Ipecac

Ipecac is a prepared form of the Cephaelis acuminata or Cephaelis ipecacuanha plants. Vomiting within 30 minutes after administration is caused by local irritation of the gastric mucosa. Vomiting after 30 minutes is centrally induced.²

Gastric Lavage

For gastric lavage, a large-bore (36F-40F) orogastric tube is passed, after which small volumes (200-300 mL) of liquid are alternately administered and aspirated. Endotracheal intubation should precede this procedure in comatose patients. An oral airway prevents biting of the tube. The amount of stomach contents removed via this procedure is highly variable and decreases with time.^4–6 The procedure can actually push stomach contents into the intestine.⁷ Contraindications include loss of protective airway reflexes (unless the patient is endotracheally intubated), ingestion of a corrosive substance or a hydrocarbon, gastrointestinal pathology, and other medical conditions that could be worsened by the use of lavage. Complications of the procedure include aspiration, laryngospasm, hypoxia, hypercapnia, mechanical injury, and fluid and electrolyte imbalances in children.⁸

Single-Dose Activated Charcoal

Activated charcoal is made when coconut shells, peat, wood, or other materials undergo controlled pyrolysis and are subsequently activated by heating in steam or air at high temperatures. Activation creates multiple internal pores and the small particle size necessary for adsorption. The particles have a large surface area and are capable of adsorbing poisons with varying affinities. Although in vitro studies demonstrate adsorption of many drugs to activated charcoal, animal studies reveal variable reductions in the systemic uptake of marker substances.⁹ Volunteer and clinical studies have not demonstrated that single-dose administration of activated charcoal improves outcome. Contraindications to the administration of activated charcoal include decreased level of consciousness and unprotected airway, ingestion of caustic substances or hydrocarbons, gastrointestinal pathology, and medical conditions that could be further compromised by the administration of activated charcoal. Complications include aspiration and direct administration of charcoal into the lung.¹⁰

Because activated charcoal is an inert substance, it is thought that lung injury after aspiration of activated charcoal is caused by gastric contents. Aspiration of gastric contents causes neutrophils to release neutrophil elastase, which increases pulmonary vascular permeability.¹¹ In comparison, intratracheal administration of activated charcoal does not increase elastase in the bronchoalveolar fluid.¹² Activated charcoal can activate alveolar macrophages, which are a potent source of oxygen radicals, proteases, and other inflammatory mediators. Charcoal also causes obstruction of small distal airways Overdistention of alveolar segments in areas not occluded by charcoal leads to volutrauma in those areas, which increases microvascular permeability.¹³ Although case reports reveal long-term pulmonary pathology after aspiration or instillation of activated charcoal,^14,15 the true incidence of chronic problems after charcoal aspiration is unknown.

Cathartics

Whole-Bowel Irrigation

Whole-bowel irrigation consists of administration through a nasogastric tube of an osmotically balanced, polyethylene glycol–based electrolyte solution to decontaminate the entire gastrointestinal tract by physically expelling intraluminal contents. As much as 1500 to 2000 mL/h can be administered to an awake patient. Negotiations to let the patient attempt to drink the solution only cause delay, because patients are unable to drink at a constant rate. Contraindications include bowel pathology, unprotected or compromised airway, hemodynamic instability, and intractable vomiting. Complications are nausea, vomiting, and abdominal cramps.¹⁸

Clinical Implications of Gastrointestinal Decontamination

There is no role for syrup of ipecac in the hospital setting. Gastric lavage may be considered for obtunded patients if it can be instituted within one hour after the ingestion. Single-dose activated charcoal should not be routinely administered to patients with mild to moderate degrees of poisoning. Whole-bowel irrigation should be considered for awake patients within the first hours after ingestion of a sustained-release preparation, ionic compounds (e.g., lithium), or packets of illicit drugs.

These guidelines refer to the routine management of poisoned patients. Cellular toxins require special consideration. The physician should always call the Poison Center (1-800-222-1222 in the United States) to discuss a patient with a potentially life-threatening ingestion.

