Diagnosis of Poisoning

Diagnosis of Poisoning

A poisoning case can present to a doctor or hospital in any one of a number of ways. Broadly, there are four types of presentation:

·      Fulminant—Produced by a massive dose. Death occursvery rapidly, sometimes  without preceding symptoms, the patient appearing to collapse suddenly.

·      Acute—Produced by a single dose or several small dosestaken in a short period. Onset of symptoms is abrupt.

·      Chronic—Produced by small doses taken over a longperiod. Onset is insidious.

·      Subacute—Characterised by a mixture of features of acuteand chronic poisoning.

The majority of poisoned patients presenting to the casualty (emergency) department are victims of acute exposure. Most of them are usually coherent enough to tell the doctor what the problem is, and indeed what they have taken or been exposed to. However, in an unconscious or uncooperative patient the diagnosis will have to be made on the basis of circumstantial or third party evidence. It is important to inter-rogate the persons accompanying the patient (relatives, friends, ambulance personnel, etc.), and to contact his or her family doctor as soon as possible. In spite of all this, unfortunately, in a significant proportion of cases the diagnosis remains uncertain. This is because unlike in other clinical conditions arising out of natural disease, there are only a very few toxicsyndromes characterised by specific signs and symptoms(Table 2.1). In most cases, the poisoned patient presents with one or more of the following non-specific features:

·      Impairment of consciousness

·      Respiratory/Cardiovascular depression

·      Dehydration due to vomiting/diarrhoea

·      Hypothermia

·      Convulsions

·      Cardiac arrhythmias

However, there are some valuable clues afforded on detailed clinical examination which can help narrow down the differen-tial diagnosis. Most of these will be dealt with in a subsequent section (General Management), but a few are discussed here for the sake of convenience.

·              Ocular clues: Several drugs/poisons affect the pupils of theeyes producing either miosis or mydriasis. A few produce nystagmus. These have been laid out in Table 2.2. Normally, both the pupils are equal in size, 3 to 4 mm under typical conditions, round, and react directly as well as consensu-ally to increased light intensity by constricting.

Pupillary constriction also occurs as part of the near reflex when a person focusses on near objects. All these functions result from the balance between cholinergic innervation of the iris sphincter (constrictor) by the oculomotor nerve, and sympathetic innervation of the radial muscle of the iris (dilator). Mydriasis can occur due to increased sympathetic stimulation by endogenous catecholamines or from systemic or ocular exposures to sympathomimetic drugs. Mydriasis can also result from inhibition of cholinergic mediated pupil-lary constriction. Because pupillary constriction in response to light is a major determinant of pupil size, blindness from ocular, retinal, or optic nerve disorders also leads to mydriasis. Pupillary constriction or miosis can result from increased cholinergic stimulation, or inhibition of sympa-thetic dilation. Other ophthalmological manifestations along with their respective causes are mentioned in Table 2.3.

·      Olfactory clues: Some poisons have distinctive odourswhich may be perceived in the vicinity of a poisoned patient, especially in the breath. Some important examples are mentioned in Table 2.4.

·              Dermal clues: Some poisons have characteristic dermalmanifestations in acute toxicity, while certain others demonstrate skin signs on chronic exposure (Table 2.5).

Several therapeutic drugs produce irritant dermatitis even in non-toxic doses, e.g. most antibiotics, INH, phenothiazines, sulfonamides, thiazides, NSAIDs, etc.

·              Oral clues: Careful examination of the mouth can afford valuable information about the aetiology of poisoning in some cases (Table 2.6).