Tox Tunes #90: Junco Partner (The Clash)

//www.youtube.com/watch?v=RZOPte4hlqE

“Tox Tunes” has previously featured versions of “Junco Partner” by Dr. John and Professor Longhair. I love this reggae/punk take on the song from The Clash’s 1980 triple album Sandanista!. According to Dr. John, by the 1950s the song was known as an “anthem of the dopers, the whores, the pimps, the cons.” Joe Strummer of The Clash had already recorded “Junco Partner” with the previous band, the 101ers.

By the way, the best use of the name “The Clash” in someone else’s song undoubtedly occurs in Richard Thompson’s great break-up  anthem “Tear Stained Letter”:

//www.youtube.com/watch?v=8hEWFsXrXv4

 

Related posts:

Tox Tunes #88: Junco Partner (Professor Longhair)

Tox Tunes #81: Junko Partner (Dr. John)

Tox Tunes #31: Junker’s Blues (Champion Jack Dupree)

Pop quiz: cardiac arrhythmia from an herbal medicine

Fu_Zi3 out of 5 stars

Life-threatening cardiovascular toxicity following ingestion of Chinese herbal medicine. Martinez A et al. Emerg Med Australas 2014 Oct;26:512-13.

Abstract

This case report describes a 46-year-old Chinese woman in Melbourne who presented with peri-oral and facial paresthesias, gastronintestinal disturbance (nausea, vomiting, diarrhea,  abdominal pain,) tachycardia and hypotension. She also had decreased level of consciousness and ventricular tachycardia. Symptoms started 30 minutes after ingesting a Chinese herbal medicine.

The following is a pop quiz based on this presentation. Click on the question to reveal the answer.

The differential diagnosis of this presentation includes cardiac glycoside poisoning from plants such as lily of the valley, foxglove, and oleander. However, many Chinese medicine such as Fu Zi contain aconite (wolfsbane or monkshood), which can also present with gastrointestinal, cardiac, and neurologic manifestations. Other Chinese preparations that contain aconite include “Chuan Wu” and “Cao Wu.”

Aconite alkaloids maintain sodium channels in an open position,  interfering with  transmission and impairing normal function of excitable cardiac and neurological tissue. It also has a muscarinic effect on the vagus nerve.

Neurological: peri-oral and facial numbness and tingling, muscle weakness

Cardiovascular: hypotension, bradycardia, tachycardia, ventricular arrhythmias

Gastrointestinal: nausea, vomiting, diarrhea, abdominal paint

There is no specific readily available text to diagnosis aconite exposure. The diagnosis should be suspected in a patient who presents with a history of exposure to a plant or herbal medicine, and has cardiovascular, neurological, and gastrointestinal signs and symptoms.

Since there is no specific antidote good supportive care is essential. Some anecdotal reports suggest but do not prove that it is reasonable to use amiodarone and flecanide for ventricular arrhythmias.

In 2010, Lakvir Kaur Singh — the so-called “curry killer” — was convicted in a London court of murdering her lover by lacing his curry dinner with aconite.


Related posts:

Aconite killer convicted

Aconite: a modern case with an ancient poison

 

 

What’s better for amatoxin poisoning: silibinin or leprechaun luck?

Amanita phalloides

Amanita phalloides

2 out of 5 stars

Survival Following Investigational Treatment of Amanita Mushroom Poisoning: Thistle or Shamrock? Gores KM et al. Chest 2014 Oct 1 [Epub ahead of print]

Abstract

Amatoxins are potent RNA inhibitors, shutting down protein synthesis and producing hepatonecrosis and, occasionally, renal injury.

There is not generally accepted treatment for amatoxin-induced hepatotoxicity aside from supportive care, early multi dose activated charcoal, and liver transplant if indicated. There are, however, a number of unproven therapies that have been used and advocated in the past.

This case report, from the University of Iowa College of Medicine, describes a 71-year-old man who presented with vomiting, diarrhea and weakness 3 days after ingesting mushrooms foraged in northwestern Iowa. Laboratory examination revealed elevated AST (2313 IU/L) and ALT (2730 IU/L), but only slightly elevated total bilirubin and an INR of 1.3 (normal up to 1.2). There was evidence of renal insufficiency with a creatinine  of 2.7 mg/dL (normal, 0.51 – 1.2 mg/dL). Treatment was started with IV N-acetylcysteine and penicillin. The next day he became encephalopathic and was started on the experimental drug silibinin.

Silibinin is derived from the milk thistle plant (Silybum marianum). It is has not been FDA approved, but was available as part of a phase 2/3 Open Multicenter Clinical Trial. The drug apparently inhibits entry of amatoxin into hepatocytes. It is generally believed that, if it is to be effective at all, it must be given early. In this patient, who had already developed hepatic encephalopathy, it is unlikely it provided any benefit.

In any case, the encephalopathy and kidney injury resolved on hospital day 3 and was discharged two days later. Even the authors admit that it is not clear whether this seemingly miraculous recovery could be attributed to the thistle (silibinin) or the shamrock (luck).

