Latest posts by the anesthesia consultant (see all)
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Prior to surgery your patient tells you, “I always have a hangover after general anesthesia. I sleep for hours and I’m nauseated. All my life I’ve been very sensitive to medications. I never drink alcohol, and even a ½ dose of Nyquil or cold medicine knocks me out all night.”
What do you do with this information?
I’ve been a full time anesthesiologist for 34 years, and I’ve heard this monologue from patients countless times. My impression? The patient is always right. They’ve had the same body all their lives, and they know their reaction to central nervous system depressants. Listen to them and adjust your care.
Hangover after general anesthesia (HAGA) describes a patient who has a safe general anesthetic, but who then feels hungover, sedated, and wasted for a time period exceeding two hours afterwards. There is significant overlap between HAGA and postoperative nausea and vomiting (PONV).
The four established risk factors for PONV are: 1) the use of postoperative narcotic pain relievers, 2) female sex, 3) a non-cigarette smoker, and 4) a previous history of PONV.1 In my experience, these same four characteristics are risk factors for HAGA. Painful surgeries require more narcotics, which can lead to more nauseated patients. If the surgery isn’t painful, an anesthesia provider can work to eliminate postoperative narcotics, and minimize both PONV and HAGA.
With modern pharmacology and anesthetic techniques, HAGA should be uncommon. Propofol and sevoflurane are the mainstays of 21st century general anesthesia. Both are ultra-short acting medications that enable anesthesiologists to produce alert, awake patients within an hour of most general anesthetics.
Propofol has a quick onset and quick offset clinical effect, because the drug is highly lipid soluble and is rapidly distributed out of the bloodstream to other tissues of the body. When administration of propofol is discontinued, the initial fall in the plasma concentration is 50% due to this redistribution and 50% due to liver metabolism. The time to awakening after a 2-hour anesthetic is rapid (8-19 minutes).2 The elimination (hepatic) half-life is 3 to 12 hours, but propofol is not known to cause nausea. Hangover symptoms from propofol are rare. Sleepiness is the most common side effect, and this clears quickly.
Sevoflurane also has a quick onset and quick offset. Sevoflurane vapor is primarily eliminated via ventilation from the lungs. Because the drug has low solubility in the bloodstream, the pulmonary elimination is rapid, and only 5% of sevoflurane remains in the body to be metabolized by the liver and excreted via the kidneys. Pertinent mild side effects of sevoflurane include nausea/early 25%, vomiting/early 18%, dizziness/early 4%.3 These incidences of nausea and vomiting are higher than for propofol, so utilization of propofol over sevoflurane seems prudent for patients with a history of HAGA or PONV. However, because propofol is a sedative/hypnotic and does little to provide surgical analgesia, the addition of either a potent vapor such as sevoflurane or a narcotic is often necessary.
Over the years I’ve examined previous anesthetic records for many patients with a history of HAGA. The most common findings in these old records are relative overdoses of narcotics, be it fentanyl, Dilaudid, morphine, or any another narcotic. My impression is that some anesthesia providers rely on a set recipe for their narcotic dosing, and that they do not adequately alter or adjust this recipe for patients who are small, petite, elderly, or teetotalers. Narcotics are often indicated during surgery when surgical stimulus peaks, or near the conclusion of surgery to insure a patient has an adequate systemic narcotic effect and won’t wake up in agony. When a patient has a history of HAGA or PONV, I recommend minimizing the amount of intraoperative IV narcotics. Additional IV narcotics can be added post-extubation if the patient complains of significant pain.
Anesthesia providers typically judge anesthetic dosing depending on: a) patient weight, b) patient age, and c) the patient’s vital signs (i.e. high blood pressure and/or heart rates are treated by increasing doses of drugs, and low blood pressures are treated with decreasing drug administration).
A patient’s weight can be misleading. Multiple studies support that drug doses should be based on lean body weight (LBW) rather than their total weight.4,5 A 5-foot-6-inch obese patient may weight 200 pounds but have an estimated LBW of 150 pounds. Injected drug doses need to reduced by a factor of 150/200, or ¾.
