A 28-year-old man is brought to the hospital with a 6-hour history of sudden onset severe abdominal pain, persistent vomiting, and bloody diarrhea. He works in a small jewelry workshop and admits to accidentally ingesting a solution used for metal plating. On examination, he is severely dehydrated with a blood pressure of 70/40 mmHg and a heart rate of 130/min. His mucous membranes show a characteristic garlic odor on his breath. Cardiac auscultation reveals an irregular rhythm. ECG shows prolonged QT interval and multiple ectopic beats. Serum electrolytes show severe hypokalemia (K^+^ 2.1 mEq/L) and hypomagnesemia. What is the most appropriate immediate management?

Explanation

## Clinical Diagnosis: Acute Arsenic Poisoning **Key Point:** The combination of garlic odor on breath, severe GI symptoms with hemorrhagic diarrhea, cardiovascular collapse, and characteristic electrolyte abnormalities (hypokalemia, hypomagnesemia) with ECG changes (prolonged QT, arrhythmias) is diagnostic of acute arsenic poisoning. ## Why This Is Arsenic ### Pathognomonic Features - **Garlic odor** on breath and body fluids — due to volatile arsine gas production during metabolism - **Hemorrhagic diarrhea** ("rice-water" stools with blood) - **Severe cardiovascular collapse** — arsenic causes direct myocardial toxicity and peripheral vasodilation - **Electrolyte derangements:** Hypokalemia and hypomagnesemia from massive GI losses - **ECG abnormalities:** Prolonged QT interval and arrhythmias (risk of sudden cardiac death) **High-Yield:** The garlic odor is nearly pathognomonic for arsenic and is a critical diagnostic clue in toxicology exams. ## Mechanism of Arsenic Toxicity ```mermaid flowchart TD A[Arsenic ingestion]:::outcome --> B[Absorption from GI tract]:::action B --> C[Binds to sulfhydryl groups<br/>in cellular proteins]:::outcome C --> D[Inhibits pyruvate dehydrogenase<br/>and other enzymes]:::outcome D --> E[Cellular respiration failure]:::urgent E --> F[Multi-organ dysfunction:<br/>GI, cardiac, renal]:::urgent C --> G[Accumulates in tissues<br/>especially skin, hair, nails]:::outcome G --> H[Chronic manifestations:<br/>hyperkeratosis, hyperpigmentation]:::outcome ``` ## Management Algorithm ```mermaid flowchart TD A[Acute Arsenic Poisoning]:::outcome --> B[ABCs: Airway, Breathing, Circulation]:::action B --> C[Aggressive IV fluid resuscitation]:::action C --> D[Correct electrolytes:<br/>K+, Mg2+, Ca2+]:::action D --> E[Continuous cardiac monitoring]:::action E --> F{Symptomatic acute poisoning?}:::decision F -->|Yes| G[Chelation therapy:<br/>BAL or DMSA]:::action F -->|No| H[Supportive care only]:::action G --> I[Monitor urine arsenic levels]:::action I --> J[Renal function & electrolytes]:::action J --> K[Long-term follow-up for<br/>chronic toxicity]:::outcome ``` **Clinical Pearl:** Dimercaprol (BAL — British Anti-Lewisite) is the first-line chelating agent for acute arsenic poisoning. It binds arsenic and forms a water-soluble complex excreted in urine. DMSA (succimer) is an alternative oral chelator used after acute phase stabilization. ## Immediate Management Priorities ### 1. Resuscitation (First 1–2 hours) - **IV fluids:** Aggressive normal saline (0.9%) to restore intravascular volume - **Target:** Urine output >200 mL/hour (dilutes arsenic in urine, reduces renal toxicity) - **Electrolyte correction:** - K^+^ replacement (target >3.5 mEq/L) — hypokalemia increases arrhythmia risk - Mg^2+^ replacement (target >2 mg/dL) - Ca^2+^ monitoring (arsenic can cause hypocalcemia) ### 2. Cardiac Stabilization - **Continuous ECG monitoring** — watch for QT prolongation and arrhythmias - **Avoid QT-prolonging drugs** (e.g., antiarrhythmics like quinidine, sotalol) - **Treat arrhythmias:** Magnesium sulfate IV for torsades de pointes ### 3. Chelation Therapy - **Dimercaprol (BAL):** 3–5 mg/kg IM every 4–6 hours for 2 days, then daily for 10 days - Most effective if started within 24 hours of exposure - Binds As^3+^ and As^5+^ in 1:1 molar ratio - Increases urinary excretion 5–10 fold - **DMSA (succimer):** 10 mg/kg PO three times daily for 5 days (alternative, especially for chronic exposure) ### 4. Supportive Care - **Gastric decontamination:** Activated charcoal (if within 1–2 hours of ingestion) - **Avoid gastric lavage** in hemorrhagic diarrhea (risk of perforation) - **Antiemetics:** Ondansetron (avoid QT-prolonging agents) - **Renal monitoring:** Creatinine, BUN; consider dialysis if renal failure develops ## Why Each Option Is Correct or Wrong | Option | Assessment | | --- | --- | | **Aggressive IV fluid + BAL/DMSA** | ✓ CORRECT — Addresses both acute shock and arsenic toxicity | | Gastric lavage + charcoal only | ✗ Inadequate; no chelation therapy | | Sodium thiosulfate | ✗ Used for cyanide, not arsenic | | Hemodialysis alone | ✗ Does not remove arsenic; chelation is essential | **Mnemonic for Heavy Metal Chelators:** - **BAL** (Dimercaprol) → **As, Hg, Pb** (arsenic, mercury, lead) - **DMSA** (Succimer) → **Pb, Hg** (lead, mercury) + As (arsenic) - **EDTA** (Ethylenediaminetetraacetic acid) → **Pb, Ca** (lead, calcium) - **Penicillamine** → **Cu, Hg, Pb** (copper, mercury, lead) **Warning:** Do NOT use sodium thiosulfate for arsenic — it is specific for cyanide poisoning. Confusing these is a common exam trap. **Tip:** In acute arsenic poisoning with severe cardiovascular collapse, the priority is SIMULTANEOUS resuscitation (fluids, electrolytes, cardiac monitoring) AND chelation therapy. Delay in starting BAL/DMSA reduces efficacy. [cite:Parikh Textbook of Forensic Medicine Ch 15; Poisoning & Drug Overdose (Olson) Ch 3]