Tox Tunes #102: Jake Leg Blues (The Mississippi Sheiks, 1930)


“Jake Leg Blues”  by the Mississippi Sheiks is another song form the 1930s that describes the ravages wrought by Jamaica Ginger extract, an alcohol-containing patent medicine that was deliberately contaminated with the organophosphate compound tricresyl phosphate (TOCP) during prohibition. For a more complete description of this tragic episode of mass poisoning, and for references, see our previous post.

“Limber leg” refers both to the leg weakness and foot drop caused by TOCP, and also to the impotence that affected many victims.

The blog Vernacular:Shellac has a great post about Jake Leg, with wonderful illustrations.

The Mississippi Sheiks were a bawdy country blues band that recorded during the 1930s. Their biggest recording was “Sitting On Top of the World':

Related post:

Tox Tunes #101: Alcohol and Jake Blues (Tommy Johnson, 1930)

Case report: seizures after exposure to 25B-NBOMe (N-Bomb)

Blue Batman pills (25C-NBOMe)

Blue Batman pills (25C-NBOMe)

3 out of 5 stars

Beware of blotting paper hallucinogens: severe toxicity with NBOMes. Isbister GK et al. Med J Aust 2015 Sep 21;203:266-267


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 the sympathomimetic toxidrome (α effects.) Since these drugs are so potent, they are often sold in the form of impregnated blotter paper and misrepresented as LSD. Street names include N-Bomb, Wizard, Smiles, and Blue Batman.

This brief case report Australia describes a 16-year-old boy who ingested blotter paper that he believed had been impregnated with LSD. He was brought to hospital after having 3 seizures; after a 4th seizure in the emergency department he was intubated, placed on mechanical ventilation, and admitted to the intensive care unit.

Despite laboratory tests suggesting some degree of rhabdomyolysis and renal insufficiency, the patient recovered and was discharged after 5 days in hospital. A blood sample drawn 22 hours after exposure showed a 25B-NBOMe level of 0.089 μg/L.

In their discussion, the authors make the following points:

  • exposure to LSD generally does not produce severe medical complications such as those seen with the NBOMe agents
  • NBOMe toxicity can present with:
    • hallucinations and acute behavioral abnormalities, and/or
    • medical complications such as seizures, rhabdomyolysis, and acute kidney injury (one could add hyperthermia and multiorgan failure
  • supportive treatment includes sedation and IV volume repletion

Related posts:

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

N-Bomb: a potent psychedelic stimulant

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”)



Tox Tunes #101: Alcohol and Jake Blues (Tommy Johnson, 1930)

One of the most interesting, and tragic, episodes of mass poisoning in U.S. history involves “jake paralysis“. The first depiction in the medical literature was in a June 1930 New England Journal of Medicine article, that described an epidemic of motor neuropathy that occurred in the midwestern and southern states. As I explained in the “Toxicology Rounds” column in Emergency Medicine News:

Onset of this condition was usually heralded by lower leg muscular pain and tingling, rapidly followed by weakness that often also involved the upper extremities. Distal deep tendon reflexes were diminished. Sensory function remained intact or was only minimally affected.

The author of the NEJM article, Dr. Benjamin T. Burley, wrote that “The exact etiological factor i this paralysis has thus far escaped identification.” It is unfortunate he seems not to have followed popular culture closely, because earlier in 1930 blues musicians such as Tommy Johnson were already recording songs like “Alcohol and Jake Blues” that not only described the ravages of this epidemic, but also pointed to the causative agent:

I drink to much of Jake, till it done give me the limber leg
(And that’s sure to mess you up)
Drinking so much of Jake, till it done give me the limber leg
If I don’t quit drinking it every morning, sure gonna kill me dead

“Jake” was Jamaica Ginger Extract, a preparation that was 80% ethanol by weight. During prohibition (1919-1933), it could be legally sold in pharmacies for treatment of various ailments such as menstrual cramps and indigestion.

Of course, jake could also be used as a legal alternate source of intoxicating alcohol. In an attempt to assure that jake was unpalatable in undiluted form, U.S.P. standards required that a certain amount of solid or resinous material remain after the volatile liquid was boiled off. Although this residual solid was assumed to be ginger, manufacturers would sometimes use other additives to reduce costs.

In 1930, one make of jake, Hub Products of Boston, started adding tricresyl phosphate, an industrial organophosphate. Thus, “jake paralysis” was a manifestation of organophosphate-induced delayed neuropathy (OPIDN). By the end of the epidemic, thousands of individuals were left with residual persistent paralysis and paresis.

To read my Emergency Medicine News column about jake paralysis, click here.

There was an excellent New Yorker magazine article about jake leg in 2003. To read it, click here.

A very interesting 2-part film about “The Jake Leg Infamy” was presented at the 2009 North American Congress of Clinical Toxicology. It is a definite must-watch:


Related post:

Adulterated Drugs Now and Then: Cocaine and Jamaican Ginger Extract


Implications of obesity for pharmacology and toxicology

3.5 out of 5 stars

A Review of the Toxicologic Implications of Obesity. Zuckerman M et al. J Med Toxicol 2015 Sep;11(3):342-54


The authors of this thought-provoking study propose that obese patients be considered a “special population” — similar to children, the elderly, and pregnant women — for matters of medical toxicology.

