associated with postoperative atelectasis is fever, which often prompts diagnostic evaluation or therapeutic intervention for potential infectious causes.
Intraoperative ventilation with high partial pressures of oxygen provides clinicians additional time to diagnose and treat inadvertent extubation, laryngospasm, and breathing‐circuit disconnections.

Although it is not associated to an increase of mortality in patients with COPD admitted to ICU18 tracheal intubation may entail spirometric worsening at postoperative of healthy patients.19 However it is not known whether this worsening observed in the spirometric pattern of healthy patients, also takes places in patients with COPD and whether it may contribute to increased mortality or postoperative cost - when compared to patients who have used NIMV in the intraoperative.
Management of an obese patient with severe COPD submitted to hip arthroplasty under spinal anesthesia and BIPAP was previously described.12 Risks of general anesthesia with tracheal intubation in this population are reported, as well as need for compliance to the method as the essential problem. In the case reported, previous knowledge of the patient's tolerance regarding NIMV facilitated its use. The patient of the study was discharged 7 days after surgery, while the patient in this case remained in the ICU for 10 days. It is noteworthy that although intensive care length of stay is longer in the report on our patient, he showed more severity factors in surgery (lower FEV1, older, obesity).
NIMV has also been reported in patients with acute ventilation impairment. One case of worsened chronic respiratory failure, submitted to spinal anesthesia and support with NIMV avoiding general anesthesia, was reported.13 Warren et al. described the case of a patient with myasthenia gravis and acute respiratory failure submitted to obstetric surgery under peridural anesthesia using noninvasive ventilation support.14 The position required for the surgical procedure often involves undesirable and intolerable ventilatory alterations in pulmonary sick patients.10 An English group described use of NIMV in a severe COPD patient submitted to resection of a carcinoma of the rectum, under spinal anesthesia in lithotomic position11. NIMV allowed the patient to tolerate the respiratory restriction imposed by the position of lithotomy, avoiding general anesthesia.
In view of this evidence, NIMV has been evaluated in patients with chronic and acute ventilation impairment. However, other groups of patients and surgical procedures may benefit from this intraoperative ventilation mode.
NIMV was also described by a Japanese groupfor patients submitted to craniotomy for cerebral mapping16. NIMV allowed for a sufficient anesthetic depth during bone opening and closure, total awareness during mapping, smooth transition between anesthesia and consciousness, suitable ventilation and immobility with comfort for the patient.

However, unless the patient is connected to a ventilator, or has a tight-fitting face mask, the appliance used to deliver oxygen to the face will always result in an inhaled FIO2. less than 100%.
6. The body does not store oxygen.
Athletes who inhale a few minutes of oxygen, and then return to the playing field, are not benefitted in any physiologic way. If a patient needs supplemental oxygen it should be for a specific physiologic need, e.g., hypoxemia during sleep or exercise, or even continuously (24 hours a day) as in some patients with severe, chronic lung disease.
7. Supplemental O2 is an FIO2 > 21%.
Supplemental oxygen means an FIO2 greater than the 21% oxygen in room (ambient) air. When you give supplemental oxygen you are raising the patient's inhaled FIO2 to something over 21%; the highest FIO2 possible is 100%. To give more oxygen requires a hyperbaric chamber, an expensive piece of equipment found in relatively few hospitals.
8. Supplemental oxygen is a drug.
Like any other drug, it has indications, contra-indications, and side effects. Unlike the situation with most drugs, there are also easily measurable "levels" of oxygen (either PaO2 with a blood gas measurement or SaO2 with a pulse oximeter).
9. Supplemental oxygen is the most commonly prescribed drug
An estimated 1/4 to 1/3 of all patients admitted to a hospital will receive supplemental oxygen at some point. It is the only prescription drug in common use on all inpatient services (except perhaps Psychiatry).
10. A reduced PaO2 is a non-specific finding.
It can occur from any parenchymal lung problem, and only signifies a disturbance of gas exchange (usually due to V/Q imbalance). A low PaO2 should not be used to make any particular diagnosis, including pulmonary embolism.
11. A normal PaO2 and Alveolar-arterial PO2 difference (A-a
gradient) do not rule out pulmonary embolism.
About 5% of confirmed cases of PE manifest a normal A-a gradient.
12. High FIO2 doesn't affect COPD hypoxic drive.

Oxygenation during One Lung Ventilation (OLV) depends not only on the magnitude of shunt fraction but also on the oxygenation of the shunted blood . Thus, factors leading to a decrease in the oxygenation of the shunted (venous) blood (states of increased oxygen extraction, low cardiac output, low hemoglobin levels) compromise the ‘buffering’ capacity against tissue hypoxia. Under limited circumstances, pursuing increases in cardiac output may benefit arterial oxygenation during one-lung ventilation; for example SpO2 less than 90% may be tolerated poorly in anaemic patients with right to left cardiac shunts . Furthermore, low hemoglobin concentrations can increase shunt fraction and decrease oxygenation [29,30]. Therefore, increasing cardiac output and normalising haemoglobin concentration remain the main clinical interventions that can enhance oxygen delivery to tissues in this situation despite low SpO2 readings. However, this approach is not a panacea and does not obviate the necessity to optimize dependent lung volume .
Therefore, in venous admixture situations, attention to cardiac output, oxygen expenditure, venous saturation, and haemoglobin levels are needed to improve tissue oxygenation .
In this era of 21st century medicine, we need additional considerations to cope with increasing surgical complexity. For example, the increased recognition of the advantages of Video Assisted Thoracoscopic Surgery (VATS) in children has reiterated the need for efficient one lung ventilation . During one lung ventilation for VATS, there are additional factors that need focus: the use of positive pressure in pleural space; mechanical shift of the mediastinum; the effects of added CO2 upon vascular adaptive responses to hypoxia and the oxygen dissociation curve; and increased V/Q mismatch (due to decreased functional residual capacity and tidal volume resulting from general anesthesia, suboptimal patient positioning, surgical retraction and mechanical ventilation) .
A reliably measured  SpO2 of 92% is considered the lowest clinically acceptable level by established norms of clinical practice at any age, with an exception of 88% as the lowest in chronic lung disease. This is despite neither a SpO2 below 92% having been proven to be directly associated with tissue hypoxia, nor a SpO2 above 92% proven to exclude it.

Prospective, randomized trial comparing fluids and dobutamine optimization of oxygen delivery in high-risk surgical patients [ISRCTN42445141]
Division of Critical Care Medicine, Departments of Internal Medicine, Anesthesiology and Surgery, Medical School – FUNFARME and Hospital de Base, São José do Rio Preto, São Paulo, Brazil
Critical Care 2006, 10:R72 doi:10.1186/cc4913Published: 12 May 2006
Preventing perioperative tissue oxygen debt contributes to a better postoperative recovery. Whether the beneficial effects of fluids and inotropes during optimization of the oxygen delivery index (DO2I) in high-risk patients submitted to major surgeries are due to fluids, to inotropes, or to the combination of the two is not known. We aimed to investigate the effect of DO2I optimization with fluids or with fluids and dobutamine on the 60-day hospital mortality and incidence of complications.
A randomized and controlled trial was performed in 50 high-risk patients (elderly with coexistent pathologies) undergoing major elective surgery. Therapy consisted of pulmonary artery catheter-guided hemodynamic optimization during the operation and 24 hours postoperatively using either fluids alone (n = 25) or fluids and dobutamine (n = 25), aiming to achieve supranormal values (DO2I > 600 ml/minute/m2).
The cardiovascular depression was an important component in the perioperative period in this group of patients. Cardiovascular complications in the postoperative period occurred significantly more frequently in the volume group (13/25, 52%) than in the dobutamine group (4/25, 16%) (relative risk, 3.25; 95% confidence interval, 1.22–8.60; P < 0.05). The 60-day mortality rates were 28% in the volume group and 8% in the dobutamine group (relative risk, 3.00; 95% confidence interval, 0.67–13.46; not significant).
In patients with high risk of perioperative death, pulmonary artery catheter-guided hemodynamic optimization using dobutamine determines better outcomes, whereas fluids alone increase the incidence of postoperative complications.

No interaction was found between BMI quartile and the effect of randomized group on incidence of major complications (P = 0.34, Breslow–Day test, Table 5) nor did the effect of supplemental oxygen on major complications depend on type of surgery (P = 0.44, Breslow–Day test). Furthermore, there was no supplemental oxygen effect within laparoscopic surgery (RR: 1.06 [0.54–2.07]) or open Roux-en-Y gastric bypass surgery (RR: 0.67 [0.20–2.29], Table 6).
Within open Roux-en-Y gastric bypass surgery, the relative risks between the supplemental group and the 30% group were not different between the main trial and the pilot trial (P = 0.66, Breslow–Day test, Table 7). Since the number of complications was so low, we did not perform subanalysis of the data per surgical duration.
All surgical wounds become contaminated. What determines whether inevitable contamination progresses to clinical infection is largely the adequacy of host defense. The primary host defense against surgical pathogens is oxidative killing by bacteria, a process that depends on the partial pressure of oxygen over the entire range of physiologic values. Superoxide radical production is necessary for host defense and correlates directly with the inspired oxygen concentration.
Obese patients having laparoscopic surgery require more inspired oxygen to produce similar arterial oxygen partial pressures than lean individuals. They also have significantly lower subcutaneous oxygen tensions (36–41 vs 57 mm Hg).27,49 Supplemental inspired oxygen (80%) significantly increases subcutaneous oxygenation in the upper arm in morbidly obese patients: 58 vs 43 mm Hg. Tissue oxygenation progressively increases with supplemental oxygen to a maximal difference of about 40 mm Hg after 13 postoperative hours (94 vs 52 mm Hg).

This provides 24% to 30% inspired oxygen in most patients.35 When patients used a continuous positive expiratory pressure (CPAP) machine at home and could not maintain oxygen saturation ≥90% with the nasal cannula alone, they were switched to their CPAP machines at an inspired oxygen concentration (FIO2) to 30%. FIO2 was maintained at 30% in patients who remained intubated. Additional oxygen was given as necessary to maintain oxygen saturation ≥90%.
2. Supplemental oxygen administration: After extubation, patients were given 10 L/min of oxygen via a nonrebreathing Hi-Ox mask (Viasys Healthcare, Inc., Yorba Linda, CA), a valved manifold system. An oxygen flow of 5 L/min produces a supplemental inspired concentration of approximately 80%, even at a minute ventilation of 12 L/min, which few patients exceed.36,37 When patients used a CPAP machine at home and could not maintain oxygen saturation ≥90% with the Hi-Ox mask, they were switched to their CPAP machines at an inspired oxygen concentration of 80%. In patients who experienced claustrophobia or severe discomfort from the Hi-Ox mask, a venturi style dual-dial mask was substituted at an oxygen flow rate of 15 L/min. This mask delivers nebulized oxygen, which makes it more comfortable for patients and delivers approximately 60% inspired oxygen. FIO2 was maintained at 0.8 in patients who remained intubated.
The oxygen flowmeters were concealed from blinded surgeons and nursing staff. The nurses were instructed not to change the oxygen settings until the first postoperative morning, unless clinically indicated (oxygen saturation <90%).
The designated oxygen management was maintained until the first postoperative morning. Patients wore oxygen masks or nasal prongs while in bed but were allowed to remove them briefly as necessary (e.g., to visit the bathroom). To encourage compliance with the randomized oxygen assignment, an investigator visited patients when they first arrived on the surgical ward from the recovery room, the evening of surgery, and the first postoperative morning.
Demographic characteristics of patients were tabulated. We also recorded preoperative laboratory values (including plasma glucose concentration), smoking history, and American Society of Anesthesiologists Physical Status rating.
Fluids administered, estimated blood loss, urine output, and amount of opioids used were recorded daily throughout hospitalization.

13,14
Oxygen per se
also seems to be antiemetic, 15
which is of substantial clinical importance because uncontrollable nausea and vomiting remains the leading cause of unanticipated hospital admission after planned ambulatory surgery. 16,17
Even patients with normal arterial oxygen saturation may experience regions of inadequate tissue perfusion as result of extreme positioning, surgical retractors, and operative disruption of blood vessels. 18–20
High arterial oxygen partial pressures help limit hypoxia in these marginally perfused tissues. High inspired oxygen concentrations may similarly help oxygenate penumbra tissues surrounding the core of a stroke. 21,22
Inspired oxygen concentration is a major determinant of tissue oxygen tension, 23
which, in turn, is highly correlated with oxidative killing of bacteria by neutrophils over the range of observed values. 24
Oxidative killing is the major defense against surgical wound infection. 25
Therefore, it is not surprising that tissue oxygen tension is highly correlated with the risk of surgical wound infection. 26
Collagen deposition and scar formation are also directly dependent on tissue oxygen tension. 27–29
These data suggest that perioperative administration of high inspired oxygen concentrations may facilitate wound healing and improve resistance to surgical wound infections.
Available data thus indicate that high concentrations of inspired oxygen are associated with atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. Concern about atelectasis prompts many clinicians to forego the benefits of generous inspired oxygen concentrations. Accordingly, we tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% inspired oxygen during and for 2 h after colon resection.
The sample size for this study was based on atelectasis rates cited in previous studies. 1,11
These data suggested that a power of 95% for detecting a 50% difference in atelectasis at an α level of 0.05 would be obtained with 13 patients in each group. With approval of the ethics committee of the University of Vienna, we studied 30 patients aged 18–65 yr who were scheduled to undergo elective colon resection. These patients were among the 500 who participated in the multicenter Study of Oxygen and Surgical Wound Infection. The procedure was identical for all patients.

