SNAKEBITE (VENOMOUS SNAKEBITE)

1. INTRODUCTION AND EPIDEMIOLOGY

• An estimated 1.2 - 5.5 million snakebites worldwide each year
• 421,000 - 1,200,000 envenomations
• 63,415 deaths globally (2019 GBD data), projected to rise to ~68,799 by 2030 despite WHO's goal to halve deaths
• Wide-ranging estimates reflect poor reporting, lack of access to care, and consulting traditional healers

2. CLASSIFICATION OF VENOMOUS SNAKES

3. SNAKE ANATOMY AND IDENTIFICATION

• Venom apparatus: bilateral venom glands behind the eyes + hollow anterior maxillary fangs
• Viperids: long, mobile fangs - retracted at rest, erected to strike; triangular head, elliptical pupils, loreal heat-sensing pits (in pit vipers), rattle (rattlesnakes)
• Elapids: smaller, fixed erect fangs - fewer distinct fang marks; fangs fixed in erect position
• Colubrids: No true venom glands; Duvernoy's glands instead

• 20-25% of pit viper bites
• Up to 75% of sea snake bites

• Triangular head, elliptical pupils = vipers (but NOT exclusively - many harmless snakes mimic this)
• Color pattern identification can be misleading - do not rely solely on color

4. VENOM COMPOSITION AND PATHOPHYSIOLOGY

• Enzymes
• Polypeptides
• Glycoproteins
• Other bioactive constituents

5. CLINICAL MANIFESTATIONS

A. Local (Viper and Cytotoxic Elapid) Envenomation

• Progressive local pain
• Soft tissue swelling and ecchymosis
• Hemorrhagic or serum-filled vesicles and bullae at bite site (hours to days)
• Significant tissue loss in severe bites
• Limb circumference measurement every 15 min used to track progression

B. Systemic Manifestations (Vipers / Cytotoxic)

• Generalized fatigue, nausea, vomiting
• Changes in taste, mouth numbness
• Tachycardia or bradycardia
• Hypotension
• Muscle fasciculations
• Pulmonary edema
• Renal dysfunction
• Spontaneous hemorrhage

C. Neurotoxic Envenomation (Elapids - Kraits, Some Cobras, Australian Elapids, Some Vipers)

1. Nausea, vomiting, headache, paresthesias, altered mental status
2. Cranial nerve abnormalities: ptosis, difficulty swallowing (dysphagia)
3. Peripheral motor weakness
4. Diaphragmatic paralysis → respiratory failure → death (if untreated)

D. Sea Snake Envenomation

• Local pain (variable)
• Generalized myalgias
• Trismus
• Rhabdomyolysis
• Progressive flaccid paralysis
• Manifestations can be delayed for several hours

E. Coagulopathy

• Consumptive coagulopathy / DIC
• Thrombocytopenia
• Hemolysis / decreased hematocrit
• Usually reverses after adequate antivenom

6. LABORATORY INVESTIGATIONS

• Place 1-2 mL venous blood in a clean, dry glass tube; leave undisturbed for 20 min
• Invert: if blood is still liquid and no clot has formed = coagulopathy present
• Simple, bedside, no laboratory equipment required

7. FIELD (PREHOSPITAL) MANAGEMENT

• Rapid transport to a medical facility (most important step)
• Remove jewelry and tight-fitting clothing near bite site
• Clean wound with soap and running water; cover with sterile dressing
• Apply splint to bitten extremity; maintain at approximately heart level
• Take digital photographs of the snake from a safe distance (for identification)

• Do NOT incise or apply suction to the bite - worsens local tissue damage, no benefit
• Do NOT apply tourniquets or lympho-occlusive bandages for viperid bites - intensifies local necrosis, risks ischemia
• Do NOT attempt to capture/transport the snake
• Do NOT consult traditional healers - causes dangerous delays

• Wrap the entire bitten limb with a bandage and immobilize
• Restricts lymphatic drainage, delays systemic absorption of venom
• Pressure: 40-70 mmHg (upper limb), 55-70 mmHg (lower limb)
• Bandage should be snug but loose enough for a finger to slip under
• NOT recommended for viperid envenomation (would worsen local necrosis)

8. HOSPITAL MANAGEMENT

A. Initial Steps

1. Stabilize Airway, Breathing, Circulation (ABC)
2. Establish IV access (two large-bore IV lines)
3. Institute monitoring (vitals, cardiac rhythm, O2 saturation)
4. Remove field bandages carefully (release can cause hypotension/dysrhythmia as acidotic, venom-laden blood enters circulation)
5. Thorough history (time of bite, symptoms) + complete physical exam
6. Neurovascular assessment of envenomated site
7. Palpate axillary/inguinal lymph nodes (lymphatic spread assessment)
8. Mark leading edge of swelling/ecchymosis; measure limb circumference at 3 points every 15 min until stabilized; then every 1-2 h
9. Position bitten extremity above the level of the heart once stabilized
10. Watch for ptosis/cranial nerve signs (warning of impending airway compromise)

