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!”

Or:

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 the 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 place the patient on 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 GI obstruction, achalasia, a BMI of 70, or a reason why you need 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 down the hall?

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” is 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.

True 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 suffer from laryngospasm for multiple reasons, not solely as a response to extubation during “Stage 2”. Laryngospasm can happen due to GE reflux, or reactive airways disease, or upon induction of anesthesia. It has occurred in the PACU. I was once called into an operating room 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 deep 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.”  The persistence of many anesthesiologists in believing after more than 50 years that positive pressure will relieve complete laryngospasm confirms my impression that evidence is applied selectively to support existing belief systems, and only on occasion to alter, guide, or improve clinical care.

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 by applying substantial upward pressure at the angle of the jaw to relieve any upper airway obstruction. Watch to see if air movement resumes.

If elevating the jaw 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 workup, 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.

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.

Karen S. Sibert is an anesthesiologist who blogs at A Penned Point.  

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