Fatal caffeine overdose: useful paper despite BuzzFeed-worthy title

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2.5 out of 5 stars

Fatal Caffeine Intoxication: A Series of Eight Cases from 1999 to 2009. Banerjee P et al. J Forensic Sci 2014 May;59:865-868.

Abstract 

This article is classic example of scientific bait and switch, a deceptive tactic not dissimilar to the use of “click bait” by websites like BuzzFeed. The subtitle promises “Fatal Caffeine Intoxication: A Series of Eight Cases . . .” But by the end of the introduction this has been walked to back “eight fatal cases of caffeine intoxication-related deaths,” a concept that is hopelessly vague and undefined. The way the authors use the term, a man who gets hit by a truck leaving Starbucks after drinking two Vente cappuccinos could be considered a caffeine-related death. The authors’ attitude seems to be: Causation? We don’t need no stinkin’ causation!

In fact, a careful analysis of these cases, from the Office of the Chief Medical Examiner of Maryland, reveals that only 3 of these 8 cases (numbers 5,6 and 8) are convincingly caused by caffeine overdose. In the others, the caffeine level was lower than the generally accepted lethal concentration of 80 mg/L and/or other drugs were possibly involved (case #4 had a lethal level of butalbital).

However, the paper may be worth perusing since, as illustrated by the clip above, the availability of concentrated caffeine powders may mean that we will be seeing more cases of significant overdose. Here are some key take-home points from the discussion section:

  • Caffeine is rapidly and completely absorbed from the GI tract, with peak levels 30-60 minutes after ingestion.
  • Through its action blocking adenosine receptors, increased peripheral vascular resistance and raises blood pressure.
  • Caffeine increases the risk of cardiac arrhythmias in a dose-related fashion.
  • Presenting signs and symptoms of caffeine toxicity include: weakness, vomiting, fever, seizures, cardiac arrhythmias, hypokalemia, hyperglycemia, and coma.
  • Although treatment of caffeine toxicity is generally supportive, hemodialysis can be beneficial in massive overdose.

The authors don’t mention that the antidotes-of-choice to treat cardiotoxic effects of caffeine (tachydysrhythmias and blood pressure alteration) are β-blockers.

Earlier this year, 18-year-old Ohio high school senior Logan Stiner died from an overdose of caffeine powder:

http://www.youtube.com/watch?v=JE95w8tPSQY

Related posts:

Toxicity of high-caffeine “energy” drinks

Fatal caffeine overdose

 

Two cases of laboratory-confirmed exposure to 25B-NBOMe

25I-NBOMe blotter paper

25I-NBOMe blotter paper

3 out of 5 stars

Two cases of severe intoxication associated with analytically confirmed use of the novel psychoactive substances 25B-NBOMe and 25C-NBOMe. Tang MHY et al. Clin Toxicol 2014 Jun;52:561-565.

Abstract

The NBOMe series of drugs are substituted phenethylamines. They act as agonists at both the 5-HT2A receptors and the α-receptors. Because of these actions, they can cause both hallucinations (5-HT2A  effects) and sympathomimetic toxidrome (α effects.) Since these drugs are so potent, they are often sold in the form of impregnated blotter paper.

This paper, from Hong Kong, describes 2 laboratory-confirmed cases of 25B-NBOMe toxicity. One patient also had 25C-NBOMe in his urine. Given the basic toxicology of these compounds, the patients’ signs and symptoms were not surprising. Both ad mydriasis, agitation, hypertension, tachycardia, hyperthermia, diaphoresis, and altered mental status, One patient had seizure activity and was intubated. The other developed rhabdomyolysis and renal impairment.  Treatment included basic supportive care, fluids, and benzodiazepines.

[Photograph of blotter paper, seized in Austria in April 2013, from Belgian Early Warning System on Drugs. The blotter paper had been sold as LSD but found to contain 25I-NBOMe]
Related posts:

NBOME — it’s not your father’s LSD

Case series: 7 patients with confirmed exposure to hallucinogenic stimulant 25I-NBOMe (“N-bomb”)

25I-NBOMe: a dangerous new hallucinogen

 Case report: toxicity from designer drug 25I

Seizures, hyperthermia, and serotonin syndrome following use of designer drug 2C-I (“Smiles”)

 

 

Case report: guanfacine overdose

Intuniv (Guanfacine)

Intuniv (Guanfacine)

3 out of 5 stars

Prolonged Bradycardia and Hypotension Following Guanfacine Extended Release Overdose. Walton J et al. J Child Adolesc Psychopharmacol 2014 Jul 10 [Epub ahead of print]

Reference 

Guanfacine is a central α2-agonist with a mechanism of action similar to that of clonidine. Originally marketed as an antihypertensive agent, it is now available as an extended-release preparation (Imtuniv) for treating children ages 6-17 with attention-deficit hyperactivity disorder (ADHD). It is thought the mechanism of action in that condition may involve stimulation of α2-receptors in the prefrontal cortex.

As with clonidine, guanfacine can cause initial hypertension (from peripheral α-agonist activity) followed by prolonged bradycardia and hypotension (from central α2 effects.

This short case report describes a 9-year-old boy with ADHD who was taking dexmethylphenidate and risperidone, as well as extended-release guanfacine (3 mg in the morning.) Inadvertently, the child received an extra dose of guanfacine-ER at around noon. Four hours later he was lethargic and drowsy but arousable. On arrival at hospital, he was bradycardic (40-50 bpm) and hypotensive (~80/40 mm Hg.) He was admitted for observation and given IV fluids. He recovered uneventfully over the next 24 hours.

