Understanding the fundamentals of acute poisoning

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.