Physician anesthesiologist at Stanford at Associated Anesthesiologists Medical Group
Richard Novak, MD is a Stanford physician board certified in anesthesiology and internal medicine.Dr. Novak is an Adjunct Clinical Professor in the Department of Anesthesiology, Perioperative and Pain Medicine at Stanford University, the Medical Director at Waverley Surgery Center in Palo Alto, California, and a member of the Associated Anesthesiologists Medical Group in Palo Alto, California.
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Anoxic brain injury. These three words make any anesthesiologist cringe. In layman’s terms, anoxic brain injury, or anoxic encephalopathy, means “the brain is deprived of oxygen.”

Five minutes stopwatch


In an anesthetic disaster the brain can be deprived of oxygen. Without oxygen, brain cells die, and once they die they do not regenerate. If something dire goes wrong during anesthesia and surgery and the flow of oxygen to the brain is cut off, an anesthesia practitioner has about five minutes to diagnose the cause of the problem and treat it. Some brain cells start dying within five minutes after the oxygen supply disappears, and brain hypoxia can rapidly cause severe brain damage or death. (1,2)

In malpractice cases I’ve consulted on, a five-minute window is an accepted duration for low blood oxygen levels to cause permanent brain damage.

The good news is that catastrophic events causing sudden drops in oxygen levels are very rare during anesthesia. I’ve reviewed the risks of anesthesia in the 21st Century in a previous column, which I refer you to.

Miller’s Anesthesia is the premier textbook in anesthesiology. I respect Miller’s Anesthesia as an outstanding reference, but a keyword search for “anoxic encephalopathy” in Miller’s Anesthesia only links to two chapters: one on temperature regulation, and second on pediatric intensive care. The topic of anoxic encephalopathy as related to anesthesia disasters and brain death—a issue that can ruin both a patient’s life and an anesthesiologist’s career—is not specifically covered in Miller’s Anesthesia.

Anesthesiologists are human, and human error is known to seep into anesthesia care. Miller’s Anesthesia, Chapter 7 on Human Performance and Patient Safety,3 makes several statements pertinent to human error:

“. . . anesthesia professionals themselves, both as a profession and as individuals, have strengths and vulnerabilities pertaining to their work environment. The performance of human beings is incredibly flexible and powerful in some aspects but very limited in others. Humans are vulnerable to distractions, biases, and errors.”  

“The stakes are high because even for elective surgery in healthy patients, there is an ever-present and very real risk of injury, brain damage, or even death. A catastrophe is often the end result of many pathways that begin with seemingly innocuous triggering events. . . .”

“Because more than 70% of all errors in medicine can be attributed to problems with human factors rather than problems with knowledge or practical skills, the impact of human factors cannot be overestimated.

My impression, based on 34 years in an anesthesia career, is that some anesthesia practitioners perform better under pressure. Just like Joe Montana had the knack for doing the right thing on a football field when the pressure was on, and just like Sully (Chesley Sullenberger) made correct decisions when the jet engines of US Airways Flight 1549 were knocked out by collisions with birds shortly after takeoff, some anesthesia practitioners perform well under intense pressure . . . and some don’t.

Let me present two examples, inspired by real cases, of relatively healthy young patients who had unexpected hypoxic (low oxygen) episodes. These patients had drastically different outcomes due to different anesthetic care:


A 40-year-old male presented for outpatient septoplasty surgery. His past medical history was positive for obesity (weight=100 kg with a BMI=32) and hypertension. His preoperative vital signs were normal with an oxygen saturation of 98%.

Anesthesia was induced with propofol 250 mg, fentanyl 100 micrograms, and rocuronium 50 mg IV. An endotracheal tube was easily placed, and breath sounds were equal bilaterally. Anesthesia was maintained with oxygen, nitrous oxide, and sevoflurane 1.5%, and incremental doses of 50 micrograms of fentanyl.

The surgery concluded 2 hours later, and the nitrous oxide and sevoflurane were discontinued. The patient began to cough, and reached up to try to pull out his endotracheal tube. The anesthesiologist decided to extubate the trachea. After extubation the patient was making respiratory efforts, but no airflow was noted. A jaw thrust attempt to break suspected laryngospasm was ineffective. The oxygen saturation dropped to 78%.

