Posts Tagged ‘Laryngospasm’

The art of deep extubation

Fair warning — this post is likely to be of interest only to professionals who administer anesthesia or may have to deal with laryngospasm in emergency situations.

There are two schools of thought about how to extubate patients at the conclusion of general anesthesia:

Allow the patient to wake up with the endotracheal tube in place, gagging on the tube and flailing like a fish on a line, while someone behind the patient’s head bleats, “Open your eyes!  Take a deep breath!”


Remove the endotracheal tube while the patient is still sleeping peacefully, which results in the smooth emergence from anesthesia like waking from a nap.

It will not require much subtlety of perception to guess that I prefer option 2. It is quiet, elegant, and people who’ve seen it done properly often remark that they would prefer to wake from anesthesia that way, given the choice.

There is art and logic to it, which I had the pleasure of learning from British anesthesiologists at the Yale University School of Medicine years ago. Here are time-tested steps:

Allow the patient to resume breathing spontaneously, making sure that muscle relaxation is completely reversed and anti-emetic medication has been given. Deep extubation is most easily done with inhalation anesthesia and minimal narcotic use. Do not reduce the amount of inhaled anesthetic toward the end of the case.

Make sure that tidal volume is adequate, and that the respiratory rate is less than 25. If the patient is breathing rapidly, titrate small amounts of a long-acting IV opioid (hydromorphone, morphine) until the respiratory rate settles down.

Insert an appropriately sized oral airway, and use a suction catheter to suction down the center of the airway and beside it on each side. Secretions are the enemy.

If the patient reacts at all to suctioning, he or she is not deeply enough asleep. Titrate small amounts of IV opioid or propofol, and/or give 1 mg/kg IV lidocaine. Suction again; confirm that the level of anesthesia is deep and that the patient does not react but is still breathing well.

Deflate the cuff and remove the tube. Discontinue the inhaled anesthetic. My preference is to have the patient breathe supplemental oxygen via a transport face mask rather than to use the anesthesia circuit and mask, because there is no need for further inhaled anesthesia.

Turn the patient’s face slightly to one side and gently lift the chin and/or mandible. Make sure that the patient is exchanging air well. It is not uncommon for the patient to hold his/her breath momentarily just after extubation, but breathing will resume, I promise. There is no need to intervene. Continue to support the chin or mandible until the patient is able to maintain a patent airway without assistance. Remove the oral airway as soon as the patient begins to react to it, to avoid biting or gagging.

Frequently asked questions

Is deep extubation dangerous?

With improper patient selection, it certainly could be. This is not the technique for the patient with a full stomach, ileus, GI obstruction, achalasia, a BMI of 70, or a reason why you might choose to intubate awake. It is appropriate for most patients who walk into the hospital breathing room air, are scheduled for elective surgery, have fasted, are not morbidly obese, and are not chronic CO2 retainers. If your plan is to induce anesthesia and mask ventilate prior to intubation, it is likely that deep extubation will be safe and feasible.

What if the patient goes into “Stage 2” on the way from the OR to PACU?

This question reflects a misunderstanding of the definition of “Stage 2” anesthesia. The stages of mask induction with diethyl ether anesthesia were described by Dr. Arthur Guedel in a 1920 article, and later in a 1937 textbook. He characterized “Stage 2” as the “delirium” stage, with rapid eyeball activity, swallowing, and possible vomiting.

We no longer use diethyl ether, and modern balanced anesthesia utilizes multiple different anesthetic medications for hypnosis, analgesia, and anti-emesis. There really is no “Stage 2” anesthesia, either on induction or emergence. Today “Stage 2”, in my opinion, has become a tale handed down by attending anesthesiologists from generation to generation to frighten the children and justify the unpleasantness of awake extubation.

Occasionally patients may exhibit signs of excitement on emergence. This occurs more often with younger patients, but may happen at any age. If the patient should move unpredictably, and isn’t awake enough yet to cooperate, a small dose of IV propofol will calm the patient and this phase will pass. For this reason, the prudent anesthesiologist will always have propofol in his/her pocket during any patient transport.

Emergence delirium and postoperative cognitive dysfunction are genuine medical problems, but are not related to the timing of extubation.

What about the risk of laryngospasm?