Spinal anaesthesia was chosen after an extensive discussion of the risks and benefits involved. On arrival in the operating room, non-invasive blood pressure was 130/85 mm Hg, heart rate 80 beats min-1, and oxygen saturation 98%. Following the rapid administration of 500 ml of Ringer's solution intravenously, spinal anaesthesia was performed at the L4-L5 interspace using a 25-G Quincke type needle. Bupivacaine hydrochloride (2 ml; Marcaine(R) 0.5% spinal, AstraZeneca) was administered. Surgery was started after achieving anaesthesia at the T10 dermatome. Postoperatively, his neurologic status remained normal with no worsening of his dysphagia or extremity weaknesses. He was discharged from hospital without any neurologic complaint on the sixth postoperative day. CONCLUSION: Kennedy's disease typically presents as muscular atrophy, weakness, and fasciculations predominantly of bulbar, facial, and proximal muscles of the extremities. When a patient with Kennedy's disease is scheduled to undergo a procedure requiring anaesthesia, anaesthesiologists should carefully assess patient preoperative status, respiratory function, and inquire about swallowing difficulties or a history of intolerance to any general or local anaesthetic agent. Considerations for general anaesthesia concern possible prolonged neuromuscular blockade and consequent postoperative muscle weakness and a compromised baseline pulmonary function.1 Many inhalation agents have been reported to be well tolerated by the patients with lower motor neuron disease.2 However, it is not clear whether neuromuscular blocking agents prolong neuromuscular blockage. Depolarizing muscle relaxants, such as, succinylcholine, are not recommended. Moreover the possibility of hyperkalemia and of resultant ventricular arrhythmia or fibrillation has been reported in patients with neuromuscular and lower motor neuron diseases by several investigators.3 If muscle relaxation is required, non-depolarizing neuromuscular blocking agents should be considered, and neuromuscular transmission should be monitored closely.
As Robbie2 indicates below, there is additional information on this subject at: KDA Surgery ConcernsThis message has been edited. Last edited by: Bruce,
Location: San Luis Obispo CA
Davey - My impression is that the Dentist has several options as to how they induce numbness.

at 1L/min it delivers 24% (20% is already in the air), at 2L per min it delivers 28%, 3L/min 32%…and so on so at 6L/min it delivers 44%
- A simple face mask should be used at a minimum of 6L/min (normal minute ventilation) to prevent the patient from breathing back their own CO2.
- Application of a self inflating Bag-Valve-Mask on a patient’s face without compressing the bag is called suffocation. Due to the valves system, oxygen is only delivered ON COMPRESSING THE BAG
- Pulse oximeters consist of two light-emitting diodes, one in the red range and one in the infrared range, and a detector. Oxygenated and deoxygenated haemoglobin absorb light at different wavelengths differently. Deoxygenated or ‘‘blue’’ blood absorbs light maximally in the red band, whereas Oxygenated or ‘‘red’’ blood absorbs light maximally in the infrared band. The ratio of absorption of the two wavelengths of light are then compared with an algorithm in the microprocessor generated by empirically measuring the absorption in healthy volunteers at varying degrees of directly measured arterial oxygen saturation. The displayed value is usually an average based on the previous 3 to 6 seconds of recording.
- Nonhypoxic heart attack victims treated with oxygen endure a 25 to 30% more heart damage than patients not given oxygen
- Oxygen supplementation to nonhypoxic patients with mild or moderate strokes may increase mortality.
- High-dose oxygen therapy to produce hyperoxaemia (above normal oxygen saturation) can cause absorption atelectasis
- Oxygen is liberally administered to many critically ill patients, thereby exposing them to supranormal arterial oxygen levels.
- Hyperoxia also results in the formation of reactive oxygen species, which adversely affect the pulmonary, vascular, cnetral nervous, and immune systems.
- Though the optimal PaO2 remains unknown, recent evidence indicates that hyperoxia is associated with increased mortality in post-cardiac arrest, CVA, acute coronary syndrome, and traumatic brain injury patients.
- Take Home Point: Carefully titrate oxygen to the lowest tolerable level to meet the patient’s needs.

Infected wounds had 1.2 ± 0.4 cm greater fat thickness than noninfected wounds.55 Another study of 608 patients having digestive tract surgery reported that, after multivariable analysis, obese patients (BMI >30 kg/m2) had an adjusted odds ratio for surgical site infection of 4.8 (95% CI, 2.95–7.81).56
Fleischmann et al.49 and Kabon et al.27 demonstrated that obese patients need a greater FIO2 to reach the same arterial oxygen partial pressure than nonobese patients. And finally, obese patients had lower tissue oxygen partial pressures in both the upper arm and near the incision, even when oxygen administration was adjusted to provide comparable arterial oxygen partial pressures. Nonetheless, supplemental postoperative oxygen did not reduce the risk of infection or a composite of major complications plausibly related to infection or wound healing. Supplemental postoperative oxygen thus seems unlikely to prove beneficial in nonobese subjects also, although the theory would be well worth testing in surgical populations at special risk of infection such as colorectal surgery.
We were unable to precisely control inspired oxygen concentration in patients assigned to supplemental oxygen. Patients randomized to supplemental postoperative oxygen thus received between 65% and 95% inspired oxygen, depending on their minute ventilation and ability to tolerate a sealed mask postoperatively. Nonetheless, in a previously published substudy, we showed that supplemental oxygen substantially increases subcutaneous oxygenation in the arm and adjacent to the surgical incision, suggesting that our administration methods were effective.49
In summary, the composite risk of wound infection and major complications related to infection or wound healing was similar in gastric bypass patients who were randomly assigned to approximately 30% or approximately 80% inspired oxygen administered from tracheal extubation through the first postoperative morning. Supplemental postoperative oxygen does not appear to be beneficial in this population.
APPENDIX. SUPPLEMENTAL POSTOPERATIVE OXYGEN TRIAL (SPOT) INVESTIGATORS
SPOT investigators from the University of Louisville included Anupama Wadhwa, MD, Mukadder Orhan Sungur, MD, Ryu Komatsu, MD, Ozan Akça, MD, Jorge Rodriguez, MD, and Raghavendra Govinda, MD.

Such patients should be evaluated with an arterial blood gas and a sleep study.
Classic symptoms of sleep disordered breathing include excessive daytime sleepiness, morning headache, and restless sleep, but insomnia may also be seen. In addition:
●Some patients with OSA may awaken with choking or shortness of breath
- Perrin C, Unterborn JN, Ambrosio CD, Hill NS. Pulmonary complications of chronic neuromuscular diseases and their management. Muscle Nerve 2004; 29:5.
- Shneerson JM. Respiration during sleep in neuromuscular and thoracic cage disorders. Monaldi Arch Chest Dis 2004; 61:44.
- Bourke SC, Gibson GJ. Sleep and breathing in neuromuscular disease. Eur Respir J 2002; 19:1194.
- Guilleminault C, Shergill RP. Sleep-disordered Breathing in Neuromuscular Disease. Curr Treat Options Neurol 2002; 4:107.
- Krachman SL, Criner GJ. Sleep and long-term ventilation. Respir Care Clin N Am 2002; 8:611.
- Cirignotta F, Mondini S, Zucconi M, et al. Sleep-related breathing impairment in myotonic dystrophy. J Neurol 1987; 235:80.
- Smith PE, Edwards RH, Calverley PM. Ventilation and breathing pattern during sleep in Duchenne muscular dystrophy. Chest 1989; 96:1346.
- Smith PE, Calverley PM, Edwards RH, et al. Practical problems in the respiratory care of patients with muscular dystrophy. N Engl J Med 1987; 316:1197.
- Dolmage TE, Avendano MA, Goldstein RS. Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis. Eur Respir J 1992; 5:864.
- Steljes DG, Kryger MH, Kirk BW, Millar TW. Sleep in postpolio syndrome. Chest 1990; 98:133.
- Ellis ER, Grunstein RR, Chan S, et al. Noninvasive ventilatory support during sleep improves respiratory failure in kyphoscoliosis.

is it always a good idea?British Journal of Anaesthesia
13Th International Conference on Electrical Bioimpedance and the 8Th Conference on Electrical Impedance Tomography 2007
Analysis of ventilatory conditions under different inspiratory oxygen concentrations and positive end-expiratory pressure levels by EIT
13Th International Conference on Electrical Bioimpedance and the 8Th Conference on Electrical Impedance Tomography 2007, 17():
New England Journal of Medicine
Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection
New England Journal of Medicine, 342(3):
Anesthesia and AnalgesiaThe effect of increased FIO2 before tracheal extubation on postoperative atelectasisAnesthesia and Analgesia
HerniaThe effect of supplemental 70% oxygen on postoperative nausea and vomiting in patients undergoing inguinal hernia surgeryHernia
AnaesthesistEmergency treatment of thoracic traumaAnaesthesist
Expert Review of Anti-Infective TherapyControversies in host defense against surgical site infectionExpert Review of Anti-Infective Therapy
Annales Francaises D Anesthesie Et De ReanimationPreoxygenation and upper airway patency controlAnnales Francaises D Anesthesie Et De Reanimation
Can anaesthetic management influence surgical-wound healing?
Clinical Infectious Diseases
Nonpharmacological prevention of surgical wound infections
Clinical Infectious Diseases, 35():
Anesthesia and AnalgesiaThe influence of protocol pain and risk on patients' willingness to consent for clinical studies: A randomized trialAnesthesia and Analgesia
Perioperative management and monitoring in anaesthesia
Anz Journal of SurgeryPerioperative high-dose oxygen therapy in vascular surgeryAnz Journal of Surgery
Archives of Surgery
Perioperative Supplemental Oxygen Therapy and Surgical Site Infection A Meta-analysis of Randomized Controlled Trials
Archives of Surgery, 144(4):
Wound Repair and Regeneration
Supplemental perioperative oxygen and fluids to improve surgical wound outcomes: Translating evidence into practice
Wound Repair and Regeneration,

Acta Anaesthesiologica ScandinavicaSupplemental 80% oxygen does not attenuate postoperative nausea and vomiting after breast surgeryActa Anaesthesiologica Scandinavica
Anasthesiologie Intensivmedizin Notfallmedizin SchmerztherapiePulmonary gas exchange: Classical and modern findingsAnasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
AnaesthesistOxygen - An effective supplement of perioperative antibiotic treatment?Anaesthesist
Critical Care ClinicsPerioperative anesthesia issues in the elderlyCritical Care Clinics
Anasthesiologie & Intensivmedizin
Oxygen as carrier gas in general anoesthesic
Anasthesiologie & Intensivmedizin, 45(3):
Anesthesia and AnalgesiaThe influence of allogeneic red blood cell transfusion compared with 100% oxygen ventilation on systemic oxygen transport and skeletal muscle oxygen tension after cardiac surgeryAnesthesia and Analgesia
Archives of Surgery
Perioperative Supplemental Oxygen Therapy and Surgical Site Infection A Meta-analysis of Randomized Controlled Trials INVITED CRITIQUE
Archives of Surgery, 144(4):
The effect of auricular acupuncture on anaesthesia with desflurane
Anesthesia and AnalgesiaDosing oxygen: A tricky matter or a piece of cake?Anesthesia and Analgesia
European Journal of Cancer Care
Nausea and vomiting after surgery for colorectal cancer
European Journal of Cancer Care, 9(3):
Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie
Best evidence in anesthetic practice - Prevention: supplemental oxygen reduces the incidence of surgical-wound infection - Commentary
Canadian Journal of Anaesthesia-Journal Canadien D Anesthesie, 48(9):
British Journal of AnaesthesiaNew concepts of atelectasis during general anaesthesiaBritish Journal of Anaesthesia
The management of malignant large bowel obstruction: ACPGBI position statement
Colorectal Disease, 9():
Journal of Applied PhysiologyHypoxic pulmonary vasoconstriction does not contribute to pulmonary blood flow heterogeneity in normoxia in normal supine humansJournal of Applied Physiology
Jama-Journal of the American Medical Association
Supplemental oxygen and risk of surgical wound infection - Reply
Jama-Journal of the American Medical Association, 295():
British Journal of AnaesthesiaJust a little oxygen to breathe as you go off to sleep.

Creatinine kinase levels rise to 20,000 or more within 12 to 24 hours, putting the patient at risk for myoglobinuric renal failure. Isolated myoglobinuria in the early postoperative period should make the anesthesiologist and surgical team suspicious for Malignant hyperthermia. Masseter muscle rigidity shortly after the administration of succinylcholine has also been associated with MH as well.
Malignant hyperthermia treatment is simple. With early diagnosis and appropriate treatment, the mortality rate approaches zero. If Malignant hyperthermia is suspected, all triggering agents should be discontinued immediately. In the operating room, the patient should be ventilated with 100% oxygen at a flow of 10 L/minute. If a general anesthetic must be continued, it is safe to administer barbiturates, benzodiazepines, opioids, and propofol.
The patient should be intubated as soon as possible. Cardiac dysrhythmias, hyperkalemia, acidosis, and other medical problems should be managed appropriately. The patient should be given dantrolene as soon as possible. Dantrolene acts by inhibiting the release of calcium from the sarcoplasmic reticulum. The initial dose is a 2.5mg/kg intravenous (IV) bolus followed by 1 mg/kg IV every 6 hours for at least 24 hours.
Dantrolene’s side effects include nausea, phlebitis, and weakness for approximately 24 hours after the drug is discontinued. Each vial of dantrolene contains 20 mg of dantrolene and 3 mg of mannitol and must be mixed with 60 mL of sterile water. The initial dose for a 70-kg adult is 175 mg or 9 vials. Assistance should be sought in mixing the dantrolene as it is poorly soluble.
Dantrolene 2.5 mg/kg should be given every 5 to 10 minutes until there is a fall in heart rate, normal cardiac rhythm, a reduction in muscle tone, and a decline in body temperature. Maintenance of normal volume status is essential in the setting of rhabdomyolysis. Hyperkalemia may require treatment with insulin and glucose. Caution should be excercised with potassium-losing diuretics as hypovolemia should be avoided.