  • Succinylcholine 40 mg was administered. There was no improvement in the oxygenation or airway.
  • Two minutes later a second dose of succinylcholine 60 mg was administered. There was continued inability to move oxygen.
  • Two minutes later, a #4 LMA was placed, with continued inability to move oxygen.
  • Two minutes later the anesthesiologist attempted to reintubate the trachea. The first attempt was unsuccessful due to poor visibility. The oxygen saturation dropped to 50%.
  • Seven minutes after the initial oxygen desaturation to 78%, a second laryngoscopy using a GlideScope was successful, and a 7.0 ET tube was placed. Copious secretions were suctioned out of the ET tube. Ventilation remained difficult and peak inspiration pressures were high. The patient continued to be hypoxic. The patient’s ECG deteriorated into pulseless electrical activity (PEA), and chest compressions were initiated. Epinephrine 1 mg was administered IV twice, the peripheral pulses returned, and chest compressions were stopped.
  • Twenty minutes after the oxygen desaturation to 78%, the oxygen saturation finally rose to 94%. A chest x-ray showed pulmonary edema. The diagnosis was laryngospasm leading to negative pressure pulmonary edema. Furosemide 20 mg was administered IV. The patient remained on a ventilator in the ICU for seven days, at which time he was declared brain dead.


A 30-year-old male was scheduled for maxillary and mandibular osteotomies for obstructive sleep apnea. He was otherwise healthy. He weighed 80 kg and had a BMI=26. His preoperative vital signs were normal.

Anesthesia was induced with propofol 250 mg and rocuronium 50 IV, and a right cuffed nasal endotracheal tube was placed. Breath sounds were bilateral and equal. Anesthesia was maintained with sevoflurane 1.5%, nitrous oxide 50%, propofol 50 mcg/kg/hr, and incremental doses of 50 mcg fentanyl. The surgery concluded 4 hours later. The surgeons wired the upper and lower teeth together. The propofol, sevoflurane, and nitrous oxide were discontinued.

The patient opened his eyes ten minutes later, and responded appropriately to conversation. The endotracheal tube was removed, and the patient’s airway was patent. He was moved to the gurney, the back of the gurney was elevated 30 degrees, and a non-rebreather mask with a 10 liters/minute flow rate of oxygen was strapped over his face. The anesthesiologist then transported the patient down the hallway to the PACU. En route the patient became more somnolent and developed upper airway obstruction resistant to jaw thrust maneuvers.

  • On arrival at the PACU the patient was nonresponsive, and his initial oxygen saturation was 75%. The anesthesiologist began mask ventilation via an Ambu bag, and the oxygen saturation rose to 90%. The patient was making ventilatory efforts without significant air movement.
  • The wires fixating the maxilla and mandible together were severed with a wire cutter.
  • The anesthesiologist attempted laryngoscopy with a Miller 2 blade, and was unable to visualize the larynx because of frothing fluid bubbling in the oropharynx. A presumptive diagnosis of negative pressure pulmonary edema was made, and a GlideScope was called for. The oxygen saturation was 88%.
  • After suctioning the frothy fluid which filled the oropharynx, a second laryngoscopy attempt with the GlideScope yielded successful placement of a 7.0 oral endotracheal tube. Pulmonary edema fluid was suctioned from the lumen of the endotracheal tube, and furosemide 20 mg was injected IV. The oxygen saturation rose to 98% on 100% oxygen.

The duration of time from when the patient’s oxygen level was discovered to be 75% until his oxygen level rose above 90% was two minutes. The duration of time from when the patient’s oxygen level was discovered to be 75% until the trachea was successfully reintubated was four minutes.

The patient remained intubated in the ICU for two nights, with diagnoses of upper airway edema post maxillary-mandibular osteotomies and negative pressure pulmonary edema. He was extubated on post-op day #3, when he successfully passed a cuff-leak test. His oxygen saturations were normal and his brain was undamaged. He walked out the hospital alive and well.

Case #1 and Case #2 were similar in that both patients were young relatively healthy men having head and neck surgery. The expected risk of serious complication for each procedure was low. The expected risk of death, or of brain death, was extremely small. Yet one man died and the other survived.


