INTRAVENOUS ACETAMINOPHEN: AN IMPORTANT NON-OPIOID THERAPY, OR AN EXORBITANTLY PRICED VERSION OF AN OVER-THE-COUNTER MEDICATION?

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IV acetaminophen (Ofirmev)

 

tylenol-tylenol-extra-strength-500-mg-150-units

Oral acetaminophen

Healthcare costs continue to skyrocket in the United States. In 2016 Americans spent $435 billion on prescription drugs.1 This month the Trump administration released a 44-page blueprint for executive action on drug pricing entitled “American Patients First.” Their goal is to drive prescription drug costs down by increasing competition. At this time it’s too early to tell how effective these efforts will be.

Anesthesiologists are the only physicians who prescribe and then directly administer medications themselves. CRNAs are the only nursing professionals who prescribe and then directly administer medications themselves. Because anesthesiologists and CRNAs typically don’t pay for the medications, there can be a disconnect regarding costs and value.

If you were in charge of pharmaceutical purchasing at a hospital or an ambulatory surgery center, and you had an identical acetaminophen molecule available for either 5 cents per dose or $42 per dose, which would you choose? The answer is obvious, but as an administrator you are not prescribing the drug.

Acetaminophen (Tylenol) has been available in oral and rectal forms for decades. Intravenous acetaminophen was introduced in Europe in 2002. The United States Food and Drug Administration approved IV acetaminophen (Ofirmev, Cadence Pharmaceuticals) in 2010 for management of mild to moderate pain, moderate to severe pain with adjunctive opioid analgesics, and reduction of fever.

A 2014 study showed that patients who received IV acetaminophen reported superior satisfaction with pain control compared to patients who received placebo.2 In inpatient and postoperative settings, intravenous acetaminophen became a route of choice for rapid analgesia, and appeared to reduce the need for other analgesics such as opioids. Disadvantages of IV acetaminophen included the time and equipment needed for IV drug administration, as well as increased costs.

In a publication from the Canadian Journal of Hospital Pharmacy, Jibril wrote, “The study drug (acetaminophen, either oral or IV) was given when patients first awakened after surgery, and additional doses were given every 6 h until 0900 the next morning. . . . The use of opioids was significantly lower in the group receiving acetaminophen by the IV route than in the group receiving acetaminophen by the oral route (p < 0.05). However, this difference did not translate into a significant difference in rates of postoperative nausea and vomiting or any significant difference in pain scores on a 100-mm visual analogue scale (VAS) at any time. . . . A major finding of this review was the absence of strong evidence suggesting superiority of IV acetaminophen administration over oral routes. . . . IV acetaminophen may be useful for opioid-sparing in postoperative pain. To date, no strong evidence exists that IV acetaminophen should replace any form of standard care. At most, the evidence indicates that this formulation could function as an adjunctive agent in patients unable to take oral forms. . . . . In the United States, there has been great debate regarding use of this formulation, which has led many hospitals to adopt policies and procedures that restrict use for a limited period or for patients not able to take medications by mouth. These restrictions are required because of the cost of the product, in addition to other administration-related inconveniences. Canadian hospitals and formulary committees should be aware of the available efficacy and safety data if the formulation is marketed in Canada and its use becomes widespread. Given the high cost and the lack of superiority over oral forms, Canadian hospitals may need to restrict use of the IV formulation, as their US counterparts have already done.”3

In a study of IV acetaminophen use in neurosurgical ICU patients at Virginia Commonwealth University, Gretchen Brophy, PharmD, of the departments of pharmacy and neurosurgery wrote, “We and every institution I’ve spoken to have restricted its use, because we don’t have data saying it’s more effective. At $33 a dose” – recently up from $10 – “it’s harder to justify. At least in the 0-3 hour window, it didn’t have any additional benefit over oral. It might still be better at 1 hour; kinetically, that would make sense, but there’s nothing yet to say from what we did that it’s better.”4 VCU restricted intravenous acetaminophen use to one dose per patient.

Mallinckrodt purchased Cadence Pharmaceuticals in 2014, and increased the price of Ofirmev from $17.70 to $42.48 per vial. (A full case of Ofirmev includes 24 vials.) Sales increased to $71 million during their fiscal first quarter, double the amount for the same period the previous year. Hospitals noted the rise in expenses and sought alternatives such as oral acetaminophen, and the volume of sales dropped. Robert Press, chief of hospital operations at NYU Langone, which anticipated $1 million in additional costs because of Ofirmev, was quoted to say, “We found out a lot of the use was really not necessary and we found we could give alternative products.”5

Some hospitals removed Ofirmev from their formularies after the price went up. Others simply switched to alternatives such as oral acetaminophen. Others increased their budgets to cover the cost of the drug, but the net effect of Mallinckrodt’s price hike was to reduce the doses of Ofirmev prescribed. Mallinckrodt’s U.S. headquarters are located in Missouri. Senator Claire McCaskill (D-Missouri) wrote a letter to Mallinckrodt CEO Mark Trudeau demanding information about pricing and revenue numbers. In the letter she also suggested that Ofirmev, expensive as it was, might actually be saving hospitals money because of opioid-sparing. Senator McCaskill wrote, “Any obstacle to prescribing non-opioid alternatives, even those used solely in a hospital setting, is cause for concern.” It should be noted that McCaskill received $2,500 in campaign financing from Mallinckrodt during the 2016 election cycle.6

Mallinckrodt released a statement that read, “One recent analysis of health economic data on the use of Ofirmev coupled with a one-level reduction in opioid use was linked to decreasing hospital stays, potential opioid-related complications and related costs for the treatment of acute surgical pain. . . . The study showed a potential of $4.7 million in annual savings for a typical, medium-sized hospital.”6

The clinical benefit of reduced opioid consumption with Ofirmev has not been evaluated nor demonstrated in prospective, randomized controlled trials. In a review in the journal Pharmacotherapeutics, Yeh wrote, “Although use of intravenous acetaminophen has reduced other postoperative resource utilization (e.g., hospital length of stay) in some studies outside the United States in patients undergoing abdominal surgery, a full economic evaluation in the United States has yet to be undertaken.”7

The research study anesthesiologists would like to read is a prospective, randomized, double-blind trial of 1000 mg of preoperative oral acetaminophen, versus 1000 mg of IV acetaminophen administered just prior to the end of surgery. Will this research ever be performed? I hope so, but you can bet Mallinckrodt is never going to fund that study.

I repeat Jibril’s conclusion to sum up the answer to our initial question above:“An absence of strong evidence suggesting superiority of IV acetaminophen administration over oral routes. . . . To date, no strong evidence exists that IV acetaminophen should replace any form of standard care. At most, the evidence indicates that this formulation could function as an adjunctive agent in patients unable to take oral forms. . . . Therefore, on the basis of current evidence, if a patient has a functioning gastrointestinal tract and is able to take oral formulations, IV formulations are not indicated.”3

And what is the solution regarding anesthesia providers who frequently choose to prescribe IV acetaminophen despite these recommendations? The hospital I work at, Stanford University Hospital, restricts Ofirmev usage to patients who are NPO (nothing by mouth), and each Ofirmev order has a hard stop after 24 hours, eliminating further usage. The owners of the surgery center I medically direct have an even more decisive solution: Ofirmev is not on the facility formulary at all.

