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Emergency Management of Marijuana Psychosis

Details: Published: Tuesday, 28 July 2015 12:44

Marijuana is a commonly used drug. In some states it is legal. The following article appeared in the Western Journal of Emergency Medicine, and it describes the correct approach and standard of practice in the treatment of marijuana overdose resulting in psychosis in the emergency department. The citation is noted at the bottom of the article.

Abstract and Introduction

Abstract

We use a case report to describe the acute psychiatric and medical management of marijuana intoxication in the emergency setting. A 34-year-old woman presented with erratic, disruptive behavior and psychotic symptoms after recreational ingestion of edible cannabis. She was also found to have mild hypokalemia and QT interval prolongation. Psychiatric management of cannabis psychosis involves symptomatic treatment and maintenance of safety during detoxification. Acute medical complications of marijuana use are primarily cardiovascular and respiratory in nature; electrolyte and electrocardiogram monitoring is indicated. This patient's psychosis, hypokalemia and prolonged QT_c interval resolved over two days with supportive treatment and minimal intervention in the emergency department. Patients with cannabis psychosis are at risk for further psychotic sequelae. Emergency providers may reduce this risk through appropriate diagnosis, acute treatment, and referral for outpatient care.

Introduction

Already the most commonly used illicit drug in the United States, marijuana (or cannabis) is becoming more widely used and more potent with expanded legalization.^[1–3] Legalization has also popularized "edible" forms of marijuana, including teas and food products. Although often portrayed as a harmless drug with potential therapeutic uses, marijuana has detrimental effects on brain development, psychiatric health (eg, psychosis, schizophrenia, depression and anxiety), lungs (eg, chronic bronchitis and lung cancer) and heart (eg, myocardial infarction and arrhythmias).^[2] Public perception of these risks decreases with legalization, and no guidelines exist to help patients gauge the personal safety of use.^[4,5] As emergency providers treat more patients with cannabis use disorders, they must educate patients about these chronic health risks and also manage the acute medical and psychiatric complications of marijuana intoxication.

To illustrate the management of acute complex marijuana intoxication and psychosis, we present a case of a woman requiring prolonged emergency department management after ingestion of edible tetrahydrocannabinol (THC), the active ingredient in marijuana.

Case Report

A 34-year-old woman with no significant psychiatric history presented to the emergency department (ED) with erratic and disruptive behavior. She broke into a neighbor's home, requesting to "go to heaven." She feared people were stealing from her and that "something bad" was going to happen. She reported insomnia, racing thoughts, and euphoria for the past week.

Upon arrival to the ED, her vital signs were temperature of 36.4°C, heart rate of 96bpm, blood pressure 148/111mmHg, and respiratory rate of 11. She was difficult to redirect and her mental status revealed a thin, "nervous," well-groomed woman with a labile affect and pressured speech. The patient's thought process was loose and disorganized with thought blocking. She was paranoid, grandiose, hyper-religious, and endorsed auditory hallucinations. She denied suicidal or homicidal ideation. Her attention and memory were considered impaired though not formally tested.

The patient admitted to using cannabis lip balm and consuming edible cannabis chocolate bars daily over the past week, most recently the day of presentation. She could not quantify her consumption. She believed her paranoia and insomnia onset coincided with her THC ingestion last week. The patient denied other recent substance or alcohol use. She denied any falls or history of traumatic brain injuries. A friend of the patient confirmed this history. Her other medications included propranolol 20mg twice a day for hypertension and infrequent sumatriptan as needed for migraines. Family history of mental illness was unknown since the patient was adopted.

For this presentation of acute psychosis, emergency medical providers conducted a comprehensive work-up to exclude organic etiologies of psychosis or concurrent medical morbidity. A basic metabolic panel was significant for a potassium level of 3.2mg/dL (reference range: 3.5–5.0); her electrocardiogram (EKG) demonstrated a prolonged QT_c of 508ms, a pulse of 86, and no U waves or T wave changes. A 9-carboxy-THC level was over 500ng/mL; her urine toxicology screen was negative for cocaine, amphetamines, benzodiazepines, and opioids. A B12 level was elevated at 1186pg/mL. Her complete blood count and a noncontrast head computerized tomography (CT) study were unremarkable.

The patient refused supplemental potassium, and it was thought that her EKG findings did not warrant emergent, forcible repletion. She also removed her intravenous line while agitated. She was placed in two-point soft restraints for her safety. After consultation with psychiatry, the patient was deemed medically appropriate for transfer to the ED's psychiatric emergency service (PES) for further evaluation and treatment.

In the PES, the patient was hypersexual, hyperactive, and intrusive, entering other patients' rooms and touching them. As she could not be safely re-directed, physical restraints were again ordered for the patient's and others' safety. Risperidone 0.5mg PO q6hr and lorazepam 1mg PO q6hr were ordered as needed for management of psychosis and anxiety; the patient required one dose of each during her PES stay.

Twenty-four hours after presentation, her psychotic symptoms and anxiety persisted: she suggested that her food was poisoned and asked whether she was African-American (though she was Caucasian). The patient claimed to have forgotten her father's name, did not know where she was currently living, and was oriented only to person and place. She received her scheduled propranolol for hypertension and 40meq of oral potassium chloride (which she had earlier refused). Her consciousness and attention were intact.

Forty-eight hours after presentation, the patient's paranoia and hallucinations improved dramatically. The patient was able to reflect on the unreality of her paranoia and "odd thoughts" of being African-American. With improved insight, she confirmed heavy use of multiple edible THC products in addition to frequent coffee and energy drink consumption, which she had difficulty quantifying. The patient was diagnosed with cannabis-induced psychotic disorder and severe marijuana use disorder; she was instructed to follow up with outpatient mental health to ensure resolution of her psychosis and begin substance abuse treatment.