In Case #1, a case study based on a closed claim malpractice settlement, the delays in anesthesia care led to prolonged low oxygen levels, and these prolonged low oxygen levels caused anoxic brain damage. The deviations from the standard of care included:

  1. The patient was extubated too early, at a time when he was still partially anesthetized, in a transitional phase of anesthesia, and not yet awake. The safest technique for extubation is awake extubation, when the patient is an awake state of eye opening and obeying commands. Per the Difficult Airway Society Guidelines for the Management of Tracheal Extubation, an awake intubation is when “the patient’s eyes are open and the patient is responsive to commands.”4 This patient had head and neck surgery, and was at risk for post-operative airway problems. Extubating before the patient opened his eyes and obeyed verbal commands was a deviation from the standard of care.
  2. Once the patient developed post-extubation laryngospasm, the standard of care was for the anesthesiologist to act immediately to relieve airway obstruction and correct hypoxemia. Laryngospasm can lead to hypoxia, as it did in this case. The order of treatment is A-B-C, or Airway–Breathing–Circulation. When the immediate application of jaw thrust and continuous positive airway pressure via facemask was unsuccessful, and the oxygen saturation dropped into the 70’s, the standard of care was to immediately paralyze the patient with an intubating dose of succinylcholine (1 mg/kg IV) and to reinsert an endotracheal tube. Per Difficult Airway Society Guidelines for the Management of Tracheal Extubation, “If laryngospasm persists and/or oxygen saturation is falling: (administer) succinylcholine 1 mg/kg intravenously. Worsening hypoxia in the face of continuing severe laryngospasm with total cord closure . . . requires immediate treatment with intravenous succinylcholine. The rational for 1 mg/kg is to provide cord relaxation, permitting ventilation, re-oxygenation and intubation should it be necessary.”4 The entire time from the onset of laryngospasm to the successful control of the airway and ventilation of the lungs in Case #1 exceeded 20 minutes.

When a bad outcome like this occurs in a hospital or surgery center, a facility’s Quality Assurance Committee examines the details of the case—not to assign blame—but to identify flaws in patient care systems which must be improved in the future.

When a patient’s family hires a lawyer to investigate a bad outcome, the same analysis of the medical record and the medical details occurs, but the stakes are different. Physicians and facilities carry malpractice insurance with limits in the millions of dollars. If a physician or a facility is found to have performed below the standard of care, and if that negligent performance is found to have caused patient damage, they may well lose a malpractice settlement. The minute-by-minute pulse oximetry data will be scrutinized during any ensuing malpractice trial or deposition, with an aim to document how many minutes the oxygen saturation was critically low. A time frame of five minutes or greater of hypoxia in the medical record can be damning for the anesthesiologist’s case.

In the Miller’s Anesthesia chapter titled Human Performance and Patient Safety, Drs. Rall and Gaba describe 15 Key Points of Crisis Resource Management (CRM).3 Highlights of the Key Points include:

  • CRM Key Point 2. Anticipate and Plan. “Anesthesia professionals must consider the requirements of a case in advance and plan for the key milestone. They must imagine what could go wrong and plan ahead for each possible difficulty. Savvy anesthesia professionals expect the unexpected, and when it does strike, they then anticipate what could happen next and prepare for the worst.”
  • CRM Key Point 3. Call for Help Early.
  • CRM Key Point 4. Exercise Leadership and Followership With Assertiveness. “A team needs a leader. Someone has to take command, distribute tasks, collect information, and make key decisions. . . . Followers are key members of the team who listen to what the team leader says and do what is needed.”
  • CRM Key Point 8. Use All Available Information. “Information sources include those immediately at hand (the patient, monitors, the anesthesia record), secondary sources such as the patient’s chart, and external sources such as cognitive aids (see later) or even the Internet.”
  • CRM Key Point 11. Use Cognitive Aids. “Cognitive aids—such as checklists, handbooks, calculators, and advice hotlines—come in different forms but serve similar functions. They make knowledge “explicit” and “in the world” rather than only being implicit, in someone’s brain.” An example cognitive aid is the Stanford Emergency Manual, which I recommend.5

Dr. David Gaba, one of the authors of this chapter, is a longtime friend of mine and a pioneer in the fields of anesthesia simulator design and crisis management. I respect this list of 15 CRM Key Points, but I also know that when the clock is ticking on those five minutes of patient hypoxia, there is no time to think through 15 items. There is no time for any wasted effort or motions. The anesthesia provider must captain the ship and restore oxygenation without delay. The anesthesia provider needs a plan embedded in his or her brainstem that allows them to keep the patient safe.