If the cardiac output is doubled in this situation, the oxygen delivery to tissues can be increased by well over 60% without any change in SpO2. Nevertheless, hypoxemia (low PaO2) is the most common cause of tissue hypoxia , hence the need to support acute reductions in SpO2 with oxygen therapy until the cause in resolved.
Despite the poor association between tissue hypoxia and SpO2, patients with chronic lung disease are strongly advised to use oxygen if their SpO2 drops below 88% during exercise. Yet athletes are subjected to high intensity and high volume training to promote enhanced performance without additional oxygen . In this context, prompting patients with chronic lung disease to use oxygen if their SpO2 fall below 88% during exercise is unfair, especially in the absence of credible evidence to claim that SpO2 less than 88% during exercise is damaging. Although submaximal oxygen saturation during exercise has not led to any untoward cardiac events in lung disease , empirical use of oxygen may prevent the triggering of natural mechanisms for tolerance or recovery. This kind of patient advice based on ‘logical’ thinking in the absence of sufficient evidence could therefore bring needless harm whilst adding unnecessary expense to health care services.
Indeed the evidence for the harmful effects of oxygen is becoming more widely recognised. One example is the withdrawal of oxygen use for neonatal resuscitation, where decades ago, use of oxygen was the norm . This practice is now considered harmful [13,14]. Similarly, evidence against the use of oxygen in adult CPR is emerging . On the contrary, it should be noted that long term use of oxygen for symptomatic relief has benefited selected patients with hepatopulmonary syndrome, a situation of hypoxemia in chronic liver disease resulting from pulmonary vascular dilation characterised by anatomical shunting .
There are a number of changes in the heart and pulmonary circulation occurring in humans living permanently at high altitudes i.e., in low oxygen tension environments. These adaptations are not quite comparable to that of temporary residents at high altitudes, nor those experimentally exposed to acute hypoxia [17-20]. Thus, the natural adaptation to one’s surrounding should be another caveat in the decision-making process behind providing oxygen therapy [21,22].
During exercise, high cardiac output may compensate and deliver adequate oxygen to tissues despite lower recordings of SpO2. Hypoxia ensues when aerobic metabolism in tissues turn to anaerobic for energy production.

Laboratory results were part of routine perioperative blood sampling. Induction of general anesthesia was performed intravenously with fentanyl and etomidate, and a muscle relaxant (pancuronium) to allow tracheal intubation. Maintenance of general anesthesia was inhalational, using sevoflurane with additional doses of fentanyl and a muscle relaxant. After the surgery patients were transferred to a postoperative cardiac ICU, still intubated and mechanically ventilated, sedated to achieve adequate sedation depth (Richmond Agitation Sedation Scale [RASS] between −1 and +1) with adequate pain control, using intravenous morphine infusion and a non-opioid analgesic. The initial mode for mechanical ventilation was synchronized intermittent mechanical ventilation with continuous positive airway pressure when the patient regained their respiratory drive and the weaning process was initiated. Patients were extubated when they met pre-defined criteria: normal body temperature, Glasgow Coma Scale 14–15 points, no focal neurological deficit, pain under control, drainage <100 mL/h, hemodynamic stability (noradrenaline or adrenaline <0.05 μg/kg/min), absence of significant arrhythmias, PaO2 >60 mmHg, PaCO2 <45 mmHg, SpO2 >95% with FiO2 <0.45, no respiratory distress and normal respiratory rate. Patients were extubated to passive oxygen therapy (facial mask with O2 at 5–7 L/min). An arterial blood gas was obtained 30 minutes after extubation to ensure patient safety.
The study was performed in accordance with the Declaration of Helsinki due to its retrospective character a waiver was granted from the Bioethical Committee of the Pomeranian Medical University in Szczecin, Poland, decision no KB-0012/254/06/18. The data entered into the prospectively collected database required written informed consent for surgery, anesthesia and data collection at the time of hospital admission from each patient, as part of routine preoperative assessment, therefore patient consent to review their medical documentation was waived by the Bioethical Committee. To ensure patient data safety only de-identified data was used for analysis.

When these fail to bring up the oxygen saturation, we proceed to mechanical ventilatory support which could be Non invasive or Invasive. If ventilatory support also fails, Extracorporeal Membrane Oxygenation (ECMO) can be considered.
When and how should oxygen be given?
Oxygen is a drug with specific indications, methods of delivery and targets. A prescription for oxygen should reflect all these features. For instance, an adequate prescription for a COVID pneumonia patient with mild hypoxemia in the ward would be “Oxygen at 6 litres per minute to be given by nasal cannula and titrated to an oxygen saturation of 92-94%. Remove when the patient is maintaining a saturation of greater than 90 % on room air.”
Let us consider the indications, the methods of delivery and the targets in sequence.
Indications for oxygen delivery
Oxygen supplementation is indicated in COVID patients with hypoxemia; there is no benefit of giving oxygen prophylactically. Hypoxemia is a low arterial oxygen tension below the normal expected value of (85-100 mmHg). The British Thoracic Society (BTS) guideline defines hypoxemia as PaO2 < 60 mmHg or SaO2 < 90%. Hypoxia on the other hand, refers to oxygen lack at a tissue level, and is generally inferred from evidence of tissue hypoperfusion (increasing serum lactate).
Sources of Oxygen Supply
Oxygen is available in three forms; in a cylinder, which is what one sees in smaller hospitals; from a liquid oxygen plant, generally present in larger hospitals and from oxygen concentrators/ Oxygen generators. Oxygen cylinders are generally available in two size- a size ‘E’ cylinder, which when full contains 680 litres of oxygen, and a type ‘F’ cylinder which contains between 1200 and 1300 litres of oxygen. It is important to know this, because when one is transporting a patient, dividing the capacity of the cylinder by the oxygen required in litres per minute will let one know how long the supply will last. The oxygen cylinder manifold supply has a main bank and a reserve bank of cylinders, with a selector switch, which the technician uses to switch from one bank to the other when the pressure drops below a critical limit. This gives the technician time to attach filled cylinders after removing the empty ones.
Liquid oxygen is nearly always supplied from a central location through a system of pipeline to patient outlets.

Simonds AK, Ward S, Heather S, Bush A, Muntoni F. Outcome of pediatric domiciliary mask ventilation in neuromuscular and skeletal disease. Eur Respir J. 2000;16:476-81. [ Links ]
17. Make BJ, Hill NS, Goldbery AI, Bach JR, Dunne PE, Heffner JE, et al. Mechanical ventilation beyond the intensive care unit. Report of a consensus conference of the American College of Chest Physicians. Chest. 1998;113(5 Suppl):289S-344. [ Links ]
18. Katz S, Selvadurai H, Keilty K, Mitchell M, MacLusky I. Outcome of non-invasive positive pressure ventilation in pediatric neuromuscular disease. Arch Dis Child. 2004;89:121-4. [ Links ]
19. Khan Y, Heckmatt JZ, Dubowitz V. Sleep studies and supportive ventilatory treatment in patients with congenital muscular disorders. Arch Dis Child. 1996;74:195-200. [ Links ]
20. Suresh S, Wales P, Dakin C, Harris MA, Cooper DG. Sleep-related breathing disorder in Duchenne muscular dystrophy: disease spectrum in the pediatric population. J Paediatr Child Health. 2005;41:500-3. [ Links ]
21. Mellies U, Dohna-Schwake C, Stehling F, Voit T. Sleep disordered breathing in spinal muscular atrophy. Neuromuscul Disord. 2004;14:797-803. [ Links ]
22. Hill N. Noninvasive ventilation: does it work, for whom, and how? Am Rev Respir Dis. 1993;147:1050-5. [ Links ]
23. Kramer N, Hill N, Millman R. Assessment and treatment of sleep-disordered breathing in neuromuscular disease and chest wall diseases. Top Pulm Med. 1996;3:336-42. [ Links ]
24. Annane D, Quera-Salva MA, Lofaso F, Vercken JB, Lesieur O, Fromageot C, et al.

—To assess the effect of deliberate perioperative increase in oxygen delivery on mortality and morbidity in patients who are at high risk of both following surgery.
—Prospective, randomized clinical trial.
—A teaching hospital general intensive care unit, London, England.
—A total of 107 surgical patients, who were assessed as high risk from previously identified criteria, were studied during an 18-month period.
—Patients were randomly assigned to a control group (n=54) that received best standard perioperative care, or to a protocol group (n=53) that, in addition, had deliberate increase of oxygen delivery index to greater than 600 mL/min per square meter by use of dopexamine hydrochloride infusion.
—Mortality and complications were assessed to 28 days postoperatively.
—Groups were similar with respect to demographics, admission criteria, operation type, and admission hemodynamic variables. Groups were treated similarly to maintain blood pressure, arterial saturation, hemoglobin concentration, and pulmonary artery occlusion pressure; however, once additional treatment with dopexamine hydrochloride had been given, the protocol group had significantly higher oxygen delivery preoperatively (median, 597 vs 399 mL/min per square meter; P<.001) and postoperatively (P<.001). Results indicate a 75% reduction in mortality (5.7% vs 22.2%; P=.015) and a halving of the mean (±SEM) number of complications per patient (0.68 [±0.16] vs 1.35 [±0.20]; P=.008) in patients randomized to the protocol group.
—Perioperative increase of oxygen delivery with dopexamine hydrochloride significantly reduces mortality and morbidity in high-risk surgical patients.(JAMA. 1993;270:2699-2707)

11(6):
Anasthesiologie Intensivmedizin Notfallmedizin SchmerztherapieRoutine use of high inspired oxygen concentration - ProAnasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
Anaesthesia and Intensive Care
A review of the risks and benefits of nitrous oxide in current anaesthetic practice
Anaesthesia and Intensive Care, 32(2):
Journal of Clinical Monitoring and Computing
Atelectasis formation during anesthesia: Causes and measures to prevent it
Journal of Clinical Monitoring and Computing, 16():
Anesthesia and AnalgesiaSupplemental oxygen does not reduce the incidence of postoperative nausea and vomiting after ambulatory gynecologic laparoscopyAnesthesia and Analgesia
Hemodyinamic effects of several inspired oxygen fractions in spontaneously breathing dogs submitted to continuous infusion of propofol
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Obesity SurgerySupplemental Postoperative Oxygen and Tissue Oxygen Tension in Morbidly Obese PatientsObesity Surgery
Anesthesia and AnalgesiaSupplemental oxygen, but not supplemental crystalloid fluid, increases tissue oxygen tension in healthy and anastomotic colon in pigsAnesthesia and Analgesia
Jama-Journal of the American Medical Association
Effect of High Perioperative Oxygen Fraction on Surgical Site Infection and Pulmonary Complications After Abdominal Surgery The PROXI Randomized Clinical Trial
Jama-Journal of the American Medical Association, 302():
Pulmonary atelectasis in dogs during general anesthesia
Ciencia Rural, 40(1):
Archivos De BronconeumologiaPen-Operative Atelectasis and Alveolar Recruitment ManoeuvresArchivos De Bronconeumologia
Anesthesia and Analgesia
Ondansetron is no more effective than supplemental intraoperative oxygen for prevention of postoperative nausea and vomiting
Anesthesia and Analgesia, 92(1):
Mayo Clinic Proceedings
A randomized controlled trial of oxygen for reducing nausea and vomiting during emergency transport of patients older than 60 years with minor trauma
Mayo Clinic Proceedings, 77(1):
TrialsPerioperative oxygen fraction - effect on surgical site infection and pulmonary complications after abdominal surgery: a randomized clinical trial.

To help prevent potential complications from oxygen administration, reach for the nasal cannula before the non-rebreather mask, and apply just enough oxygen to maintain normal saturations.
1. Morton PG, et al, eds., Critical Care Nursing, a Holistic Approach, 8th edition. Philadelphia, PA: Lippincott, Williams & Wilkins, 2005.
2. Des Jardins T, Burton GG. Clinical Manifestations and Assessment of Respiratory Disease, 5th edition. St. Louis, MO: Elsevier, 2006.
3. O’Connor RE, et al. Acute Coronary Syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 122: S787–817, 2010.
4. Shapiro BA, et al. Clinical Application of Blood Gases, 5th Edition. St. Louis, MO: Elsevier, 1994.
5. Kattwinkel J, et al, Neonatal Resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 122: S909–S919, 2010.
6. Ntoumenopolus G. Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease (COPD) saves lives. J Physiother 57(1):55, 2011.
7. Austin MA, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomized controlled trial. BMJ 341: c5462, 2010.
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also the performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at firstname.lastname@example.org.
Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California San Francisco and a former New York City paramedic for 10 years. Contact him at email@example.com.

A recent Cochrane review combined this trial with a smaller similar one, which generated a composite RR of mortality of 3.03 (95% CI, 0.93-9.83).1 In acute decompensated heart failure, no clinical studies are available, despite the rather abundant evidence from preclinical studies, suggesting that such patients may experience the adverse effects caused by coronary and systemic vasoconstriction (Table).
In accordance with existing guidelines, supplemental oxygen is often administered during CPR. In the postresuscitation phase, evidence exists that 30% oxygen is more brain protective than pure oxygen.2 Recently, an observational study in 6326 patients showed that supplemental oxygen induced postresuscitation hyperoxia was independently associated with increased mortality (odds ratio [OR], 1.8; 95% CI, 1.5-2.2). A subsequent analysis of the same cohort indicated that each 25–mm Hg increase in PaO2 was associated with a statistically significant 6% increase in the relative risk of death.3 Finally, a comparable cohort of 12 108 patients was analyzed in New Zealand and Australia. Again, the hyperoxia group showed an increased risk of mortality compared with the normoxia group (OR, 1.2; 95% CI, 1.1-1.6). Although the statistical significance of this finding was not maintained after multivariable adjustment, certainly no beneficial effects of hyperoxia were found.4
In the management of ischemic stroke, a randomized trial suggested that hyperbaric oxygen may adversely affect stroke severity.5 With regard to normobaric oxygen, 3 randomized trials were performed. One showed no benefit on clinical outcome.6 Another trial in nonhypoxic patients found lower survival at 1 year (OR, 0.45; 95% CI, 0.23-0.90) in those who received supplemental oxygen during initial treatment.7 The third randomized trial was terminated in 2009 after enrolling 85 patients because of excess mortality in the hyperoxia group (40% vs 17% [P = .01 by our own calculation]) (Clinical Trial of Normobaric Oxygen Therapy in Acute Ischemic Stroke [not published]; clinicaltrials.gov Identifier: NCT00414726).