Discussion

New-onset psychosis is a medical emergency with a broad differential.^[6] Signs and symptoms concerning for a medical etiology of psychiatric symptoms include abnormal vital signs, altered consciousness, or lack of prior psychiatric history in a patient over 40 years old.^[7] The acute onset of symptoms with marijuana use, high serum marijuana metabolite levels, and symptomatic resolution with detoxification suggest these symptoms were secondary to marijuana use.

Cannabis-induced psychotic disorder ("cannabis psychosis") is diagnosed when psychotic symptoms persist beyond acute intoxication and may require clinical management.^[8] Psychiatric symptoms include paranoia, derealization, disorganized thinking, persecutory and grandiose delusions, hallucinations, and cognitive impairment. Patients pose a danger to others and themselves due to their altered sense of reality. Safe cannabis detoxification typically requires 24 hours, but sometimes longer for patients with unstable vital signs and persistent psychosis. Benzodiazepines are recommended for agitation related to stimulant intoxication – unless psychosis is present, in which case oral atypical antipsychotics are considered first-line.^[9]

Cannabis blood levels reflect the extent and chronicity of marijuana use. A free THC level below 3ng/mL (μg/L) suggests occasional consumption (≤1 joint/week) while a concentration higher than 40ng/mL corresponds to heavy use (≥10 joints/month).^[10] Levels above 10ng/mL impair motor function, leading two states with legal recreational marijuana to establish the legal limit for driving at 5ng/mL. In clinical practice, measuring an inactive metabolite of THC, 9-carboxy THC, is preferred due to the rapid decrease in free serum THC levels.^[11] In a prior case report, oral cannabis-induced psychosis resolved within 24 hours after recorded serum THC levels below 20ng/mL, or 9-carboxy-THC levels below 50ng/mL; the authors suggested that oral administration may not achieve high serum THC levels.^[12] Our patient's 9-carboxy-THC level over 500ng/mL demonstrates that oral administration can achieve high serum THC levels and suggests a dose-response relationship between serum metabolite levels and the severity of psychosis. Moreover, serum drug levels may anticipate a patient's clinical course.

The medical risks of acute cannabis use are primarily cardiovascular in nature. THC enhances sympathetic tone, thereby increasing heart rate and blood pressure.^[13] Marijuana increases the risk of myocardial infarction within one hour of use, and cardiovascular events have been reported in otherwise healthy patients.^[5,14,15] A Norwegian autopsy study suspected THC-induced arrhythmias (including ventricular tachycardia and fibrillation) as the culprit in six patients who died suddenly.^[15,16] Electrocardiograms should be obtained for patients with severe cannabis intoxication; telemetry monitoring may be considered for patients with known cardiac pathology.

Electrolyte abnormalities reported in marijuana users contribute to this cardiac pathology. Chronic marijuana users have lower serum sodium and potassium than non-users.^[17] The heavy consumption of carbohydrates while intoxicated leads to an increase in serum insulin levels, driving potassium into cells and causing serum hypokalemia.^[18] This hypokalemia can produce reentrant arrhythmias by decreasing conductivity and increasing the resting membrane potential, duration of the action potential, and duration of the refractory period.^[19] EKG changes include the decrease in T-wave amplitude, presence of U waves and a prolonged QTc. This patient's very high THC metabolite level, prolonged QTc, and hypokalemia increased her risk for an arrhythmia. The hypokalemia observed in this case was likely related to acute intracellular potassium shifts superimposed on chronic hypokalemia.

Clinicians must manage other, non-vascular risks of acute marijuana use. Respiratory symptoms include shortness of breath, wheezing, and even respiratory failure when marijuana has been smoked "wet" with phenylcyclidine or embalming fluid.^[20,21] Patients with pre-disposing genetic vulnerabilities may develop hypokalemic periodic paralysis.^[18] And, marijuana use correlates with fatal motor vehicle collisions – clinicians should educate patients and ensure a safe transportation plan on discharge.^[22]

Patients with toxic ingestion must be screened for co-ingestion. The persistence and intensity of the patient's symptoms warranted consideration of multiple involved substances. Co-ingestion may also be signaled by an abnormal osmolar or anion gap, positive urine toxicology screen, or QTc or QRS prolongation (Only QTc prolongation was present here).^[23,24] However, in many cases, the presence of co-ingestion may only be detected once the patient is able to provide a reliable history. In this case, an elevated B12 level was found on work up of the patient's psychiatric symptoms and suspected to have been caused by energy drink consumption; only later did the patient confirm this suspicion. By its effects on mesolimbic dopamine activity, caffeine may precipitate psychosis, exacerbate chronic psychosis, or worsen affective lability and mood states.^[25–28] This patient's high THC metabolite level and medical course are consistent with cannabis psychosis; however, we cannot exclude excessive caffeine use as a contributor to this presentation.

What is this patient's prognosis? Marijuana correlates with the onset of psychosis in patients with schizophrenia and perhaps bipolar disorder as well.^[29–32] About half of patients with cannabis psychosis will later be diagnosed with a primary psychotic disorder.^[8,33] This high rate may reflect high rates of marijuana use among patients with schizophrenia. Younger age, greater frequency of marijuana use, family history of psychosis, trauma history, and schizotypal personality correlate with higher risk of a later diagnosis of primary psychosis.^[8] ED providers can mitigate the risk of psychopathology by addressing the patient's substance use disorder. Safe detoxification is a primary goal and was accomplished here; brief interventions like motivational interviewing and referral for treatment in the ED may reduce use on discharge.^[34,35]