 

References:

  1.  Cortez J. Prescription Drug Spending Hits Record $425 Billion in U.S. Bloomberg, April 13, 2016.                                                https://www.bloomberg.com/news/articles/2016-04-14/prescription-drug-spending-hits-record-425-billion-in-u-s
  2. Apfel CC et al. Patient satisfaction with intravenous acetaminophen: a pooled analysis of five randomized, placebo-controlled studies in the acute postoperative setting. J Healthc Qual. 2014 Jan 16.
  3. Jibril F, et al. Intravenous versus Oral Acetaminophen for Pain: Systematic Review of Current Evidence to Support Clinical Decision-Making, Can J Hosp Pharm. 2015 May-Jun; 68(3): 238–247.
  4. Otto MA et al. No pain benefit found for IV acetaminophen vs. oral in the neuro ICU. Clinical Neurology News. January 30, 2015.
  5. Staton T. Price hikes aren’t always sustainable: Just ask Mallinckrodt about Ofirmev. Fierce Pharma. Oct 12, 2015. https://www.fiercepharma.com/pharma/prie-hikes-aren-t-always-sustainable-just-ask-mallinckrodt-about-ofirmev
  6. Staton T. Mallinckrodt’s pain med Ofirmev gets scrutiny in Senate—but this pricing probe has a twist. Fierce Pharma. May 30, 2017. https://www.fiercepharma.com/pharma/mallinckrodt-s-pain-med-ofirmev-gets-scrutiny-senate-but-pricing-probe-has-a-twist
  7. Yeh Y et al. Reviews of Therapeutics: Clinical and Economic Evidence for Intravenous Acetaminophen. Pharmacotherapeutics. 08 May 2012.

 

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41wlRoWITkL

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.

KIRKUS REVIEW

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:

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LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

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LEARJET ANESTHESIA – THE EARLY DAYS OF HEART TRANSPLANTATION

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Anesthesia can be a glamorous specialty. During my Stanford training in 1984-1986 I flew on Learjets more times than I can count, during missions to harvest donor hearts from throughout the western United States.

Norman Shumway MD PhD, a Stanford surgical professor and legend, invented the heart transplantation procedure and performed the first heart transplant in the USA on January 6, 1968 in operating room 13 of Stanford University Hospital. Survival rates for heart transplantation patients increased markedly in 1983 with the adoption of cyclosporine as an effective anti-rejection drug. During the 1980’s Stanford was the only prominent heart transplantation program in the western United States, and the quantity of brain dead heart donors was modest. In order to expand their volume of transplants, Stanford created a fixed-wing aircraft harvesting and transportation program to bring donor hearts to Palo Alto from distant locations.

One registered nurse had a fulltime job locating appropriate brain dead heart donors within a 60-90 minute Learjet trip from Stanford. A separate team of physicians and nurses was responsible for assembling a waitlist of prospective heart transplant recipients, and for arranging housing for them within the San Francisco Bay Area.

When Stanford learned of a brain dead donor with a normal heart at a distant location, the following choreography occurred: 1) a matching donor was identified and told to come to Stanford Medical Center immediately; 2) a team of surgeons, anesthesiologists, nurses, and a heart-lung perfusionist was paged to Stanford Medical Center immediately to prepare the recipient patient for his or her transplant surgery; and 3) a transport team of two surgeons (a chief resident in cardiac surgery and a second surgical resident), one anesthesia fellow or resident, one scrub nurse, one circulating nurse, and the nurse in charge of the transport team were all paged to the Stanford Medical Center immediately.

Note that the anesthesia transport team member was only an anesthesia fellow or a resident. The eligible residents were second-year residents (anesthesia residency training was only two years in duration during the 1980’s). As a second-year resident, I was a partially trained anesthesiologist who had done only 800-1000 anesthetics at that time, and was not yet eligible to sit for the American Board of Anesthesia exam.

An ambulance transported our team to the Moffett Field Air Force Base, 10 miles southeast of the Stanford campus, where we boarded a Learjet for the flight to the donor hospital. The donor harvesting catchment area was as far north as Seattle, as far south as Las Vegas, and as far east as Boise. We had no medical tasks to do in flight, and we spent our time looking out the windows and small talking. Upon arrival at the airport in the donor city, an ambulance transported us to the hospital.

At the hospital we proceeded to the intensive care unit where we found the donor’s brain dead body connected to a ventilator and ICU monitors. At this point my work began. Even though the patient was brain dead, it was imperative to maintain his or her vital signs and oxygenation at optimal levels to preserve the cardiac function for the eventual recipient. My first tasks were to insert an arterial line in the radial artery to monitor blood pressure, and to insert a central venous pressure catheter in the internal jugular vein to administer medication infusions as needed to decrease or increase the blood pressure during the upcoming surgery. We would then transport the patient through the hallways of this foreign hospital, accompanied by the surgeons, and directed by staff of that hospital who knew the floor plan. I’d be squeezing an Ambu bag full of oxygen to ventilate the patient, all the while vigilant of the vital signs displayed on a portable monitor during the transport.

We’d arrive in the operating room—a room we’d never seen or worked in before—and prepare the patient for surgery. My job was to connect the patient to the operating room ventilator and the standard cardiac surgery monitors: ECG, oximeter, arterial line, and central venous pressure. The manufacturers of the monitoring equipment varied from hospital to hospital, and it was not unusual for the equipment to be different than machines I’d worked with before. My next task was to prepare vasoactive drips such as nitroprusside and connect them to the central venous pressure IV line. No anesthetic drugs were used, because the donor was brain dead, but surgical stimulus always caused increases in blood pressure and heart rate. It was critical that pumping against a high resistance or pumping at a high rate not tax the donor heart. I also had to fill out a written anesthesia medical record to document what I was doing to the patient.

The scrub tech, nurse, and the two surgeons prepped and draped the patient for surgery, and the initial incision was made over the sternum. A power saw was used to cut the breastbone down the midline to enter the chest. A rib-spreader was used to widen the cavity and improve visualization. The surgeons inspected the heart in terms of its general appearance, size, contractility, and the state of the coronary arteries. Once they’d determined the heart was indeed normal, the transplant nursing coordinator made a phone call to the Stanford operating room in California to inform them it was a green light to anesthetize the heart recipient there.

