Diagnostic Assessment and Risk Stratification in Poisoned Patients

Diagnostic Assessment and Risk Stratification in Poisoned Patients

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Objective

Describe the clinical and diagnostic framework for rapid recognition, laboratory evaluation, and risk stratification of poisoned patients in the ICU.

1. Clinical Toxidromes and Bedside Diagnosis

Rapid identification of a toxidrome—a constellation of signs and symptoms characteristic of a specific class of poison—is the cornerstone of initial management. This allows for empiric therapy while definitive laboratory results are pending.

Key Toxidrome Features

The five classic toxidromes are distinguished by their effects on vital signs, mental status, pupils, and secretions. The table below provides a rapid comparison for bedside differentiation.

Bedside Comparison of Major Toxidromes
Feature Anticholinergic Cholinergic Opioid Sympathomimetic Sedative-Hypnotic
Mental Status Agitated, Delirious Confused, Seizures Depressed, Coma Agitated, Paranoid Depressed, Ataxic
Pupils Mydriasis (dilated) Miosis (constricted) Miosis (constricted) Mydriasis (dilated) Normal or Miosis
Heart Rate Tachycardia Bradycardia Bradycardia Tachycardia Bradycardia/Normal
Skin/Secretions Dry, Flushed, Hot Diaphoretic, Wet Normal Diaphoretic Normal
Mnemonic “Mad as a hatter, blind as a bat, red as a beet, hot as a hare, dry as a bone” “SLUDGE” or “DUMBELS” Classic Triad: CNS depression, miosis, respiratory depression “Fight or flight” Generalized depression
Agents TCAs, Antihistamines Organophosphates Fentanyl, Morphine Cocaine, Amphetamines Benzodiazepines
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: The Great Discriminators

When a patient presents with agitation and tachycardia, the differential narrows to anticholinergic vs. sympathomimetic toxidromes. The fastest way to distinguish them at the bedside is by examining the skin. Sympathomimetic patients are diaphoretic (sweaty), while anticholinergic patients are dry.

Editor’s Note Icon A pencil icon, indicating an editor’s note or a gap in evidence. Editor’s Note: Overlapping Features and Diagnostic Pitfalls

Mixed or polypharmacy overdoses often present with conflicting or atypical features, confounding simple toxidrome classification. For example, co-ingestion of an opioid and a sympathomimetic may result in a normal heart rate. Avoid anchoring bias and be prepared to reassess the diagnosis if the patient does not respond to initial therapies as expected. Insufficient source material exists for a definitive algorithm on managing mixed toxidromes; clinical judgment and frequent reassessment are paramount.

2. Laboratory Diagnostics in Poisoning

Laboratory and imaging data are essential to confirm exposures, quantify the severity of poisoning, identify co-ingestions, and guide targeted therapies like antidotes or extracorporeal removal.

Key Metabolic Markers

Essential Metabolic Calculations in Toxicology
Marker Calculation / Threshold Clinical Significance & Common Causes
Anion Gap Na⁺ – (Cl⁻ + HCO₃⁻)
Normal: ≤12 mmol/L
Elevated gap suggests accumulation of unmeasured anions. A gap >27 mmol/L is highly suggestive of methanol or ethylene glycol poisoning. Other causes include salicylates, metformin (lactic acidosis), and uremia.
Osmolal Gap Measured Osm – Calculated Osm
Normal: <10 mOsm/kg
Elevated gap indicates the presence of osmotically active, low-molecular-weight substances. Primarily used to screen for toxic alcohols (methanol, ethylene glycol, isopropanol).
Lactate >2 mmol/L (concerning)
>4 mmol/L (severe)
Marker of tissue hypoperfusion (shock) or direct mitochondrial toxicity. Key causes include cyanide, carbon monoxide, metformin, and severe sympathomimetic or salicylate poisoning.
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Mind Both Gaps

When toxic alcohol ingestion is suspected, always calculate both the anion and osmolal gaps. Initially, the parent alcohol (e.g., methanol) causes a high osmolal gap but no anion gap. As it is metabolized to toxic acids (e.g., formic acid), the osmolal gap decreases while the anion gap rises. A patient can present anywhere along this timeline.

Serum Toxin Levels & Specialized Tests

  • Quantitative Levels: Specific levels are crucial for agents with nomogram-based treatments (acetaminophen) or where levels correlate with severity and guide therapy (salicylates, digoxin, lithium).
  • Co-oximetry: A specialized blood gas analysis that directly measures carboxyhemoglobin and methemoglobin levels, which is essential for diagnosing carbon monoxide poisoning and methemoglobinemia, respectively. Standard pulse oximetry is unreliable in these conditions.
  • Toxicology Screens: Rapid urine immunoassays are often used for initial screening but have significant limitations, including false positives and false negatives. They should not be used to rule out exposure, and confirmatory testing (e.g., GC-MS) is often required.

3. Severity Scoring and Risk Stratification

Standardized scoring systems help to objectively assess the severity of poisoning, facilitate clear communication, guide the appropriate level of care, and track the patient’s clinical trajectory.

Poisoning Severity Score (PSS)

The PSS is a simple, widely used tool to grade the overall severity of a poisoning case.

  • 0 None: No symptoms or signs related to poisoning.
  • 1 Mild: Mild, transient, and spontaneously resolving symptoms.
  • 2 Moderate: Pronounced or prolonged symptoms requiring medical intervention.
  • 3 Severe: Severe or life-threatening symptoms.
  • 4 Fatal: Death resulting from poisoning.

Glasgow Coma Scale (GCS) and ICU Scores

  • Glasgow Coma Scale (GCS): A fundamental tool for assessing level of consciousness. A score of GCS ≤ 8 is a critical threshold often indicating the need for definitive airway protection (intubation).
  • General ICU Scores (APACHE II, SAPS II): While these scores can estimate overall mortality risk in critically ill patients, they are not specifically validated for poisoned patients and may not accurately reflect risks associated with specific toxins.
Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: Use Trends, Not Snapshots

A single severity score is a snapshot in time. The true value of these tools lies in serial assessments. A declining GCS or an increasing PSS is a red flag that signals clinical deterioration and the need to escalate care, even if the initial score was not in a critical range.

4. Clinical Decision Algorithms

Effective management of the poisoned patient requires a systematic approach that integrates bedside findings, laboratory data, and risk scores into a cohesive management plan.

Toxicology Patient Management Algorithm A flowchart showing the management pathway for a poisoned patient, starting with ABC stabilization, moving to bedside toxidrome assessment and lab diagnostics, then to risk stratification using scores, and finally to a decision on the level of care and specific treatments. Step 1: Stabilize Airway, Breathing, Circulation Step 2a: Bedside Assessment History, Vitals, Exam Identify Toxidrome Step 2b: Diagnostic Data Labs (Gaps, Levels) ECG, Imaging Step 3: Risk Stratify Calculate PSS & GCS Step 4: Intervene Supportive Care, Antidotes, Triage
Figure 1: Integrated Management Pathway for the Poisoned Patient. This algorithm emphasizes the parallel processes of clinical assessment and diagnostic evaluation, which converge for risk stratification and guide the final decisions on intervention and level of care.

Linking Scores to Triage and Care Levels

  • Low Risk (e.g., PSS 0-1, GCS 15, asymptomatic): Can often be managed with observation on a medical floor. Requires serial exams to ensure no delayed toxicity.
  • Moderate Risk (e.g., PSS 2, GCS 9-14, mild symptoms): Warrants admission to an intermediate care or step-down unit with continuous cardiac and pulse oximetry monitoring.
  • High Risk (e.g., PSS ≥3, GCS ≤8, critical lab values, hemodynamic instability): Requires immediate ICU admission for invasive monitoring, potential airway protection, and administration of antidotes or consideration for extracorporeal toxin removal.

References

  1. Emergency Care BC. Common toxidromes – diagnosis & treatment. Emergency Care BC Clinical Resource. 2018.
  2. Royal College of Emergency Medicine. Management of Patients with Suspected but Unidentified Poisoning in the Emergency Department. RCEM; 2025.
  3. Hovda KE, Hunderi OH, Rudberg N, et al. Anion and osmolal gaps in the diagnosis of methanol poisoning. Intensive Care Med. 2004;30(9):1842–1846.
  4. Marts LT. Mind the Gap. Ann Am Thorac Soc. 2014;11(5):701–704.