References

Choo EK, Benz M, Zaller N, et al. The impact of state medical marijuana legislation on adolescent marijuana use. J Adolescent Health. 2014;55(2):160–166.
Volkow ND, Baler RD, Compton WM, et al. Adverse health effects of marijuana use. N Engl J Med. 2014;370(23):2219–2227.
Sevigny EL, Pacula RL, Heaton P, et al. The effects of medical marijuana laws on potency. Int J Drug Policy. 2014;25(2):308–319.
Schuermeyer J, Salomonsen-Sautel S, Price RK, et al. Temporal trends in marijuana attitudes, availability and use in Colorado compared to non-medical marijuana states: 2003–11. Drug Alcohol Depend. 2014;140:145–155.
Rezkalla SH, Sharma P, Kloner RA. Coronary no-flow and ventricular tachycardia associated with habitual marijuana use. Ann Emerg Med. 2003;42:365–369.
Nordstrom K, Zun LS, Wilson MP, et al. Medical evaluation and triage of the agitated patient: consensus statement of the American association for emergency psychiatry project BETA medical evaluation workgroup. Western J Emerg Med. 2012;13(1):3–10.
Sood, TR, McStay CM. Evaluation of the psychiatric patient. Emerg Med Clin North Am. 2009;27(4):669–683.
Radhakrishnan R, Wilkinson ST, D'Souza DC. Gone to pot - a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:1–24.
Wilson MP, Pepper D, Currier GW, et al. The psychopharmacology of agitation: consensus statement of the american association for emergency psychiatry project BETA psychopharmacology workgroup. Western J Emerg Med. 2012;13(1):26–34.
Fabritius M, Favrat B, Chtioui H, et. al. THCCOOH concentrations in whole blood: are they useful in discriminating from heavy smokers? Drug Test Anal. 2014;6(1–2):155–63.
Sharma, P, Murthy P, Bharath MM. Chemistry, metabolism, and toxicology of cannabis: clinical implications. Iran J Psychiatry. 2012;7(4):149–156.
Favrat B, Menetrey A, Augsburger M, et al. Two cases of "cannabis acute psychosis" following the administration of oral cannabis. BMC Psychiatry. 2005;5:17.
Aryana A, Williams MA. Marijuana as a trigger of cardiovascular events: Speculation or scientific certainty? Int J Cardiol. 2007;118(2):141–144.
Mittleman MA, Lewis RA, Maclure M, et al. Triggering myocardial infarction by marijuana. Circulation. 2001;103:2805–2809.
Charles R, Holt S, Kirkham N. Myocardial infarction and marijuana. Clin Toxicol. 1979;14(4):433–438.
Bachs L, Morland H. Acute cardiovascular fatalities following cannabis use. Forensic Sci Int. 2001;124:200–203.
Osadolor HB, Emokpae AM. Effects of marijuana on sodium and potassium ions homeostasis among smokers in benin city - a metropolitan city in nigeria. International Journal of Pharma and Bio Sciences. 2010;1(3):1–3.
Feldman ML, Hadfield S. Pot paresis: marijuana and a case of hypokalemic periodic paralysis. J Emerg Med. 2009;36(3):236–238.
Helfant, RH. hypokalemia and arrhythmias. Am J Med. 1986;80(4):13–22.
Lutchmansingh D, Pawar L, Savici D. Legalizing cannabis: a physician's primer on the pulmonary effects of marijuana. Curr Respir Care Rep. 2014;3(4):200–205.
Gilbert CR, Baram M, Cavarpocchi NC. "Smoking west": respiratory failure related to smoking tainted marijuana cigarettes. Tex Heart Inst J. 2013;40(1):64–67.
Asbridge M, Hayden JA, Cartwright JL. Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis. BMJ. 2012;344.
Holstege C, Borek H. Toxidromes. Crit Care Clin. 2012;28:479–498.
Mokhlesi B, Leiken JB, Murray P, et al. Adult toxicology in critical care – part I: general approach to the intoxicated patient. CHEST. 2003;123:577–592.
Nehlig A, Daval JL, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev. 1992;17(2):139–169.
Hedges DW, Woon FL, Hoopes SP. Caffeine-induced psychosis. CNS Spectrum. 2009;14(3):127–129.
Shaul PW, Farrell MK, Maloney MJ. Caffeine toxicity as a cause of acute psychosis in anorexia nervosa. J Pediatr. 1984;105(3):493–495.
Szpak A, Allen D. A case of acute suicidality following excessive caffeine intake. J Psychopharmacol. 2012;26(11):1502–1510.
Moore THM, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370(9584):319–328.
Large M, Sharma S, Compton MT, et al. Cannabis use and earlier onset of psychosis: a systematic meta-analysis. Arch Gen Psychiatry. 2011;68(6):555–561.
Gibbs M, Winsper C, Marwaha S, et al. Cannabis use and mania symptoms: a systematic review and meta-analysis. J Affect Disord. 2014;171C:39–47.
Bally N, Zullino D, Aubry JM. Cannabis use and first manic episode. J Affect Disord. 2014;165:103–108.
Arendt M, Rosenberg R, Foldager L, et al. Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: followup study of 535 incident cases. Br J Psychiatry. 2005;187:510–515.
Woodruff SI, Eisenberg K, McCabe CT, et al. Evaluation of california's alcohol and drug screening and brief intervention project for emergency department patients. West J Emerg Med. 2013;14(3):263–270.
Magill M, Barnett NP, Apodaca TR, et al. The role of marijuana use in brief motivational intervention with young adult drinkers treated in an emergency department. J Stud Alcohol Drugs. 2009;70(30):409–413.

