In the emergency setting, patient stabilization takes precedence over a meticulous physical examination. However, a rapid directed examination can yield important diagnostic clues. Once the patient is stable, a more comprehensive physical examination can reveal additional signs suggesting a specific poison/exposure. Additionally, a dynamic change in clinical appearance over time may be a more important clue than findings on the initial examination. Taking note of odors emanating from the patient or the environment can provide valuable information. Some poisons produce odors characteristic enough to suggest the diagnosis upon first encounter (Table 46.1). A complete set of vital signs can further assist the provider in narrowing the differential diagnosis [5]. The skin should be carefully examined by removing patient clothes and assessing for color, temperature, and the presence of dryness or diaphoresis. Absence of diaphoresis is an important clinical distinction between anticholinergic and sympathomimetic poisoning. The presence of bites or similar marks may suggest spider or snake envenomations. The presence of erythema or bullae over pressure points may suggest rhabdomyolysis in the comatose patient, while track marks suggest IV or subcutaneous drug abuse. Finally, a systematic neurological evaluation is important, particularly with patients exhibiting altered mental status. While the Glasgow Coma Scale (GCS) is useful for evaluating trauma victims, it has little role in predicting the prognosis of the poisoned patient [6].

Seizures are a common presentation of an unknown overdose, and the list of toxins that can induce a convulsion is lengthy (Table 46.2). Ocular findings helpful in narrowing the differential diagnosis include miosis and mydriasis (Table 46.3). Other useful general neurological signs include fasciculations (from organophosphate poisoning), rigidity (tetanus and strychnine), tremors (lithium and theophylline), and dystonic posturing (neuroleptic agents).

Toxidromes

A toxidrome is a toxic syndrome or constellation of signs and symptoms associated with a certain class of poisons. Rapid recognition of a toxidrome can determine the class or, in some cases, the specific poison responsible for a patient’s condition. Table 46.4 lists characteristics of selected toxidromes. It is important to note that patients may not present with every component of a toxidrome and that toxidromes are difficult to identify in mixed ingestions.

Certain aspects of a toxidrome can have great significance. For example, noting dry axilla may differentiate an anticholinergic patient from a sympathomimetic patient, and miosis may distinguish opioid toxicity from a benzodiazepine overdose. There are notable exceptions to the recognized toxidromes. For example, several opioid agents (meperidine, propoxyphene, and tramadol) are not always associated with miosis. In most cases, a toxidrome will not indicate a specific poison but rather a class of poisons. Several poisons have unique presentations that make their presence virtually diagnostic. For example, clonidine is associated with sedation, miosis, bradycardia, shallow respirations, and hypotension, yet the patient will become alert with stimulation and then drift rapidly back to sedation with no stimulation.

Cardiac monitor and electrocardiogram

Electrocardiogram interpretation of in the poisoned patient can be challenging. Numerous drugs can cause ECG changes. The incidence of ECG changes in the poisoned patient is unclear, and the significance of various changes may be difficult to define [7]. Despite the fact that drugs have widely varying indications for therapeutic use, many unrelated drugs share common electrocardiographic effects if taken in overdose. Toxins can be placed into broad classes based on their cardiac effects. Agents that block the cardiac fast sodium channels and agents that block cardiac potassium efflux channels cause characteristic ECG changes, QRS prolongation, and QT prolongation, respectively. The recognition of specific ECG changes associated with other clinical data (toxidromes) can be potentially life saving [8].

The ability of drugs to induce cardiac sodium channel blockade prolonging the QRS complex has been well described in the literature [9]. Cardiac voltage-gated sodium channels reside in the cell membrane and open in conjunction with cell depolarization. Sodium channel blockers bind to the transmembrane sodium channels, decreasing the number available for depolarization. This creates a delay of sodium entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens [10]. In some cases, the QRS complex may take the pattern of recognized bundle branch blocks [11,12]. With tricyclic antidepressant poisoning, rightward axis deviation of the terminal 40 msec of the QRS axis can be present, in addition to QRS widening [13,14]. In the most severe cases, QRS prolongation becomes so profound that it is difficult to distinguish between ventricular and supraventricular rhythms [15,16]. Continued QRS prolongation may result in a sine wave pattern and eventual asystole. It has been theorized that the sodium channel blockers cause slowed intraventricular conduction, unidirectional block, the development of a reentrant circuit, and a resulting ventricular tachycardia [17]. This can then degenerate into ventricular fibrillation. Differentiating a QRS prolongation due to sodium channel blockade in the poisoned patient versus other non-toxic etiologies can be difficult.

Drugs blocking myocardial sodium channels comprise a diverse group of pharmaceutical agents (Box 46.1). Patients poisoned with these agents have varied clinical presentations. For example, sodium channel-blocking medications such as diphenhydramine, propoxyphene, and cocaine may also develop anticholinergic, opioid, and sympathomimetic syndromes, respectively [18–20]. In addition, specific drugs may affect not only the myocardial sodium channels but also calcium influx and potassium efflux channels, resulting in ECG changes and rhythm disturbances not related entirely to the drug’s sodium channel-blocking activity [21,22]. All the agents listed in Box 46.1 induce myocardial sodium channel blockade and may respond to therapy with sodium bicarbonate or hypertonic saline. Displacement of the sodium channel-blocking agents by hypertonic saline or sodium bicarbonate can improve inotropy and prevent arrhythmias.[9] It is therefore reasonable to treat poisoned patients with prolonged QRS intervals, particularly those with hemodynamic instability, empirically with 1–2 mEq/kg of sodium bicarbonate (the gold standard for treatment of sodium channel blockade). Shortening of the QRS can confirm the presence of a sodium channel-blocking agent.

Approximately 3% of all non-cardiac prescriptions are associated with the potential for QT prolongation [23]. Myocardial repolarization is driven predominantly by outward movement of potassium ions [24]. Blockade of the outward potassium currents prolongs the action potential [25]. This subsequently results in QT interval prolongation and the potential emergence of T- or U-wave abnormalities on the ECG [26]. The prolongation of repolarization causes the myocardial cell to have less charge difference across its membrane, which may result in the activation of the inward depolarization current (early after-depolarization) and promote triggered activity. These changes may lead to reentry and subsequent polymorphic ventricular tachycardia (VT), most often as the torsades de pointes variant of polymorphic VT [27]. QT prolongation is considered to occur when the QTc interval is greater than 440 msec in men and 460 msec in women, with arrhythmias most commonly associated with values greater than 500 msec. However, the potential for an arrhythmia for a given QT interval will vary from drug to drug and patient to patient [24]. Drugs associated with QT prolongation are listed in Box 46.2

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