In their discussions, the authors suggest that — as illustrated by their case — a prolonged hypotensive response can follow even a mild overdose of guanfacine, and any overdose of this agent should mandate medical evaluation.

To read my Emergency Medicine News column discussing the toxicology of newer ADHD drugs, click here.

 

Review of cannabinoid hyperemesis syndrome

potleaf205-thumb-205x2053 out of 5 stars

A hot mess: A case of hyperemesis. Cheung E et al.  Can Fam Physician 2014 Jul;60:633-637.

Full Text

With medical marijuana now legal in 23 states plus the District of Columbia, and recreational marijuana legal in 2 states, it is essential that all emergency and primary care physicians become familiar with the adverse effects that can ensue from regular use of cannabis.

One of the most striking and unexpected complications of chronic cannabis exposure is violent cyclic vomiting. This has been called “cannabinoid hyperemesis syndrome” (CHS). In this review article, the authors propose the following criteria of CHS:

  • Chronic regular use of marijuana
  • Cyclic nausea and vomiting with or without abdominal pain
  • Relief of symptoms by taking hot baths or showers
  • Lack of alternative cause
  • Resolution of symptoms within days of abstinence
  • Return of symptoms on re-exposure to cannabinoid products

This short review is worth reading, especially for those unfamiliar with this often unrecognized syndrome.

HT: @EMCases
Related posts:

First case of cyclic hyperemesis associated with synthetic cannabinoids

Cannabinoid hyperemesis syndrome: largest case series to date

Review: cannabinoid hyperemesis syndrome

More on cannabinoid hyperemesis syndrome

The anti-munchies: cannabinoid hyperemesis syndrome

 

Tox Tunes #84: Pass the Dutchie (Musical Youth)

http://www.youtube.com/watch?v=dFtLONl4cNc

The term “dutchie” now refers to a marijuana product, possibly a “blunt” made from a cigar such as a Dutch Masters. But it probably didn’t in 1982 when the British reggae band Musical Youth released this hit. The song is a cover of the Mighty Diamonds’ “Pass the Koutchie” — a “koutchie” being a pipe used to smoke marijuana.

However, then Musical Youth’s version was released, the record company thought it unseemly for young teenagers to be singing about drugs, so the title was changed to “Pass the Dutchie”. A “dutchie” at that time referred to a large, heavy cooking pot such as a dutch oven. It is not clear if the pun on the word “pot” was intentional.

Another change: In this version, Musical Youth sing: “How does it feel when you’ve got no food?” The Mighty Diamonds original asked: “How does it feel when you’ve got no herb?”

Here is the Magic Diamonds’ original “Pass the Koutchie”:

http://www.youtube.com/watch?v=k05n4xpXFeI

Acute respiratory distress syndrome following intralipid emulsion therapy

intralipid2.5 out of 5 stars

Acute respiratory distress syndrome following verapamil overdose treated with intravenous lipid emulsion; A rare life-threatening complication. Martin C et al.  Ann Fr Anesth Reanim 2014 [Epub ahead of print]

Reference

This interesting French case report is a textbook example of how not to use intralipid emulsion therapy (ILE) in calcium-channel-block (CCB) overdose.

It describes a 51-year-old woman who present to the emergency room 8 hours after ingesting forty 240 mg verapamil, a total of 9.6 grams. She was hypotensive and bradycardic, although alert and oriented. Initial echocardiography showed good systolic function. She was given fluids and calcium, and a temporary transvenous pacemaker placed.

Six hours after presentation the patient was intubated after her oxygen saturation decreased and she required high-dose pressors. At that point, “A literature review suggested the use of lipid therapy as a possible antidote,” and an intralipid bolus was given followed by continuous infusion. After 4 hours of infusion, the patient developed signs of acute respiratory distress syndrome (ARDS). Echocardiography at this point showed impaired systolic function with an ejection fraction of 35%.

Veno-arterial extracorporeal membrane oxygenation (ECMO) and continuous veno-venous hemofiltration (CVVH) was started, as well as plasmapharesis. The patient slowly recovered. She was extubated on day 9 and discharged from the ICU on day 18, with intact pulmonary and neurological function.

In a recent column in Emergency Medicine News, I wrote about how CCB overdose produces a “perfusion salad.” with hypotension caused by impaired myocardial function, vasodilation, or a combination of the two. Apparently in this case systolic function was initially intact, which might be why high-dose insulin (HDI) was withheld and the clinical team relied on high-dose pressors. When these proved insufficient, it would have made sense to re-evaluate systolic function and move on to HDI if it was impaired. Most toxicologists would save ILE for a last-ditch effort if response to other modalities was inadequate. It is puzzling why the infusion was continued for 4 hours if the response was not sufficient.

The authors conclude that this paper is “the first one to our knowledge to report a case of ARDS induced by an ILE administration.” Although the authors do not do so, it is worth pointing out that, in terms of likelihood,  applying the Naranjo Algorithm reveals that this was only a possible or at best probable adverse drug reaction to ILE. A simple PubMed search would have determined that this was not true. A 1984 paper reported a similar case, although in that instance ILE was administered for nutritional purposes, not to treat a toxic overdose.