Emergency Treatment of Marijuana Psychosis

Details: Published: Tuesday, 28 July 2015 12:30

Abstract and Introduction

Abstract

Introduction

Case Report

Discussion

References

Choo EK, Benz M, Zaller N, et al. The impact of state medical marijuana legislation on adolescent marijuana use. J Adolescent Health. 2014;55(2):160–166.
Volkow ND, Baler RD, Compton WM, et al. Adverse health effects of marijuana use. N Engl J Med. 2014;370(23):2219–2227.
Sevigny EL, Pacula RL, Heaton P, et al. The effects of medical marijuana laws on potency. Int J Drug Policy. 2014;25(2):308–319.
Schuermeyer J, Salomonsen-Sautel S, Price RK, et al. Temporal trends in marijuana attitudes, availability and use in Colorado compared to non-medical marijuana states: 2003–11. Drug Alcohol Depend. 2014;140:145–155.
Rezkalla SH, Sharma P, Kloner RA. Coronary no-flow and ventricular tachycardia associated with habitual marijuana use. Ann Emerg Med. 2003;42:365–369.
Nordstrom K, Zun LS, Wilson MP, et al. Medical evaluation and triage of the agitated patient: consensus statement of the American association for emergency psychiatry project BETA medical evaluation workgroup. Western J Emerg Med. 2012;13(1):3–10.
Sood, TR, McStay CM. Evaluation of the psychiatric patient. Emerg Med Clin North Am. 2009;27(4):669–683.
Radhakrishnan R, Wilkinson ST, D'Souza DC. Gone to pot - a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:1–24.
Wilson MP, Pepper D, Currier GW, et al. The psychopharmacology of agitation: consensus statement of the american association for emergency psychiatry project BETA psychopharmacology workgroup. Western J Emerg Med. 2012;13(1):26–34.
Fabritius M, Favrat B, Chtioui H, et. al. THCCOOH concentrations in whole blood: are they useful in discriminating from heavy smokers? Drug Test Anal. 2014;6(1–2):155–63.
Sharma, P, Murthy P, Bharath MM. Chemistry, metabolism, and toxicology of cannabis: clinical implications. Iran J Psychiatry. 2012;7(4):149–156.
Favrat B, Menetrey A, Augsburger M, et al. Two cases of "cannabis acute psychosis" following the administration of oral cannabis. BMC Psychiatry. 2005;5:17.
Aryana A, Williams MA. Marijuana as a trigger of cardiovascular events: Speculation or scientific certainty? Int J Cardiol. 2007;118(2):141–144.
Mittleman MA, Lewis RA, Maclure M, et al. Triggering myocardial infarction by marijuana. Circulation. 2001;103:2805–2809.
Charles R, Holt S, Kirkham N. Myocardial infarction and marijuana. Clin Toxicol. 1979;14(4):433–438.
Bachs L, Morland H. Acute cardiovascular fatalities following cannabis use. Forensic Sci Int. 2001;124:200–203.
Osadolor HB, Emokpae AM. Effects of marijuana on sodium and potassium ions homeostasis among smokers in benin city - a metropolitan city in nigeria. International Journal of Pharma and Bio Sciences. 2010;1(3):1–3.
Feldman ML, Hadfield S. Pot paresis: marijuana and a case of hypokalemic periodic paralysis. J Emerg Med. 2009;36(3):236–238.
Helfant, RH. hypokalemia and arrhythmias. Am J Med. 1986;80(4):13–22.
Lutchmansingh D, Pawar L, Savici D. Legalizing cannabis: a physician's primer on the pulmonary effects of marijuana. Curr Respir Care Rep. 2014;3(4):200–205.
Gilbert CR, Baram M, Cavarpocchi NC. "Smoking west": respiratory failure related to smoking tainted marijuana cigarettes. Tex Heart Inst J. 2013;40(1):64–67.
Asbridge M, Hayden JA, Cartwright JL. Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis. BMJ. 2012;344.
Holstege C, Borek H. Toxidromes. Crit Care Clin. 2012;28:479–498.
Mokhlesi B, Leiken JB, Murray P, et al. Adult toxicology in critical care – part I: general approach to the intoxicated patient. CHEST. 2003;123:577–592.
Nehlig A, Daval JL, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev. 1992;17(2):139–169.
Hedges DW, Woon FL, Hoopes SP. Caffeine-induced psychosis. CNS Spectrum. 2009;14(3):127–129.
Shaul PW, Farrell MK, Maloney MJ. Caffeine toxicity as a cause of acute psychosis in anorexia nervosa. J Pediatr. 1984;105(3):493–495.
Szpak A, Allen D. A case of acute suicidality following excessive caffeine intake. J Psychopharmacol. 2012;26(11):1502–1510.
Moore THM, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370(9584):319–328.
Large M, Sharma S, Compton MT, et al. Cannabis use and earlier onset of psychosis: a systematic meta-analysis. Arch Gen Psychiatry. 2011;68(6):555–561.
Gibbs M, Winsper C, Marwaha S, et al. Cannabis use and mania symptoms: a systematic review and meta-analysis. J Affect Disord. 2014;171C:39–47.
Bally N, Zullino D, Aubry JM. Cannabis use and first manic episode. J Affect Disord. 2014;165:103–108.
Arendt M, Rosenberg R, Foldager L, et al. Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: followup study of 535 incident cases. Br J Psychiatry. 2005;187:510–515.
Woodruff SI, Eisenberg K, McCabe CT, et al. Evaluation of california's alcohol and drug screening and brief intervention project for emergency department patients. West J Emerg Med. 2013;14(3):263–270.
Magill M, Barnett NP, Apodaca TR, et al. The role of marijuana use in brief motivational intervention with young adult drinkers treated in an emergency department. J Stud Alcohol Drugs. 2009;70(30):409–413.

Surprising Verdicts In Med-Legal Cases

Details: Published: Monday, 01 June 2015 22:13

A recent article by Dr. Segal in Medscape discusses two defensible cases that resulted in surprising horrific outcomes for the two doctors who were sued. There is a take home message and lesson to be learned embedded in these two cases.

How Would You Have Handled Patients Like These?

Being sued for malpractice is a traumatic experience. The odds of being sued at least once over one's career are high.[1] Doctors typically have sufficient professional liability coverage to prevent financial loss. But not all cases get resolved as expected, and doctors may end up with unforeseeable financial loss.

In addition, disciplinary action by a state medical board can also result in onerous remediation, the cost of which can also be surprisingly steep.

