Comprehensive Guide to Managing Poisoning in the Intensive Care Unit: Best Practices and Protocols

Diagnosis and Clinical Evaluation of Poisoned Patients in ICU

History and Physical Examination in Poisoning Cases

A comprehensive patient history is essential but may sometimes need to be more accurate or complete. Information from family members, friends, the patient's pharmacist, and electronic media can provide valuable insights (Mokhlesi et al., 2003; Brent et al., 2017). Without a reliable history, a physical examination helps form a differential diagnosis. Vital signs are crucial for assessing severity and determining immediate interventions. Continuous monitoring of vital signs offers valuable information about the patient's changing status or response to treatment (Brent et al., 2017).

Vital Signs and Neurological Examination in Poisoning Management

Sympathomimetic and anticholinergic substances typically increase heart rate, blood pressure, and body temperature,

Fig 1: Mindmap of substances that can cause hyperthermia

Fig 2: Mindmap of medications and toxins associated with tachycardia

Substances like barbiturates, opiates, organophosphates, beta-blockers, alcohol, benzodiazepines, and clonidine may cause bradycardia, hypothermia, and respiratory depression.

Fig 3: Mindmap of medications and toxins linked to bradycardia.

A thorough neurological examination is beneficial for suspected intoxication. It assesses consciousness, speech, focal deficits, muscle tone, pupil size, and deep tendon reflexes (Brent et al., 2017).

Fig 4: Mindmap of substances that can cause hypothermia

Identifying Toxidromes in Poisoned Patients

Clinical evaluations may reveal specific toxidromes, which are sets of symptoms indicative of certain drugs or toxins. The most frequently encountered toxidromes include:

• Sympathomimetic (Stimulant): These substances can cause Restlessness, tremors, excessive speech and motor activity, mydriasis, hyperthermia, tachycardia, hallucinations, and insomnia (amphetamines, cocaine, phencyclidine).

• Sedative/Hypnotic: Confusion, sedation, coma, slurred speech, delirium, hallucinations, paresthesia, blurred vision, ataxia, nystagmus (benzodiazepines, barbiturates).

• Opioids: These substances can cause miosis, altered mental status, unresponsiveness, shallow respiration, bradypnea, bradycardia, hypotension, hypothermia, and decreased bowel sounds (narcotic agents, clonidine, heroin).

Fig 5: Mindmap of substances causing miosis.

• Anticholinergic: These substances can cause Flushing, fever, dry skin, tachycardia, urinary retention, mydriasis, blurred vision, decreased bowel sounds, ileus, myoclonus, seizures, hallucinations, psychosis, coma (cyclic antidepressants, scopolamine, muscle relaxants).

Fig 6: Mindmap of substances causing mydriasis

• Cholinergic: Salivation, lacrimation, urination, defecation, gastrointestinal distress, emesis, bradycardia (organophosphorus insecticides, black widow spider bites).

Diagnostic Tests for Poisoned Patients

Electrocardiogram (ECG) Interpretation in Poisoning

Medications affecting the ECG when taken in overdose include those that block potassium efflux channels, leading to QT interval prolongation, and those blocking fast sodium channels, resulting in QRS interval prolongation (Holstege et al., 2005, 2008). The QTc interval is considered prolonged if it exceeds 460 milliseconds in women and 440 milliseconds in men; arrhythmias are most frequently associated with QTc values greater than 500 milliseconds (Holstege et al., 2008).

Arterial Blood Gases (ABGs) in Poisoning Management

ABGs are crucial for evaluating critically ill poisoned patients, providing insights into acid-base status (pH), ventilation (PCO2), and oxygenation (PO2). Serial ABGs monitor changes in condition or response to treatment. The most common acid-base imbalance in poisoned patients is anion gap metabolic acidosis (Brent et al., 2017).

Anion Gap (AG) Calculation and Interpretation

A high anion gap, calculated using the formula [Na+] - [Cl- + HCO3-], aids in diagnosing metabolic acidosis. A normal AG ranges from 4 to 12 milliequivalents per liter. An elevated AG (>20 mEq/L) indicates conditions such as lactic acidosis, uremia, ketoacidosis, or intoxication (Mokhlesi et al., 2003). The mnemonic MUDPILES CAT lists common causes of elevated AG.

Fig 7: Mindmap of the MUDPILES CAT mnemonic, detailing common causes of an elevated anion gap.

Osmol Gap and Toxic Alcohols: Diagnosis and Management

Measuring serum osmolality helps estimate concentrations of toxic alcohols like isopropanol, ethylene glycol, and methanol. The osmol gap (OG), calculated as the difference between measured and calculated osmolarity, detects osmotically active compounds. Elevated OG levels can be caused by substances such as ethanol, methanol, ethylene glycol, isopropanol, lactate, glycine, glycerol, mannitol, sorbitol, excipients like propylene glycol, hypermagnesemia, ketones, and shock states (Mokhlesi et al., 2003; Levine et al., 2011).

