Understanding the fundamentals of acute poisoning

Iwan Darmansjah, Jakarta

The alleged poisoning of human rights activist Munir attracted nationwide attention, although the poisoning of adults and children has become an alarming phenomenon these days. This article will discuss the basis and fundamentals of poisoning, poison identification, management of outbreaks, and the clinical management of the poisoned patient.

It is important to distinguish between chronic and acute poisonings. Chronic poisoning is more subtle and rare; it develops within a long period of time, during which it is difficult to diagnose poisoning and its causative factors. Quite often, chronic poisoning is revealed as the side effects of drugs, which may not be recognized by the attending physician. These may be on the borderline of an adverse reaction to drugs, rather than poisoning.

Symptoms like nausea, vomiting, anorexia, decrease in body weight, loss of hair, skin changes, decreased alertness, irritability or convulsion may mimic the side effects of drugs or are symptoms of disease entities, and, therefore, may be treated erroneously. Chronic poisoning with xenobiotics is also seldom, but may arise as an epidemic (mercury poisoning in Japan, Iraq, etc.). It may also take the form of a sub-acute or sub-chronic poisoning, whereby the build-up of small doses in the body could erupt into an acute manifestation.

To develop the symptoms of poisoning one has to ingest a large enough quantity, because "the dose determines whether a chemical is a poison". Therefore, even the most lethal poison may be given in a minute dose that would not affect a human. Likewise, one may kill a man with almost any harmless chemical when the dose given is large enough.

This principle of relative toxicity in relation to dose is the most important single principle in poisoning, but, ironically, also the factor most often misunderstood in the management of poisoned patients, and in drug treatment as well. The second important issue is that very few true antidotes exist to counteract poisons, and most poisonings have to be treated symptomatically.

This does not mean, however, that the latter is useless. The human body is usually strong enough to withstand poisoning if one can maintain the vital functions (heart and respiration) long enough so as to allow the body to metabolize and excrete the poison through the kidneys, liver and the gut.

Treatment should be minimized to the most needed and over- treatment may lead to the worsening of the condition and even death. Sometimes this is referred to as a "nihilistic approach", but it works best. This was exemplified by the fact that, when in the 1950s barbiturate poisoning was treated with all kinds of stimulants, some 25 percent of the patients died, but when nothing was given (no stimulants nor blood-pressure-increasing drugs), only one percent to two percent of patients succumbed.

Outbreaks of poisoning occur now and then in any community; it is so rare, however, that it is almost forgotten when the previous one is over. But any time it pops up again the same problems and deficiencies in management reappear. The nitrite case caused by contaminated biscuits in W. Java some time ago is perhaps still in our memories. It took the authorities three months to find the nature of the poison.

The key to appropriate outbreak management lies in the early clinical diagnosis of the patients and the identification of possible causative factors. Treatment will usually follow without too many problems, as soon as the diagnosis is established. In difficult cases, the role of the laboratory in detecting the causative poison is very important, but this may only be initiated after the clinician has given an indication of the possible poison that one should identify in the lab.

What went wrong in the nitrite case? The initial presumptive clinical diagnosis was pesticide poisoning, and, therefore, the laboratory was misled and the search for pesticides in the laboratory may indeed produce a positive (albeit small quantity) result, especially when only qualitative methods were used. The laboratory should also be able to quantify the poison detected, even if it was semi-quantitatively. Not least important is the capacity to evaluate the result, because what has been "found" may not always be the causative poison.

The basic problem lies in the unrecognized fact that the average doctor knows very little about poisoning, while the clinical toxicologist's presence on the scene seem to be urgently needed to direct the search in the laboratory. How the clinical toxicologist identifies the class of chemicals that the laboratory should look for is beyond the scope of this short article and covers, in fact, the toxicology of the whole area of drugs and possible xenobiotics. A short introduction into its clinical management will be attempted below:

To begin with, it may be stated that, for the expert working in a specialized poisoning ward, there are very few problems with acute poisoning management in adults, as well as in children. The principles are simple and clear-cut and very few ramifications develop during the management of a poisoned patient in contrast with disease entities. But even though it looks simple, great problems may arise when one is ignorant of the basic principles of diagnosis and treatment, and faulty management may even endanger the patient's life.

Acute poisoning may present itself as a most dramatic case. But, as with chronic poisoning, all possible symptoms of acute poisoning and signs can be mimicked by disease and, therefore, one should be able to distinguish between disease and poisoning. Any bizarre symptoms occurring in a previously healthy adult or child should be reason to suspect poisoning. Symptoms develop within a few minutes to about a few hours after acute exposure to a poison.

It should be possible for a clinical toxicologist to group the signs and symptoms of poisoning into specific classes, and thereby direct the search for the causative poison in the laboratory. Thus, central nervous system (CNS) depression in various stages with flaccid extremities, no extrapyramidal signs, and perhaps a moderate fall of blood pressure should point toward a pure CNS depressant drug. Tachycardia with dry skin and mucus membranes, and dilated pupils -- with or without CNS involvement -- should point definitely toward an anticholinergic drug. Coma with hypersecretion of the mouth, bronchial airway, and sweat glands of the skin, plus constricted (or dilated) pupils, and a slow -- or fast -- heart rate is typical for organophosphorus or carbamate insecticides, so that no laboratory confirmation is needed and swift treatment with massive doses of atropine sulfate is mandatory.

Insecticides have been the cause of many poisoning outbreaks but they were also falsely incriminated in some. It should be realized that there are many classes of pesticides with different actions and, therefore, different antidotes are needed; but most do not even have a specific antidote. When diagnosis is established -- with or without laboratory confirmation -- the management of the poisoned patient becomes an important consequence.

It has been previously stated that very few antidotes exist; they are a.o. naloxone for opiate drugs, atropine for organophosphorus and carbamate insecticides, sodium nitrite and sodium thiosulfate for cyanide, methylene blue for nitrites, and chelating agents for heavy metals. Then we have activated charcoal as a non-specific, general antidote to delay the absorption of or adsorb poisons in the gut. It has been shown convincingly that many chemicals are bound to charcoal and poison levels in the blood may be diminished by 30-40 percent, hereby hastening the recovery time.

The writer is Emeritus Professor of Pharmacology, School of Medicine of University of Indonesia.