It's one thing when a physician clearly did something wrong and as a result suffers the consequences. But what if the wrongdoing isn't clear-cut—yet the financial hit to the doctor is still severe? Consider two unusual cases in point.

Did This Doctor Instruct His Patient?

In 2012, a Georgia jury awarded $3 million dollars to the estate of William Martinez.[1] Martinez was 31 years old when he entered his cardiologist's office. He complained of chest pain radiating into his arm. His cardiologist noted that Martinez was at "high risk" of having coronary disease and ordered a nuclear stress test. The test was scheduled to take place 8 days later.

The day before his test, however, Martinez apparently engaged in some "exertional activity."[2] He participated in a threesome with a woman who was not his wife and a male friend. While in the midst of this three-way sexual experience, Martinez died. Naturally, his family then sued the cardiologist, arguing that no instruction to avoid exertional activity had been given. The family's rationale was that had Martinez been properly instructed to avoid high-risk activities, he would have complied.

During the trial, the cardiologist alleged that Martinez was instructed to avoid exertional activity until after the test was completed.[2]

The family initially claimed $5 million in damages, but this claim was reduced by a finding that Martinez was 40% liable for his own death.[2] So the patient was 40% liable; the liability of the doctor was 60%. If the cardiologist's malpractice policy coverage was for the typical $1 million, it probably leaves him $2 million short.

In states that have implemented substantive tort reform, the sizeable award might have been reduced as a matter of law—if a large portion of that award was attributable to "pain and suffering." In 2010, however, the Georgia Supreme Court overturned that state's law, which set a $350,000 limit on damages paid out for pain and suffering in medical malpractice cases.[1] It ruled that the 5-year-old Georgia law violated a person's constitutional right to trial by jury and a plaintiff's right to allow a jury to calculate noneconomic damages as it sees fit.

That prior decision has concrete implications for physicians—particularly given that most doctors carry only $1 million in malpractice coverage. As such, understand what your policy limits are if you are sued; assess the likelihood that a judgment will exceed those limits in a particular case if you lose; and see whether limiting your downside risk while still allowing you to have your day in court would be helpful, an option discussed next.

Hedging Your Risk if You Go to Court

The patient died young, with decades of unrealized earning capacity. For the physician being sued, this means that if the plaintiff wins, there is a sizable chance of a multimillion-dollar award. Juries are unpredictable. How can a doctor protect himself against a financially crippling judgment when the alternative is to give the carrier permission to pay an amount up to and including the policy limits?

The answer is a high/low agreement. A high/low agreement allows the doctor to both have his day in court and potentially be vindicated with a verdict of "not liable," without having his carrier simply pay the plaintiff an amount up to and including his policy limits (a tacit admission of liability) and not risking his entire nest egg should he lose the judgment.

In a high/low agreement, the each side agrees that there is risk to their case. A doctor may be concerned that an injured patient (such as someone in a wheelchair) will elicit a strong emotional reaction from a jury when testifying about an expensive life-care plan. Or a young widow with little earning capacity may likewise generate sympathy with a jury when they learn that her children will not be able to afford college. Such judgments could be as high as $10 million and bankrupt a doctor.

On the other hand, a plaintiff may be concerned that although the injury was great, the doctor did not violate the standard of care—and even if he did, the doctor's actions did not cause the injury. If the jury agrees, the plaintiff may get nothing.

A contractual high/low agreement between both parties can create settlement "bookends" of, say, $100,000 and $1 million. The doctor gets his day in court. The jury renders its verdict. But each side hedges its risk. If the jury says the doctor is liable for $10 million, the doctor only has to pay the "high" value—or $1 million, typically his policy limit. If the jury finds the doctor not liable, the plaintiff still gets something—in this example, $100,000. In addition, because the jury finds the doctor not liable, there's no report to the National Practitioner Data Bank.

Because there was no way to prove whether the cardiologist had properly advised his patient—because the advice was not documented, it was the doctor's word against that of the family of the deceased—the jury could just as easily have found for 100% for the plaintiff or 100% for the defendant. Given this possibility, a high/low strategy might have helped mitigate risk for the cardiologist.

If you are in a situation with a potentially catastrophic payout, consider bringing up the possibility of this arrangement with your carrier.

Was This Surgeon "Grossly Negligent"?

On December 4, 2010, at 11:47 AM, a patient was admitted to the emergency department (ED) of a hospital in California's Bay Area with a self-reported history of having inserted a bottle into his rectum 2 days earlier.[4] He was in pain and had gone 2 days without a bowel movement. A physician assistant documented distention and diffuse tenderness. A plain abdominal radiograph showed a glass bottle in the mid-pelvis. There was no free air, although the patient was in the supine position.

The surgeon arrived at 2:11 PM and ordered 25 μg of fentanyl for pain.[4]

What happened next resulted in a complaint to the California Board of Medicine. An interview with the surgeon by a board investigator provided the details.[4] The surgeon explained that she had given the patient two options: He could have the bottle removed surgically, or it could be extracted manually in the ED. The surgeon stated that the patient chose the ED route because he did not want to lose his new job. (It is unclear whether this decision was related to a longer perceived recovery time if he had surgery, a higher bill for a surgical procedure, or something else.)

During the interview, the surgeon said that she could feel the bottom of the bottle with one finger but could not move it at all.[4] However, the history and physical documented something else: The surgeon "was able to palpate the bottle and was able to manipulate the bottle and move the foreign body around but was unable to rectally extract it."

During the first part of her interview, the surgeon stated that she placed her hand into the rectum to remove the bottle while the patient pushed.[4]

Nursing notes indicated that the surgeon placed her arm into the rectum up to her bicep, and the patient was screaming in pain.[4] This same nurse said the surgeon did not want the patient to receive any additional pain medication, because she needed the patient conscious for him to help push the bottle out.