Toxicology Screening: Methods and Interpretation

Toxicologic screening guides treatment. While urine tests often do not change clinical management, serum toxicology screens provide valuable information for specific toxins like acetaminophen and salicylates. False positives and negatives are common; results should be interpreted based on clinical presentation.

Radiographic Studies in Poisoning Diagnosis

Radiographic evaluations identify conditions and injuries associated with acute toxicity, such as aspiration pneumonitis and anoxic brain injury. They are particularly useful for radiopaque substance ingestion, visualized using the mnemonic COINS: cocaine packets, Chloral hydrate, calcium, opium packets, iron, and other heavy metals, neuroleptic agents, and sustained-release or enteric-coated agents.

Management Strategies for Poisoned Patients in ICU

Supportive Measures for Poisoning Management

Prioritize supportive measures, including the ABCs (airway, breathing, and circulation). Ensure a patent airway and adequate ventilation; endotracheal intubation may be necessary. For hypotension, initiate intravenous crystalloid fluids and, if unresponsive, consider vasopressor therapy. Frequent neurological examinations and continuous cardiac and oxygen saturation monitoring are essential.

Coma Cocktail for Altered Mental Status in Poisoning

For patients with altered mental status, administer a "coma cocktail" of thiamine (100 mg), dextrose (50 g IV), and naloxone (0.4–2.0 mg IV). Due to safety concerns, flumazenil and physostigmine should be avoided in cases of unknown ingestion (Brent et al., 2017).

Gastrointestinal Decontamination Techniques

Activated charcoal (AC) is the most common intervention but is effective only within 60 to 120 minutes post-ingestion. It should not be used for caustics, heavy metals, hydrocarbons, or toxic alcohols. Whole-bowel irrigation (WBI) benefits sustained-release medications, heavy metals, or body packers.

Enhanced Elimination Methods: Hemodialysis and Hemoperfusion

Hemodialysis (HD) is used for xenobiotics with low molecular weight, high water solubility, low volume of distribution (Vd), and low protein binding. It corrects fluid and electrolyte abnormalities and removes substances like methanol, ethylene glycol, salicylates, and theophylline. Hemoperfusion is effective for drugs with high protein binding. Extracorporeal membrane oxygenation (ECMO) provides temporary support for cardiorespiratory failure.

Fig 8: Mindmap showing drugs and toxins removed by hemodialysis

Urinary Alkalization for Poison Elimination

Urinary alkalization enhances the elimination of specific drugs by maintaining a pH of 7.5 or greater. It involves administering intravenous sodium bicarbonate (1–2 mEq/kg every 3–4 hours), with potassium chloride added to prevent hypokalemia.

Fig 9: Mindmap showing drugs and toxins removed by urinary alkalinization.

Managing Metabolic Acidosis in Poisoned Patients

Sodium bicarbonate therapy treats severe metabolic acidosis. For salicylate poisoning, urinary alkalization using sodium bicarbonate is recommended. Hyperinsulinemia euglycemia (HIE) therapy treats severe calcium channel blockers and beta-blocker poisoning.

Seizure Management in Poisoning Cases

Administer parenteral benzodiazepines for toxin-induced seizures. If ineffective, use phenobarbital as a second-line agent. Avoid phenytoin, which can increase toxicity in some cases (Wills & Erickson, 2005).

Common Antidotes for Poisoning

• Acetaminophen: N-acetylcysteine (NAC)

• Benzodiazepines: Flumazenil (with caution)

• Anticholinergics: Physostigmine

• Opioids: Naloxone

• Botulism: Botulinum antitoxin

• Beta-blockers: Glucagon

• Cholinergic toxins: Atropine, pralidoxime

• Calcium channel blockers: Calcium, glucagon

• Carbon monoxide: Oxygen therapy, hyperbaric oxygen

• Anticoagulants: Vitamin K1, protamine

• Toxic alcohols: Fomepizole, ethanol, hemodialysis

• Iron: Deferoxamine

• Isoniazid: Pyridoxine (vitamin B6)

• Methemoglobinemia: Methylene blue

• Cyanide: Hydroxocobalamin, amyl nitrate, sodium thiosulfate, sodium nitrate

• Sulfonylureas: Dextrose, octreotide

• Tricyclic antidepressants: Sodium bicarbonate

• Digoxin: Digoxin-specific antibody fragments (Digibind)

   

Conclusion: Effective Management of Poisoning in the ICU

Effective management of poisoned patients requires immediate supportive care, accurate diagnosis, and targeted treatment. Recognizing toxidromes, understanding diagnostic tests, and utilizing appropriate antidotes and therapies can significantly improve patient outcomes.

Reading more: https://medicaltoxic.com/guidelines/comprehensive-guidelines-for-managing-poisoning-in-adults