Based on my experience as both a practicing anesthesiologist for over 30 years and an expert witness for over 15 years, when your patient’s oxygen level drops acutely, these are the things you need to DO:

  1. First off, turn your oxygen supply to 100% oxygen. Turn off all nitrous oxide or air input.
  2. Call for help.
  3. Think A-B-C, or Airway-Breathing-Circulation, in that order.
  4. Examine the patient, particularly their airway and lungs.
  5. If the patient is not already intubated, and you cannot mask ventilate the patient to a safe oxygen level, intubate the trachea immediately to deliver 100% oxygen via controlled ventilation. Use succinylcholine, the fastest emergency paralytic drug.
  6. If you cannot intubate the patient with a traditional Miller 2 or Mac 3 blade, request a GlideScope videoscope ASAP. (Have the American Society of Anesthesiologists Difficult Airway Algorithm committed to memory.)
  7. Have the Stanford Emergency Manual5 in your operating room suite, and ask a registered nurse to recite the Cognitive Aid Checklist for HYPOXEMIA to you, to make sure you haven’t missed something.
  8. If the patient is still not improving, reaffirm your assessments of A-B-C. Fix the Airway, fix the B, then fix the Circulation.
  9. Remember: ACLS (Acute Cardiac Life Support) is important, but ACLS is C, and if A and B are faulty, the cardiac care of ACLS will not save the brain.

Other advice to anesthesiologists:

  • Before a hypoxic emergency occurs in your practice, do yourself and your patients a favor by passing the American Board of Anesthesiologists oral board examination. The time spent studying for the oral boards will make you a safer and smarter anesthesiologist who is better prepared to handle emergency situations. A study in the journal Anesthesiology showed rates for death and failure to rescue from crises were greater when anesthesia care was delivered by non-board certified midcareer anesthesiologists.6 In the Stanford Department of Anesthesiology, Perioperative and Pain Medicine, we administer mock oral board examinations to the residents and fellows twice a year. Presenting an examinee with a sudden hypoxic episode is a common occurrence during the exam. If you can think well in a room in front of two examiners, you are more likely to think well in a true hypoxemic emergency when your patient’s life is at stake.
  • A second tip: If you have access to anesthesia simulator sessions, enroll yourself.

What if you’re a patient reading this? What if you’re contemplating surgery? How can you optimize your chances to avoid an anesthetic disaster?

I offer these suggestions:

  • Choose to have your surgery at a facility that is staffed with American Board of Anesthesiology board-certified physician anesthesiologists.
  • Ask a knowledgeable medical professional to recommend a specific anesthesiologist at your facility, and request that specific anesthesiologist for your care.
  • Inquire about who would manage your crisis if you have one during or after your surgery. Will your anesthesia professional be a physician anesthesiologist, a Certified Registered Nurse Anesthetist (CRNA), or an anesthesia care team made up of both? If an anesthesia care team is attending to you, how many rooms is each physician anesthesiologist supervising? How far away or how many minutes away will your physician anesthesiologist be while you are asleep?
  • In the future, quality of care data will be available on facilities and physicians, including anesthesiologists. These metrics will allow patients to compare facilities and physicians. Do your homework with whatever data is publicized. Research the facility you are about to be anesthetized in.
  • If you’re a higher risk patient, i.e. you have: significant obesity, obstructive sleep apnea, heart problems, breathing problems, age > 65, or you’re having regular dialysis, emergency surgery, abdominal surgery, chest surgery, major vascular surgery, cardiac surgery, brain surgery, regular dialysis, total joint replacement, or a surgery with a risk of high blood loss . . . be aware you’re at a higher risk, and ask more questions of your surgeon and your anesthesia provider.
  • If yours is an elective surgery, realize you have time to heed the advice in this column. Take your time to choose your surgeon, your facility, and your anesthesia provider if you can.

None of us, anesthesia providers or the families of patients, want to be sitting in a courtroom for a malpractice trial because there were five bad minutes without oxygen.


  3. Rall M, Gaba D, et al. Human Performance and Patient Safety. Miller’s Anesthesia, Chapter 7, Eighth Edition, p 106-166.
  4. Popat M, Mitchell V, et al. Difficult Airway Society Guidelines for the management of tracheal extubation, Anaesthesia 2012, 67, 318-340.
  5. Stanford Anesthesia Cognitive Aid Group. Emergency Manual: Cognitive aids for perioperative clinical events. *Core contributors in random order: Howard SK, Chu LK, Goldhaber-Fiebert SN, Gaba DM, Harrison TK
  6. Silber JH et al. Anesthesiologist Board Certification and Patient Outcomes. Anesthesiology.2002 May;96(5):1044-52.

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Will I Have a Breathing Tube During Anesthesia?

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