The surgeon then performed a rigid sigmoidoscopy, which showed the sigmoid colon to be dusky and swollen. A new abdominal radiograph suggested perforation. The patient was taken to an operating room (OR) for a laparotomy.[4]

The board of medicine detailed its parade of horribles[4]:

Gross negligence: Excessive force while attempting to remove the bottle demonstrated disregard for patient safety and departure from standard of care or incompetence.
Gross negligence: The decision to continue with the procedure in the ED without securing appropriate assistance from nursing staff demonstrated disregard for patient safety and constituted extreme departure from the standard of care.
Repeated negligent acts: Inadequate sedation during attempts to manually extract the bottle constituted departure from the standard of practice.
No informed consent and substandard documentation of procedure note.
No "timeout" was performed before starting the procedure. [Author's note: It's unclear whether the timeout would have been used to verify that the correct patient was about to undergo a procedure, or to confirm that the procedure addressed the correct side of the rectum.]
Dishonesty: There are multiple story lines—was a finger, hand, or arm involved? Was the bottle mobile, or not mobile?

The penalty the board imposed[4]:

25 hours a year (for each year of probation) of education addressing the deficiencies outlined in the complaint.
Complete an approved course on professionalism—at the surgeon's expense, and in addition to other continuing medical education (CME) requirements.
Complete an approved course on medical record-keeping—at the surgeon's expense, and in addition to other CME requirements.
License revoked, but revocation temporarily suspended and surgeon's license placed on probation for 3 years as long as she has no further infractions.
The surgeon will pay the costs of monitoring her probation—currently set at $3999 per year—for each year of probation.

The surgeon was licensed to practice in Ohio as well as California. The Ohio Medical Board learned of the California board's imposed discipline. The Ohio Board wrote to the surgeon stating that it was investigating whether to impose discipline in Ohio as well.[4] The board gave her 30 days from the date of mailing to request a hearing. That deadline was May 12, 2014.

The board received the surgeon's letter on May 15, 2014, and that letter did not include a request for a hearing.[4] (The record is silent on what information the letter did contain. Presumably, it was an explanation of the surgeon's treatment of the case, or why she failed to respond to the Ohio board in a timely manner.)

The board revoked her license.[4]

Ignore a State Licensing Board at Your Peril

Many doctors have licenses in more than one state. Discipline in one state often triggers discipline in another state. Most, if not all, licensing boards mandate that the licensee has an affirmative obligation to notify them of discipline in any other venue (for example, another state, the Centers for Medicare & Medicaid Services, or the US Drug Enforcement Administration) within a couple of weeks of the disciplinary action.

Most disciplinary actions are reportable to the National Practitioner Data Bank, which means that the boards of the state or states in which you are licensed will eventually learn about these actions. If you address such an action proactively, it's considered an "explanation." If you address it after it's discovered by a board, without prior notification by you first, it's considered an "excuse."

As such, if you hear from a licensing board, don't ignore it. Most of the time, they are just looking for your side of the story. Statistically, you are likely to prevail. But if you miss a deadline to respond, you will have wasted an opportunity. Make sure that you respond in a timely manner and document that you sent your response by certified mail with return receipt requested, or by FedEx or UPS with a tracking number. Not all boards will impose the same penalty as the first board. Some boards may rule the opposite of the first board.

There are times and reasons for doing a procedure in the ED instead of the OR: timeliness, OR availability, cost, and patient preference. Whatever the rationale, make sure the record supports your thinking. In this case, the surgeon was on the defensive from the beginning because the record was sparsely documented.

Next, it's okay to stop a procedure if you're not succeeding. The patient may tolerate some amount of pain if the anticipated outcome is a near-term success. At some point, however, that strategy may change—and then it's time to go to the OR. A common manifestation of that strategy is a trial of labor that turns into cesarean section.

The attending nurse's story was dramatically different from the surgeon's story. The nurse documented her story. It's hard to believe that the surgeon was able to place her arm (up to the bicep) into the patient's rectum. But there was no competing narrative in the chart.

Finally, the penalty seems steep both in cost and time. The question is how and why this matter evolved into a board complaint. Perhaps it was a dispute over a residual bill, poor communication, or verbal sparring with the nurse that escalated into score-evening retribution. The record of the case doesn't address these issues.

The Moral: Take Steps to Limit Your Risk

Even when doctors diligently care for their patients, they may be exposed to unexpected liability. If a patient's outcome is poor, judgment at trial may well exceed policy limits. Proper documentation of the medical record and timely responses to board complaints are the best ways to prevent a gray-zone set of facts from evolving into formal discipline by a medical board.

Published in Medscape: 2015, Dr. Segal

Sunscreen Dangers

Details: Published: Tuesday, 31 March 2015 09:34

The US Food and Drug Administration (FDA) is proposing to prevent two sunscreen ingredients from entering the US market unless the manufacturers can provide new data proving safety and effectiveness.

The agency published its proposal on February 25 in the Federal Register . The two ingredients — ecamsule and enzacamene — were among eight ingredients that the agency has been reviewing for years.

In early January, the FDA said that the other six were not safe or effective. Ecamsule and enzacamene are the last two in the backlog that it was required to address as part of the Sunscreen Innovation Act, which was signed into law in December.

The organization that was most active in getting that law passed — Public Access to SunScreens (PASS) Coalition — expressed dismay at the agency's proposal.

"Today's action taken by the FDA regarding ecamsule and enzacamene means that Americans will not have access to innovative products that have been used safely all over the world — in some cases for more than a decade," said Michael Werner, policy advisor to the PASS Coalition, in a statement.

"Last fall, the U.S. Surgeon General issued a Call to Action on skin cancer urging the federal government to work with the private sector and take necessary steps to respond to this public health crisis," added Werner. "FDA's latest action is inconsistent with this approach."

Need More Data

Ecamsule has been approved for use in the US since 2006, but only at a specific concentration and only in a few products manufactured by L'Oreal.