Multiple-Dose Activated Charcoal

Multiple-dose activated charcoal is the repeated oral administration of activated charcoal to enhance drug elimination. If the drug concentration in the gut is lower than that in the blood, the drug will passively diffuse back into the gut. The concentration gradient, intestinal surface area, permeability, and blood flow determine the degree of passive diffusion. As the drug passes continuously into the gut, it is adsorbed onto the charcoal particles, a process called gastrointestinal dialysis. Multiple-dose activated charcoal also interrupts the enterohepatic and enterogastric circulation of drugs. Drugs with a prolonged elimination half-life, a small volume of distribution (less than 1 L/kg), and little protein binding are the most amenable to this sort of management.¹⁹

The initial dose of charcoal is 50 to 100 g, and this treatment is followed every 1, 2, or 4 hours by a dose equivalent to 12.5 g/h. More frequent, smaller doses may prevent vomiting. Addition of a cathartic (e.g., sorbitol) can be considered for the initial one or two doses. Continuous use of a cathartic can cause diarrhea and fluid and electrolyte imbalances. Multiple-dose activated charcoal can be continued until the patient improves clinically. Contraindications include an unprotected airway, intestinal obstruction, and an anatomically abnormal gastrointestinal tract. Complications include bowel obstruction and vomiting with subsequent aspiration.¹⁹

Urinary Alkalinization

Urinary alkalinization is the administration of intravenous (IV) sodium bicarbonate to produce urine with a pH ≥ 7.5. The objective of treatment is pH manipulation, not forced diuresis. Hypokalemia is the most common complication. Alkalemia also can occur.²⁰

Dextrose

Up to 8% of patients with altered mental status are hypoglycemic.²¹ Hypoglycemia can be a result of drug or toxin exposure, nutritional deprivation, or a medical complication (e.g., sepsis, hyperthermia). Glucose should be checked at the bedside for all patients with altered mental status.

Naloxone

Endogenous and exogenous opiates produce their effects by binding at one or more opiate receptors. Naloxone, nalmefene, and naltrexone are competitive opioid antagonists that bind at the mu (µ), kappa (κ), and delta (δ) receptors and competitively prevent the binding of endogenous and exogenous opiates at these receptors. The duration of action of naloxone is 15 to 90 minutes. Its clinical effects depend on the dose and route of naloxone administration as well as the dose and rate of elimination of the opiate agonist. Naloxone can be administered by IV, intramuscular, intratracheal, or sublingual routes. After IV administration, naloxone rapidly enters the central nervous system (CNS). In patients with opiate poisoning, consciousness is restored and respiration improves within 1 to 2 minutes. Meiosis, inhibition of baroreceptor reflexes, laryngospasm, and decreased gastrointestinal motility are also reversed.²²

Certain nonopiate drugs can cause release of endogenous opiates, contributing to CNS and respiratory depression as well as hypotension. Alternatively, nonopiate drugs and naloxone can compete for an unidentified nonopiate receptor that contributes to CNS depression and hypotension. Naloxone can reverse the toxicity caused by drugs that are not opioids, such as clonidine, angiotensin-converting enzyme inhibitors, and sodium valproate. Naloxone should be administered to all patients with altered mental status or coma of unknown cause. Opiate-dependent patients should receive only small doses in an effort to prevent rapid withdrawal. If a patient is not opiate dependent, a reasonable starting dose is 2 mg, increasing to 10 mg (in increments) if there is no response. Large doses of naloxone may be necessary to reverse the effects of nonopiate drugs or of opiate drugs with high affinity for the δ and κ opiate receptors.

If respiratory depression returns, the initial dose of naloxone may have to be repeated or a constant infusion of naloxone initiated. The starting dose for a constant infusion of naloxone is hourly administration of about one-half to two-thirds of the bolus dose that reversed the opiate effects. If withdrawal is precipitated, it is short lived and not life threatening. Complications of naloxone administration are very rare.²³