This is one of the old wives’ tales of anesthesiology. A patient may experience laryngospasm for multiple reasons, not solely as a response to extubation during “Stage 2”. Laryngospasm can happen in awake patients due to GE reflux or reactive airways disease, or upon induction of anesthesia in adults or children. It has occurred in the PACU. I was called into an operating room one day to assist in the care of a patient who had gone into laryngospasm at the end of her procedure, sitting bolt upright on the gurney, desperately trying to breathe but as blue as a Smurf. Awake extubation is no guarantee of immunity from laryngospasm.

There is a tendency to confuse inspiratory stridor with true laryngospasm. Inspiratory stridor may occur briefly after extubation, and may be relieved by elevating the mandible and opening the airway. Administration of 0.5-1 mg IV lidocaine may help as well. As the patient continues to emerge from anesthesia, inspiratory stridor will resolve on its own.

True laryngospasm is characterized by the complete absence of air movement or sound despite vigorous attempts to breathe. Obstruction of the airway occurs at the level of the true vocal cords, the false cords, and the redundant supraglottic tissue. This creates a ball-valve obstruction, controlled by the intrinsic and extrinsic laryngeal muscles.

Here is the most important point:

Applying positive pressure will not relieve true laryngospasm, and may worsen it, because it will press the aryepiglottic folds more firmly against each other and reinforce the closure.

This phenomenon was described elegantly by Dr. Bernard Fink in his classic article published in Anesthesiology in 1956, “The Etiology and Treatment of Laryngeal Spasm”, and reiterated more recently in a letter to the editor. The persistence of many anesthesiologists in believing after more than 50 years that positive pressure will “break” complete laryngospasm confirms my impression that the principles of “evidence-based medicine” are applied or ignored selectively if they challenge entrenched belief systems.

How should complete laryngospasm be managed?

If a patient at any stage of care is in true laryngospasm, characterized by attempts to breathe with no sound, no air movement, no chest rise, and a visible tracheal tug, positive pressure ventilation will be useless.

The first step is to elevate the mandible and apply firm upward pressure just behind and above the angle of the jaw — the so-called “laryngospasm notch“. (Click here to watch a NEJM video of this technique, known as the Larson maneuver.) Watch to see if air movement resumes.

If this maneuver does not work within a breath or two, however, the next step is to make the patient apneic. If the patient continues to try to breathe against a closed glottis, there is a risk that the patient will develop negative pressure pulmonary edema. This will cause no end of problems, including an extremely expensive cardiac work-up, extended hospitalization, and potential lawsuit.

Apnea may be achieved with enough propofol, or with a small amount of any muscle relaxant. Succinylcholine is the classic treatment; even 10 mg IV will suffice, but make sure the patient is asleep first. Assure adequate oxygenation with mask ventilation, suction any secretions, and then permit the patient to resume spontaneous ventilation and wake up. It isn’t always necessary to reintubate.

Laryngospasm should be neither life-threatening to the patient, nor terrifying to the anesthesiologist, if the pathophysiology and treatment are clearly understood and the right plan of care is promptly initiated.

Why bother with deep extubation when awake is easier?

There are many surgical situations where deep extubation is desirable: hernia repair, thyroidectomy, plastic surgery procedures, any major abdominal procedure where coughing will strain the repair, ophthalmology procedures, cervical spine surgery — the list goes on. With today’s modern insoluble anesthetics, emergence from anesthesia is rapid and outpatient discharge need not be delayed. Deep extubation is a useful technique for any anesthesiologist to master, and it is a key part of the art as well as the science of anesthesiology.

New York Post reporter Susan Edelman revealed on January 4 the name of the unfortunate anesthesiologist allegedly present on August 28 at Yorkville Endoscopy, during the throat procedure that led to the death of comedian Joan Rivers. She is reported to be Renuka Reddy Bankulla, MD, 47, a board-certified anesthesiologist from New Rochelle, NY.

Having her name made public will be a nightmare for Dr. Bankulla, as investigators will certainly target her role in Ms. Rivers’ sedation and the management — or mismanagement — of her resuscitation.

When the news of Ms. Rivers’ cardiac arrest and transfer to Mt. Sinai Hospital became public, many of us guessed that there might have been no qualified anesthesia practitioner — either anesthesiologist or nurse anesthetist — present during the case. The gastroenterologist and then medical director of the clinic, Dr. Lawrence Cohen, argued famously that the sedative propofol, which Ms. Rivers received, could be safely given by a registered nurse under his supervision, and that no anesthesiologist is necessary.