L'Oreal got approval for those products through a new drug application process. The FDA's latest proposal applies to a different process in which L'Oreal is seeking a blanket approval for ecamsule at various concentrations and in various formulations.

Enzacamene has been under review at the agency since 2002. The application was submitted by a division of the German pharmaceutical company Merck KGaA.

According to the FDA, neither of the companies had sufficient data to prove that the ingredients were safe or effective.

L'Oreal (which is a member of the PASS Coalition) was seeking to market various products with concentrations of up to 10% ecamsule. The trials only looked at concentrations of 0.33% to 3.96%, and in the end did not support "human dermal safety of ecamsule at any concentration," according to the FDA.

The agency also said that the company needed to submit more animal data to determine potential effects from systemic exposure, and that it wanted carcinogenicity studies, in addition to other data.

L'Oreal also needs to prove effectiveness, said the FDA, which is requesting two such trials.

The FDA is also seeking more data on enzacamene, including on bioavailability, dermal safety, and toxicity. Some published studies have also indicated that the ingredient has the potential to be an endocrine disruptor, so the FDA has requested more data on hormonal changes.

In addition, the agency said that the manufacturer needed to conduct two, and possibly three, efficacy studies.

The FDA proposal is open for public comment until April 13. Manufacturers will also have a chance to meet with the FDA and submit more data.

Eventually, the agency will publish a final determination

Powdered Alcohol: Is it harmful?

Details: Published: Tuesday, 31 March 2015 09:31

Powdered alcohol is now here. This marks the beginning of an entirely new problem for toxicologists. The key question is: Powdered Alcohol--Is is harmful? Several experts have weighed in on this and have offered up their opinions. Below is a sampling of these opinions.

Substance abuse experts are concerned about the imminent availability of powdered alcohol because of its health risks and abuse potential.

The flavored, freeze-dried alcohol, which looks like powdered Jell-O, can be thrown into a back pocket and taken almost anywhere, according to Harris Stratyner, PhD, regional clinical vice president, Caron Treatment Center's New York Recovery Services, and associate professor of psychiatry, Mount Sinai School of Medicine, New York City.

"You don't have to carry around a bottle of alcohol if you're going camping or for a bike ride. And when you get to your destination, you just add water or mixer to reconstitute the alcohol ― and voilá, you've got an instant alcoholic beverage," he said.

The powdered alcohol ― known as Palcohol ― was approved for sale earlier this month by the US Alcohol and Tobacco Tax and Trade Bureau.

The product, which comes in single-serving packages, each the equivalent of one shot of alcohol and weighing about an ounce, will reportedly hit retail stores and be available online by the summer.

There are five versions: vodka, rum, and three cocktails – Cosmopolitan, Lemon Drop, and Powderita, which tastes just like a Margarita. The mixed drink cocktails have natural flavorings and use Sucralose as a sweetener.

Because it is concentrated, the product would be easier than liquid alcohol to sneak into concerts and other places where alcohol is banned, said addiction specialist Petros Levounis, MD, chair, Department of Psychiatry, Rutgers New Jersey Medical School, Newark.

Disaster Waiting to Happen?

The powdered substance makes it easy to snort the alcohol, which is "worrisome" and "dangerous," according to Dr Stratyner. He is also concerned about combining it with other drugs, such as cocaine and marijuana.

"Say you sprinkle it on a brownie made with marijuana, which is an antiemetic. Then suddenly you're going to have something that's inhibiting your ability to fight off alcohol poisoning."

Because the water has been removed, the percentage of alcohol by volume depends on how much liquid is added. When you add 6 ounces of liquid, it is equal to a standard mixed drink.

Dr Levounis is concerned about a product that "we don't know much about" bringing unanticipated problems. "We've been burned before" when products that appeared to be different formulations of a seemingly benign substance were approved and became a "completely new beast."

He used the example of Four Loko, a combination of alcohol and four shots of espresso. Alcohol has a "built-in protection" in that when you drink too much, you fall asleep. "But if you add four shots of espresso, you prolong your ability to continue to drink," he said.

Another concern is the misconception that products subject to abuse are safer when legal.

"The biggest disaster in addiction has come from cigarettes, not from marijuana," said Dr Levounis.

In addition, the novelty of the product might draw young people to try the powdered alcohol to impress their peers or seem cool, and to use it to excess, added Dr Levounis. He has seen first hand the fallout from such "crazy" behavior among kids.

Although approved at the federal level, the product is still subject to state regulations.

The powdered alcohol was approved before by the Alcohol and Tobacco Tax and Trade Bureau, but the approval was "rescinded," said Dr Stratyner. He and his colleagues at Caron Treatment Centers hope that "something can be done to take a closer look at it" again.

Sources: Interviews with Dr Stratyner and Dr Levounis, Palcohol website.

Breaking News: EMA suspends dozens of Drugs based on Flawed Studies

Details: Published: Friday, 23 January 2015 19:38

A committee of the European Medicines Agency (EMA) has just a few days ago recommended suspending the sale of roughly four dozen generic drugs that are used for conditions including diabetes, depression, and hypertension because they noted that their approvals were based on flawed clinical studies conducted only in India. The US Food and Drug Administration (FDA) has not yet taken action on the issue. But they are in the process of reviewing this issue now.

Familiar names of commonly prescribe drugs on the list include candesartan, donepezil, escitalopram, esomeprazole, and metformin. The list extends more than 120 pages because the drugs are marketed individually in multiple European Union (EU) nations in various dosages, and therefore appear over and over.

Abbott Laboratories, Actavis, Dr Reddy's Laboratories, Mylan Pharmaceuticals, Sandoz, and Takeda Pharmaceuticals are some of the many well-known manufacturers involved in this scandel.

