Poisoning cocaine

Non-cardiac Anemia, anxiety disorders, carbon monoxide poisoning, cocaine use, esophageal reflux, peptic ulcer, pleuritis, pneumonia, pneumothorax, pulmonary embolus, pulmonary hypertension, thyrotoxicosis... 

Jonsson, S. O Meara, M. and Young, J.B. Acute cocaine poisoning. 

Sc parishes the slave of cocaine. Wilh every nerve clamoring, all he can do is to renew the lash of the poison, The pharmaceutical effect is over the toxic effect accumulates, The nerves become insane. The victim begins to have hallucinations. See There is a grey cat in that chair. I said nothing, but it has been there all the time. ... 

To disinfect water (well, ponds) for stomach wash in alkaloidal poisoning (except atropine cocaine which are not efficiently oxidized). 

A frequently cited example of an important natural-product-derived drag is the neuromuscular blocker d-tubocurarine, derived from the South American plant curare, which was used by South American Indians as an arrow poison (see Chapter 26). Tubocurarine led to the development of decamethonium, which, although structurally dissimilar to tubocurarine, was nevertheless synthesized based on the then prevalent presumption that tubocurarine contained two quaternary nitrogens. Similarly, synthetic local anesthetics, such as lidocaine, benzocaine, and dibucaine, were synthesized to mimic the nerve-blocking effect of cocaine, a natural alkaloid obtained from the leaves of Coca eroxylum, but without the adverse side effects that have led to its abuse. 

The phenomena of systemic cocaine poisoning are largely those of sympathetic stimulation but not as consistently as with epinephrine. The sympathetic stimulation is mainly central (midbrain) but partly peripheral. The chief manifestations of sympathetic stimulation are (1) sensitization to epinephrine (but antagonization to ephedrine) by peripheral action, (2) mydriasis and slight exophthalmos by central and peripheral action, and (3) cardiac acceleration (chiefly central). Other sympathetic symptoms are constriction of the blood vessels, erection of hair, and relaxation of the intestines. High concentrations of cocaine paralyze all smooth muscles. Procaine also produces... 

The vomiting that frequently occurs in cocaine poisoning is perhaps due to the medullary stimulation, but its mechanism has not been fully investigated. 

Acute poisoning by local anesthetics is fairly common, especially with cocaine, and is apt to be fatal. Some accidents are due to excessive doses through mistakes or faults of technique, but the susceptibility varies greatly owing to differences of absorption and of destruction, and to varying response to the actions. Fright plays a considerable part. 

The treatment of poisoning by local anesthetics should begin with prevention and the selection, dosage, and technique of the administration gross errors and carelessness have caused many deaths. The previous administration of a sedative, especially of the barbituric series, diminishes the risk by suppressing the convulsions and their interference with respiration, so that animals survive one and a half to four times the ordinary fatal dose of cocaine or procaine if administered hypodermically. 

Central nervous system toxicity is rarely observed with catecholamines or drugs such as phenylephrine. In moderate doses, amphetamines commonly cause restlessness, tremor, insomnia, and anxiety in high doses, a paranoid state may be induced. Cocaine may precipitate convulsions, cerebral hemorrhage, arrhythmias, or myocardial infarction. Therapy is discussed in Chapter 59 Management of the Poisoned Patient. 

Cardiovascular toxicity is also frequently encountered in poisoning. Hypotension may be due to depression of cardiac contractility hypovolemia resulting from vomiting, diarrhea, or fluid sequestration peripheral vascular collapse due to blockade of -adrenoceptor-mediated vascular tone or cardiac arrhythmias. Hypothermia or hyperthermia due to exposure as well as the temperature-dysregulating effects of many drugs can also produce hypotension. Lethal arrhythmias such as ventricular tachycardia and fibrillation can occur with overdoses of many cardioactive drugs such as ephedrine, amphetamines, cocaine, tricyclic antidepressants, digitalis, and theophylline. 

Seizures, muscular hyperactivity, and rigidity may result in death. Seizures may cause pulmonary aspiration, hypoxia, and brain damage. Hyperthermia may result from sustained muscular hyperactivity and can lead to muscle breakdown and myoglobinuria, renal failure, lactic acidosis, and hyperkalemia. Drugs and poisons that often cause seizures include antidepressants, theophylline, isoniazid (INH), diphenhydramine, antipsychotics, cocaine, and amphetamines. 

Alkaloids are compounds of biosynthetic origin that contain nitrogen, usually in a heterocyclic ring. These compounds are produced by plants in which they are usually present as salts of organic acids. They tend to be basic and to have a variety of physiological effects. One of the more notorious alkaloids is cocaine, and alkaloidal strychnine is a deadly poison. The structural formulas of these compounds and three other alkaloids are given in Figure 15.10. 

Several SM have been used by mankind for thousands of years22,27 as dyes (e.g., indigo, shikonine), flavors (e.g., vanillin, capsaicin, mustard oils), fragrances (e.g., rose oil, lavender oil and other essential oils), stimulants (e.g., caffeine, nicotine, ephedrine), hallucinogens (e.g., morphine, cocaine, mescaline, hyoscyamine, scopolamine, tetrahydrocannabinol), insecticides (e.g., nicotine, piperine, pyrethrin), vertebrate and human poisons (e.g., coniine, strychnine, aconitine) and even therapeutic agents (e.g., atropine, quinine, cardenolides, codeine, etc.). 

Mild cases of alkaloid poisoning can produce psychological effects that resemble peacefulness, euphoria, or hallucinations. People seeking these effects often become addicted to alkaloids. Alkaloid addiction frequently ends in death. Current estimates are over 400,000 deaths from alkaloid addiction in the United States per year, including both natural alkaloids like nicotine and cocaine, and synthetic alkaloids like metham-phetamine. Most of these deaths result from addiction to nicotine in tobacco, a particularly difficult addiction to overcome. 

Alkaloids are widespread in plants and include some very well-known poisons (notably coniine and strychnine), hallucinogens (morphine, cocaine and muscimol) and other potentially lethal compounds that are nevertheless used in medical practice (e.g. atropine, codeine, colchicine and morphine). As indicated by the preliminary snap-shot above, alkaloids typically have names ending in -ine and which are often related to the plant source or properties. Thus, morphine was named after Morpheus (the God of sleep) and coniine derives from Conium maculatum (hemlock), the plant used in the judicial murder of Socrates (399 BC). Various chemical tests for alkaloids are used as preliminary indicators of alkaloid presence in crude plant extracts. Finally, it should be noted that alkaloids can also exist as jVoxides of the alkaloid base. 

This young man had been poisoned by GHB that was added to his soft drinks without his knowledge. It is worth noting that primary toxicological screens did not identify the presence of GHB. There must be a strong suspicion of GHB use or abuse in order to test for its presence. It is not one of the five drugs—forms of marijuana, cocaine, amphetamines, heroin, and PCP—for which standard drug tests normally screen. 

Jonsson S, O Meara M, Young JB. Acute cocaine poisoning. Importance of treating seizures and acidosis. Am J Med 1983 75(6) 1061-4. 

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