I am curled up in a fetal position on the bathroom floor, my forehead pressed firmly against the cool tile to soothe a fierce pounding headache. Waves of nausea lap at my solar plexus and then retreat, leaving me exhausted in a drenching cold sweat. Any attempt to stand is greeted by the nausea gurgling back, along with lightheadedness and a feeling of pre-syncope. Saliva pools in my mouth.
A differential diagnosis flashes through my mind. Have I been inadvertently exposed to an organophosphate insecticide? A carbamate? Sarin or some other cholinergic nerve agent?
Actually, none of the above. I am, in fact, the victim of another cholinergic syndrome, this one caused by the evil weed. No, not that weed. I'm talking about tobacco. Just 40 minutes before, I had finished a Churchill Humongo, a cigar so gargantuan that the band might well have read Louisville Slugger. My symptoms represented a classic case of nicotine toxicity.
The tobacco plant — Nicotiana tabacum—is native to the Americas. Before Christopher Columbus, smoking of any kind was unknown in Europe. The missionary André Thevet described the effects tobacco had on nicotine-naïve Europeans:
“The Christians that do now inhabit [Brazil] are become very desirous of this herb and its perfume, although that the first use thereof is not without danger, before that one is accustomed thereto, for this smoke causes sweats and weakness, even to fall into a syncope. (The New Found World, 1568. Historical information and the passage from The New Found World are found in Iain Gately's fascinating book, Tobacco: A Cultural History of How an Exotic Plant Seduced Civilization [Grove Press].)
Signs and Symptoms
The specific cholinergic receptors that bind nicotine are found throughout the peripheral and central nervous systems, including autonomic ganglia, the spinal cord, the neuromuscular junction, and many areas of the brain and brainstem. They also are present in the adrenal medulla. With significant exposure, nicotine causes initial stimulation of these receptors, followed by more prolonged receptor blockade and paralysis.
Signs and symptoms of nicotine toxicity can be varied and even contradictory. (See table.) In severe cases, respiratory failure can occur from paralysis of the neuromuscular junctions in the diaphragm and intercostal muscles, as well as airway obstruction from increased secretions.
Fortunately, severe nicotine toxicity is virtually never seen anymore. Before 1950, highly concentrated nicotine solutions (40%) were available for use as a “natural” insecticide, and were not infrequently involved in cases of suicidal ingestion or inadvertent exposure. Now that such products are not generally marketed, seizures and respiratory arrest caused by nicotine toxicity are extremely rare.
It is not at all unusual for emergency physicians and toxicologists, however, to be presented with a child who has ingested a product containing nicotine. Cigarettes and cigarette butts rarely produce clinically significant symptoms; the vomiting that frequently occurs following such ingestions accomplishes a measure of gastrointestinal decontamination, and the relatively low pH minimizes absorption for the gastrointestinal tract. Smolinske et al (Human Toxicol 1988;7:27) prospectively reviewed 51 cases of pediatric tobacco ingestion, and found that severe symptoms (which they defined as limb jerking and unresponsiveness, although they don't use the term “seizure”) occurred only in children who had ingested more than one cigarette or three cigarette butts. They recommended that kids who have ingested these amounts be referred to a health care facility for evaluation and treatment.
Other nicotine products — chewing tobacco (smokeless tobacco), snuff, and gum — contain relatively larger amounts of nicotine, and have an alkaline pH to increase absorption across the oral and nasal mucosae. Significant symptoms appear more commonly after these forms are ingested, and most such cases should probably be referred for evaluation, especially if exposure has occurred in the preceding four hours or the child already is symptomatic.
When indicated, treatment of nicotine ingestion includes basic supportive measures. Gastric lavage is rarely indicated. Because nicotine appears to undergo enterohepatic and enteroenteric circulation, administering multidose activated charcoal (for example, 20 g every two hours after an initial loading dose) would be reasonable after a significant ingestion. Increased secretions can be treated with atropine and seizures with a benzodiazepine. Patients who remain asymptomatic after four hours of observation can be discharged.
An unusual but ancient method of administering nicotine was by tobacco enema, a device used in some religious and supernatural ceremonies. The tomb of a 5th century Colombian shaman was found to contain a primitive clyster, with a nozzle made of bone or cane and a bulb of animal skin. Occasionally, reports appear in the medical literature of tobacco administered rectally in an attempt to treat pinworms. This route can produce serious toxicity.
A 2-year-old boy, for example, was given an enema composed of half a package of Bull Durham tobacco mixed in a cup of water. Within 15 minutes, he seized and went on to develop vasomotor collapse and intercostal paralysis. With treatment he recovered completely. (Pediatrics 1953;11:338.) At that time — more than half a century ago — treatment included administration of caffeine. While this is not the recommended therapy for nicotine toxicity, it may explain the popularity, especially in Cuba, of accompanying a cigar with a cup of strong java.