This paper has many defects. The exact mushroom consumed was never identified. The complete treatment regimen is never identified. And although the authors make a big thing about the importance of shared decision-making when administering experimental drugs, they never disclose exactly how that worked in this case.

For an interesting article on Amanita phalloides in Slate, click here.

[Photograph of Amanita phalloides from wikipedia.org]
Related posts:

Treating Amanita phalloides poisoning: is silibinin superior to chicken dung?

Silibinin or Silly Putty for Mushroom Poisoning?

 

Crayola toxicology: life-threatening causes of bluish vomiting

BlueVomit_Lp2 out of 5 stars

 Bluish vomiting: a rare clinical presentation of poisoning. Higny J et al. Acta Clin Belg 2014;69:299-301.

Abstract

This case report describes a 65-year-old man who ingested an unknown substance and subsequently present with pharyngitis and mucositis, nausea, diarrhea, abdominal pain, and blue-green vomitus. The remainder of the physical exam and basic laboratory results were unremarkable.

The authors use the case to discuss 3 life-threatening ingestions that can cause bluish emesis. Unfortunately, their discussion of these causes is confusing and superficial. And, of course, must blue green vomitus will be due to food dye, blue raspberry Gatorade, or some other benign but brightly colored substance.

This article does serve to remind us of 3 important not-to-miss ingestions on the differential when a patient shows up barfing blue. Unfortunately, the authors misses an obvious mnemonic: Cerulean Blue Puke = Copper sulfate, Boric acid, Paraquat.

Related posts:

Green urine

Propofol causes green urine

An elderly woman with purple urine

Snorting bupropion

150px-Wellbutrin2.5 out of 5 stars

An 11-year review of bupropion insufflation exposures in adults reported to the California Poison Control System. Lewis JC et al. Clin Toxicol 2014 Nov;52:969-972.

Abstract

The abuse of bupropion by pulverizing and snorting the medication has been described at least as far back as 2002. Bupropion inhibits re-uptake of dopamine and norepinephrine, but apparently has little or no effect on serotonin. It is abused for its psychotropic effects that resemble those of amphetamine and cocaine..

A hallmark of overdose with sustained-release or extended-release bupropion formulations is delayed onset of seizures — sometimes more than 8 hours after ingestion. When these preparations are crushed and insufflated, absorption is rapid and manifestations would be expected to come on more quickly.

This observational case series from the California Poison Control System describes 67 cases of pure bupropion insufflation over an 11-year period. Although this study is certainly impaired by inherent limitations — including reporting bias and small sample size — some of its findings are worth noting:

  • the median dose reported was 1500 mg (range, 100-9000 mg; therapeutic 150-300 mg/day)
  • 30% of patients had seizure in the prehospital setting
  • there were not seizures after arrival at hospital
  • tachycardia was the most frequent manifestation
  • agitation and tremor also occurred

The authors conclude that “once the mechanical delayed release mechanism is disabled by crushing . . . no patient in this case series had a repeat seizure after arrival to [hospital].”

A major problem with this is that, as the authors admit, “there was no reliable way to correlate time from insufflation to seizure.” Therefore, there is no way of knowing whether the seizures seen occurred fairly immediately after insufflation, or were in fact delayed.

Methoxphenidine: a designer dissociative drug

methoxphenidine-mxp-2-meo-diphenidine-250x2503 out of 5 stars

Acute toxicity associated with the recreational use of the novel dissociative psychoactive substance methoxphenidine. Hofer KE et al. Clin Toxicol 2014 Oct 28 [Epub ahead of print]

Abstract

Methoxphenidine  (MXP) is a dissociative drug with actions apparently similar to those of phencyclidine (PCP), ketamine, and methoxetamine (MXE). It is often sold as a “research chemical” and labelled as “Not for Human Consumption.” The pharmacology and toxicology of MXP has not been well studied. Anecdotal reports on some drug forums describe anterograde amnesia and prolonged duration of effects (up to 18 hours).

Since it is as yet not highly regulated, MXP seems to be used more frequently as the other dissociative agents are put under legal restrictions.

This case report, from Switzerland, describes a 53-year-old man who presented after an apparent MXP ingestion, later confirmed in the laboratory. Presenting manifestations included somnolence, confusion, echolalia, miosis, hypertension, tachycardia, nystagmus, and apparent seizure activity.

The authors conclude:

. . .methoxphenidine appears to have a similar acute toxicity profile to other arylcyclohexylamines, such as PCP, ketamine and MXE. On the basis of the very limited evidence available, management of patients presenting with acute toxicity related to methoxphenidine use should be as for other dissociative drugs.”

Related posts:

Methoxetamine: a ketamine analog that is NOT bladder friendly

A “big Christmas cardigan”: recreational use of ketamine and methoxetamine

Acute cerebellar syndrome? Think methoxetamine

Methoxetamine: a designer ketamine analogue