The first priorities in the management of seriously poisoned patients are the same as with all patients. The patency of the airway must be ensured, followed by assistance of breathing and support of circulation. Cardiac monitoring, pulse oximetry, and intravenous access should be established as indicated by the patient’s clinical condition. CNS toxicity should also be addresses under stabilization especially in the setting of seizures.
Airway & Breathing
The most common factor contributing to death from drug overdose or poisoning is loss of airway-protective reflexes with subsequent airway obstruction caused by the flaccid tongue, pulmonary aspiration of gastric contents or respiratory arrest. All poisoning patients should be suspected of having a potentially compromised airway irrespective of their presentation. Look for signs of airway obstruction such as dyspnea, air hunger or hoarseness and signs of airway comprise such as stridor, intercostal/ subcostal retractions, cyanosis, diaphoresis, and tachypnea.
Along with airway problems, breathing difficulties are the major cause of morbidity and death in patients with poisoning or drug overdose. Patients may have one or more of the following complications:
a) Ventilatory failure from toxins that cause failure of the ventilatory muscles (Eg. organophosphates), central depression of respiratory drive (Eg. opiates), and severe pneumonia or pulmonary edema (Eg. hydrocarbons).
b) Hypoxia (Eg. Cyanide, methemoglobinemia, carbon monoxide).
c) Bronchospasm (Eg. organophosphates).
Airway management should focus on correcting hypoxia and respiratory acidosis and avoiding pulmonary aspiration. Continuous arterial blood gas (ABG) analysis should be done. Acidemia due to respiratory depression can exacerbate the toxicity of drugs, such as cyclic antidepressants and salicylates. Certain toxic conditions can pose problems in the performance of standard airway management techniques. For example, severe upper airway injury that occurs following a caustic ingestion may preclude routine endotracheal intubation, necessitating surgical management of the airway. The use of succinylcholine for rapid-sequence intubation can result in prolonged paralysis in patients with organophosphate toxicity. Sometimes, elective intubation may be warranted despite the patient exhibiting no signs of compromise in case of substances that may produce sudden hemodynamic compromise or stridor without prodromal signs, eg, Endosulphan or Super-Vasmol poisoning. Routine ventilator settings may be grossly inadequate for the patient with severe metabolic acidosis who requires significant respiratory compensation.
A. General Assessment and Initial Treatment:
a. Check blood pressure, pulse rate and rhythm: Perform cardiopulmonary resuscitation (CPR) if there is no pulse and perform advanced cardiac life support (ACLS) for arrhythmias and shock. Standard advanced cardiac life support (ACLS) protocols may be inadequate or inappropriate for resuscitation of poisoned patients with life-threatening cardiac dysrhythmias or cardiac arrest. Eg. The use of procainamide is contraindicated for ventricular dysrhythmias caused by cyclic antidepressants and other myocardial sodium channel-blocking agents.
b. Begin continuous electrocardiographic (ECG) monitoring. Arrhythmias may complicate a variety of poisoning (Eg. Oleander), and all patients with potentially cardiotoxic drug poisoning should be monitored in the emergency department or an intensive care unit for at least 6 hours after the ingestion.
c. Secure venous access. Antecubital or forearm veins are usually easy to cannulate and should be done so with large-bore IV cannulas. Alternative sites include femoral, subclavian, internal jugular, and other central veins. Access to central veins allows measurement of central venous pressure and placement of a pacemaker or pulmonary artery lines.
d. Advanced hemodynamic monitoring with CVP, pulmonary capillary wedge pressure (PCWP), and intra-arterial pressure measurement (IAPM).
e. Draw blood for routine studies (see Diagnostic Testing).
f. Begin intravenous infusions as needed and to keep vein open.
g. In seriously ill patients (eg, those who are hypotensive, obtunded, convulsing, or comatose), place a Foley catheter in the bladder, obtain urine for routine and toxicologic testing, and measure hourly urine output.
B. Fluid Resuscitation & Vasopressors: Most hypotensive patients following toxic ingestions respond well to fluid resuscitation. Initial fluid of choice is normal saline and dextrose-normal saline. Sometimes, low-dose vasopressors may be needed (dopamine 5–15 mcg/kg/min). Note that dopamine may be ineffective in some patients with depleted neuronal stores of catecholamines (eg, tricyclic antidepressant overdose) or in cases where alpha-adrenergic receptors may be blocked (phenothiazines). In such cases norepinephrine, 0.1 mcg/kg/min IV may be more effective. Sympathomimetics may also cause refractory arrhythmia in certain toxin-induced myocardial suppression like endosulphan.
C. Dysrhythmias: Common dysrhythmias encountered are bradycardia and atrioventricular (AV) block, QRS interval prolongation, sinus tachycardia, ventricular arrhythmias, torsade de pointes, and ventricular fibrillation. Rule out electrolyte abnormalities and correct any if present.
Do not treat bradycardia or AV block unless the patient is symptomatic (eg, exhibits signs of syncope or hypotension). Administer atropine, 0.01–0.03 mg/kg IV. If this is not successful, use isoproterenol 1–10 mcg/min IV, titrated to the desired rate, or use an emergency transcutaneous or transvenous pacemaker.
For management of ventricular tachycardias, agents that prolong QT interval like Class Ia, Class Ic, and Class III antiarrhythmic drugs are contraindicated as these may predispose to torsades de pointes (although amiodarone is an exception in Class II drugs). Use lidocaine, 1–3 mg/kg IV or amiodarone 300 mg IV or 5 mg/kg in children. For torsades de pointes, administer intravenous magnesium sulfate, 1–2 g in adults, over 20–30 minutes.