Preoperative investigations were within normal limits.
The patient was premedicated with Inj. Glycopyrolate 0.2mg, Inj. Pentazocine 0.5
mg/kg, Inj.Midazolam 1mg and Inj.Diclofenac 75mg i.m. The patient was preoxygenated and
anesthesia was induced with Inj.Propofol 2mg/kg and Inj.Vecuronium 0.1mg/kg till the
loss of eyelash reflex.. The patient was ventilated with oxygen, nitrous oxide and sevoflurane
1% for five minutes and intubated orally with 7.0mm flexometallic cuffed endotracheal
tube. Anesthesia was maintained with sevoflurane at an inspired concentration of
approximately 1% with mixture of N2O/O2 50:50 (3 liters/min). The intraoperative
monitoring included NIBP, ECG, SPO2 and EtCO2. Ventilation was adjusted to maintain
normocarbia. The surgery lasted for three hours. All the vitals parameters were normal
throughout the surgery. Arterial oxygen saturation determined using pulse oximetry
remained greater than 98% during the intraoperative course. No episodes of hypoxemia
Sevoflurane and nitrous oxide was discontinued upon completion of the procedure and neuromuscular blockade was reversed. Suddenly the patient started having focal seizures involving the left upper extremity and left side face lasting 30- 40seconds. Inj.Propofol 20mg IV was administered with immediate cessation of seizure activity. Patient blood pressure dropped to 80/40 mmHg. 6mg of inj. Ephedrine was given with restoration of blood pressure. The patient was shifted to intensive care unit (ICU). During transportation she had another episode of similar seizure lasting around 30seconds. The patient was awake, confused and slow in responding to oral commands in between the convulsive episodes. On arrival in the ICU she had another episode of similar seizures with hypotension. A bolus dose of midazolam 2mg i.v was given to suppress the seizures. Inj. Noradenaline was started to correct the hypotension.

There were 2 withdrawals before surgery; no further data were collected in these 2 patients, and thus 400 patients were included in the final analysis; 198 were assigned to nasal cannula oxygen and 202 to supplemental oxygen (Fig. 1).
Many patients had laparoscopic Roux-en-Y gastric bypass (91%); the remainder had open Roux-en-Y gastric bypass (9%). The type of surgery and approach varied among the sites. Twenty-three percent of patients in the supplemental oxygen group received antibiotics more than 1 hour before the start of incision; 72% received antibiotics within 1 hour before incision, while 5% received antibiotics after incision; 8% of patients who received antibiotics in the 30% group were given antibiotics >1 hour before the start of surgery, 78% received antibiotics within 1 hour before incision, and 14% received antibiotics after incision; 31% in the supplemental and 34% in the 30% group were given cephalosporin; 7% in the supplemental group and 6% in the 30% group were given vancomycin; and 1 patient in the supplemental group received ciprofloxacin.
The 2 groups had similar baseline and demographic variables (standardized difference <0.30, Table 2). Preoperative and intraoperative glucose concentrations were comparable in the 2 groups (Tables 2 and 3). Both groups were given similar amounts of intraoperative crystalloids and opioids. The median duration of surgery was 2.7 hours in the 80% oxygen group and 2.6 hours in the 30% oxygen group (Table 3). Nasal cannula oxygen was well tolerated. Among the patients randomized to supplemental oxygen (n = 202), only 32 patients (16%) did not tolerate the tightly fitting Hi-Ox mask and were instead given supplemental oxygen with an open humidified mask at a flow rate of 15 L/min.
Among the observed complications, surgical wound infection was the most common, occurring in 8.5% of patients. The incidence of surgical wound infection was similar in patients randomized to either supplemental oxygen (8%, 16 of 202) or 30% oxygen (9%, 18 of 198). The observed median ASEPSIS score was 1 (interquartile range: 0–4) within each group.

Author Affiliations: Departments of Internal Medicine (Drs Cornet, Kooter, Peters, and Smulders) and Intensive Care Medicine (Dr Cornet), VU University Medical Center, and Institute for Cardiovascular Research ICaR-VU (Drs Cornet, Kooter, Peters, and Smulders), Amsterdam, the Netherlands.
In medical emergencies, such as acute coronary syndrome, cardiopulmonary resuscitation (CPR), stroke, and exacerbations of chronic obstructive pulmonary disease (COPD), supplemental oxygen is often routinely administered. Most physicians believe this intervention is potentially lifesaving, and many guidelines support the routine use of high-dose supplemental oxygen.
Over the decades, however, potential detrimental effects of supplemental oxygen appear to have been ignored. Many clinicians are unaware of the variety of preclinical studies that have been executed, showing that hyperoxia causes both coronary and systemic vasoconstriction, resulting in deterioration of several important (hemodynamic) parameters (Table). The prime candidate mechanism for these unintended effects is believed to be the formation of reactive oxygen species. In this Research Letter, we draw attention to the collective clinical evidence, which argues against the routine use of high-dose oxygen. Awaiting more thorough studies, we strongly recommend a policy of careful, titrated oxygen supplementation.
We conducted a search of the literature in MEDLINE and EMBASE to identify articles addressing the effect of oxygen therapy in acute coronary syndrome, cardiopulmonary resuscitation, stroke, and exacerbations of chronic obstructive pulmonary disease.
Large (randomized) clinical studies addressing oxygen supplementation are scarce. In 1976, a double-blind randomized trial was performed in 200 patients with suspected acute myocardial infarction. In the supplemental oxygen group, 9 of 80 patients (11%) died, as opposed to 3 of 77 (3.9%) in patients breathing compressed air (relative risk [RR] of mortality, 2.9; 95% CI, 0.8-10.3).

The BTS has appointed 'Oxygen Champions' in most acute UK hospitals to help introduce the guidelines to improve oxygen use, enhance patient safety and audit usage.
National documents are available providing advice on the safe use of oxygen; these are:
British Thoracic Society (October 2008): Guidelines for emergency oxygen use in adult patients
These comprehensive clinical guidelines cover all aspects of the emergency use of oxygen in pre-hospital care and hospital settings. Note that they do not cover children under 16 years or critical care (ITU and HDU facilities). The key recommendations are: o Oxygen therapy will be adjusted to achieve target saturations rather than giving a fixed dose to all patients with the same disease. o Nurses will make these adjustments without requiring a change to the prescription on each occasion. o Most oxygen therapy will be from nasal cannulae rather than masks. o Oxygen will not be given to patients who are not hypoxaemic (except during critical illness). o Pulse oximetry must be available at all locations where emergency oxygen therapy is used. o Oxygen will be prescribed in all situations except for the immediate management of critical illness.
In Appendix 2 of the report, a number of resources and good practice examples relating to the key risks and actions recommended are stated including:
Action 6: Pulse oximetry is available in all locations where oxygen is used.
It is recommended in the BTS guidelines that:
- Pulse oximetry must be available in all locations where emergency oxygen is used;
- Oxygen saturation, ''the fifth vital sign'', should be checked by pulse oximetry in all breathless and acutely ill patients (supplemented by blood gases when necessary) and the inspired oxygen concentration should be recorded on the observation chart with the oximetry result (the other vital signs are pulse, blood pressure, temperature and respiratory rate);
- All patients should have their oxygen saturation observed for at least five minutes after starting oxygen therapy.

In practice, only a limited set of neuromuscular conditions is accompanied by respiratory failure with appreciable frequency (table). Patients who could potentially develop respiratory muscle weakness should have their vital capacity and mouth pressures measured at least once. Whether to repeat the testing will depend on the diagnosis and the rate of progression of muscle weakness. A serial fall in the vital capacity (particularly a fall below 1.2–1.5 l or <40–50% of predicted), or a fall in MIP to <60% of predicted, are indications for further respiratory assessment. Onset of daytime hypercapnia (PaCO2 >45 mmHg or 6 kPa) indicate that the patient needs urgent assessment and may imminently require non-invasive ventilation.
Motor neuron disease
All neurologists are familiar with the clinical features of this disorder. Presentation with respiratory muscle weakness or with hypercapnic respiratory failure is rare but well-recognised. Whatever the mode of onset of their disease, most patients eventually develop respiratory muscle weakness, and this can be anticipated by serial measurement of the VC and MIP. Symptoms include exertional dyspnoea, orthopnoea, fatigue, non-refreshing sleep and morning headache. There is good evidence that non-invasive ventilation can improve these symptoms and quality of life. It also significantly improves survival (to a much greater extent than does riluzole) in those patients with only mild or moderately impaired bulbar function.5 Where resources are available, a respiratory physician with an interest in non-invasive ventilation should be part of the management team in motor neuron disease (see below).
Spinal muscular atrophy
Types 1, 2 and 3 are recognised, depending on age of onset. All forms have the same genetic basis—homozygous deletion of the telomeric survival motor neuron gene. Respiratory muscle involvment in spinal muscular atrophy type 1 (Werdnig-Hoffman disease) is universal. It occurs to a variable extent in Type 2, and is uncommon in Type 3.
In the congenital myopathies, onset of hypotonia and weakness occur in early life. Unlike congenital muscular dystrophy, distinct structural alterations (for example, rod bodies in nemaline myopathy) are apparent within the muscle fibres at biopsy. If the child survives infancy, there is usually minimal or no progression of weakness in later life.

- Should I remove the nasal cannula (NC) prior to intubating once the patient is paralyzed?
- “Apneic oxygenation” allows for continuos oxygenation through a passive process driven by oxygen gradients in the alveoli that are still performing their function of gas exchange.
- Can I can rely on a finger pulse oximetry probe for current oxygenation information?
- Pulse ox results can lag anywhere from 30 seconds to 3 minutes depending on cardiac status of patient. Ear probes can provide more current information due to their lack of vasoconstriction and central blood supply.

During implant of the medullary cemented prosthesis, patient presented with temporary oxygen desaturation to 80% and bronchospasm which was reverted by adjusting parameters to IPAP 17 cmH2O and EPAP 8 cmH2O associated with administration of inhalatory β-agonist and ipatropium. He was then referred to intensive care unit (ICU) hemodynamically stable, with a 94% saturation on BIPAP, lucid, oriented and painless.
Postoperative progressed with hemodynamic stability; good control of pain using dipyrone associated to tramadol and continued use of NIMV/BIPAP during the first 24 hours following procedure. Thereafter, the patient resumed use of nasal oxygen and intermittent NIMV. Post-procedure arterial gasometry showed: pH - 7.38, pCO2 - 54 mmHg, pO2 -63 mmHg, HCO3 - 31.2 mmol/L, base excess: 4.8, sO2: 92%. Patient was transferred to the semi-intensive care unit 10 days after procedure.
Prevalence of COPD is estimated at 6% and became the main cause of mortality among respiratory diseases.1,4 Adequate pre and intraoperative assessments estimates of surgery cost-benefit, type of anesthesia, ventilation assistance and hemodynamic support increase survival of these patients at postoperative.
The patient presented a pulmonary condition with severe restrictions; however acute disease worsened the condition requiring a planning of intraoperative ventilation support appropriate for the situation.
While, among the general population the rate of postoperative pulmonary complications ranges from 5% to 12%5-6, in patients with COPD, the number and type of complications increase substantially (37% of cases)3 for this reason in the decade of 1970, some authors recommended that only life-saving surgeries should be carried out in patients with a FEV1 < 0.5L. The option of not operating this patient was considered, because of the severity of the condition, however this would mean an increase of morbidity, mortality (60 to 70%)7 and would increase the patient's physical impairment.
A recent study3 stated that, in patients with COPD, the most common postoperative complications are an increase in ICU length of stay and bronchospasm.

Although an external monitor judged the excess mortality as “unrelated to oxygen treatment,” these results are important because this was the largest randomized trial investigating oxygen treatment for ischemic stroke, and it is remarkable that these results have not (yet) been published.
In the management of COPD, the risks of oxygen supplementation are widely acknowledged. Administration of oxygen in patients with COPD may cause hypercapnia due to ventilation-perfusion mismatching, the Haldane effect, inhibition of hypoxic drive, and atelectasis. Guidelines recommend a maximum FIO2 of 0.28. However, patients with COPD often receive higher doses, especially during ambulance transportation, causing hypercapnia and increased mortality. Recently, a randomized trial compared high concentration oxygen with titrated oxygen in prehospital patients with exacerbation of COPD. Mortality was lower in patients receiving titrated oxygen (RR, 0.42; 95% CI, 0.20-0.89). In those with later-confirmed COPD, mortality reduction was even stronger (RR, 0.22; 95% CI, 0.05-0.91).8
In conclusion, there appear to be potential dangers of routine administration of supplemental oxygen during a variety of medical emergencies. Hyperoxia is associated with hemodynamic alterations that may increase myocardial ischemia and impair cardiac performance, and the results from relatively unknown preclinical studies appear to be supported by the available clinical evidence. Moreover, hyperoxia also seems to be associated with adverse outcomes in different noncardiac emergencies. Finally, in our extensive literature review, we did not find a single study contradicting the reported hazards of hyperoxia or, in fact, suggesting benefits.
We acknowledge that additional clinical research is warranted to determine whether routine high-dose supplemental oxygen in medical emergencies indeed causes more harm than benefit. Until that time, however, we call for appropriate caution in applying supplemental oxygen. Hypoxemia should be treated carefully with stepwise increases in inhaled oxygen concentration in an attempt to avoid arterial hyperoxia.
Correspondence: Dr Cornet, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, the Netherlands (email@example.com).
Published Online: January 9, 2012. doi:10.1001/archinternmed.2011.624
Author Contributions:Study concept and design: Cornet, Kooter, Peters, and Smulders.

In a previous publication we reported that, although intercurrent chest colds can necessitate intensive care and intubation, tracheotomy can be avoided for many SMA children by using a protocol in which, in addition to conventional medical, respiratory therapy, and nutritional support, mechanical insufflation-exsufflation (MI-E) (In-exsufflator™, J. H. Emerson Company, Cambridge, MA) is used via the translaryngeal tube and it along with high span nasal PIP+PEEP are used post-extubation.3 Care providers are trained and equipped with oximetry as feedback to use high span PIP+PEEP, MI-E, and manually assisted coughing to reverse decreases in SaO2 below 95%. The purpose of this work is to report the long-term outcomes of tracheostomy, and extubation protocol/noninvasive approaches. There have been no previous long term studies of SMA1 patients and only one report of a SMA1 patient who survived to 3.7 years of age with a tracheostomy.4
The status of all 65 SMA1 patients who visited one Jerry Lewis Muscular Dystrophy Association Clinic from June 1996 until October 2001 was reviewed. This included contact by telephone in October 2001. SMA1 was diagnosed on the basis of DNA evidence of chromosome 5 exon 7 and 8 deletion in 56 of 65 children, affected siblings in 4 patients, and characteristic laboratory, muscle biopsy, and electromyography results in 5 children. Inclusion criteria included inability to roll or sit unsupported at any time. In addition, all patients had to develop respiratory failure and the respiratory failure had to occur before 2 years of age. All patients attaining 2 years of age had to have lost the ability to receive nutrition by mouth. By 18 months of age all of the patients had little more than residual finger, toe, and facial movements. Sixty-three of the 65 children had paradoxical chest wall movement, whereas for 2 children, the chest walls neither expanded nor retracted upon inspiration. One of these two, a 12 month old, has not been prescribed PIP+PEEP and has not been hospitalized for respiratory failure.

