Kitchen Tox: beware of the durian



3 out of 5 stars

Durian Induced Hyperkalaemia. Leo CLB et al. Med J Malaysia 2011 Mar;66:66-67.

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Durian, a spiky, coconut-sized fruit native to Malaysia and grown throughout southeast Asia, is known for its distinctive aroma that some have compared to ripe Limburger cheese. The Oxford Companion to Food notes that others have compared the smell of durian to “the civet cat, sewage, stale vomit, onions, and cheese; while one disaffected visitor to Indonesia declared that the eating of the flesh was not much different from having to consume used surgical swabs.”

Anthony Bourdain has remarked that after eating durian “Your breath will smell as if you’d been French-kissing your dead grandmother.” Yet many people, especially those from southeast Asia, love durian, and when it’s in season will spend much of their time-consuming fruit after fruit. This can cause problems much worse that halitosis.

In fact, the custardy durian flesh contains even more potassium per 100g than bananas. This is usually not a problem for those with health kidneys, but can cause life-threatening hyperkalemia in people with renal insufficiency. This case report, from Malaysia, describes a 48-year-old woman with diabetes mellitus and end-stage renal failure requiring hemodialysis who suffered a cardiac arrest after eating a “moderate” amount of durian. Her potassium was 9.1 mmol/L and her EKG showed the sine wave pattern typical of hyperkalemia. The patient was resuscitated and ultimately discharged with instructions not to eat durian.

This is not only a problem in southeast Asia. I have a friend whose mother in New York City had renal failure and similarly developed severe hyperkalemia after eating copious amounts of durian.

The following amusing video shows how some children reacted after being exposed to durian:



Must-read: review of single-dose activated charcoal

4 out of 5 stars

Activated charcoal for acute overdose: a reappraisal. Juurlink D. Br J Clin Pharmacol 2015 Sep 26 [Epub ahead of print]


The British Journal of Clinical Pharmacology seems to be publishing a series of articles on basic management of the poisoned patient. Several weeks ago we reviewed (and highly recommended) Marco Sivilotti’s excellent discussion of flumazenil, naloxone and the coma cocktail. This current article looking at single-dose activated charcoal (SDAC) is similarly well done, and essential reading.

The author points out that although most poisons bind to activated charcoal some — most notably hydrocarbons, caustics, and the metals lithium and iron — do not. Other factors that might increase the potential benefit of administering SDAC include:

  • anticipation of severe toxicity
  • absence of contraindications (such as decreased mental status, unprotected airway, uncooperative patient, ileum, or intestinal obstruction)
  • lack of effective antidote
  • ingestion of modified-release formulation
  • ability to administer a reasonable dose of charcoal (50-100 grams) that will be at least 10-40 times the dose of poison

Although in the absence of contraindications charcoal is relatively safe, there are definite risks, including pulmonary aspiration and intestinal obstruction or perforation. The decision whether or not to treat a poisoned patient with SDAC is a clinical one. An important concept hinted at in the paper is that giving SDAC is never mandatory. That decision should be made at the bedside after carefully weighing the possible risks and benefits. I have reviewed a number of cases where the treating clinician was exposed to medical-legal vulnerability because he or she administered SDAC thinking that not doing so would be negligence or a violation of “standard of care.” In many of these cases, SDAC was given through a nasogastric tube to an uncooperative or lethargic patient.

There are several things I especially liked about this paper. The author critically evaluates much of the literature he cites, and refrains from merely relying on the abstract or conclusions. In addition, although many commentators claim — nonsensically, in my view — that SDAC is ineffective if given more than 1 hour after ingestion, this paper argues sensibly that in large potentially severe overdoses or those involving drugs that slow gastric emptying, SDAC may be a reasonable option even hours later if the clinician suspects significant amounts of drug may remain in the gastrointestinal tract.

Related post:

Point of View: Activated Charcoal


Review: recreational marijuana use

Stanimir G. Stoev/

Stanimir G. Stoev/

3 out of 5 stars

Recreational cannabis use: Pleasures and pitfalls. Rella JG. Cleve Clin J Med 2015 Nov;82:765-72.

Full Text

This somewhat superficial but relatively well done review article gets extra credit for being available via open access. The author covers the history, pharmacology, toxicology, and acute and chronic effects of cannabis use, as well as withdrawal and the cannabinoid hyperemesis syndrome.

My main problem with this paper involves the author’s casual use of references. For example, he states that previous literature had reported “a fivefold increased risk of myocardial infarction in the 60 minutes following cannabis use . . .” The reference for this is a 2001 paper by Mittleman et al. This statement does have some face validity, since acute marijuana use can cause tachycardia and hypertension, in addition to exposure to products of combustion. However, the study was based on a case-crossover design, a technique that uses patients as their own controls and is susceptible to many biases, including incomplete data, flawed recall that underestimates exposure during the control period. These are, in my opinion, crippling problems with this design, and should have been at least mentioned in the review.

Finally, the author states that during cannabis intoxication the user may experience  that “time seems to pass quickly.” This is not always the case:


Related Posts:

Death after consuming a marijuana edible

Colorado’s experience with medical effects of legalizing marijuana

Review: marijuana and health

Effects of marijuana on driving ability

Does smoking marijuana cause stroke?




Therapeutic plasma exchange in poisoned patients

1 out of 5 stars

Therapeutic plasma exchange in poisoning: 8 years’ experience of a university hospital. Disel NR et al. Am J Emerg Med 2015 Oct;33:1391-1395.


In therapeutic plasma exchange (TPE), blood is removed from the body, and plasma is separated from components such as RBCs, WBCs, and platelets. Those components are re-infused along with a replacement fluid such as fresh-frozen plasma or albumin. This procedure is usually used to removed pathological immunoglobulins in various conditions such as thrombotic thrombocytopenic purpura.