B. Supportive Treatment

• Respiratory failure (neurotoxic): Endotracheal intubation + mechanical ventilation (may be required for days to weeks)
• Rhabdomyolysis: IV fluids, monitor urine output
• Acute renal failure: Nephrologist consult; hemodialysis or peritoneal dialysis as needed
  • Acute tubular necrosis: usually reversible
  • Bilateral cortical necrosis: less favorable prognosis, may need long-term dialysis/transplant
• Compartment syndrome: If intracompartmental pressure >30-40 mmHg → fasciotomy (after ruling out pure coagulopathy; manage coagulopathy first)
• Blood products: Rarely needed; give only after adequate antivenom (to avoid fueling consumptive coagulopathy)
• Tetanus immunization: Administer as needed
• Prophylactic antibiotics: Unnecessary unless prehospital care included incision or mouth suction
• Pain management: Paracetamol/acetaminophen and/or opioids; avoid NSAIDs and aspirin (risk of worsening coagulopathy/bleeding)

C. Acetylcholinesterase Inhibitors (for Neurotoxic Elapid Bites)

• Give a trial of neostigmine (with atropine pretreatment) if cranial nerve abnormalities are present
• If positive response, continue therapy

9. ANTI-SNAKE VENOM (ASV) THERAPY

Production

• Produced by injecting animals (horses or sheep) with snake venoms
• Antibodies are harvested from the animals' serum and isolated for antivenom preparation
• May be monospecific (one species) or polyspecific (covers several regional species)
• Antivenoms generally do not cross-protect against species not used in production

Indications for ASV

• Rapidly spreading soft-tissue swelling
• Swelling involving >half the bitten limb
• Extensive blistering/bruising
• Severe pain
• Any systemic signs or lab abnormalities (coagulopathy, renal dysfunction, hemolysis)

• At the first sign of neurotoxicity (e.g., cranial nerve dysfunction, peripheral neuropathy)

Administration

• Administer intravenously only (never IM)
• Start infusion slowly with treating clinician at bedside
• In absence of reaction: increase rate gradually; full starting dose over ~1 hour
• Continue if: clinical condition worsens, fails to stabilize, or venom effects recur

10. SIDE EFFECTS OF ANTI-SNAKE VENOM

A. Early Hypersensitivity (Anaphylaxis)

• Tachycardia
• Rigors
• Vomiting
• Urticaria
• Dyspnea
• Laryngeal edema
• Bronchospasm
• Hypotension

• Rates of acute anaphylaxis exceed 50% for some low-quality antivenoms worldwide
• Newer purified products (e.g., CroFab): incidence ~1.1%

1. Stop infusion immediately
2. Epinephrine (adrenaline) IM (or IV only in severe hypotension)
3. IV antihistamines
4. IV glucocorticoids
5. Once reaction controlled: restart antivenom as soon as possible at slow rate (5-10 mL/h), titrate up as tolerated
6. In refractory hypotension: IV epinephrine infusion while continuing antivenom

B. Late Hypersensitivity (Serum Sickness)

• Myalgias
• Arthralgias
• Fever and chills
• Urticaria
• Lymphadenopathy
• Renal dysfunction
• Neurologic dysfunction

• Systemic glucocorticoids: oral prednisone 1-2 mg/kg/day until symptoms resolve, then taper over 1-2 weeks
• Oral antihistamines
• Analgesics for symptom relief

11. WOUND CARE AND FOLLOW-UP

• Wound care: Careful aseptic debridement of clearly necrotic tissue (only after coagulopathy is fully reversed)
• Intact vesicles/bullae: leave undisturbed; if ruptured, debride with sterile technique
• Damaged muscle: conservative debridement (may recover significantly after antivenom)
• Physical therapy: Start as soon as possible; long-term functional loss (reduced range of motion, sensory impairment) is substantial

12. OBSERVATION AND DISCHARGE CRITERIA

• Wound infection signs
• Serum sickness symptoms (1-2 weeks post-ASV)
• Recurrent coagulopathy (up to 2-3 weeks after bite; venom antigens persist longer than antivenom)
• Pituitary insufficiency (complication of Russell's viper bite - Sheehan-like syndrome)
• Avoid elective surgery and high-trauma activities during the coagulopathy-recurrence window
• Schedule repeat CBC, PT, fibrinogen at follow-up

13. MORBIDITY AND MORTALITY

• Mortality is low (<1%) in regions with rapid access to antivenom
• Morbidity (permanent functional loss: reduced range of motion, sensory deficits, scar contracture) is substantial and underreported
• Worst consequences in the developing world where victims lose ability to work

• Cobras (Naja spp.)
• Carpet/saw-scaled vipers (Echis spp.)
• Russell's vipers (Daboia russelii)
• Large African vipers (Bitis spp.)
• Lancehead pit vipers (Bothrops spp.)
• Tropical rattlesnakes (Crotalus durissus)

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