As comorbidities he has hypothyroidism and diabetes mellitus type II with regular use of prednisone, bamifylline, inhalatory β-agonist and ipatropium, acetylsalicylic acid and pantoprazole.
At pre-operative evaluation he was bedridden, with pain in the lower right limb, tachypnea, hemodynamically stable and with 88% oxygen saturation. Patient alternated use of NIMV/ /Bi-level Positive Airway Pressure (BIPAP) with nasal 3L/min oxygen O2. Complementary exams showed hematocrit 36%; normal leukogram and coagulogram; echocardiogram with mild ventricular dysfunction; chest X-ray (Figure 2). arterial pre-operative gasometry under O2 at 4 L/min showed pH - 7.38, pCO2 - 54 mmHg, pO2 -93 mmHg, HCO3 - 31.2 mmol/L, base excess: 4.9, SpO2: 96%.
After monitoring by cardioscope, noninvasive pressure and pulse oximetry, a peripheral venous access was punctured and cefazolin 2 g and hydrocortisone 200 mg were administered. NIMV with BIPAP under full face mask (Figure 3) was administered with the parameters expiratory positive airway pressure (EPAP) of 7cmH2O, inspiratory positive airway pressure (IPAP) 15 cmH2O and O a flow of 3 L/min.
Diazepam 1 mg and cefotamine 5 mg both intravenous, for positioning on left lateral decubitus were administered. Simple isobaric spinal anesthesia was given in the subdural space in the L3-L4, spaces, needle 25G. First trial, liquor was clear and injection of isobaric bupivacaine 16mg with final sensory level at T10. Continuous infusion of dexmedetomidine 0. 2 µg/kg/min was begun for sedation. The surgical procedure was comprised of partial bipolar arthroplasty of the hip with the contemporary technique of femoral stem cementing, on the left lateral decubitus for some 75 minutes.

The proposed pharmacodynamic model of respiratory depression integrates respiratory physiology principles and allows the clinician to estimate the level of CO2 as a function of propofol and remifentanil in patients sedated although breathing spontaneously. Such a model opens many possibilities to study in deeper detail respiratory response to anesthetic drugs or to be used as a learning tool to train anesthesiologist to perform safer sedation or to be used as an alert system while performing sedation-analgesia in real patients.
The prevalence of OSA in surgical patients may be as high as 70%. These patients pose a significant clinical challenge to health-care professionals, and the lack of evidence behind the current guidelines recommendations and significant costs of guideline implementation have created a dilemma between potentially improved postoperative adverse events and increased health-care resource utilizations. This review examines the evidence regarding the use of CPAP in the perioperative period.
For surgical patients with OSA it is clear that those who are treated and adherent to CPAP should continue their CPAP in the postoperative period. Those patients with diagnosed OSA who are not adherent to therapy or undiagnosed OSA pose a more significant clinical challenge. CPAP has been shown to have beneficial effects on postoperative adverse events.
There are several barriers to effective diagnosis and treatment of OSA in the perioperative setting. In both clinical and research settings, a significant proportion of patients who may have suspected OSA refuse to undergo additional testing for establishing an OS diagnosis. Also, for those patients that actually are on home CPAP therapy only one third used their CPAP during the postoperative stay in the hospital.
Individual evaluation is important to determine the best course of action. Referral to sleep medicine for CPAP therapy may have to be taken in the absence of overwhelming evidence from RCTs in certain groups of patients. Patients with severe OSA, COPD or overlap syndrome, obesity hypoventilation syndrome, or pulmonary hypertension would definitely benefit from further evaluation and workup. Patients who have preoperative resting hypoxemia on room air with no known cardiopulmonary cause are potential candidates for further preoperative evaluation. Patients with decreased respiratory responses to hypoxia/hypercapnia stimuli and a high arousal threshold presenting with recurrent severe hypoxemia may benefit from preoperative CPAP.

If decreased lung capacity is the result of kyphoscoliosis, corrective spinal fusion surgery may be indicated (Note: since muscular dystrophies can often be associated fatal malignant hyperthermia triggered by neuromuscular blocking anaesthetic agents, these should be prohibited in case of muscular dystrophy patients and special precautions e.g. availability of dantrolene and hyperthermia remedial measures, should be taken. Further progression of respiratory insufficiency requires more invasive measures such as a tracheostomy and portable ventilation.
The mainstay of muscular dystrophy ‘treatment’ comprises of rehabilitative and nutritional measures. Low-intensity physical therapy in order to maintain independence with ADL’s (activities of daily living) and quality of life, maintain joint flexibility, muscle tone and to prevent joint contractures and deformities such as scoliosis, is essential throughout the course of the disease. Hydrotherapy/aquatic therapy can be exceedingly beneficial as water provides buoyancy as well as resistance. The former helps a weak patient stand in the pool and possibly take steps maintaining function and improving his overall sense of wellbeing somewhat. The latter helps strengthen muscles in a low-impact, non-jarring fashion. (Note: high-intensity, isometric, weight-training exercises are strictly NOT RECOMMENDED for muscular dystrophy patients as they do not have the capacity to overcome the wear and tear induced by such. Any exercise involving ‘eccentric’ muscle contraction (stretching of an already contracted muscle by manual resistance or weight loading) is unequivocally prohibited.
As the functional strength, gross and fine motor control and independence in daily tasks diminish, the services of an occupational therapist may become essential in helping the patient be as self-sufficient as possible. At various stages of the disease, the muscular dystrophy patient may need orthotics (to prevent joint contractures), canes, walkers, standing frames, wheelchairs or motorized scooters, air mattress (to prevent bedsores), custom-made or modified utensils, aids for writing, turning book pages or for computer use as well as toilet and shower modifications and safety devices as well as accessibility needs such as ramps, chairlifts and car/van modifications.
Lastly, the importance of adequate and balanced nutrition in muscular dystrophy cannot be understated. It is crucial that the patient maintain muscle mass but not gain weight in the form of fat that can further hamper mobility.

This report was previously presented, in part, at the American Society of Anesthesiologists Meeting, 2010.
Reprints will not be available from the authors.
Address correspondence to Anupama Wadhwa, MD, Department of Anesthesiology, University of Louisville, 530 S. Jackson St, Louisville, KY 40202. Address e-mail to email@example.com.
Surgical site infections and healing-related complications are among the most common serious complications of anesthesia and surgery.1–4 The morbidity and related cost associated with surgical infections and the resulting major complications are considerable; estimates of prolonged hospitalization vary from 5 to 20 days per infection.5–7
Oxidative killing is the most important immune defense against surgical pathogens, with killing intensity increasing throughout the range of 0 to ≥150 mm Hg oxygen.8,9 Oxidative killing requires molecular oxygen that is enzymatically transformed into the bactericidal radical superoxide.10 Subcutaneous tissue oxygen values near 60 mm Hg are typical in euthermic, euvolemic, healthy volunteers breathing room air.11 Perioperative subcutaneous oxygen partial pressures <40 mm Hg are associated with high infection risk, whereas partial pressures >90 mm Hg are rarely associated with infection.12,13 Adequate tissue oxygenation is also necessary for collagen deposition (scar formation), which is an essential step in wound healing and tissue repair.14
The partial pressure of oxygen in subcutaneous tissues (PsqO2) varies widely, even in patients whose arterial hemoglobin is fully saturated. Factors known to influence tissue oxygen tension include core15 and local temperature,16 smoking,17 anemia,18 perioperative fluid management,19 neuraxial anesthesia,20 and uncontrolled surgical pain.21 As might be expected, increasing the fraction of inspired oxygen augments tissue oxygen tension.22 Supplemental perioperative oxygen was found to reduce the risk for anastomotic leak23 and wound infection in some randomized studies,22,24 but not in others.25,26
Morbidly obese patients are at high risk of wound infection and healing-related complications. Low tissue oxygenation presumably contributes to infection risk in these patients.

Respiratory failure results initially from recurrent chest infections caused by atelectasis, which progresses to nocturnal hypoventilation from muscle weakness, and reduced sensitivity to carbon dioxide during sleep. Sleep-related breathing disorders - nocturnal hypoventilation18-21 and obstructive sleep apnea,19 are well documented in children with neuromuscular diseases. Untreated sleep-related disorders can then lead to the development of respiratory failure through disordered ventilatory control resulting from adaptation and down-regulation of ventilatory responses to hypoxemia and hypercarbia.22
It has been hypothesized that NIV works by several mechanisms in the chronic lung: 1) improving ventilatory mechanics; 2) resting fatigued respiratory muscles; or 3) enhancing ventilatory sensitivity to carbon dioxide.22,23 Investigations into a mixed group of patients with neuromuscular diseases showed that NIV improved daytime blood gases,16,24,25 ventilatory response to CO2, but did not demonstrate improvement in pulmonary mechanics or respiratory muscle strength.24,25
In a retrospective review by Duiverman, which included 114 adult patients with restrictive lung diseases (mainly post-poliomyelitis and idiopathic kyphoscoliosis), NIV improved both daytime blood gases and pulmonary function.26
The differing results in the pulmonary function may be due to the differences in the natural progression of the diseases studied. Its use, in a small study of children with neuromuscular diseases, was associated with lower hospitalizations after initiation of NIV.18 The use of NIV has also been effective in improving polysomnography (PSG) indices as well as sleep architecture and sleep-related symptoms.20,21,25
It therefore follows that NIV should be considered in patients who have evidence of nocturnal hypoventilation. The 1999 Consensus Conference Report27 suggested the use of noninvasive positive pressure ventilation for restrictive lung disease in the presence of symptoms (fatigue, dyspnea, morning headache, etc) with one of the following parameters: PaCO2 ≥ 45 mmHg, nocturnal oximetry demonstrating oxygen saturation ≤ 88% for 5 consecutive minutes; or progressive neuromuscular disease, maximal inspiratory pressures < 60 cm/H2O or FVC < 50% predicted.
In a study involving Duchenne muscular dystrophy, Craig et al.

Of the more than 12 well-characterised congenital myopathies, respiratory muscle involvement is best recognised in nemaline myopathy (fig 1), myotubular (centronuclear) myopathy and multiminicore disease. If it occurs at all, respiratory failure is usually evident in the neonatal period. However, in a rare variant of nemaline myopathy—sporadic late-onset nemaline myopathy—the onset of limb and respiratory muscle weakness occurs in adult life.6
Congenital muscular dystrophy
In this rare set of disorders, hypotonia, weakness, and contractures occur within the first six months of life. In some forms there may be structural brain disease and impaired cognitive function. Respiratory muscle involvement and respiratory failure are common features and often prove fatal in childhood or the second decade.
Duchenne muscular dystrophy and its less severe allelic counterpart, Becker muscular dystrophy, arise from mutations of the gene encoding dystrophin. In Duchenne, weakness of the respiratory muscles is universal. After the normal rise in childhood, the vital capacity begins to decline after age 10. The assessment of respiratory function may be complicated by scoliosis, and by cardiac dysfunction. Non-invasive ventilation (fig 2) has been one factor which has increased the survival beyond age 24 to 53% in one large centre.7 In Becker muscular dystrophy, respiratory failure is less common but lung function should be checked at intervals.
Myotonic dystrophy (DM1) results from a CTG expansion in the gene encoding DMPK. It is a multisystem disorder, but the clinical features are highly variable in different patients. Respiratory failure, pneumonia or cardiac conduction defects are the usual causes of death. As well as weakness of the respiratory muscles, patients can have a central defect of respiratory control, and be predisposed to respiratory infection due to bulbar weakness. Monitoring should include periodic checks on the vital capacity, and an annual ECG as the PR interval and QRS duration each increase by a few percent per year. The alterations of personality and cognitive function found in patients with DM1 can hinder compliance with non-invasive ventilation.
Limb girdle muscular dystrophy
Limb girdle muscular dystrophy is a steadily expanding set of autosomal dominant or recessive myopathies which have in common weakness of the shoulder and pelvic girdle muscles.

Picture an emergency where an anesthetized patient’s temperature unexpectedly rises to over 104 degrees Fahrenheit due to hypermetabolic acidotic chemical changes in the patient’s skeletal muscles. The disease requires rapid diagnosis and treatment with the antidote dantrolene, as well as acute medical measures to decrease temperature, acidosis, and high blood potassium levels which can otherwise be fatal.
- An intraoperative myocardial infarction (heart attack). Picture an anesthetized 60-year-old patient who develops a sudden drop in their blood pressure due to failed pumping of their heart. This can occur because of an occluded coronary artery or a severe abnormal rhythm of their heart. Otherwise known as cardiogenic shock, this syndrome can lead to cardiac arrest unless the heart is supported with the precise correct amount of medications to increase the pumping function or improve the arrhythmia.
- Any massive trauma patient with injuries both to their airway and to their major vessels. Picture a motorcycle accident victim with a bloodied, smashed-in face and a blood pressure of near zero due to hemorrhage. The placement of an airway tube can be extremely difficult because of the altered anatomy of the head and neck, and the management of the circulation is urgent because of the empty heart and great vessels secondary to acute bleeding.
- The syndrome of “can’t intubate, can’t ventilate.” You’re the anesthesiologist. Picture any patient to whom you’ve just induced anesthesia, and your attempt to insert the tracheal breathing tube is impossible due to the patient’s anatomy. Next you attempt to ventilate oxygen into the patient’s lungs via a mask and bag, and you discover that you are unable to ventilate any adequate amount of oxygen. The beep-beep-beep of the oxygen saturation monitor is registering progressively lower notes, and the oximeter alarms as the patient’s oxygen saturation drops below 90%. If repeated attempts at intubation and ventilation fail and the patient’s oxygen saturation drops below 85-90% and remains low, the patient will incur hypoxic brain damage within 3 – 5 minutes. This situation is the worst-case scenario that every anesthesia professional must avoid if possible. If it does occur, the anesthesia professional or a surgical colleague must be ready and prepared to insert a surgical airway (cricothyroidotomy or tracheostomy) into the neck before enough time passes to cause irreversible brain damage.

