Snakebite Poisoning:

Introduction

Snakebite poisoning is a life-threatening emergency that requires prompt diagnosis and management. Globally, snakebites cause over 100,000 deaths annually, with India contributing significantly due to its high snake population. The severity of envenomation depends on the species, venom composition, and time to treatment.

1. General Features of Venomous vs. Non-Venomous Snakes

🔷 2. The “Big Four” Venomous Snakes in India

 Identification of Major Venomous Snake Families

Elapidae (Neurotoxic)

• Cobra (Naja spp.)
• Expands hood, spits venom in some species.
• Causes neurotoxicity, ptosis, respiratory failure.
• Krait (Bungarus spp.)
• Small, black with white bands; nocturnal.
• Causes descending paralysis, quiet bites with delayed symptoms.

Viperidae (Hemotoxic & Cytotoxic)

• Russell’s Viper (Daboia russelii)
• Large, brown snake with distinct chain-like pattern.
• Causes spontaneous bleeding, AKI, DIC.
• Saw-scaled Viper (Echis carinatus)
• Small, fast, produces “sizzling” sound.
• Causes severe coagulopathy, bleeding.

Hydrophiidae (Myotoxic)

• Sea Snake (Hydrophis spp.)
• Found in coastal waters; small head, flattened tail.
• Causes muscle necrosis, rhabdomyolysis, renal failure.

Clinical Features of Snakebite Envenomation

1. Local Symptoms

• Elapid Bites: Minimal local swelling, progressing to paralysis.
• Viper Bites: Severe pain, swelling, blistering, necrosis.
• Sea Snake Bites: Painless initially, later causing severe muscle pain.

2. Systemic Manifestations

🔷 Complications

🔷 Diagnosis

🧪 20-Minute Whole Blood Clotting Test (WBCT20)

• Simple bedside test:
• Place 2 ml blood in a dry glass tube.
• Wait 20 minutes without disturbance.
• Tilt the tube: If blood is still liquid → positive (abnormal clotting)

🧪 Labs: PT/INR, aPTT, platelets, creatinine, ABG, CK, electrolytes, urine for myoglobin

🧠 NCV/EMG: For neurotoxic weakness

🔷  Management Approach (ABCDE + ANTIVENOM)

🅰️ Airway, Breathing, Circulation

• Secure airway in neurotoxicity
• Ventilate if needed
• Manage shock (fluids, vasopressors)

🧪 Antivenom Therapy

🔹 Indian Polyvalent Antivenom

• Effective against Russell’s viper, saw-scaled viper, cobra, krait
• Dose:
• Initial 8–10 vials IV over 1 hour
• Repeat based on clinical/lab response
• Severe cases: 20 or more vials may be required

🔹 Indications

• Neurotoxicity (ptosis, bulbar signs)
• Hemostatic abnormality (positive WBCT, bleeding)
• Rapidly progressing local swelling
• AKI or hypotension

🔹 Precautions

• Give IV slowly (over 1 hour)
• Monitor for anaphylaxis (rash, bronchospasm, hypotension)
• Premedication: Hydrocortisone ± antihistamines (controversial)

🅱️ Supportive Management

• Neurotoxic: Mechanical ventilation, neostigmine test (for cobra bites), atropine
• Hemotoxic: FFP, platelets, whole blood
• Renal failure: Dialysis (HD or CRRT)
• Local necrosis: Debridement, fasciotomy only if compartment syndrome
• Tetanus prophylaxis
• Pain management

3. ASV Adverse Reactions & Management

• Anaphylaxis: Treat with IM epinephrine (0.5 mg adults, 0.01 mg/kg in children).
• Serum Sickness: Occurs 5-14 days post-ASV; treat with steroids & antihistamines.

Advanced Critical Care Management

1. Neurotoxic Envenomation (Cobra, Krait)

• Mechanical Ventilation: If respiratory paralysis develops.
• Neostigmine Trial: 0.5 mg IV with atropine for cobra bites (NOT for krait).

2. Hemotoxic Envenomation (Vipers)

• Blood Products: FFP, cryoprecipitate if severe coagulopathy.
• Hemodialysis: If AKI develops due to DIC or rhabdomyolysis.

3. Myotoxic Envenomation (Sea Snakes)

• Aggressive IV Fluids: To prevent renal failure.
• Sodium Bicarbonate Infusion: To prevent acidosis, hyperkalemia.
• Hemodialysis: If AKI or hyperkalemia is refractory.

Surgical & Wound Management

• Debridement for necrosis.
• Fasciotomy ONLY if confirmed compartment syndrome.
• Tetanus prophylaxis, broad-spectrum antibiotics for secondary infections.

Prognosis & Long-Term Follow-Up

• Early ASV + supportive care = survival rates >95%.
• Late presentations may develop chronic kidney disease (CKD), neuropathy.

Why Atropine is Given with Neostigmine Instead of Glycopyrrolate in Snakebite Management?

In the management of neurotoxic snakebite envenomation, neostigmine (a reversible acetylcholinesterase inhibitor) is used as a therapeutic trial in cobra bites (not krait bites) to reverse neuromuscular blockade. Neostigmine, however, can cause bradycardia, excessive salivation, and bronchospasm due to its muscarinic effects.

To counteract these effects, an anticholinergic agent is co-administered. While both atropine and glycopyrrolate are anticholinergics, atropine is preferred over glycopyrrolate in snakebite cases for the following reasons:

1. Atropine Crosses the Blood-Brain Barrier (BBB)

• Cobra venom-induced paralysis affects both central and peripheral nervous systems.
• Atropine crosses the BBB and can mitigate central cholinergic effects (like excessive secretions and bradycardia).
• Glycopyrrolate does not cross the BBB and primarily acts on peripheral muscarinic receptors.

2. Faster Onset of Action

• Atropine acts within 1-2 minutes when given IV, which is crucial in a critical setting where rapid bradycardia reversal is needed.
• Glycopyrrolate has a slower onset (~5 minutes), which may delay the desired response.

3. More Effective Bronchodilation in Secretions-Induced Airway Obstruction

• Neurotoxic envenomation can cause excessive salivation, bronchospasm, and pulmonary secretions.
• Atropine provides superior bronchodilation and dries secretions more effectively than glycopyrrolate.

4. No Inhibition of Neostigmine’s Nicotinic Effects

• Glycopyrrolate mainly blocks peripheral muscarinic effects but has no impact on nicotinic sites at the neuromuscular junction.
• Atropine, by affecting both muscarinic and central effects, complements neostigmine’s action better.

Dosage Protocol for Snakebite Envenomation (Cobra Bites Only)

• Atropine 0.6 mg IV given 5 minutes before neostigmine to prevent bradycardia.
• Neostigmine 0.5 mg IV every 30 minutes as a trial in mild-to-moderate paralysis cases.
• If no response in 2-3 doses, mechanical ventilation is required.

Why Not Use Neostigmine in Krait Bites?

• Krait venom causes pre-synaptic blockade, where neostigmine has no effect.
• Cobra venom causes post-synaptic blockade, which can be reversed by neostigmine.