In our operating room, the two surgeons clamped off the aorta and all other blood vessels leading into and out of the heart, and injected a cardioplegic solution into the coronary arteries via the root of the aorta. This solution preserved the heart function during the upcoming trip when the heart would no longer be beating. The surgeons then cut the heart out of the body, placed it in a sterile bag, and placed the bag into an Igloo chest full of ice. I turned off the ventilator, the surgeons removed their gloves and gowns, and our whole cast scurried out of the operating room with the Igloo and its precious cargo in hand.

It was always a bizarre sight to see that human carcass with an empty thorax lying on an operating room table when we left the operating room. In the later months of my Learjet experiences, a second transplant team was sometimes present to harvest the kidneys or corneas after we departed.

The original ambulance met us at the Emergency Room entrance, and we sped back to the airport Code 3 with alarms blaring. We drove onto the tarmac next to the Learjet and climbed inside. The doors closed, engines flared, and wheels up . . . we were on our way back to Palo Alto.

The flight home was relaxing. We’d spent an intense period of time at the hospital, and we had no work to do except to ride and look out the windows. Beverages and food were always supplied for the trip home. The mood was jubilant—the feeling you get with medical jobs when you realize you’ve accomplished something. We were helping the recipient patient in their journey back to health, and experiencing private jet travel at 35,000 feet at the same time.

On arrival to Moffett Field, an ambulance awaited us on the tarmac. We’d climb in and ride at top speed back to Stanford. We stopped in front of the Emergency Room, and the surgeons and the nurse coordinator ran through the doorway and up the stairs to operating room 13, where the anesthetized recipient patient lay, his or her chest open, ready to receive the new heart at once.

At this point I went home. An anesthesia resident colleague and an anesthesia faculty member were upstairs attending to the recipient. Caring for the recipient patient was their job for today—mine was finished.

How stressful was the entire journey to harvest the new heart? Pretty stressful, to be honest. At that point, I’d done less than two years of anesthesia training, and I was relatively inexperienced. During my training, a faculty member always stood right next to me during every anesthesia induction and a faculty member was immediately available at all times. On the Learjet trips I was without faculty backup for the first time. The setting at the destination hospital was always unfamiliar. The equipment on hand at the destination hospital was often unfamiliar. The cardiac chief resident surgeon was typically an intense 39-year-old who’d been training for decades and who had little interest in waiting any longer than possible while an anesthesia resident-in-training toiled to insert an arterial line and a central venous catheter. Even though the patient was brain dead, there was no tolerance for errors in ventilation or medical management, it was imperative to keep the vital signs stable throughout the donor surgical procedure, and there was time pressure to keep the process moving.

Prior to my anesthesia residency I’d completed three years as an internal medicine resident at Stanford and one year as an attending in the Emergency Room at Stanford. All my experience in internal medicine and emergency medicine was useful on those heart-harvesting trips—but I knew how lucky I was. Internal medicine residents don’t get to ride Learjets, and ER attendings don’t get to ride Learjets either.

An added motivation: We were paid $35/hour for our time, a princely sum in 1986.

Alas, none of this would happen nowadays. Currently there are hundreds of cardiac transplantation programs in the United States, and each program procures their donor hearts from close geographic proximity.

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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.

KIRKUS REVIEW

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:

41wlRoWITkL

LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

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HANGOVER AFTER GENERAL ANESTHESIA

 

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Prior to surgery your patient tells you, “I’m always hungover 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 fulltime 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:

  1. Take a history and correctly identify patients with a past history of hangover after general anesthesia.
  2. Utilize propofol > sevoflurane for patients who are petite, who never drink alcohol, or give a history of being sensitive to CNS depressants.
  3. 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.
  4. Administer intravenous doses based on lean body weight, not the actual weight, on obese patients.
  5. Administer lower doses of narcotics to patients at extremes of age, e.g. geriatric patients and the very young.
  6. 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.
  7. Decrease the amount of anesthesia you administer between the induction of anesthesia and surgical incision.
  8. Utilize local anesthetic/regional blocks to minimize postoperative pain as appropriate.
  9. 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.

References:

  1. 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.
  2. http://www.pdr.net/drug-summary/diprivan?druglabelid=1719#11
  3. http://www.pdr.net/drug-summary/Ultane-sevoflurane-32
  4. Lemmens HJ . Perioperative pharmacology in morbid obesity. Curr Opin Anaesthesiol.2010 Aug;23(4):485-91.
  5. 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.
  6. Liem EB et al. Anesthetic requirement is increased in redheads. 2004 Aug;101(2):279-83.
  7. Myles PSBuchanan FFBain CR. The effect of hair colour on anaesthetic requirements and recovery time after surgery. Anaesth Intensive Care.2012 Jul;40(4):683-9

 

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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.

KIRKUS REVIEW

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:

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LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

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THE MOST SIGNIFICANT ANESTHESIOLOGIST OF THE 20TH CENTURY

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The original Nellcor N100 pulse oximeter

The most significant anesthesiologist of the 20th century died just weeks ago, on December 21, 2017. His name was William New, MD, PhD. Many of you have never heard of Dr. New, and don’t know what he was famous for, but in my opinion he was the Most Valuable Player of the anesthesia ranks in the last one hundred years.

William New was a Stanford anesthesiologist and electrical engineer. In 1978 Bill New invented the prototype of the modern pulse oximeter. In 1981 Dr. New founded and became Chairman of the Nellcor company, the manufacturer of the first commercially available pulse oximeter.

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Nellcor pulse oximeter finger probe

For my non-medical readers, a pulse oximeter is a medical device that indirectly monitors the oxygen saturation of blood by assessing the red color of pulsatile blood, usually in the patient’s fingertip. The original pulse oximeter was a stand-alone monitor, about the size of a cigar box, that was both portable and easy to use. The monitor displayed two numbers, the pulse rate and the oxygen saturation, as well as a vertical array of LEDs that mimicked the rise and fall of each pulse. The monitor emitted an audible beep, with high tones representing adequate oxygen levels and low tones representing unsafe oxygen levels. Without looking at the monitor, a clinician knew whether the patient was in danger, simply by listening to the pitch of the beep tone from the oximeter.

Steve Jobs changed our way of life with the introduction of the iPhone. In parallel, Bill New changed the world with the introduction of the pulse oximeter. No single device in the 20th century changed medical care more than the oximeter. Nellcor’s successful production, marketing, and sales efforts of their pulse oximeter changed not just anesthesia practice, but medical practice, forever.

Prior to the pulse oximeter, anesthesiologists had only unreliable measures of tissue oxygenation, such as observing how red the blood seemed when the surgeon made the initial incision into the patient. Undetected hypoxia could present as a sudden cardiac arrest. Anesthesia was a more dangerous undertaking without true second-to-second knowledge of the patient’s oxygenation.

In July 1984 during the first week of my Stanford anesthesia residency at the Santa Clara County Hospital, the entire medical center owned only three Nellcor pulse oximeters. Each morning the attending anesthesiologists would huddle and decide which three had the greatest need for the new technology. The remaining operating rooms would proceed without oximetry. The situation was better at Stanford University Hospital, where each operating room included a pulse oximeter—but there were no oximeters in the PACUs, preoperative units, or intensive care units.