Steroids can weaken bones. To keep bones healthy, your child will take
and calcium supplements. If your child has heart problems, medications may be given to slow the damage.
As the disease progresses, the muscles that support breathing may weaken. Your child may need a ventilator. It will deliver air through a mask, tube, or sometimes through a
surgical hole in the windpipe called a
Surgery is sometimes used to treat symptoms of DMD. For severe contractures, surgery may be done to release specific tendons. Scoliosis can sometimes interfere with your child’s breathing. In this case, back surgery may be done.
There are no known guidelines to prevent this progressive muscle disease.
Duchenne muscular dystrophy. EBSCO DynaMed website. Available at:
http://www.ebscohost.com/dynamed. Updated March 15, 2013. Accessed August 6, 2013.
Duchenne muscular dystrophy. Muscular Dystrophy website. Available at:
http://mda.org/disease/duchenne-muscular-dystrophy. Accessed August 6, 2013.
Last reviewed May 2014 by Teresa Briedwell, DPT, OCS
Please be aware that this information is provided to supplement the care provided by your physician. It is neither intended nor implied to be a substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the advice of your physician or other qualified health provider prior to starting any new treatment or with any questions you may have regarding a medical condition.
Copyright © EBSCO Publishing. All rights reserved.

However, the special tests described in the Atelectasis section were performed only in the selected 30 patients.
Written informed consent was obtained from each patient. Patients with a history or current symptoms of acute or chronic pulmonary disease and patients in whom surgeons planned delayed primary closure techniques or wound healing by secondary intention were excluded, as were patients who had a history of fever or infection.
Anesthesia was induced at an inspired oxygen fraction of 100% with sodium thiopental (3–5 mg/kg), vecuronium (0.1 mg/kg), and fentanyl (1–3 μg/kg). Anesthesia subsequently was maintained with isoflurane (approximately 0.9%) in a carrier gas, described below in randomization groups. After tracheal intubation, the lungs were ventilated with a tidal volume of 10 ml/kg, with the rate adjusted to maintain end‐tidal carbon dioxide partial pressure near 35 mmHg. Ventilation was volume‐controlled with zero end‐expiratory pressure.
After induction of anesthesia, patients were assigned to two groups using a reproducible set of computer‐generated random numbers. The assignments were kept in sealed, sequentially numbered envelopes until used. For auditing purposes, both the assignment and the envelope number were recorded. The groups were: (1) 30% oxygen, balance nitrogen (not nitrous oxide); and (2) 80% oxygen, balance nitrogen.
At the end of surgery, residual neuromuscular block was antagonized with glycopyrrolate (0.4 mg) and neostigmine (2.5 mg). All patients were transported to the recovery unit after endotracheal extubation. During the first 2 h of recovery, the designated oxygen concentration was given via a nonrebreathing mask system (AirCare mask and manifold; Apotheus Laboratories, Inc., Lubbock, TX). Subsequently, all patients breathed room air. Supplemental oxygen was given to patients in either group at any time, as necessary, to maintain oxygen saturation as measured by pulse oximeter > 92%. Postoperative analgesia was provided by patient‐controlled intravenous doses of the opioid piritramid.
Appropriate morphometric characteristics of each treatment group were tabulated. Historical factors that might influence general health status of the participating patients were recorded.

Supplemental oxygen is needed to prevent hypoxia and keep cells functioning properly. However, during normal cellular metabolism oxygen is systematically changed and an O2- molecule is produced as a byproduct, which is oxygen with an extra negatively charged electron. This oxygen molecule is considered a free radical “toxic” molecule because it has the ability to damage cell membranes. Normally the body avoids damage from these toxic oxygen molecules because enzymes within each cell are produced that quickly destroy the “toxic” oxygen molecule.4 However, these enzymes are produced at a fixed rate that does not increase when metabolism (oxygen consumption) increases.
Complications of Oxygen Delivery
Like every other drug, oxygen administration has complications. Common complications include skin irritation and breakdown as well as a drying of the mucous membranes. Less common but more serious complications include oxygen toxicity, absorbative atelectasis and carbon dioxide narcosis.
The most common complications are a consequence of the delivery systems. Plastic systems, oxygen masks and nasal cannulas are used, and all of these devices are skin irritants which can cause significant skin irritation and breakdown when used long term. Patients who are on long-term oxygen systems often try to prevent skin irritation by padding their delivery systems, such as by padding their nasal cannula behind the ears with nasal tissues. Other common areas of skin breakdown are across the bridge of the nose and beneath the nares.
Typically oxygen systems deliver oxygen that has nearly zero moisture content. When this oxygen passes through the mucous membranes in the mouth and nose, it is humidified by pulling moisture from the mucous membranes so it is humid by the time it reaches the alveoli. While this protects the alveoli and bronchioles, the nasal and oral mucous membranes quickly dry out. Dry mucous membranes lose their ability to humidify the air we breathe and also become uncomfortable. Applying oxygen via a humidifier can help prevent this from occurring.
Recall from earlier in this article that under high oxygen environments, cells metabolize oxygen more quickly. This is because there is an increased pressure from the dissolved oxygen, the PaO2, forcing oxygen into the cell, thereby increasing oxygen consumption and the production of the toxic oxygen molecule byproduct O2-.

Muscle biopsy shows degenerating and regenerating muscle fibers, with connective tissue and fat replacing lost muscle tissue. DNA testing may also be helpful.
Long Term Effects
What are the long-term effects of the disease?
Duchenne muscular dystrophy causes progressive deterioration of the muscles, and loss of function. The muscle deterioration leads to the use of braces and eventually a wheelchair. Impaired lung function leads to serious lung infections, aspiration, and death.
What are the risks to others?
Duchenne muscular dystrophy is not contagious. It is an X-linked recessive disorder. This means that an unaffected woman who carries the gene can pass it, on average, to one half of her sons.
What are the treatments for the disease?
The major goal of early treatment is to keep the ability to walk as long as possible. Stretching exercises and using braces at night help avoid the tightening of tendons.
Surgery can be used to release tight tendons. Walking and body movement should be resumed immediately after surgery if possible. Inactivity makes the disease worse and can lead to rapid deterioration of lung function. Prednisone has been shown to slow the progression of the disease for up to three years.
Vaccination against influenza and pneumococcal infections is important. Also, weight control is essential. Obesity adversely impacts physical and respiratory functions.
How is the disease monitored?
Any new or worsening symptoms should be reported to the healthcare provider.
The Muscular Dystrophy Association [hyperLink url="http://www.mdausa.org/disease/dmd.html" linkTitle="http://www.mdausa.org/disease/dmd.html"]http://www.mdausa.org/disease/dmd.html[/hyperLink]

Neuromuscular blockade and proning have both shown to improve mortality in those with a PaO2:FiO2 ratio < 150 when initiated within the first few days of treatment (Alhazzani 2013, Guerin 2013). Although proning may be difficult in the ED, neuromuscular blockade with adequate sedation would be reasonable in the challenging, severely hypoxemic patients after discussion with the accepting ICU team.
When your patient has high plateau pressure and persistent hypoxemia despite appropriately high PEEP, low Vt and neuromuscular blockade ask for help from your intensivist colleagues and consider sending to a center with ECMO capabilities.
Mechanical Ventilation in Severe Metabolic Acidosis
Metabolic acidosis, as seen with DKA and salicylate toxicity, is a significant stimulus for tachypnea and a high minute ventilation. The patient is compensating for their acidosis by blowing off their CO2. The post intubation time is dangerous! During this time the patient is still paralyzed and sedated, not allowing them to compensate by breathing rapidly themselves. Do your best to match the patient’s pre-intubation minute ventilation through giving the patient appropriate volumes (starting at 8 mL/kg) and a respiratory rate like that of their pre-intubation. They will require a repeat blood gas shortly after intubation, to ensure that you are adequately ventilating and not allowing worsening of their underlying acidosis. Once the paralytic has worn off some patients may be most comfortable setting their own respiratory rate in a pressure support mode. Others may require deep sedation to allow for synchrony with a set rapid respiratory rate and a safe Vt ~ 8 mL/kg. With a faster set rate watch for air trapping in the flow waveform and avoid breath stacking.
Providing excellent care to intubated patients in the ED will save lives. When taking care of obstructive lung disease remember three principles: slow respiratory rate, tolerate hypercarbia, and check for air-trapping. These patients will need to be adequately sedated and potentially paralyzed for ventilator compliance. When taking care of hypoxemic patients, first identify if it is a unilateral or bilateral process. Refractory hypoxemia in the setting of unilateral disease should be treated with low Vt ventilation and positioning with the “good lung” down to decrease the intrapulmonary shunt.

The surgery duration was about 240 moments and this prolongation was due to further undiagnosed stenosis of the biliary tract. His medical history revealed DMD disability moderate restrictive pulmonary dysfunction mild hypokalemia and hypertension. His preoperative laboratory tests were hemoglobin 13.9?g?1 hematocrit 43.5% platelets 202 0 sodium 141?mmom·L?1 potassium 3?mmol·L?1 magnesium 0.58?mg·dL?1 creatinine 0.06?mg·dL?1 total calcium 8.72?mg·dL?1 lactic dehydrogenase (LDH) 230?U·L?1 direct bilirubin 230?U·L?1 and alkaline phosphatase 130?U·L?1. For the common difficulty to obtain a peripheral venous access in such patients a central venous access was established by ultrasound guided cannulation of the internal right jugular vein. In the preoperative room we prepared our patient by antibiotics prophylaxis: ciprofloxacin 2?gm; metronidazole 500?mg; and an antiemetic agent ondansetron 4?mg. Our patient was monitored by pulse oximetry expiratory capnography invasive and noninvasive blood pressure electrocardiogram neuromuscular transmission by train-of-four repeated every 12 seconds at the adductor pollicis muscle (TOF Guard Organon Teknika B.V Boxtel The Ercalcidiol Netherlands) and diuresis. We induced our anesthesia by oxygen propofol 150?mg fentanyl 200?mcg and rocuronium bromide 10?mg and then we proceeded to a rapid sequence endotracheal intubation (tube diameter was 7.5?mm). The maintenance of the anesthesia was achieved by fentanyl in a total dose of 400?mcg (200-100-100) rocuronium bromide 5?mg repeated every 45 minutes at T4/T1 recovery of 25% sevoflurane 2% and O2 40% in air.

For example, PsqO2 approaches 120 mm Hg when PaO2 reaches 300 mm Hg in nonobese patients compared with 50 mm Hg in the morbidly obese with similar PaO2.22 Administration of 50% inspired oxygen, a concentration that produces a PaO2 of approximately 300 mm Hg for most patients, results in critically low (approximately 40 mm Hg) perioperative subcutaneous tissue oxygenation27 in the morbidly obese, a value associated with a high risk of infection.28 Obese patients are thus on the “steep part of the curve” relating PsqO2 to neutrophil production of high-energy oxidative species.8
Morbidly obese surgical patients are not just at risk of inadequate tissue oxygenation during surgery. Obstructive sleep apnea, which is rampant in this population, is directly proportional to the body mass index (BMI).29–31 The associated arterial desaturation is especially severe after surgery because the syndrome is markedly worsened by opioid analgesics. Obstructive sleep apnea reduces arterial oxygenation during sleep30,32 and presumably also reduces tissue oxygenation intermittently. Supplemental oxygen may thus be especially helpful in the morbidly obese since baseline tissue oxygenation is low and, in many cases, will be further reduced by opioid-aggravated perioperative obstructive sleep apnea.
Morbidly obese patients may thus especially benefit from extending the duration of supplemental oxygen to include the first postoperative night, when the likelihood of hypoxia-related complications may be the highest due to residual effects of general anesthesia and opioid analgesia. We therefore tested the hypothesis that the risk of major complications related to infection or inadequate healing is lower in morbidly obese patients who are given approximately 80% supplemental inspired oxygen for 12 to 16 hours after gastric bypass surgery than in those given approximately 30% oxygen (2 L/min via nasal cannula).
Patients were recruited at 3 different hospitals: Cleveland Clinic, Cleveland, Ohio; University of Vienna, Vienna, Austria (AKH); and the Norton Hospital, Louisville, Kentucky. Approval was obtained from the IRBs of each of the 3 participating hospitals, and written informed consent was obtained from each patient. Patients having Roux-en-Y gastric bypass, either open or laparoscopic, with anticipated primary wound closure were included.

The body quickly recognizes that it can maintain the same PaO2 without having to work as hard, and over time the body adjusts to the alveolar oxygen levels to maintain their arterial oxygen levels as their baseline. The net result of this can be a decreased respiratory rate.4
The well documented and clinically important piece of this condition is that oxygen-induced hypercapnia most commonly occurs in otherwise asymptomatic, relaxed and unstimulated patients, such as a patient who is sleeping. It does not occur in patients with acute respiratory distress, who often are experiencing a catecholamine release stimulating increased respiratory and circulatory rates.2
Clinical symptoms of oxygen-induced hypercapnia include a rising CO2 level, which can be measured with a side-stream CO2 device, altered mental status including confusion, complaints of headaches, and a somnolent appearance.1
Prevention of Complications
Preventing complications from oxygen administration is fairly straightforward. To start, whenever possible, pad the straps and tubing of oxygen delivery systems, particularly on patients who receive oxygen long term. Also, consider increasing the use of humidified oxygen to prevent drying out mucous membranes. Oxygen humidifiers are inexpensive and greatly increase patient comfort. Also, elevating a patient’s head and chest at least 30 degrees promotes lung expansion and helps prevent aspiration.
Never withhold oxygen from patients who are in respiratory distress or hypoxic. Oxygen is truly a lifesaving drug. During major resuscitations, such as cardiac arrest and major traumas, 100% oxygen is indicated. However, for most all other patients, consider limiting oxygen to maintain SpO2 in the 90%–95% range; this also keeps the PaO2 above 60 mm Hg.1 Research has consistently shown that oxygen’s maximum benefit is obtained when delivered in the 22%–50% range4, and its benefit is limited after 6 hours of administration.3
Neonatal patient management requires special consideration. Whenever possible, utilize room air when initiating resuscitation. Only administer oxygen when the neonate remains bradycardic after 90 seconds of resuscitation efforts.5
The administration of oxygen is safe and effective for patients who are in respiratory distress or who are hypoxic. Never feel that oxygen needs to be withheld. However, keep in mind that there are real consequences to the long term utilization of high-flow oxygen.