However, with the publication of the Centers for Medicare & Medicaid Services (CMS) report of September 5, it became clear that an anesthesiologist was definitely present. The anesthesiologist was identified only as “Staff #2” in the report. She was interviewed by the CMS surveyors four days after the event, but said she was “advised by her legal representative not to discuss the case.”

Key pieces of information about what happened still haven’t been made public. Nonetheless, the surveyors gathered enough information to reach this conclusion:  “The physicians in charge of the care of the patient failed to identify deteriorating vital signs and provide timely intervention during the procedure.”

By any standard of care, the anesthesiologist clearly would be one of the physicians in charge.

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The ear, nose and throat specialist who treated comedian Joan Rivers on August 28 has been identified as Dr. Gwen Korovin, a prominent New York physician who is known as a voice doctor to many entertainers and Broadway stars including Hugh Jackman and Julie Andrews.

With a physician who is an expert in airway anatomy at her side, and all the technologic advantages of a modern clinic in Manhattan’s upper east side, the 81-year-old Ms. Rivers must have anticipated an uneventful procedure. Instead, she stopped breathing and suffered cardiac arrest. The question remains:  What went wrong?

Credentials questioned

Several sources have reported that Dr. Korovin had not completed usual credentialing procedures at Yorkville Endoscopy, and did not have privileges to do anything but observe on the day Ms. Rivers was treated.

In fairness, the credentialing process at a hospital or ambulatory surgery center (ASC) simply reviews documentation that the physician is qualified to perform procedures, and grants the physician privileges to practice there. Physicians choose where they want to work, and don’t necessarily maintain privileges at more than one hospital or ASC.  A lack of privileges doesn’t imply a lack of experience or training; it simply means that the physician hasn’t gone through credentialing steps at that facility.

In Dr. Korovin’s case, her attorney’s statement notes that she “maintains privileges at one of the city’s most prestigious hospitals.” Her prominence in Manhattan may have led to an assumption that her credentials at Yorkville Endoscopy were in order, although it is the responsibility of each facility and its medical director to make sure.  Dr. Lawrence Cohen, Ms. Rivers’ gastroenterologist, was the medical director of Yorkville Endoscopy at the time of Ms. Rivers’ treatment, and has since resigned.

Critical lack of oxygen?

Ms. Rivers suffered cardiac and respiratory arrest while at Yorkville Endoscopy for evaluation of why her voice was getting raspier. She was resuscitated and transferred to a nearby hospital, but died a week later after discontinuation of life support.

Initial autopsy results were inconclusive, according to CNN’s report of a statement from the medical examiner’s office, meaning that no obvious cause of death was clear, and more tests will be done.  This information appears to rule out some causes of sudden cardiac arrest such as pulmonary embolism, the formation of a large clot that stops blood flow through the lungs.

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Since the death of comedian and talk-show host Joan Rivers, more information has surfaced about the events on the morning of August 28 at Yorkville Endoscopy. But key questions remain unanswered.

News accounts agree that Ms. Rivers sought medical advice because her famous voice was becoming increasingly raspy. This could be caused by a polyp or tumor on the vocal cords, or by acid reflux irritating the throat, among other possible causes.

So Ms. Rivers underwent an endoscopy by Dr. Lawrence B. Cohen, a prominent gastroenterologist, to evaluate her esophagus and stomach for signs of acid reflux. At the same time, a specialist in diseases of the ear, nose, and throat (ENT) reportedly examined her vocal cords (also known as vocal folds).

We don’t know exactly how much or what type of sedation Ms. Rivers’ may have received, though several news sources have reported that she was given propofol, the sedative associated with the death of Michael Jackson. No physician who specializes in anesthesiology has been identified on the team taking care of Ms. Rivers, and we don’t know who was in charge of giving her propofol.

It seems clear that at some point during Ms. Rivers’ endoscopy and vocal cord examination, there was a critical lack of oxygen in her bloodstream.

Was laryngospasm the cause?

Giving sedation for upper endoscopy is tricky, as any anesthesia practitioner will tell you. A large black endoscope takes up space in the mouth and may obstruct breathing. Any sedative will tend to blunt the patient’s normal drive to breathe. But most patients breathe well enough during the procedure, and go home with no complaints other than a mild sore throat.

News reports have speculated that the root cause of Ms. Rivers’ rapid deterioration during the procedure could have been laryngospasm. This term means literally that the larynx, or voice box, goes into spasm, and the vocal cords snap completely shut. No air can enter, and of course the oxygen in the bloodstream is rapidly used up.

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