Patients at extremes of age, e.g. geriatric or neonatal patients, can have significantly reduced requirements for injected anesthetic drugs. I refer the reader to textbook chapters on pediatric and geriatric anesthesia for evidence.
Utilizing increased anesthesia depth to treat hypertension or tachycardia is appropriate if the diagnosis is inadequate depth of anesthesia. If in your clinical assessment you’re administering an adequate level of anesthesia, then it’s appropriate to treat hypertension or tachycardia with antihypertensive agents or beta blockers rather than adding extraneous anesthetic depth or narcotics.
Is there science to confirm the existence of excessive anesthesia dosing? In a February 2018 Stanford Grand Rounds lecture, Dr. Daniel Sessler of the Cleveland Clinic presented data that hypotension is a risk factor for perioperative myocardial injury. Per Dr. Sessler’s unpublished data gleaned from electronic medical records on thousands of patients, one-third of intraoperative hypotension occurs during the time period between the induction of anesthesia and the surgical incision. During this time period, general anesthesia doses are unopposed by surgical stimulus. An inference from this data is that lesser amounts of general anesthetic drugs are required between induction and incision. Options to lower the anesthetic doses pre-incision include: a) less or no narcotic until the time of incision, b) utilizing 60% nitrous oxide without sevoflurane until incision, or c) utilizing sevoflurane without any nitrous oxide until incision. My preference is a combination of options a) and c), i.e. minimizing or avoiding narcotics until incision, and avoiding nitrous oxide until incision.
Conflicting data exist regarding redheaded patients and general anesthesia. A 2004 study of 10 redheads and 10 controls showed the inhaled desflurane requirement in redheads was significantly greater than in dark-haired women.6 This conclusion was refuted in a 2010 prospective study of 468 patients which showed no significant difference in recovery times, pain scores or quality of recovery scores in patients with red hair.7
Whenever possible it’s advisable for the surgeon to inject local anesthesia near the surgical site, or the anesthesiologist to use local anesthetic via a nerve block or a neuroaxial block to minimize postoperative pain.
Should we use intraoperative BIS monitors to guide minimalization of intraoperative anesthetics and narcotics? Although the idea is intriguing, I’m not aware of any data to support that BIS monitors provide a significant solution to the problem of intraoperative overmedication.
When a patient has a past history of HAGA or PONV, prior to surgery I discuss a metaphorical postoperative teeter-totter. On one end of the teeter-totter, the patient will have minimal postoperative pain but will be at risk for the systemic side effects of IV narcotics, namely sedation and nausea. On the opposite end of the teeter-totter, the patient will have some postoperative pain but will also benefit from lower systemic side effects of IV narcotics, namely lower levels of sedation and nausea. I tell the patient that after the surgery, in the Post Anesthesia Care Unit, they will be awake and able to make their own decisions whether they desire additional doses of intravenous narcotics or not, with the full knowledge that extra doses of narcotics may bring extra risk of sedation and nausea.
Can anything be done to predict the risk of HAGA? I attempt to identify teetotalers preoperatively. I routinely ask every patient, “Do you drink alcohol at times?” Their answers vary from, “No, I do not drink at all,” to “Yes, once or twice a month,” to “Yes, two glasses of wine every day.” It’s been my experience that patients who never drink alcohol (the most prevalent central nervous system depressant in the world) are more sensitive to anesthetic medications. It’s easy to postulate that a teetotaler’s brain is more sensitive to CNS depressants, and that their hepatic metabolism is less efficient clearing CNS depressants than a patient who ingests alcohol or other CNS depressants daily.
This column conveys what I’ve learned based on my clinical experiences over decades. When you attend to patients with a past history of hangover after general anesthesia, try the suggestions discussed above:
- Take a history and correctly identify patients with a past history of hangover after general anesthesia.
- Utilize propofol > sevoflurane for patients who are petite, who never drink alcohol, or give a history of being sensitive to CNS depressants.