Implications for Cardiac Function Following Rescue of the Dystrophic Diaphragm in a Mouse Model of Duchenne Muscular Dystrophy.
Betts CA., Saleh AF., Carr CA., Muses S., Wells KE., Hammond SM., Godfrey C., McClorey G., Woffindale C., Clarke K., Wells DJ., Gait MJ., Wood MJA.
Duchenne muscular dystrophy (DMD) is caused by absence of the integral structural protein, dystrophin, which renders muscle fibres susceptible to injury and degeneration. This ultimately results in cardiorespiratory dysfunction, which is the predominant cause of death in DMD patients, and highlights the importance of therapeutic targeting of the cardiorespiratory system. While there is some evidence to suggest that restoring dystrophin in the diaphragm improves both respiratory and cardiac function, the role of the diaphragm is not well understood. Here using exon skipping oligonucleotides we predominantly restored dystrophin in the diaphragm and assessed cardiac function by MRI. This approach reduced diaphragmatic pathophysiology and markedly improved diaphragm function but did not improve cardiac function or pathophysiology, with or without exercise. Interestingly, exercise resulted in a reduction of dystrophin protein and exon skipping in the diaphragm. This suggests that treatment regimens may require modification in more active patients. In conclusion, whilst the diaphragm is an important respiratory muscle, it is likely that dystrophin needs to be restored in other tissues, including multiple accessory respiratory muscles, and of course the heart itself for appropriate therapeutic outcomes. This supports the requirement of a body-wide therapy to treat DMD.

Respir Physiol 7: 7-29.
- Luks AM, Swenson ER (2007) Travel to high altitude with pre-existing lung disease. Eur Respir J 29: 770-792.
- Lenfant C, Sullivan K (1971) Adaptation to high altitude. N Engl J Med 284: 1298-1309.
- Lenfant C, Torrance JD, Reynafarje C (1971) Shift of the O2-Hb dissociation curve at altitude: mechanism and effect. J Appl Physiol 30: 625-631.
- Bateman NT, Leach RM (1998) ABC of oxygen. Acute oxygen therapy. BMJ 317: 798-801.
- Goonasekera C, Kunst G, Mathew M (2017) End tidal carbon dioxide (ETCO2) and peripheral pulse oximetry (SpO2) trends and right-to-left shunting in neonates undergoing non cardiac surgery under general anesthesia. Pediatric Anesthesia and Critical Care Journal 5: 40-45.
- Ng A, Swanevelder J (2011) Hypoxaemia associated with one-lung anaesthesia: new discoveries in ventilation and perfusion. BJA 106: 761-763.
- Dimitriou G, Greenough A, Pink L, McGhee A, Hickey A, et al. (2002) Effect of posture on oxygenation and respiratory muscle strength in convalescent infants. Arch Dis Child Fetal Neonatal Ed 86: F147-F150.
- Schwarzkopf K, Schreiber T, Bauer R Schubert H, Preussler NP, et al. (2001) The effects of increasing concentrations of isoflurane and desflurane on pulmonary perfusion and systemic oxygenation during one-lung ventilation in pigs. Anesthesia & Analgesia 93: 1434-1438.
- Tripathi RS, Papadimos TJ (2011) "Life-threatening" hypoxemia in one-lung ventilation. Anesthesiology 115: 438; author reply 439-441.
- Deem S, Bishop MJ, Alberts MK (1995) Effect of anemia on intrapulmonary shunt during atelectasis in rabbits. J Appl Physiol 79: 1951-1957.

Duchenne’s muscular dystrophy (DMD) is the most common and severe type of myopathy. by fentanyl rocuronium bromide O2 and sevoflurane. We report in cases like Rac1 this the safety usage of sugammadex to antagonize the neuromuscular stop and speedy recovery in such group of sufferers. 1 Launch Duchenne muscular dystrophy (DMD) is normally a rare hereditary X-linked recessive disorder nonetheless it is among the most frequent hereditary conditions affecting around 1 in 3 500 man births worldwide. It really is recognized between three and six years usually. DMD is seen as a weakness and spending (atrophy) from the muscles from the pelvic region accompanied by the participation of the make muscles. As the condition progresses muscles weakness and atrophy pass on to have an effect on the trunk and forearms and steadily improvement to involve extra muscles of your body [1 2 The anesthetic administration of Ercalcidiol these sufferers is complicated not merely by muscles weakness but also by cardiac and pulmonary manifestations. Nevertheless there is absolutely no definite suggestion for possibly regional or general anaesthesia. Succinylcholine and volatile anaesthetics have already been best avoided since there is a threat of hyperkalemic cardiac arrest or serious rhabdomyolysis . Some authors possess recommended intubation and anesthesia without resorting to muscles relaxants to avoid postoperative respiratory system failure linked to using muscles relaxants as well as the various other problems induced by acetylcholinesterase inhibitors. Nevertheless anesthesia without muscles relaxants may not always be ideal for some surgical treatments like such as for example in our individual . Case reviews in sufferers with myasthenia gravis record the successful usage of sugammadex (six case reviews). For various other rare muscular illnesses like Duchenne muscular dystrophy latest reviews document the effective reversal of rocuronium with sugammadex in pediatric sufferers [5-9]. And in this complete case survey we record the sugammadex basic safety within an adult Duchenne disease individual. 2 Case Display A 25-year-old man with DMD using a improved Ercalcidiol Barthel index of 23 (Barthel index can be an ordinal level used to measure overall performance in activities of daily living)  (BMI 25 6 ASA III) was scheduled for open cholecystectomy under general anesthesia.

Tips For The Use Of Supplemental Oxygen
1. Keep away from any flame or spark such as gas stoves, fireplaces and candles. Even electric razors can cause sparks so do not use your oxygen whilst shaving. Oxygen isn’t flammable but it is combustible and can aid in the starting of a fire.
2. Do not allow any smoking anywhere near. Some people put signs up in their homes for visitors to let them know.
3. When cooking try not to wear loose fitting clothes and stay as far away from the heated surface as possible.
4. Avoid using any aerosol products as they can ignite in the presence of a spark.
5. Do not allow flammable liquids to get on your clothing or body as unless washed thoroughly, these could become a hazard.
6. Do not place your oxygen concentrator in an unventilated area, such as a closet. Not only does the concentrator generate a lot of heat but it uses the surrounding air to produce oxygen so the oxygen in the atmosphere will quickly become depleted in small spaces.
7. Secure all cylinders to prevent them from falling over. A falling oxygen cylinder can cause damage to the valve, releasing the pressure, which may cause it to become a dangerous projectile.
8. Call your electric company to inform them that you are using oxygen. Firstly some electric companies have a program that allows a reduction of your rates to help lower the cost of running the air concentrator. Secondly, they will generally put you first in line when restoring power after an outage. They may also be able to provide specialist adaptors or devices to aid you with your mobility and medical equipment to make life easier.
9. Oxygen hoses can be a tripping hazard so try to have your concentrator in a position for maximum mobility but also where the hose will not cause you or others to trip. Use a coloured hose to make it more visible.
10. Keep the hoses clean and replace on a regular basis. Make sure the filters are replaced regularly, wipe it down with a damp cloth to remove dust and clean tubing to prevent mould if you use water to humidify your oxygen.
Ensure you have an emergency plan arranged in case there is a power outage.
• Inform your power company that you are oxygen-dependent. Many companies offer oxygen-dependent patients priority service and will inform you of upcoming maintenance/outages and ensure your power is restored as a priority.

The practice of using supplemental oxygen to treat all patients with MI became standard nearly a century ago, after oxygen was found in 1900 to relieve angina, and led to clinical improvement in four MI patients in a 1930 case series.5,6
It was not studied in a controlled trial until 1976, when J.M. Rawles, MD, and colleagues randomized 157 patients with MI to 24 hours of oxygen at 8 L/min or to ambient air. They found no difference in mortality between the groups, but they did find a higher burden of MI in the intervention arm receiving supplemental oxygen, as measured by mean serum aspartate aminotransferase levels.7
The topic was not addressed again in a significant randomized trial until this century. Most notably, two recent studies again demonstrated no benefit of supplemental oxygen in normoxemic patients with MI.
In the AVOID trial in 2015, Dion Stub, MD, PhD, and colleagues randomized 441 patients with STEMI to oxygen at 8 L/min – from diagnosis in an ambulance until after cardiac catheterization – or to ambient air. They found no difference in death at 6 months, but did find an increased rate of in-hospital recurrent MIs, with 0.9% of the control group and 5.5% of the oxygen intervention arm suffering recurrence (P = .006).8 They also showed a larger area of myocardial infarct in the oxygen group, as measured by peak creatine kinase levels and cardiac MRI at 6 months.
Proposed mechanisms of increased myocardial injury from hyperoxia include increased coronary vascular resistance resulting in decreased myocardial perfusion, and increased reperfusion injury from formation of free radicals.9
Where does all this leave us in the treatment of suspected MI?
Morphine should only be used when the patient has pain, and is probably best reserved for severe pain, as the safety of its use is not clear. While hypoxemia is a common consequence of MI – and may correlate with worse outcomes – treatment with supplemental oxygen in the absence of hypoxemia is not supported by current evidence, and may carry risk of harm. Nitroglycerin should be avoided in patients with right ventricular infarcts, and in patients who present with hypotension.

About Duchenne Supporting Therapies Diet It is important that children with Duchenne muscular dystrophy eat a well-balanced diet. Children on steroids, and those with reduced mobility, tend to put on weight, which in turn can add pressure to already weakened muscles. A high protein diet is recommended. Care should be taken to avoid fatty meats like beef, lamb or pork, instead some dieticians suggest that there should be an emphasis on protein in the form of fish, leaner meats like chicken, or vegetable protein like beans or soya. As for all children, it is suggested that refined foods such as white bread, sugars and pasta are reduced or excluded. Constipation can be a problem, caused by a combination of weak stomach muscles and immobility, so a high fibre diet - rich in fresh fruits and vegetables - is suggested. It is important too, to keep hydrated. Some people use supplements including calcium and vitamin D to keep muscles and bones strong. Dietary considerations when starting Corticosteroids Duchenne patients using corticosteroids like prednisone or deﬂazacort, and those with heart problems, may need a low salt diet. They may also experience gastroesophageal reﬂux (GORD). A low-fat, high-fibre diet that's heavy on whole grains, fruits and vegetables, and lean meats may help. They are also at risk of osteoporosis - a thinning and weakening of the bones. Vitamin D, calcium supplements and bisphosphonate infusions can help with this. Foods naturally high in vitamin D include fatty fish, liver, and egg. Vitamin D is also made naturally when skin is exposed to sunshine. Foods containing calcium include dairy products, green vegetables such as broccoli and kale, figs, oranges, salmon, sardines, soya and almonds.

Sharkey KM, Machan JT, Tosi C, Roye GD, Harrington D, Millman RP. Predicting obstructive sleep apnea among women candidates for bariatric surgery. J Womens Health (Larchmt). 2010;19:1833–41
32. Ahmad S, Nagle A, McCarthy RJ, Fitzgerald PC, Sullivan JT, Prystowsky J. Postoperative hypoxemia in morbidly obese patients with and without obstructive sleep apnea undergoing laparoscopic bariatric surgery. Anesth Analg. 2008;107:138–43
33. Kurz A, Kurz M, Poeschl G, Faryniak B, Redl G, Hackl W. Forced-air warming maintains intraoperative normothermia better than circulating-water mattresses. Anesth Analg. 1993;77:89–95
34. Hynson JM, Sessler DI. Intraoperative warming therapies: a comparison of three devices. J Clin Anesth. 1992;4:194–9
35. Bazuaye EA, Stone TN, Corris PA, Gibson GJ. Variability of inspired oxygen concentration with nasal cannulas. Thorax. 1992;47:609–11
36. Slessarev M, Somogyi R, Preiss D, Vesely A, Sasano H, Fisher JA. Efficiency of oxygen administration: sequential gas delivery versus “flow into a cone” methods. Crit Care Med. 2006;34:829–34
37. Kabon B, Rozum R, Marschalek C, Prager G, Fleischmann E, Chiari A, Kurz A. Supplemental postoperative oxygen and tissue oxygen tension in morbidly obese patients. Obes Surg. 2010;20:885–94
38. Haley RW, Culver DH, Morgan WM, White JW, Emori TG, Hooton TM. Identifying patients at high risk of surgical wound infection. A simple multivariate index of patient susceptibility and wound contamination. Am J Epidemiol. 1985;121:206–15
39.

Women and/or couples need to consider carefully which test to have and to discuss this with their genetic counselor. Earlier testing would allow early termination which would probably be less traumatic for the couple, but it carries a slightly higher risk of miscarriage than later testing (about 2%, as opposed to 0.5%).
Appearance of the Patient
There is no known cure for Duchenne muscular dystrophy yet although recent stem-cell research is showing some ways to replace damaged muscle tissue. Treatment is aimed at control of symptoms to maximize the quality of life.
- Corticosteroids such as prednisone and deflazacort increase energy and strength and defer severity of some symptoms.
- Mild, non-jarring physical activity such as swimming is encouraged. Inactivity (such as bed rest) can worsen the muscle disease.
- Physical therapy may be helpful to maintain muscle strength and function.
- Orthopedic appliances (such as braces and wheelchairs) may improve mobility and the ability for self-care. Form-fitting removable leg braces that hold the ankle in place during sleep can defer the onset of contractures.
- Appropriate respiratory support as the disease progresses is important
Duchenne muscular dystrophy eventually affects all voluntary muscles and involves the heart and breathing muscles in later stages. Survival is rare beyond the early 30s,  although recent advancements in medicine are extending the lives of those afflicted. Death typically occurs from respiratory failure or heart disorders.
Physiotherapists are concerned with enabling children to reach their maximum physical potential. Their aim is to:
- minimize the development of contractures and deformity by developing a programme of stretches and exercises where appropriate
- anticipate and minimise other secondary complications of a physical nature
- monitor respiratory function and advise on techniques to assist with breathing exercises and methods of clearing secretions
Mechanical Ventilatory Assistance: Volume Ventilators
Modern "volume ventilators," which deliver a preset volume (amount) of air to the person with each breath, are valuable in the treatment of people with muscular dystrophy related respiratory problems. Ventilator treatment usually begins in childhood when the respiratory muscles begin to fail.
When the vital capacity has dropped below 40 percent of normal, a volume ventilator may be used during sleeping hours, a time when the person is most likely to be underventilating ("hypoventilating").