D. Hypertension is frequently overlooked in drug-intoxicated patients and often goes untreated. Eg. Anticholinergics (datura, amphetamines). Nicotinic cholinergic stimulators (organophosphates) may initially cause hypertension and tachycardia followed by hypotension and bradycardia. For hypertension with little or no tachycardia, use nitroprusside, 2–10 mcg/kg/min IV. For hypertension with tachycardia, use labetalol (0.2–0.5 mg/kg IV) or esmolol (500 mcg/kg over one minute loading dose followed by 40-200 mcg/kg/min infusion).
A. Seizures Seizures are a major cause of morbidity and mortality from drug overdose or poisoning. Seizures may be single and brief or multiple and refractory. They can cause airway compromise, resulting in apnea or pulmonary aspiration. Multiple or prolonged seizures may cause severe metabolic acidosis, hyperthermia, rhabdomyolysis, and brain damage.
Since most toxins are GABA antagonists, the treatment of choice for toxin-induced seizures are GABA agonists like benzodiazepines (lorazepam, 0.05–0.1 mg/kg IV or midazolam, 0.05–0.1 mg/kg IV. Refractory seizures may be treated with phenobarbitone, 10–15 mg/kg IV; slow infusion over 15–20 minutes (caution as barbiturates may mimic brain death), propofol, 2–5 mg/kg IV followed by 2-4 mg/kg/hour (watch for propofol infusion syndrome) or thiopentone (3-5 mg/kg loading followed by 3-5 mg/kg/hr infusion).
Phenytoin is considered the anticonvulsant of last choice for most toxin-induced seizures.
Monitor for cerebral edema, hyperthermia, and rhabdomyolysis. Neuromuscular paralysis with a nondepolarizing neuromuscular blocker may be used to prevent hyperthermia and rhabdomyolysis associated with refractory seizures. Monitor ECG, electrolytes, and blood glucose levels when administering anticonvulsants.
B. Coma and stupor: A variety of drug overdose and poisonings produce coma and stupor. Coma is most often a result of global depression of the brain’s reticular activating system, caused by anticholinergic agents, sympatholytic drugs, generalized CNS depressants, or toxins that result in cellular hypoxia. Hypoglycemia is one of the major causes of coma and bedside glucose testing should be done at the earliest. Coma sometimes represents a postictal phenomenon after a drug- or toxin-induced seizure.
Coma cocktail may be useful in unknown overdoses and where bedside glucose testing is unreliable; dextrose (50% 50 ml IV), thiamine (100 mg in IV bottle or IM), and naloxone (0.1 mg IV, followed by 0.4 mg and 2 mg IV if no response in 2 minutes).
Consider flumazenil only if benzodiazepines are the only suspected cause of coma and there are no contraindications. Be aware that use of flumazenil can precipitate seizures. Do not use analeptics in coma as they may cause seizure and have been proved to be not beneficial.
C. Hypothermia: Hypothermia may mimic or complicate drug overdose and poisonings and should be suspected in every comatose patient. Re-warming should be done slowly (using blankets, warm intravenous fluids, and warmed-mist inhalation) to prevent rewarming arrhythmias.
D. Hyperthermia: It may be caused by excessive heat generation because of sustained seizures, rigidity, or other muscular hyperactivity; an increased metabolic rate or impaired dissipation of heat secondary to impaired sweating (eg, anticholinergic agents). Untreated, severe hyperthermia is likely to result in hypotension, rhabdomyolysis, coagulopathy, cardiac and renal failure, brain injury, and death. Survivors often have permanent neurologic sequelae.
Immediate rapid cooling by mechanical means is essential to prevent death or serious brain damage. Begin external cooling with tepid (lukewarm) sponging and fanning. This evaporative method is the most efficient method of cooling. Antipyretics and salicylates are ineffective in controlling toxin-induced hyperthermia and may worsen any hepatic derangements if present and are therefore contraindicated. The most rapidly effective and reliable means of lowering the temperature is neuromuscular paralysis. Administer a nondepolarizing agent such as pancuronium, 0.1 mg/kg IV, or vecuronium,
0.1 mg/kg IV once the patient has been intubated and ventilated.
Neuroleptic malignant syndrome (NMS) is a hyperthermic disorder characterized by hyperthermia, muscle rigidity, metabolic acidosis, and confusion. It is seen rarely in organophosphates poisoning and in antipsychotic overdoses. Bromocriptine or dantrolene (1–10 mg/kg IV) are the treatments of choice.
E. Agitation, Delirium, or Psychosis: Administer benzodiazepines, midazolam or lorazepam as stat doses.
Anaphylactic and Anaphylactoid Reactions
Examples of toxins that cause anaphylactic or anaphylactoid reactions include pyrethrins, colchicine, additives in chemical formulations etc. These reactions are characterized by bronchospasm and increased vascular permeability that may lead to laryngeal edema, skin rash, and hypotension. Maintain airway and administer epinephrine 0.3–0.5 mg intramuscularly (IM) (children: 0.01 mg/kg, maximum 0.5 mg) for mild-to-moderate reactions and for severe reactions, administer 0.05–0.1 mg IV bolus every 5 minutes or give an infusion starting at a rate of 1–4 mcg/min and titrating upward as needed. Diphenhydramine and IV corticosteroids may also be used as needed.