There have been some case reports and small case series on the use of TPE in poisoned patients, but nothing that even comes close to demonstrating that it may be beneficial. Unfortunately, this paper from Çukurova University in Turkey adds nothing to the discussion. The authors retrospectively reviewed 36 adult toxicology cases (from January 2007 to May 2015) in which TPE was used, and claim this is the largest such case series in the literature. I have not reason to doubt them. But we have no idea why TPE was chosen in these cases, or how the patients would have done without the intervention. Poisons involved included organophosphates (25 cases,) carbamazepine, baclofen, acetaminophen, seroquel, and paraquat.There were 12 deaths, including 10 patients exposed to an organophosphate.

As the authors point out, plasma exchange can remove large, highly protein-bound molecules that would not be amenable to hemodialysis. They suggest that it would be effective eliminating substances with protein-binding capacity > 80% and a low volume of distribution (< 0.2 L/kg.)  Yet many of the toxicants in these patients did not at all meet these criteria — for example, carbamazepine has a volume of distribution of 2-3 L/kg.

The authors conclude:

When applicable, TPE may be a promising extracorporeal elimination and treatment technique in poisoned patients when performed in selected cases.

Well, almost anything may be true, and the paper gives no real clue about how to selected appropriate cases. TPE is expensive and comes with risk of infection. I am not at all enthusiastic that this is a promising technique in toxicology cases. The only possible exception might be in neonates and small infants where hemodialysis may be technically difficult.

Use of flumazenil and naloxone in poisoned patients

flumazenil4 out of 5 stars

Flumazenil, naloxone and the ‘coma cocktail’ Sivilotti MLA Br J Clin Pharmacol 2015 Aug 7 [Epub ahead of print]


This very smart paper reviews factors affecting the clinical use of two antidotes that reliably reverse  coma caused by two major classes of poisons: flumazenil for benzodiazepines, and naloxone for opiates.

Both these antidotes are specific, rapid-acting, short-lived, and titratable. However, significant adverse effects have been associated with each of them. Unwise or overly aggressive administration of flumazenil can cause acute benzodiazepine withdrawal, agitation, seizures, and fatal cardiac arrhythmias. Since many of the severe adverse effects occur in cases of mixed overdoses, use is generally discouraged in the comatose poisoned patients where detailed history is often not available.

Although naloxone is often considered safe, it can precipitate acute opiate withdrawal that, though rarely fatal, can present a risk to medical staff and other patients. The author notes:

There is a growing awareness that widely recommended initial doses [of naloxone] of 0.4 mg to 2 mg are unnecessary and that 40 μg is a more appropriate initial dose in many cases.

Actually, there is considerable controversy regarding the proper starting dose of naloxone, with some maintaining that 40 μg is a dose so low as to be almost homeopathic. Sivilotti argues (convincingly, to my mind) that in opiate-induced respiratory depression, “non-pharmacological approaches to treating respiratory depression take precedence,” and that titration of naloxone should be accomplished simultaneously with ventilatory support based on airway management and bag-valve-mask ventilation/oxygenation.

When discussing the so-called “coma cocktail” — a combination of antidotes that in the past were given empirically to awaken comatose poisoned patients  — Sivilotti points out that this cookbook approach was outdated long ago, and now seems “antiquated” and “antediluvian.” In addition is was based on a mistaken emphasis on reversing coma rather than providing good supportive care that addressed airway control, oxygenation and ventilation.

His conclusion:

. . .the modern approach to a patient with an altered level of consciousness should not be protocolized, empirical administration of fixed doses with an end point of analepsis, but rather the targeted correction of immediate threats to life. . . . With both flumazenil and naloxone, even pharmacologically ideal antidotes are no substitute for basic airway management and modern principles of targeted resuscitation and supportive care.

This is exactly right. The paper is important reading.
Related posts:

Is ED use of flumazenil safe?

Flumazenil-induced seizures

Is use of flumazenil in poisoned pediatric patients safe?




Hemodialysis in lithium poisoning: there is no evidence. Full stop.

0Lithium Carbonate, 300mg, 1,000 Capsules per Bottle McGuffMedical.com3.5 out of 5 stars

Hemodialysis for lithium poisoning. Lavonas EJ, Buchanan J. Cochrane Database Sys Rev 2015 Sep 16 [Epub ahead of print]


At a session at the ACEP Scientific Assembly last year, Jerry remarked: “Guidelines should regularly conclude that there is no evidence. Full stop.”

I really like this Cochrane review of hemodialysis in lithium poisoning because [SPOILER ALERT] that is exactly what the authors conclude. They note that although hemodialysis undoubtedly increases clearance of lithium, there is no agreement as to whether this enhanced elimination actually improves clinical outcome.

In an attempt to answer that question, they used explicit criteria to review the literature, looking for randomized controlled trials that studied the effect of extracorporeal techniques (hemodialysis, hemofiltration, and continuous renal replacement methods) on outcomes in patients with lithium toxicity.

Their conclusion:

[T]here is no evidence from randomized controlled trials to support nor refute the use of hemodialysis in the management of patients with lithium poisoning.

Full stop.

This seems right on, and is useful counterpoint to the recent ExTRIP review that, based on no logic or evidence that was apparent to this reader, came up with precise lithium levels for which to recommend extracorporeal treatment.

Although this Cochrane review included no studies, the paper is worth reading for the general discussion of lithium toxicity and the logical (if not evidentiary) basis for hemodialysis.

Related post:

Hemodialysis in lithium poisoning: what is the evidence?