Obesity — defined as a body mass index (BMI) > 30 kg/m2 — is associated with a number of pharmacokinetic and pharmacodynamic changes that can impact on toxicology:

  • increased blood volume and cardiac output
  • impaired respiratory function
  • alterations in gastric emptying (especially after bariatric surgery)
  • altered volume of distribution

These are all important issues, and will become more so in the future as the rate of obesity increased. One group estimated that by the year 2030 obese Americans will constitute over half the population.

Unfortunately, since little hard research has been done on this topic, there is little hard data here one can bring to the beside at this point. One important consideration: When dosing lipid rescue therapy, the initial bolus is 1.5 mL/kg lean body weight.

Colchicine in acute gout: high-dose or low-dose or no-dose?

003206 Colchicine, 0.6mg, 1,000 Tablets per Bottle McGuffMedical.com3.5 out of 5 stars

Does Colchicine Improve Pain in an Acute Gout Flare? Turner J, Cooper D. Ann Emerg Med 2015 sep;66:260-1.


The 7th edition of Tintinalli’s Emergency Medicine (2011) has this to say about using colchicine to treat gout:

Oral colchicine is typically administered in a dose of 0.6 milligrams/h until intolerable side effects (vomiting or diarrhea) or efficacy ensues.

This “typical” dosing schedule goes back decades, and even when I was a medical student who didn’t know an Ewald tube from an Ewok it never made sense to me. The instructions might as well have been “Take this until you’re better or you find you’re shitting and puking your guts out.”

And this dosing made even less sense when I realized that the “intolerable side effects” were actually symptoms of colchicine toxicity which can be — and not infrequently is — life-treatening.

Is there any evidence on this issue? This short synopsis summarizes a recent article updating the 2006 Cochrane review of the topic. The authors of that review found only 2 randomized controlled trials that met inclusion criteria. One trial (43 patients) gave 1 mg colchicine orally, then 0.5 mg  every 2 hours until complete relief or toxicity, or placebo. The second study (575 patients) compared placebo v. high-dose colchicine (4.8 mg over 6 hours) v. low-dose colchicine (1.2 mg then 0.6 mg one hour later.)

The take-home message:

“Low-quality evidence suggests that both high- and low-dose colchicine decreases [sic] pain in acute gout flares; however, high-dose regimens are associated with more frequent adverse effects.”

Note that there were adverse effects associated with use of the low-dose regimen. (For that matter, there were also adverse effects in the placebo groups.) This synopsis gives no indication of the nature or severity of these effects. Unfortunately, there are no trials comparing colchicine to other modalities such as non-steriodal anti-inflammatory agents in these patients.

Also remember that renal insufficiency is a contraindication to the use of colchicine, especially in high doses.

To read my Emergency Medicine News column on colchicine toxicity, click here.

Related posts:

Colchicine: tips for avoiding fatal in-hospital toxicity

Colchicine: be afraid, be very afraid

Case report: use of ECMO in colchicine poisoning

Colchicum autumnale (Autumn crocus)

Colchicum autumnale (Autumn crocus)

3.5 out of 5 stars

Extracorporeal life support in the treatment of colchicine poisoning. Boisramé-Helms J et al. Clin Toxicol 2015;53:827-829.


Colchicine toxicity occurs roughly in 3 phases. During the initial 24 hours, severe gastrointestinal symptoms — nausea, vomiting, and diarrhea — can cause hypotension and shock if fluid losses are not adequately replaced. During the second phase, severe toxicity can manifest with pancytopenia, sepsis, rhabdomyolysis, and renal failure. In addition, within days after ingestion, patients can develop cardiogenic shock and sudden cardiac death.

This fascinating case report describes the use of veno-arterial extracorporeal membrane oxygenation (ECMO) as a bridge to recover in a patient with colchicine toxicity. A 68-year-old woman inadvertently ingested the Colchicum autumnale plant, thinking it was wild leek. The plant contains colchicine,  especially concentrated in the bulb and seeds. Several hours later she developed severe vomiting and diarrhea. By day 3 (phase 2) she developed shock and multi-organ failure. She was intubated and admitted to the intensive care unit.

On or about day 4 (the paper is somewhat vague on the exact time course) V-A ECMO was started because of hypotension resistant to fluids and pressors, along with an ejection fraction of 5-10%. Despite an unsurprisingly complicated hospital course she slowly recovered cardiac function and ECMO was discontinued on day 10. The authors report: “She completely recovered from multi-organ failure and was discharged from the ICU 24 days after the poisoning.” On subsequent outpatient follow-up appointments she was doing well.

This is to my knowledge only the second description of the use of ECMO to treat colchicine poisoning in the literature. (The first case can be found here.)  Although the evidence is sparse, this is undoubtedly an exciting and promising modality for treating what is often a devastating toxic exposure.

To read my Emergency Medicine News column on ECMO in the poisoned patient, click here.

Several months back, Steve Aks and I discussed the potential use of ECMO in the critical toxicology patient with Joe Bellezzo, Zack Shinar and Scott Weingart  from the ED ECMO website. To listen to that podcast, click here.

Related posts:

Case report: veno-venous ECMO as a bridge to lung transplantation in paraquat poisoning

Poisoned patients treat with ECMO: 10 cases from the ToxIC Registry

Lipid rescue therapy and ECMO in the poisoned patient: can they be used together?

ECMO and the poisoned patient: ready for prime time?


[Photograph of C autumnale from]