It may be difficult for you to imagine the increased stress level when administering anesthesia without knowing what the patient’s arterial oxygen saturation is. The reassuring audible “beep-beep-beep” treble notes from the Nellcor were reassuring, and the descending bass notes of an acute desaturation struck terror into every one of us.

The market for the Nellcor pulse oximeter exploded between 1984 and 1986, and eventually all ICUs and acute care areas had oximeter monitoring. The oxygen saturation became recognized as “the fifth vital sign,” joining heart rate, blood pressure, respiratory rate, and temperature. On October 21, 1986, the American Society of Anesthesiologists made pulse oximetry a required standard monitor for all anesthetic care. The new standard read: “During all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed. When the pulse oximeter is utilized, the variable pitch pulse tone and the low threshold alarm shall be audible to the anesthesiologist or the anesthesia care team personnel.”

In 1990 an American Society of Anesthesiology Closed Claims Study examined 1541 malpractice settlements, and showed that adverse respiratory events constituted the single largest class of injury (522 of 1541 cases; 34%).  Death or brain damage occurred in 85% of these cases. Three-fourths of the adverse respiratory events were due to inadequate ventilation (196 cases; 38%), esophageal intubation (94 cases; 18%), and difficult tracheal intubation (87 cases; 17%). Most of the adverse respiratory outcomes (72%) were considered preventable with better monitoring (i.e. pulse oximetry plus capnography).

After the adoption of pulse oximetry and end-tidal carbon dioxide monitoring as standards, unexpected cardiac arrests from hypoxia or esophageal intubation became rare. Malpractice cases from respiratory events decreased, and malpractice insurance for anesthesiologists decreased in cost. In its landmark 1999 publication To Err is Human, the Institute of Medicine cited anesthesiology as the specialty that had made the most significant advances in patient safety.

Over the ensuing years, multiple companies produced pulse oximeters to mimic and compete with Nellcor. At the present time oximeters are ubiquitous, and are found in all clinics, emergency rooms, ICUs, PACUs, operating rooms, ambulances, critical care transport aircraft, and even in many homes. Today you can purchase a tiny finger oximeter from Walmart for $11.95

How big is the business of selling oximeters? The global pulse oximeter market was valued at $1.5 billion in 2015, and is projected to grow with a CAGR (Compound Annual Growth Rate) of 6.15%. Escalating healthcare costs are driving the market toward more home care, boosting the demand for remote patient monitoring devices, and increasing the demand for pulse oximeters.

I didn’t know Dr. New personally, although he and I attended the same alumni gatherings many times. He was congenial, humble, smart, and shunned the spotlight. He didn’t even have a Wikipedia page. He was nonetheless a celebrity among us. All Stanford anesthesia alumni knew the importance of his contribution to medical history. Dr. New continued his work as an engineer, entrepreneur and educator, and volunteered as an advisor for the Stanford Anesthesia Innovation Lab (SAIL), a medical device incubator focused on accelerating the development of anesthesia-related medical devices.

We anesthesiologists keep our patients alive, one at a time, aided by Dr. New’s discovery, and in total his discovery has kept millions of patients safe. The Stanford anesthesia department emailed out this brief note that Bill New wrote some years ago, which captured his thoughts regarding the future of our specialty:

As I ponder the future of ‘anesthesiology’ in a world where human physiology is unchanged but technology expands exponentially, the challenges and opportunities loom large. Moore’s Law and corollaries Rock’s Law + Edholm’s Law are driving us toward a technology singularity in anesthesia and critical life support, converting our human role to empathy and advocacy and no longer direct administration of agents/agonists, pills or potions, biochemical or otherwise.

I think back on academic departments and even entire schools/institutes of study at Stanford some fifty years ago that no longer exist or have morphed to fit the present world order.  I see anesthesiology morphing over the next fifty in a comparable way, with technology (as in many fields) becoming the dominant paradigm.

Stanford needs to lead us into this new unknown vortex — and one of the best ways is how we train/acculturate our residents/fellows to embrace the 21st century, which is unlikely to become simply the elongation of the 20th century shadow.  The past generation in academia blossomed to maturity with NIH grants, Medicare funding, peer review, publish or perish, tenure, big labs, hierarchical seniority, hospital hubs, risk-adverse regulation and a plethora of other customs and traditions.  The accoutrements of academia yesterday will vanish.  Anesthesia can — and must — join the new paradigm that technology now offers.

– Bill 

 

In a future column I’ll discuss the implications of Dr. New’s vision for the future of anesthesiology.

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William New MD PhD

MYOCARDIAL INJURY AFTER NONCARDIAC SURGERY . . . COMMON, SILENT, AND DEADLY. WHAT CAN WE DO?

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You’re a 55-year-old man with hypertension. How likely is it you will die within the next 30 days?

Extremely unlikely.

You’re a 55-year-old man with hypertension scheduled for a right colon removal for colon cancer. How likely is it that you could die within 30 days after surgery?

Higher than you would think. Your 30-day morality following this inpatient surgery is 1.2%. What can we do to improve myocardial injury after noncardiac surgery? Read on…

Dr. Daniel Sessler, Chairman of the Department of Outcomes Research at the Anesthesia Institute of the Cleveland Clinic, spoke at the Stanford Anesthesia Grand Rounds last week. His lecture, titled “Perioperative Myocardial Injury,” answered the questions above. Let me share what Dr. Sessler had to say:

  1. Myocardial injury after noncardiac surgery, abbreviated as MINS, is a common, silent, and deadly problem. Dr. Sessler described mortality related to surgery as the third leading cause of death in America, behind cardiovascular disease and cancer, and he cited myocardial injury as the leading cause of death after surgery.
  2. Devereaux, Sessler, and colleagues measured postoperative hsTnT (high sensitive troponin T) in 21,842 patients over the age of 45 who had inpatient noncardiac surgery at 23 medical centers in 13 countries.1 (For my nonmedical readers: hsTnT or cardiac troponin is a biomarker for acute myocardial infarction, i.e. heart attack.) Two hundred sixty-six patients died within 30 days after surgery, for an overall mortality rate of 1.2%. A total of 3904 patients had elevated hsTnT, diagnostic for MINS, for an overall incidence of tropinin elevation = 18% of the patients. Ninety-three percent of these patients had no ischemia-related symptoms, and would not have been detected without the hsTnT measurements.
  3. Puelacher published similar data in an older population (all patients over the age of 65).2 He studied postoperative hsTnT levels in 2018 consecutive inpatients and found perioperative myocardial injury (PMI) occurred in 397 (16% of the patients). Only 24 (6% of the patients) had typical chest pain, and only 72 (18% of the patients) had ischemic symptoms. The 30-day mortality was 8.9% for patients with PMI, compared to 1.5% for patients without PMI.
  4. hsTnT isn’t commonly measured in current practice, which means the majority of MINS patients go undiagnosed. Sessler recommended that all patients diagnosed with MINS be seen by a cardiologist, to consider further diagnostic or therapeutic intervention. He specifically mentioned the possibilities of statin and/or aspirin therapy, as well as smoking cessation and weight loss.
  5. Sessler suggested that a future approach to MINS detection would be to measure postoperative hsTNT for three days in every inpatient noncardiac surgery patient over 65 years old, and in those over 45 with one or more cardiovascular risk factor.
  6. What about preoperative clearance for noncardiac surgery? Sessler described exercise tolerance and the echocardiogram cardiac stress test as two inaccurate screening tools. He rated the two most effective screening tools as the Revised Cardiac Risk Index (see below), and the preoperative measurement of BNP (Brain Natriuretic Peptide).
  7. The Revised Cardiac Risk Index (RCRI) evaluates these 6 patient factors:

■ High-Risk Surgery – the following surgeries are deemed high risk for perioperative cardiac complications:

-­ Intraperitoneal

– Intrathoracic

– Suprainguinal vascular

■ History of ischemic heart disease – characterized by either a history                                     of a positive test, a diagnosed MI, current chest pain suspicion of                                                 myocardial ischemia, nitrate therapy, or evidence of                                                             pathological Q waves on electrocardiogram.

■ History of congestive heart failure – described as the presence of                                     either:

– Pulmonary edema, bilateral rales or S3 gallop;

– Paroxysmal nocturnal dyspnea;

– A CXR showing pulmonary vascular redistribution.

■ History of cerebrovascular disease – e.g. a prior TIA or stroke.

■ Pre-operative insulin treatment.

■ Pre-operative creatinine more than 2 mg/dL.

 

Positive findings of these factors define 4 classes of postoperative                                     cardiac complication percentage rates:

■ 0 factors – Class I – risk 0.4%;

■ 1 factor – Class II – risk 0.9%;

■ 2 factors – Class III – risk 6.6%;

■ 3 to 6 factors – Class IV – risk 11%. 

  1. Preoperative BNP concentration is a powerful independent predictor of perioperative cardiovascular complications.3 At best, clinicians can utilize both a low score in the preoperativeRevised Cardiac Risk Index plus a low value of the BNP or the N-terminal proB-type natriuretic peptide (NT-proBNP) plasma level.4 Sessler stated that a BNP test costs 1/20th as much as an echo stress test, and is more accurate in predicting postoperative cardiac mortality. He stated that a NT-proBNP level of < 300 ng/mL correlated well with a safe perioperative cardiovascular course.
  2. Elevated preoperative troponin or hsTnT concentrations were also significantly associated with postoperative MI and long-term mortality after noncardiac surgery.5
  3. Metoprolol, aspirin, and clonidine all failed as preoperative interventions to decrease cardiac risk. Metoprolol decreased postoperative myocardial infarction, but there were more deaths and an increased rate of stroke in the metoprolol group than in the placebo group.6 Aspirin before surgery and throughout the early postsurgical period had no significant effect on the rate of death or nonfatal myocardial infarction, and increased the risk of major bleeding.7 Low-dose clonidine did not reduce the rate death or nonfatal myocardial infarction, and increased the risk of clinically important hypotension and nonfatal cardiac arrest.8
  4. Eliminating nitrous oxide from the anesthetic regimen had no effect in decreasing myocardial injury.9
  5. Intraoperative hypotension correlated with postoperative myocardial injury. Mascha studied the time-weighted average intraoperative mean arterial pressure (TWA-MAP), and found that lower mean arterial pressure strongly correlated with mortality.10 Sessler stated that a mean blood pressure of 50 torr for even one minute was a risk factor for postoperative myocardial injury. Targeting a specific systolic blood pressure reduced the risk of postoperative organ dysfunction.11
  6. Sessler stated that 1/3 of intraoperative hypotension occurred during the time between induction of anesthesia and time of the surgical incision. By analyzing large databases from electronic anesthesia recording systems, hypotension was documented during this time period when general anesthesia lacked any surgical stimulus to keep blood pressure elevated. Sessler’s recommendation was to maintain the MAP > 65 torr throughout noncardiac surgery.
  7. The use of vasopressors to treat hypotension was safe.
  8. Tachycardia was not a risk factor. “It hardly matters,” Sessler said.
  9. Preoperative angiotensin-converting-enzyme inhibitors (ACE inhibitors), e.g. lisinopril, Lotensin, or Altace, and Angiotensin II receptor blockers (ARBs), e.g. Diovan or Cozaar, were risk factors for intraoperative hypotension and cardiovascular morbidity. Roshanov studied data from 14,687 patients aged 45 years or older for inpatient noncardiac surgery.12 Four thousand eight hundred and two of these patients were taking ACE inhibitors or ARBs preoperatively. The patients who withheld their ACE inhibitors/ARB drugs in the 24 hours before surgery were less likely to suffer the outcomes of death, stroke, or myocardial injury. The authors recommended that patients withhold these drugs for 24 hours before surgery.

 

Dr. Sessler closed his lecture with the following recommendations:

  • In the future, clinicians should measure high-sensitivity troponin (hsTnT) for three days postoperatively on inpatient surgery patients of age > 65, or patients age >45 with one cardiovascular risk factor. Elevated shTnT will identify patients who with MINS, and these MINS patients should be referred for cardiology/internal medicine follow up.
  • In the future, clinicians should screen for preoperative cardiovascular risk by a combination of the BNP and hsTnT assays prior to surgery.
  • There is no known preoperative medical prophylaxis against MINS.
  • Maintain intraoperative mean arterial pressure > 65.
  • Hold ACE inhibitors/ARBs for 24 hours prior to surgery.

One of our professors asked Dr. Sessler if the current practice at the Cleveland Clinic included measuring preoperative BNP and three-day postoperative hsTnT. Sessler’s answer was, “not yet, but we’re working on it.”

What about your practice and mine?

This is a new topic and a cutting edge issue to most anesthesiologists, with the key studies only published in the last year. I’m impressed by the MINS data, and I don’t want any patient of mine joining the MINS mortality list. I already withhold ACE inhibitors/ARBs for 24 hours preoperatively. I will continue to be vigilant to maintain MAP > 65, using vasopressors as necessary. I currently use the Revised Cardiac Risk Index as well as cardiology consultations as indicated to screen patients preoperatively. At the present time both the cardiologists and I depend on exercise tolerance history and echo treadmill tests for preoperative cardiac clearance. I expect in the near future our healthcare systems will adopt the standards of checking BNP preoperatively and hsTnT for three days postoperatively for inpatient surgery patients of age > 65, or patients age >45 who have one cardiovascular risk factor. Stay tuned for future recommendations.