- Administer significantly less IV narcotics to patients who are petite, who are elderly, who never drink alcohol, or give a history of being sensitive to CNS depressants.
- Administer intravenous doses based on lean body weight, not the actual weight, on obese patients.
- Administer lower doses of narcotics to patients at extremes of age, e.g. geriatric patients and the very young.
- Regarding intraoperative hypertension and/or tachycardia, if the anesthetic depth is already adequate, consider treating with antihypertensive medications or beta blockers rather than adding additional anesthetic.
- Decrease the amount of anesthesia you administer between the induction of anesthesia and surgical incision.
- Utilize local anesthetic/regional blocks to minimize postoperative pain as appropriate.
- Ask patients “Do you drink alcohol at times?” For teetotalers, utilize decreased doses, particularly decreased doses of narcotics.
These patients will likely fare better in your hands than what they’ve experienced after previous surgeries, and they will rank you above the historical control of anesthetists who’ve overdosed them in the past.
- Apfel CC et al. A simplified risk score for predicting postoperative nausea and vomiting: conclusions from cross-validations between two centers. Anesthesiology 1999 Sep;91(3):693-700.
- Lemmens HJ . Perioperative pharmacology in morbid obesity. Curr Opin Anaesthesiol.2010 Aug;23(4):485-91.
- Chassard D et al. Influence of bodycompartments on propofol induction dose in female patients. Acta Anaesthesiol Scand. 1996 Sep;40(8 Pt 1):889-91.
- Liem EB et al. Anesthetic requirement is increased in redheads. 2004 Aug;101(2):279-83.
- Myles PS, Buchanan FF, Bain CR. The effect of hair colour on anaesthetic requirements and recovery time after surgery. Anaesth Intensive Care.2012 Jul;40(4):683-9
Published in September 2017: The second edition of THE DOCTOR AND MR. DYLAN, Dr. Novak’s debut novel, a medical-legal mystery which blends the science and practice of anesthesiology with unforgettable characters, a page-turning plot, and the legacy of Nobel Prize winner Bob Dylan.
In this debut thriller, tragedies strike an anesthesiologist as he tries to start a new life with his son.
Dr. Nico Antone, an anesthesiologist at Stanford University, is married to Alexandra, a high-powered real estate agent obsessed with money. Their son, Johnny, an 11th-grader with immense potential, struggles to get the grades he’ll need to attend an Ivy League college. After a screaming match with Alexandra, Nico moves himself and Johnny from Palo Alto, California, to his frozen childhood home of Hibbing, Minnesota. The move should help Johnny improve his grades and thus seem more attractive to universities, but Nico loves the freedom from his wife, too. Hibbing also happens to be the hometown of music icon Bob Dylan. Joining the hospital staff, Nico runs afoul of a grouchy nurse anesthetist calling himself Bobby Dylan, who plays Dylan songs twice a week in a bar called Heaven’s Door. As Nico and Johnny settle in, their lives turn around; they even start dating the gorgeous mother/daughter pair of Lena and Echo Johnson. However, when Johnny accidentally impregnates Echo, the lives of the Hibbing transplants start to implode. In true page-turner fashion, first-time novelist Novak gets started by killing soulless Alexandra, which accelerates the downfall of his underdog protagonist now accused of murder. Dialogue is pitch-perfect, and the insults hurled between Nico and his wife are as hilarious as they are hurtful: “Are you my husband, Nico? Or my dependent?” The author’s medical expertise proves central to the plot, and there are a few grisly moments, as when “dark blood percolated” from a patient’s nostrils “like coffee grounds.” Bob Dylan details add quirkiness to what might otherwise be a chilly revenge tale; we’re told, for instance, that Dylan taught “every singer with a less-than-perfect voice…how to sneer and twist off syllables.” Courtroom scenes toward the end crackle with energy, though one scene involving a snowmobile ties up a certain plot thread too neatly. By the end, Nico has rolled with a great many punches.
Nuanced characterization and crafty details help this debut soar.
Click on the image below to reach the Amazon link to The Doctor and Mr. Dylan:
LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW: