A 58-year-old man from Jharkhand presents with a 6-month history of progressive peripheral neuropathy, hyperpigmentation, and hyperkeratosis on his palms and soles. He works as a traditional pesticide applicator without protective equipment. On examination, he has stocking-glove distribution sensorimotor neuropathy, Mees' lines on fingernails, and raindrop hyperpigmentation on the trunk. Nerve conduction studies show axonal sensorimotor polyneuropathy. Serum arsenic is 15 µg/dL (normal

Question

A 58-year-old man from Jharkhand presents with a 6-month history of progressive peripheral neuropathy, hyperpigmentation, and hyperkeratosis on his palms and soles. He works as a traditional pesticide applicator without protective equipment. On examination, he has stocking-glove distribution sensorimotor neuropathy, Mees' lines on fingernails, and raindrop hyperpigmentation on the trunk. Nerve conduction studies show axonal sensorimotor polyneuropathy. Serum arsenic is 15 µg/dL (normal <5 µg/dL), and 24-hour urine arsenic is 120 µg/L. Which of the following is the most appropriate initial management and the primary reason for its use in chronic arsenic neuropathy?

Accepted Answer

D. DMSA (meso-2,3-dimercaptosuccinic acid) 10 mg/kg TDS orally for 5 days, then 10 mg/kg BD for 14 days, because it chelates arsenic and reduces tissue burden while being safer than BAL for chronic exposure. ## Chronic Arsenic Poisoning: Neuropathy and Chelation Strategy

### Clinical Diagnosis: Chronic Arsenic Exposure

**Key Point:** The constellation of occupational exposure, progressive axonal neuropathy, Mees' lines (horizontal white lines on nails), and raindrop hyperpigmentation are hallmark features of chronic arsenic toxicity.

**High-Yield:** Mees' lines appear 2–3 months after exposure and persist for months; they are not pathognomonic but highly suggestive of arsenic (also seen in thallium, mercury, and chemotherapy).

### Pathophysiology of Chronic Arsenic Neuropathy

1. **Arsenic accumulation** in peripheral nerves, particularly in myelin sheaths
2. **Oxidative stress** — increased reactive oxygen species (ROS) and lipid peroxidation
3. **Axonal degeneration** — distal sensorimotor axonal loss in a stocking-glove pattern
4. **Mitochondrial dysfunction** — impaired energy production in nerve terminals

**Clinical Pearl:** Chronic arsenic neuropathy is typically **axonal** (not demyelinating), affecting sensory fibers more than motor, and is dose- and duration-dependent.

### Chelation Therapy: DMSA vs. BAL

| Parameter | DMSA (Succimer) | BAL (Dimercaprol) |
|-----------|-----------------|-------------------|
| **Route** | Oral | IM/IV (painful) |
| **Mechanism** | Binds As³⁺ and As⁵⁺ | Binds As³⁺ only |
| **Use in acute** | Second-line | First-line |
| **Use in chronic** | **Preferred** | Avoid (mobilizes tissue stores) |
| **Adverse effects** | Mild GI upset, rash | Pain, fever, hypertension, tachycardia |
| **Dosing** | 10 mg/kg TDS × 5 days, then BD × 14 days | 3–5 mg/kg IM q4–6h |

**Key Point:** In **chronic arsenic poisoning**, DMSA is preferred because:
1. **Oral route** — better compliance and tolerability
2. **Safer profile** — fewer systemic adverse effects
3. **Reduces tissue burden** — mobilizes arsenic without the inflammatory response seen with BAL
4. **Prevents progression** — early chelation can halt or slow neuropathy if started before irreversible axonal loss

**Mnemonic: DMSA CHRONIC** — **D**imercaptosuccinic acid, **M**ild side effects, **S**afe oral route, **A**rsenic reduction; **C**hronic exposure, **H**igh tissue burden, **R**educed progression, **O**ral compliance, **N**europathy stabilization, **I**nitial therapy, **C**helation choice

### Treatment Course in Chronic Arsenic Neuropathy

```mermaid
flowchart TD
  A[Chronic arsenic exposure confirmed]:::outcome --> B{Acute or chronic?}:::decision
  B -->|Acute| C[BAL 3-5 mg/kg IM q4-6h]:::action
  B -->|Chronic| D[DMSA 10 mg/kg TDS × 5 days]:::action
  D --> E[Then DMSA 10 mg/kg BD × 14 days]:::action
  E --> F[Monitor serum/urine arsenic]:::action
  F --> G{Levels normalized?}:::decision
  G -->|Yes| H[Supportive care + repeat cycles if needed]:::action
  G -->|No| I[Repeat DMSA course]:::action
  H --> J[Neurological monitoring]:::outcome
  I --> J
```

### Prognosis and Supportive Care

**Clinical Pearl:** Early chelation (within months of exposure cessation) can stabilize or slow progression of neuropathy, but established axonal loss is irreversible. Supportive measures include:
- **B-complex vitamins** — for nerve regeneration
- **Alpha-lipoic acid** — antioxidant, may reduce neuropathic pain
- **Occupational/physical therapy** — for functional recovery
- **Pain management** — gabapentin or pregabalin for neuropathic pain

**Warning:** Penicillamine is contraindicated in chronic arsenic poisoning because it mobilizes arsenic from tissue stores, potentially worsening toxicity and increasing urine arsenic without clinical benefit.

[cite:Forensic Medicine & Toxicology, Reddy 34e, Ch. Poisoning; Parikh's Textbook of Medical Jurisprudence, 7e, Ch. Toxicology]

Answer

A. Supportive care with vitamin B12 and alpha-lipoic acid only, because chronic arsenic neuropathy is irreversible and chelation therapy does not prevent progression

Answer

B. BAL (dimercaprol) 5 mg/kg IM every 4–6 hours for 2 weeks, because it is the gold standard for all arsenic poisoning

Answer

C. Penicillamine 250 mg QID for 3 months, because it mobilizes arsenic from tissue stores and enhances urinary excretion

Explanation

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