References:

  1. Devereaux PJ et al. Association of Postoperative High-Sensitivity Troponin Levels With Myocardial Injury and 30-Day Mortality Among Patients Undergoing Noncardiac Surgery. 2017Apr 25;317(16):1642-1651.
  2. Puelacher C et al. Perioperative Myocardial Injury After Noncardiac Surgery. Circulation. 2018;137, 1-12.
  3. Rodseth RN et al. The prognostic value of pre-operative and post-operative B-type natriuretic peptides in patients undergoing noncardiac surgery: B-type natriuretic peptide and N-terminal fragment of pro-B-type natriuretic peptide: a systematic review and individual patient data meta-analysis. J Am Coll Cardiol.2014 Jan 21;63(2):170-80.
  4. Vetrugno L et al. The Possible Use of PreoperativeNatriuretic Peptides for Discriminating Low Versus Moderate-High Surgical Risk Patient. Semin Cardiothorac Vasc Anesth. 2018 Jan 1.
  5. Nagele P et al. High-sensitivity cardiac troponin T in prediction and diagnosis of myocardial infarction and long-term mortality after noncardiac surgery. Am Heart J.2013 Aug;166(2):325-332.
  6. Devereaux PJ et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. 2008 May 31;371(9627):1839-47.
  7. Devereaux PJ et al. Aspirin in patients undergoing noncardiac surgery. N Engl J Med.2014 Apr 17;370(16):1494-503.
  8. Devereaux PJ et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med.2014 Apr 17;370(16):1504-13.
  9. Myles PS et al. The safety of addition of nitrous oxide to general anaesthesia in at-risk patients having major non-cardiac surgery (ENIGMA-II): a randomised, single-blind trial. Lancet. Volume 384, No. 9952, October 2014, 1446-1454.
  10. Mascha EJ. Intraoperative Mean Arterial Pressure Variability and 30-day Mortality in Patients Having Noncardiac Surgery. 2015 Jul;123(1):79-91.
  11. Futlier E et al. Effect of Individualized vs Standard Blood Pressure Management Strategies on Postoperative Organ Dysfunction Among High-Risk Patients Undergoing Major Surgery: A Randomized Clinical Trial. 2017Oct 10;318(14):1346-1357.
  12. Roshanov PS et al. Withholding versus Continuing Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers before Noncardiac Surgery: An Analysis of the Vascular events In noncardiac Surgery patIents cOhort evaluatioN Prospective Cohort. 2017Jan;126(1):16-27.

 

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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.

KIRKUS REVIEW

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:

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LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

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TEN REASONS WHY PHYSICIAN ANESTHESIOLOGY IS AN ESTEEMED PROFESSION

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Some people have difficulty seeing the outstanding merits of the profession of anesthesiology. I understand where these opinions come from, but the phenomenon still bothers me. Today I read a thoughtful and well-written essay in Anesthesiology News titled, Anesthesiologists-The Utility Players of the Medical Field written by anesthesiologist David Stinson MD from my native state of Minnesota. His thesis is that, like utility players on a baseball team, we are valuable but suffer an identity crisis. He writes, “Our specialty, anesthesia, has suffered an identity crisis for decades. Are we the ‘captain of the ship’ or is the surgeon? . . . It is never quite clear and the answer changes with location and context. Are we physicians or are we glorified advanced practice nurses?”

To me, the appropriate headline should read, “Anesthesiologists—the Most Valuable Players of the Medical Team.” I’d like to see an anesthesiologist saying, “I’m going to Disney World” at the end of the Super Bowl before picking up his (or her) MVP trophy.

Why would I say this? Two anecdotes will illustrate why I understand the problem. In the late 1970’s I was a third-year medical student at a prominent Midwestern medical school, where an unspoken rank system existed in the operating room. The surgical attendings were the kings, the students were the peasants, the nurses and techs were serfs, and the anesthesiologists were the whipping boys for the surgeons. I witnessed consistent verbal abuse, bullying, condescending barking commands, and lack of respect directed from surgeons toward anesthesiologists. One day I was scrubbed in as a retractor-holding medical student on a 12-hour esophagectomy, and at the conclusion of the procedure the attending surgeon removed his gloves and gown and left the room to talk to the family. Five minutes later, the patient had a cardiac arrest. The resuscitation was not successful, and the patient died. Afterward the surgeon bellowed his disapproval regarding how the anesthesia team had failed to keep the patient alive after he had spent all day “curing” the patient. It was an unforgettable experience to me, and one of the take-home messages was that I never wanted to be an anesthesiologist.

Fast-forward three years into the future, when I was an internal medicine resident at Stanford serving my medical intensive care unit rotation. The anesthesiology department ran the ICUs at Stanford during the 1980’s. The ICU attendings were charismatic, smart, decisive, impressive role models. The ICU attendings had respectful peer relationships with all the surgeons, including the private-practice cardiac surgeons whose post-operative patients were housed in the ICU. Morning rounds, evening rounds, and the eight hours in between were filled with action, procedures, upbeat emotions, and encouraging talk about the specialties of anesthesiology and critical care medicine. The Stanford anesthesia residents boasted of weekdays off after their nights on call, Learjet trips to harvest donor hearts for Dr. Norm Shumway’s cardiac transplant patients, weeklong trips to third-world countries to perform anesthetics on cleft lip and palate patients, and best of all, the excitement of inserting endotracheal tubes, arterial lines, central lines, Swan Ganz catheters, spinal and epidural needles into patients of all sizes and surgical needs. This was alluring to internal medicine residents. Each year a significant number of internal medicine residents applied for admittance to anesthesiology residencies, which is what I did. Were surgeons hollering at the anesthesiologists at Stanford? In a word . . . no. The department had the respect of the surgeons. This was the environment I grew up in, and the professional spirit we all should aspire to.

Here are 10 reasons why anesthesiologists should hold their heads high and never have a molecule of low self esteem around their medical center:

  1. All of acute care medicine is based on A-B-C, or Airway-Breathing-Circulation. Operating room medicine, intensive care medicine, emergency room medicine, trauma helicopter medicine, and battlefield medicine are all based on A-B-C, or Airway-Breathing-Circulation. Who are the experts of the A, or Airway? Anesthesiologists are the experts. There can be no acute care resuscitation without someone managing the airway, usually with an endotracheal tube. It’s true that other medical professionals have abilities to place endotracheal tubes, but none of them have the breadth of skills, techniques, and volume of attempts as anesthesiologists do. Hold your heads high. Read my column on bullying in the operating room. Don’t put up with condescending behavior from a surgeon. Surgeons know how to wield a scalpel. You know how to wield the most valuable tool of all medical equipment, the laryngoscope.78432-7985650
  2. It’s true that surgeons bring the patients to the operating room for surgery. It’s just as true that none of those patients would agree to the operations without having an anesthetic. The anesthesiologist’s role is vital.
  3. Clinic doctors are important. They manage primary care as well as outpatient specialty care. They make diagnoses and prescribe therapeutic medicines. Anesthesiologists also partake in clinic care in preoperative clinics and pain clinics. An anesthesiologist’s knowledge of internal medicine isn’t as comprehensive as a board-certified internist, but the consider the flip side: None of the internists can administer general anesthesia, regional anesthesia, or manage the A of the A-B-Cs like an anesthesiologist can. I was an internal medicine doctor who lacked these skills and then acquired them during anesthesia residency. Trust me—internists envy the skills of anesthesiologists.
  4. Anesthesiologists deal with life and death situations on a regular basis. Clinic doctors, including surgeons on their days in clinic, listen to and talk to patients. There is no peril in outpatient clinic medicine. On any given day at your job as an anesthesiologist you could be attending to a morbidly obese adult, a tiny child, a frail geriatric patient, or an emergency thoracic case. Your heart rate will climb as high as the patient’s, and you’ll manage the circumstances. Anesthesiologists are goalies at the Pearly Gates, and we should be proud of it.
  5. Physician anesthesiologists have a fascinating job. Anesthesiologists administer anesthetics to virtually every specialty: general surgery, cardiac surgery, neurosurgery, obstetrics, gynecology, otolaryngology, orthopedic surgery, podiatry, ophthalmology, plastic surgery, psychiatry for electroshock therapy, invasive radiologists, cardiologists, oral surgeons, dentists, and pediatric surgeons. The breadth of knowledge across specialties is unrivaled by any other physician.
  6. Who is the captain of the ship in the operating room? Is it the surgeon or is it the anesthesiologist? My advice is: don’t concede the role to your surgical colleague alone. He or she knows how to do the operation. You know how to do the anesthetic. It is a symbiotic relationship. Do not lay yourself down on the ground in reverence. In the words of the Eagles song “Peaceful Easy Feeling,” “she can’t take you anywhere you don’t already know how to go.” If you see and feel yourself as the servant, second in command, that’s where you’ll find yourself . . . as the servant, second in command. Step up. Be an equal. Be in control of your domain, a critical domain.
  7. Physician anesthesiologists are well paid. Per U. S. News and World Report, an anesthesiologist is the highest paying job in America. Think about that. There are 325 million people in our country, and there are thousands of different job descriptions. Your profession is the highest paid. Be proud of that.
  8. Physician anesthesiologists are in demand. As I write this in 2018, I receive multiple emails per day seeking attending anesthesiologists for jobs around the USA. If you’re willing to relocate and be mobile, you’ll find numerous suitors competing for your services as an attending anesthesiologist. Per U.S. News and World Report, the unemployment rate for anesthesiologists is a paltry 0.5%.
  9. Physician anesthesiologists help people every day. You could be selling Coca Cola or cell phones or cell phone data networks or stocks. Would you be serving humanity as well if you were working in some business job? You have the opportunity to change lives for hundreds of patients per year.
  10. Maybe you’re worried that nurse anesthetists will take your job away. I have no crystal ball to foretell the future, but consider these things: (a) Most CRNAs work in anesthesia care team models with our physician anesthesiologist colleagues, and this MD-CRNA relationship is a well accepted model of patient care that will persist into the future; (b) Physician anesthesiologists are needed for leadership roles in clinical care, administration, committees, and quality assurance; and (c) Remember that you are a physician and CRNAs are not. Keep up your skills. The large medical systems of the future will tier their anesthesia coverage. Complex cases will always require MD anesthesiologists. It’s likely that simple cases such as cataracts, lymph node biopsies, and knee arthroscopies can be safely done with CRNA anesthesia. Continue to seek out and perform difficult anesthetic cases only an MD would feel comfortable doing. If you find yourself attending to only ASA I an ASA II patients for straightforward surgeries, you may indeed find your job taken by someone with less training. Instead, step up. Be proud of your training, your unique skills, the heritage of your profession, and the esteem of your standing among your fellow physicians.

 

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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.

KIRKUS REVIEW

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:

41wlRoWITkL

LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

DSC04882_edited

 

FRAILTY AND ANESTHESIA

 

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What if your patients, especially elderly patients, could enter their personal data and symptoms into an iPad app, and what if that information could help you determine if their risk for anesthesia was too great to risk having surgery? Can you imagine this? It will happen someday soon.

Webster’s Dictionary defines frailty as “the condition of being weak and delicate.”

Frailty is also a medical term with an accepted definition of “a multisystem loss of physiologic reserve that makes a person more vulnerable to disability during and after stress.”1

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The majority of frail patients are elderly. My training was in both internal medicine and anesthesiology, and the intersection of these two fields is geriatric anesthesia. I have both an interest and expertise in the evaluation and management of geriatric surgery patients. Metrics of frailty exist, and the evaluation of a patient’s frailty index will become an important part of geriatric anesthesia care.

The geriatric population is increasing in size, and the number of elderly patients undergoing surgery is increasing as well. More than half of all operations in the United States are performed on patients of ages ≥65 years, and this proportion will continue to increase.2

In the past a physician’s assessment of a patient’s frailty was an “eyeball” judgment, dependent on how robust versus how frail a patient looked, and dependent on an interpretation of the patient’s active medical problems. Medical researchers began to seek a quantitative metric for frailty, and they proposed frailty evaluation tools.

Dr. Linda Fried developed one of the first frailty indexes in 2001. She studied 5317 men and women 65 years of age or older, and tabulated their answers to questions regarding these five criteria of the Fried Frailty Index: 1,3

  1. Unintentional weight loss. The patient is asked the question, “In the last year, have you lost more than 10 lb unintentionally (i.e., not as a result of dieting or exercise)?” Patients answering “Yes” are categorized as frail by the weight loss criterion.
  2. The patient is read the following two statements: (1) I felt that everything I did was an effort; (2) I could not get going. The question is asked, “How often in the last week did you feel this way?” The patient’s response is rated as follows: 0 = rarely or none of the time (<1 day); 1 = some or little of the time (1 to 2 days); 2 = a moderate amount of the time (3 to 4 days); or 3 = most of the time.
  3. Muscle weakness. The patient is asked about weekly physical activity. Patients with low physical activity are categorized as frail by the physical activity criterion.
  4. Slowness while walking. The patient is asked to walk a short distance and timed. Patients who are slow walkers are categorized as frail by the walk time criterion.
  5. Grip strength. The patient’s grip strength is measured. Patients with decreased grip strength are categorized as frail by the grip strength criterion.

Frailty was defined as a clinical syndrome in which three or more of these five criteria were present. The overall prevalence of frailty in this age>65 patient population was 6.9%. The prevalence of frailty increased with age, and was higher in women than men. The frailty phenotype was predictive of falls, worsening mobility or disability, hospitalization, and death. Fried’s conclusion, a novel one at the time, was that “frailty was not synonymous with either comorbidity or disability, but that comorbidity was an etiologic risk factor for frailty, and disability was an outcome of frailty.”