- The patient and the health care team should be aware that known, treated, partially treated and untreated OSA as well as suspected OSA may be associated with increased postoperative morbidity.
- Consideration should be given to obtaining the results of the sleep study and the recommended Positive Airway Pressure (PAP) setting before surgery.
- If resources allow, facilities should consider having PAP equipment for perioperative use, or have patients bring their own PAP equipment with them to the surgical facility.
- Additional evaluation for preoperative cardiopulmonary optimization should be considered in patients with known, partially treated/untreated and suspected OSA who have uncontrolled systemic conditions e.g. i) hypoventilation syndromes, ii) severe pulmonary hypertension, and iii) resting hypoxemia in the absence of other cardiopulmonary disease.
- Patients with known OSA, partially treated/untreated and suspected OSA with optimized co-morbid conditions may proceed to surgery provided strategies for mitigation of postoperative complications are implemented.
- The risks and benefits of the decision should include consultation and discussion with the surgeon and the patient.
- The use of PAP therapy in previously undiagnosed but suspected OSA patients should be considered case by case. Due to the lack of evidence from randomized controlled trials, we cannot recommend its routine use.
- Continued use of PAP therapy at previously prescribed settings is recommended during periods of sleep while hospitalized, both preoperatively and postoperatively. Adjustments may need to be made to the settings to account for perioperative changes such as facial swelling, fluid shifts, recent pharmacotherapy, and pulmonary function.
The primary goal of this SASM guideline is to ensure optimal pre-operative evaluation of patients with known or suspected OSA in order to improve patient safety. It is hoped that the recommendations from this guideline will influence clinical practice as well as stimulate additional research to address the questions for which there is currently insufficient evidence to support recommendations.
Adequate control of respiratory function under sedation-analgesia remains a challenge for the anesthesiologist because neither respiratory rate, tidal volume, pulse oximetry nor capnography are sensitive and specific enough measures. The present study uses a continuous transcutaneous noninvasive measure of CO2 which directly reflect the efficiency of ventilatory function as a pharmacodynamic endpoint of respiratory depression in response to propofol and remifentanil predicted concentrations to construct a mathematical model based on the data collected from 136 patients.

Meyhoff CS, Wetterslev J, Jorgensen LN, Henneberg SW, Høgdall C, Lundvall L, Svendsen PE, Mollerup H, Lunn TH, Simonsen I, Martinsen KR, Pulawska T, Bundgaard L, Bugge L, Hansen EG, Riber C, Gocht-Jensen P, Walker LR, Bendtsen A, Johansson G, Skovgaard N, Heltø K, Poukinski A, Korshin A, Walli A, Bulut M, Carlsson PS, Rodt SA, Lundbech LB, Rask H, Buch N, Perdawid SK, Reza J, Jensen KV, Carlsen CG, Jensen FS, Rasmussen LSPROXI Trial Group. . Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA. 2009;302:1543–50
26. Pryor KO, Fahey TJ 3rd, Lien CA, Goldstein PA. Surgical site infection and the routine use of perioperative hyperoxia in a general surgical population: a randomized controlled trial. JAMA. 2004;291:79–87
27. Kabon B, Nagele A, Reddy D, Eagon C, Fleshman JW, Sessler DI, Kurz A. Obesity decreases perioperative tissue oxygenation. Anesthesiology. 2004;100:274–80
28. Choban PS, Heckler R, Burge JC, Flancbaum L. Increased incidence of nosocomial infections in obese surgical patients. Am Surg. 1995;61:1001–5
29. Knorst MM, Souza FJ, Martinez D. [Obstructive sleep apnea-hypopnea syndrome: association with gender, obesity and sleepiness-related factors]. J Bras Pneumol. 2008;34:490–6
30. Gallagher SF, Haines KL, Osterlund LG, Mullen M, Downs JB. Postoperative hypoxemia: common, undetected, and unsuspected after bariatric surgery. J Surg Res. 2010;159:622–6
31.

It is recommended to choose anesthetic methods and medicine with minimal impact on child on the basis of ensuring safety and painlessness of children, as well as safety of medical workers meanwhile. For pediatric patients that cry more often and do not cooperate, appropriate sedation can be applied before surgery to reduce the risk of transmission of saliva and droplet. The three-level protection measures are required for anesthesiologists, and one more layer of gloves is necessary before intubation during the endotracheal intubation for general anesthesia, then be removed after the completion of intubation. Medication should be used on those who have venous access as soon as possible to get sedation after entering the room, and sevoflurane inhalation can be applied on those without venous access to get sedation, followed by the establishment of venous access. Before anesthesia induction, double layer of warm and moist gauzes should be used to cover the mouth and nose of patient, followed by mask sustained high flow preoxygenation. It is recommended that to choose rapid anesthesia induction, moderate sedation and sufficient muscle relaxant are necessary to avoid choking cough, and intubation should be performed by skilled pediatric anesthesiologists under optimal conditions for high success rate. In case of difficult airway, the laryngeal mask should be placed after the failure of the first endotracheal intubation (attempt) to avoid the risk of infection caused by repeated attempts of endotracheal intubation. To avoid being close to operating area, the use of visual laryngoscope will be required. The patients with oral secretions could be cleaned with a closed suction system after completion of endotracheal intubation to avoid secretion contamination, if there is no obstruction of respiratory tract. Monitoring should be strengthened during operation, and severe patients are required to be closely monitored and dealt with in time due to the possible existence of acute lung injury, ARDS, heart failure, acid-base imbalance, and electrolyte disorders. At the end of the operation, the endotracheal tube should be removed under deep sedation with strengthening monitoring. It is recommended that complete the sputum suction work before the child wake up and appropriate injection of lidocaine before extubation. The mouth and nose of patient should be covered with two warm and moist gauzes to reduce the secretion spatter caused by choking cough as much as possible.

Morray JP, Geiduschek JM, Caplan RA, Posner KL, Gild WM, Cheney FW: A comparison of pediatric and adult anesthesia closed malpractice claims. A NESTHESIOLOGY 1993; 78: 461–7
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Hypoventilation during sleep is determined by a thorough history of sleep disorder with an oximetry study and a capillary blood gas (See Pulmonary Function Testing). The ventilator requires a nasal or facemask for connection to the airway. The masks are constructed of comfortable plastic with Velcro straps to hold them in place during sleep.
As the vital capacity declines to less than 30 percent of normal, a volume ventilator may also be needed during the day for more assistance. The person gradually will increase the amount of time using the ventilator during the day as needed. A mouthpiece can be used in the daytime and a nasal or facemask can be used during sleep. The machine can easily fit on a ventilator tray on the bottom of a power wheelchair.
There may be times such as during a respiratory infection when a person needs to rest his/her respiratory muscles during the day even when not yet using full-time ventilation. The versatility of the volume ventilator can meet this need, allowing tired breathing muscles to rest and also allowing aerosol medications to be delivered.
Researching a cure
Promising research is being conducted around the globe to find a cure, or at minimum a therapy that is able to mitigate some of the devastating effects of the disease. Finding a cure is made more complex by the number and variation of genetic mutations in the dystrophin gene that result in DMD.
In the area of stem cell research, a recent paper was published in Nature Cell Biology that describes the identification of pericyte-derived cells from human skeletal muscle. These cells have shown to fulfill important criteria for consideration of therapeutic uses. That is, they are easily accessible in postnatal tissue, they are able to grow to a large enough number in vitro to provide enough cells for systemic treatment of a patient, they have been shown to differentiate into skeletal muscle, and, very importantly, they can reach skeletal muscle through a systemic route. This means that they can be injected arterially and cross through arterial walls into muscle, unlike past hopeful therapeutic cells such as muscle satellite cells which require the impractical task of intramuscular injection. These findings show great potential for stem cell therapy of DMD. In this case a small biopsy of skeletal muscle from the patient would be collected, the pericyte-derived cells would be extracted and grown in culture, and then these cells would be injected into the blood stream where they could navigate into and differentiate into skeletal muscle.

"We used a failure mode effect and analysis [FMEA] to identify the potential risks for surgical fire and to look at how we could minimize those risks," says Leanne Bales, RN, CNOR, administrator of the center.
"I like the FMEA approach to potential problems because it is a proactive way to make changes and it gets staff members involved in the process," she notes. The five nurses who worked on the FMEA for fire in the operating room presented their findings to the staff in training sessions that included fire hats for the presenters and fireball jawbreakers for audience members who could answer questions about surgical fire risks, Bales says.
One key to reducing the risk of fire is to recognize the potential for one to happen, she adds.
Awareness of the increased risk of fire when oxygen is in use is key, Greco explains. In fact, he suggests surgeons evaluate their need for oxygen prior to any procedure.
When patients are sedated without an anesthesiologist in an office-based program, surgeons tend to give oxygen routinely because it does ensure the patient maintains a good oxygen saturation rate, Greco says.
However, this is not always necessary, he adds. "If a surgeon uses pulse oximetry to monitor the patient during the procedure and administers oxygen only when necessary, the potential risk of fire is minimized because you’ve removed a combustible gas from the operating room," Greco explains.
If oxygen is used, use the lowest concentration necessary and use it in the open as opposed to allowing it to pool under surgical drapes, he recommends. "If it has to be administered under drapes, be sure you vent or suction the extra oxygen from under the drape," he says.
Finally, if you must use oxygen and you will be using an ignition source such as a laser or Bovie, be sure to turn off the oxygen and allow it to dissipate before turning on the laser or Bovie, Greco suggests. "There is no magic number for the amount of time you must wait for oxygen to dissipate, but any delay before activating a Bovie or laser will reduce the risk of ignition," he says.
The oxygen-use policy at Effingham Surgery Center requires the oxygen to be turned off one minute prior to activating a device such as a cautery, Bales says. "If the cautery is used on the face or neck area, the oxygen must stay off one minute after the cautery is turned off," she adds.

A 21-year-old primigravida was posted for elective caesarean section because of anticipating difficult vaginal delivery in view of the disease at 37 weeks of gestation. There was no family history of polymyositis. On general physical examination, blood pressure was 124/72 mm Hg and pulse was 90/min. Cardiovascular and respiratory systems were normal. Neurological examination revealed a muscle power of 4/5 in most proximal muscle group, compared to distal muscle groups (5/5). Blood biochemistry revealed creatine kinase levels 526 U/L (n <167 U/L). EMG showed myopathic pattern. ECG and echo were normal. She was on the tablet prednisolone 50 mg once a day. Because of fetal distress the obstetrician planned an emergency caesarean section. She was premedicated with metoclopramide 10 mg and ranitidine 50 mg intravenous (iv). Subarachnoid block was given in L3-L4 interspace using 1.8 ml of 0.5% hyperbaric bupivacaine. Adequate sensory block was achieved up to T4. A female baby weighing 2 kg was delivered with APGAR score of 7 and 9 at 5 and 10 min respectively. She had one episode of hypotension, which was corrected by mephentermine 3 mg iv. Postoperative course was uneventful. The patient was continued on oral prednisolone in the postoperative period.
Patients with polymyositis are at increased risk of pulmonary aspiration. Further, there are other implications of general anesthesia in these patients. Volatile anesthetic agents may not only serve as a trigger of malignant hyperthermia but also potentiate the effects of muscle relaxants. It is recommended that these agents should be avoided in these patients more so with raised plasma creatine phosphokinase levels. These patients are supposed to be sensitive to nondepolarizing muscle relaxants, and use of their antagonist drugs may cause muscle weakness and dysrhyhmias.  Vecuronium and pancuronium are associated with prolonged neuromuscular paralysis though atracurium has been implemented as a safe drug under neuromuscular monitoring.

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- Fukushima KY, Yatsuhashi H, Kinoshita A, Ueki T, Matsumoto T, et al. (2007) Two cases of hepatopulmonary syndrome with improved liver function following long-term oxygen therapy. J Gastroenterol 42: 176-180.
- Peñaloza D, Sime F, Banchero N, Gamboa R, Cruz J, et al. (1963) Pulmonary hypertension in healthy men born and living at high altitudes. Am J Cardiol 11: 150-157.
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Currently Schwann cell transplantation is under investigation.
[Table 1] shows the clinical picture in MS with its anaesthetic implications. ,,
Literature regarding anaesthetic management contains use of general anaesthesia (GA), spinal and epidural techniques. GA and epidural with low concentrations of LA are considered safe. ,, Spinal anaesthesia has been implicated in postoperative exacerbation, , so also epidurals with higher concentrations and longer duration. , The demyelinated neurons appear susceptible to the neurotoxicity of LA and aggravate the conduction blockade. ,, As regards conduct of G.A no particular agent among induction agents/inhalation agents is preferred. , Succinylcholine is best avoided as it can produce hyperkalemia due to denervation sensitivity by upregulation of acetylcholine receptors. sup>,
The latter can also cause resistance to non-depolarizing blocking agents (NDBA).  Sensitivity to NDBAs can also be present due to muscle wasting and use of medications such as baclofen, dantrolene , [Table 1]. N-M monitoring is recommended with titration of the NDBA as required for the surgery. , Even a 0.5°C rise of temperature can slow the conduction along the demyelinated segment ,, resulting in relapse, hence maintenance of O.T temperature and temperature monitoring is essential.
In spite of prolonged periods of immobility, MS patients surprisingly showed the absence of thrombophlebitis and pulmonary embolism (PE) in contrast to other immobile patients suffering from stroke, quadriplegia and flaccid paraplegia.  The presence of lower extremity spastic disease in MS patients appears to protect them from thrombophlebitis and PE, as the occurrence of muscle spasms could prevent venous stasis.
Cerebral venous thrombosis (CVT) has been reported in MS exacerbation patients who underwent lumbar puncture (L.P) and were receiving I.V. methylprednisolone.  Following L.P, high dose corticosteroids are considered as risk factors for CVT and prophylactic anticoagulant treatment may be warranted when other risk factors of CVT also exist. sup>
As MRI scan of our patient showed involvement of cervical and upper thoracic segments, to detect autonomic dysfunction preoperatively we tested heart rate response to deep breathing.