The EMA recommendation to suspend the drugs would apply across the entire EU. Drug regulators in France, Germany, Belgium, and Luxembourg have already acted to stop the sales of 25 of these drugs.

The clinical studies in question were conducted by GVK Biosciences, a contract research organization in Hyderabad, India.

The recommendation of the EMA's Committee for Medicinal Products for Human Use to suspend the drugs was based on an independent French inspection of GVK Biosciences that revealed "data manipulations of electrocardiograms during the conduct of some studies of generic medicines," apparently over the course of at least 5 years. The systematic and prolonged nature of these manipulations and the number of staff involved "cast doubt" on the integrity of the trial methodology and the reliability of the data generated according to the EMA.

FDA Has Taken No Action After Its Own GVK Inspection

When queried the FDA said that some 40 drug applications received from 2007 to March 2012 contained GVK clinical data, and that some of these applications were approved.

The FDA declined to identify the drugs in question or indicate those that had been approved.

According to the FDA statement, the agency inspected GVK Biosciences in September 2014 on the heels of the French inspection in May 2014 and failed to find any evidence "that affects the safety or efficacy of drug products subject to pending applications or products approved in the US."

The agency promised to take "swift and appropriate action" to protect American consumers if it "identifies issues concerning GVK Biosciences that relate to products approved by the FDA."

Exceptions Can Be Made

The EMA investigation of drugs studied at GVK Biosciences encompassed more than 1000 individual generics in various forms and strengths as individually approved in 29 EU nations. Of this group, 300 generics had enough supporting clinical data from other sources to warrant staying on the market, according to the EMA.

That left roughly 700 generics — reiterations of the core four dozen or so drugs — that should be suspended, the EMA said. However, individual countries can make an exception for drugs that are critically important because there are no alternatives to meet patients' needs.

The EMA recommendation goes to the European Commission, the EU's executive agency, for a legally binding decision that will apply to all EU nations, including those that already have suspended the generics in question.

In the meantime, American physicians are waiting for the results of the independent FDA evaluation of this situation. If the FDA concurs, then this will be the biggest debacle ever in U.S. pharmaceutical history.

Stay tuned!

Statins: A new side effect

Details: Published: Sunday, 28 December 2014 23:37

Statins are one of the most popular drugs. They reduce serum lipids implicated in producing cardiac and vascular disease. Statins have side effects and are well-known, such as liver disease and muscle pain. Now a new side effect has been discovered.

Statin therapy significantly elevates the risk of developing cataracts severe enough to warrant surgery, suggests analyses of two distinct cohorts, one from Canada and another from the US.

For now, the possibility of such a risk from statins and its potential mechanisms should be explored in prospective trials, "especially in light of increased statin use for primary prevention of cardiovascular disease and the importance of acceptable vision in old age, when cardiovascular disease is common," according to the report, published in the December 2014 issue of the Canadian Journal of Cardiology with lead author Dr Stephanie J Wise (University of British Columbia, Vancouver).

"However, because the relative risk is low and because cataract surgery is effective and well tolerated, this association should be disclosed but not be considered a deterrent to use of statins when warranted for cardiovascular risk reduction," they write.

"For those of us who have prescribed high doses of statins for almost 3 decades, there is certainly no epidemic of cataracts among our longtime lipid-clinic patients," write Drs Steven E Gryn and Robert A Hegele (Western University, London, ON) in an accompanying editorial in the same journal.

"Nevertheless, if the findings of Wise et al are confirmed, physicians might need to factor in this potential risk when discussing statin use with patients," they continue.

And, in patients at high CV risk, "the prevention of CVD, stroke, and their associated morbidity and mortality vastly outweighs the risk of cataracts. Even among lower-risk patients, for whom the benefit/risk ratio is less dramatic, most patients would still probably prefer having to undergo earlier non–life-threatening cataract surgery over suffering a major vascular event."

Pain Meds Linked to Hypoglycemia

Details: Published: Sunday, 28 December 2014 23:24

A popular pain medication called Tramadol (Ultram) has been found to cause serious hypoglycemia (low blood sugar). This adverse reaction is potentially fatal. Tramadol is not a narcotic. It is used in lieu of narcotics. The study can be found in JAMA.

JAMA Intern Med. Published online December 8, 2014.

The authors of the study wrote: "The increased prescribing of tramadol most likely reflects aggressive marketing coupled with the perception that it is a safe analgesic not prone to abuse. Whereas the drug's analgesic effects are at best moderate, its toxic effects are dangerous and merit respect, particularly when doses are escalated."

Other adverse effects include seizures, serotonin syndrome, and drug interactions, as well as well-known opiate adverse effects, namely respiratory depression.

New Synthetic Hallucinogens

Details: Published: Sunday, 28 December 2014 23:13

A novel class of synthetic hallucinogens that is being sold as a cheaper, more readily available LSD substitute, or even as LSD itself, is emerging as a particularly deadly drug, especially for young males, new research shows. A recent paper was published discussing the advent of this new class of drug. See: American Academy of Addiction Psychiatry (AAAP) 25th Annual Meeting and Symposium: Abstract 54, presented December 6, 2014.

This paper shows that a systematic review of published reports about use in humans of 251-NBOMe, or simply NBOMe, showed that doses as small as 50 µg can produce powerful effects ― and ingestion was associated with a variety of serious adverse events, from severe agitation and delirium that can last for days to seizures and even death. In fact, several deaths have already been reported. In fact, the drug is far more toxic and dangerous than prior hallucinogens like LSD.

Drug-related adverse events included severe agitation and aggression, delirium, tachycardia and hypertension, pyrexia, respiratory and metabolic acidosis, impaired renal function, elevation of creatine kinase levels, and elevated transaminase levels. A total of 40% of the patients presented with seizures; there was one case of status epilepticus. This differs dramatically from the side effect profile of LSD which wore off with time and only required sedation in some cases. These new drugs require ICU admission, and treatment of severe status epilepticus.