Multiple frailty indexes have been proposed. Velanovich et al proposed a modified Frailty Index using 11 pre-operative variables:4

  1. History of diabetes
  2. Impaired functional status
  3. History of chronic obstructive pulmonary disease or pneumonia
  4. History of congestive heart failure
  5. History of MI within 6 months
  6. History of percutaneous coronary intervention
  7. Cardiac surgery or angina
  8. Antihypertensive medication use
  9. Peripheral vascular disease or rest pain
  10. Impaired sensory faculties
  11. History of transient ischemic attack or cerebrovascular accident with persistent residual deficit

This modified Frailty Index correlated positively with the 30-day morbidity and mortality among almost a million patients who underwent surgery between 2005 and 2009 across all surgical specialties.

Other researchers, using a variety of frailty scales, have found that increasing frailty correlates with poorer outcomes after surgery. Researchers at the Seoul National University Bundang Hospital enrolled 275 consecutive elderly patients (aged ≥65 years) who were undergoing intermediate-risk or high-risk elective operations.5

A comprehensive geriatric assessment (CGA) was performed before surgery. The CGA included 6 areas: burden of comorbidity, polypharmacy, physical function, psychological status, nutrition, and risk of postoperative delirium. 9.1% of the patients died during the follow-up period of 11.5-16.1 months, including 4 in-hospital deaths after surgery. 10.5% of the patients experienced at least one complication (e.g., pneumonia, delirium, or urinary tract infection) after surgery, and 8.7% required discharge to inpatient nursing facilities. This CGA frailty score predicted all-cause mortality rates more accurately than the American Society of Anesthesiologists classification. The following factors were associated with increased mortality rates: burden of comorbidity, dependence in activities of daily living, dependence in instrumental activities of daily living, dementia, risk of delirium, short midarm circumference, and malnutrition.

Why was the frailty score more predictive than the ASA score? Geriatric patients often have multiple comorbidities and physiological changes that impair their functional reserve. The assessment of frailty is used to account for these factors.

Contrast the frailty indexes described above to the American Society of Anesthesiologists preoperative assessment scores of ASA 1, 2, 3, 4 , and 5, below:6

ASA I A normal healthy patient Healthy, non-smoking, no or minimal alcohol use
ASA II A patient with mild systemic disease Mild diseases only without substantive functional limitations. Examples include (but not limited to): current smoker, social alcohol drinker, pregnancy, obesity (30 < BMI < 40), well-controlled DM/HTN, mild lung disease
ASA III A patient with severe systemic disease Substantive functional limitations; One or more moderate to severe diseases. Examples include (but not limited to): poorly controlled DM or HTN, COPD, morbid obesity (BMI ≥40), active hepatitis, alcohol dependence or abuse, implanted pacemaker, moderate reduction of ejection fraction, ESRD undergoing regularly scheduled dialysis, premature infant PCA < 60 weeks, history (>3 months) of MI, CVA, TIA, or CAD/stents.
ASA IV A patient with severe systemic disease that is a constant threat to life Examples include (but not limited to): recent ( < 3 months) MI, CVA, TIA, or CAD/stents, ongoing cardiac ischemia or severe valve dysfunction, severe reduction of ejection fraction, sepsis, DIC, ARD or ESRD not undergoing regularly scheduled dialysis
ASA V A moribund patient who is not expected to survive without the operation Examples include (but not limited to): ruptured abdominal/thoracic aneurysm, massive trauma, intracranial bleed with mass effect, ischemic bowel in the face of significant cardiac pathology or multiple organ/system dysfunction

 

ASA scores are the currently accepted way physicians stratify patient surgical risk. An ASA IV patient with a severe systemic disease that is a constant threat to life will likely have a high frailty index, but the correlation is not absolute. A chronically ill, weak, elderly patient who is losing weight and is inactive may not have an obvious severe systemic disease such as coronary artery disease, cerebral vascular disease, end-stage renal disease, or sepsis, which would qualify them as ASA IV. But a chronically ill, weak, elderly patient who is losing weight and is inactive may have a very high frailty index, and may have a perioperative risk equivalent to any ASA IV patient.

Kennedy created a 30-item Frailty Index in the Canadian Multicentre Osteoporosis Study.7 Their frailty index proved to be a sensitive measure to quantify fracture risk over the next 10 years. McMaster University professors then authored the Fit-Frailty App (available at Apple or Google App Store), a smartphone/iPad app based on the 30-item Canadian Multicentre Osteoporosis Study Frailty Index from the Kennedy study. It takes only minutes for a patient to answer the questions on the app, and the app generates a frailty score, which ranges from 0 to 1.0.

The Edmonton Frail Scale (available at Apple or Google App Store) is a 9-criteria survey which quantifies a frailty score from 0–17. It’s easy to use, and takes about 2–3 minutes to complete.

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I predict you’ll see patients filling out frailty apps such as these on iPads in the future, with anesthesiologists and internal medicine doctors using the frailty score as part of their preanesthetic evaluation. You can also expect research on whether intervention or modification of frailty criteria prior to surgery results in lower postoperative complication rates. Frailty index research may lead us to stratify surgical treatments for healthier subsets of geriatric patient populations who are at a lower risk of complications, and provide guidance regarding the proper management of the more frail geriatric patients found to have a higher risk of adverse outcomes after surgery.

Fire up your iPads, download these frailty apps, and see how fit or frail your patients are right now.

References:

  1. Sieber F, Pauldine R, Geriatric Anesthesia, Miller’s Anesthesia, Chapter 80, 5th edition, 2407-2422.
  2. Etzioni  DA, et al. The aging population and its impact on the surgery workforce. Ann Surg. 2003;238(2):170-177.
  3. Fried LP et al. Frailty in Older Adults: Evidence for a Phenotype, The Journals of Gerontology: Series A, Volume 56, Issue 3, 1 March 2001, Pages M146–M157.
  4. Velanovich V, Antoine H, Swartz A, Peters D, Rubinfeld I. Accumulating deficits model of frailty and postoperative mortality and morbidity: its application to a national database. Journal of Surgical Research2013; 183: 104–10.
  5. Kim S-W et al, Multidimensional Frailty Score for the Prediction of Postoperative Mortality Risk, JAMA Surg. 2014;149(7):633-640.
  6. https://www.asahq.org/resources/clinical-information/asa-physical-status-classification-system
  7. Kennedy CC et al, A Frailty Index predicts 10-year fracture risk in adults age 25 years and older: results from the Canadian Multicentre Osteoporosis Study (CaMos) Osteoporosis International, December 2014, Volume 25, Issue 12, pp 2825-2832.

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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.

KIRKUS REVIEW

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:

41wlRoWITkL

LEARN MORE ABOUT RICK NOVAK’S FICTION WRITING AT RICK NOVAK.COM BY CLICKING ON THE PICTURE BELOW:

DSC04882_edited