Tox Tunes #109: I Killed Robert Johnson (The Stone Foxes)

More myths and legends are attached to the life of Robert Johnson (1911 – 1938) than surround any other American blues artist. It’s said that he sold his soul to the devil down at a Mississippi crossroads in return for the ability to play guitar with a technique that musicians like Eric Clapton are still trying to replicate. It’s said that his death at age 27 established a precedent for other great American musicians who also died at that same age, including Jimi Hendrix, Janis Joplin, Jim Morrison, and Al “Blind Owl” Wilson. And it is said that Johnson was poisoned with strychnine in Greenwood, Mississippi after making advances on another man’s wife. This has never been proven.

The story of Robert Johnson has fascinated other musicians from the time of his death up through the present. This song, by The Stone Foxes, is from the Bears & Bulls disc. It is the imagined confession of a club owner who poisoned the musician:

Now I’m not saying he deserved it, oh for crossing the line
But I killed Robert Johnson, with strychnine

There is some dispute as to whether, if Johnson was in fact poisoned, the agent was strychnine. Some argue that the smell and taste of nux vomica is so strong and distinct that it could be hidden even if combined with whiskey. In addition, it apparently took Johnson 3 days to die after the presumed exposure. Strychnine would have acted much more rapidly.

Here is Johnson’s recording of “Sweet Home Chicago“:

And here is Eric Clapton’s cover of “Love in Vain“:

 

 

 

Labetalol in acute cocaine toxicity: is it safe?

Cocaine-medical-grade3 out of 5 stars

Acute Toxicity from Topical Cocaine for Epistaxis: Treatment with Labetalol. Richards JR et al. J Emerg Med 2017 Mar;52:311-313.

Abstract

There has long been a debate among toxicologists — still unresolved — as to whether it is safe to use a beta-blocker to treat cocaine-related hypertension and tachycardia. The (theoretical) concern is that since cocaine is both an α- and a β-agonist, blocking the β-receptors could lead to unopposed α stimulation with increased severe hypertension.

Some authors contend that in this setting, labetalol would be safe since it blocks both α and β receptors.  Others argue that since labetalol has β blocking that is 7 times as potent as its α effect, the potential problem of increased blood pressure would remain. For some papers discussing this issue, see “Related Posts” below.

This case report describes a 56-year-old man who received 4 ml of 4% cocaine solution (160 mg) applied to the nasal mucosa to treat epistaxis. Within 10 minutes after the cocaine was applied, the patient described a “sense of light-headedness and impending doom.” Evaluation revealed hypertension (155/108 mm Hg) and tachycardia (96/min, increased from 76/min.)

He was treated with IV labetalol (10 mg,) with immediate resolution of his symptoms and autonomic instability. The clinicians treated his nasal bleeding with topical nitrate and an epistaxis device without further event.

The authors conclude that:

Labetalol represents an effective first-line treatment, which, unlike benzodiazepines, directly counters the pharmacologic effects of cocaine and has no respiratory or sedative side effects. Labetalol, with its mixed β/α-blocking properties, also mitigates the potential for “unopposed α-stimulation.”

It seems to me quite a stretch to base such a conclusion on a single case report. Certainly the debate goes on, and evidence on either side is sparse and inconclusive. For the record, the current (Tenth) edition of Goldfrank’s Toxicologic Emergencies says:

. . .”adrenergic antagonism increases lethality in cocaine-toxic animals and in humans, exacerbates cocaine-induced coronary vasoconstriction, and produces severe paradoxical hypertension. Mixed alpha and beta adrenergic antagonists do not appear to offer any advantage in the treatment of patients with cocaine associated chest pain.”

Related posts:

Cocaine, chest pain, and beta-blockers:time for re-evaluation?

Cocaine-associated cardiotoxicity: a systematic review yields no asnwers