Cobra Envenomation (Neurotoxic)
Description: Bite by the Indian Cobra (Naja naja), releasing neurotoxins that block nerve-muscle signals.
Symptoms: Local swelling and pain, drooping eyelids (ptosis), difficulty swallowing, respiratory paralysis.
Causes: Cobra bite injecting neurotoxic venom.
Risk Factors: Agricultural work, walking barefoot in rural areas at night.
Diagnosis: Clinical signs of neurotoxicity, prolonged clotting tests.
Treatment: Immediate Anti-Snake Venom (ASV) infusion, mechanical ventilation if respiratory failure occurs.
Krait Envenomation (Neurotoxic)
Description: Bite by the Common Krait (Bungarus caeruleus), causing near-painless bites but severe neurological blockage.
Symptoms: Often minimal local pain, severe abdominal pain, muscle cramps, progressive muscle paralysis.
Causes: Krait bite injecting presynaptic neurotoxins.
Risk Factors: Sleeping on the floor in rural settings, warm monsoon months.
Diagnosis: Clinical presentation, rising pulse rate, ptosis.
Treatment: Polyvalent ASV infusion, close airway monitoring, mechanical ventilation.
Russell's Viper Bite (Hemotoxic & Nephrotoxic)
Description: Bite by Russell's Viper (Daboia russelii), causing coagulation failure and acute kidney injury.
Symptoms: Severe local swelling, blistering, bleeding from gums/bite site, dark urine, decreased urine output.
Causes: Viper bite injecting hemotoxic and nephrotoxic venom.
Risk Factors: Harvesting crops, walking in tall grass without boots.
Diagnosis: 20-minute whole blood clotting test (20WBCT), renal function tests (elevated creatinine).
Treatment: Immediate polyvalent ASV, IV fluids, dialysis support for renal failure, wound care.
Saw-Scaled Viper Bite (Vasotoxic)
Description: Bite by the Saw-scaled Viper (Echis carinatus), causing local tissue destruction and systemic bleeding.
Symptoms: Intense local pain, severe swelling, bruising, bleeding from mucous membranes, prolonged clotting.
Causes: Viper bite injecting metalloproteinases and coagulopathic toxins.
Risk Factors: Dry, rocky agricultural landscapes, handling firewood.
Diagnosis: 20WBCT, platelet count, coagulation profile.
Treatment: Anti-snake venom (ASV) therapy, local wound management, monitoring blood counts.
Neurotoxic Respiratory Paralysis
Description: Complete failure of respiratory muscles due to neurotoxic snake venom, representing an emergency.
Symptoms: Inability to clear secretions, shallow rapid breathing, cyanosis, loss of consciousness.
Causes: Advanced neurotoxic envenomation blocking diaphragm and intercostal muscles.
Risk Factors: Delayed presentation to the hospital after a cobra or krait bite.
Diagnosis: Clinical assessment of breathing effort, arterial blood gas showing hypercapnia.
Treatment: Urgent endotracheal intubation, mechanical ventilation, continued ASV infusion.
Venom-Induced Consumption Coagulopathy (VICC)
Description: A condition where venom toxins consume clotting factors, leading to severe bleeding risks.
Symptoms: Continuous bleeding from gums, nose, venipuncture sites, blood in vomit or urine.
Causes: Hemotoxic viper venom acting as clotting factor activators.
Risk Factors: Delayed ASV administration after a viper bite.
Diagnosis: Prolonged PT/aPTT, low fibrinogen levels, positive 20WBCT.
Treatment: Neutralization of venom using ASV, transfusion of fresh frozen plasma (FFP) or cryoprecipitate.
Acute Kidney Injury (AKI) in Viper Bites
Description: Sudden decline in kidney function due to direct nephrotoxicity and hemolytic products from viper venom.
Symptoms: Drastic decrease in urine output, swelling of legs/face, nausea, vomiting.
Causes: Direct action of Russell's viper venom on renal tubules, hypotension.
Risk Factors: Severe systemic envenomation, pre-existing kidney disease, dehydration.
Diagnosis: Daily creatinine and blood urea nitrogen (BUN) monitoring, urine output tracking.
Treatment: Intravenous hydration, renal dose-adjusted medications, hemodialysis.
Local Tissue Necrosis (Snake Bite)
Description: Severe tissue death around the bite area, common in viper and cobra bites.
Symptoms: Blackening of skin, foul-smelling discharge, severe local pain, skin sloughing.
Causes: Cytolytic enzymes in venom destroying cell membranes and local blood vessels.
Risk Factors: Tight tourniquets applied to the limb, high local venom load.
Diagnosis: Visual inspection, wound swab cultures, ultrasound of soft tissues.
Treatment: Surgical debridement, antibiotics for secondary infection, reconstructive skin grafting.
ASV Anaphylaxis (Hypersensitivity)
Description: Severe allergic reaction to anti-snake venom serum, requiring immediate treatment.
Symptoms: Hives, itching, flushing, difficulty breathing, drop in blood pressure during ASV infusion.
Causes: Immune response to foreign horse proteins present in ASV.
Risk Factors: Prior exposure to equine serum products.
Diagnosis: Clinical signs developing during or shortly after ASV infusion.
Treatment: Temporarily stopping ASV, administering subcutaneous epinephrine, IV hydrocortisone, and pheniramine.
Dry Bite Syndrome
Description: A snake bite where no venom is injected, requiring clinical monitoring but no ASV.
Symptoms: Visible fang marks, mild local pain, no progressive swelling, no systemic symptoms.
Causes: Defense bite by the snake without venom gland discharge.
Risk Factors: Accidental encounters where the snake does not feel deeply threatened.
Diagnosis: 24-hour monitoring showing normal coagulation (20WBCT) and no neurological deficits.
Treatment: Wound cleaning, tetanus prophylaxis, observation for 24 hours, reassurance.
Compartment Syndrome (Bite Limb)
Description: Increased pressure within a muscle compartment, threatening limb viability.
Symptoms: Severe pain out of proportion to injury, pain on passive stretching, numbness, pale cold skin.
Causes: Massive local edema caused by cytolytic viper venom within tight muscle fascial boundaries.
Risk Factors: Use of tight ligatures/tourniquets on the bitten limb, deep muscle injections.
Diagnosis: Measuring compartment pressure, clinical evaluation of peripheral pulses.
Treatment: Elevating limb (moderate), ASV to reduce swelling, surgical fasciotomy if pressures are elevated.
Secondary Bacterial Infection (Bite Wound)
Description: Bacterial infection at the bite wound, requiring targeted antibiotic therapy.
Symptoms: Increasing redness, warmth, pus discharge, throbbing pain, fever starting 48 hours post-bite.
Causes: Bacteria from the snake's mouth (Proteus, Pseudomonas) invading the damaged tissue.
Risk Factors: Traditional incising of the wound, applying cow dung or herbal pastes to the bite.
Diagnosis: Wound swab culture and sensitivity.
Treatment: Surgical drainage, culture-specific antibiotics, sterile dressings.
Hemorrhagic Stroke (Viper Bite)
Description: Intracranial bleeding caused by severe coagulopathy after a viper bite, requiring intensive care.
Symptoms: Sudden severe headache, vomiting, seizures, altered consciousness, pupillary changes.
Causes: Severe consumption coagulopathy combined with venom-induced blood vessel damage.
Risk Factors: Untreated severe hemotoxic envenomation, severe hypertension.
Diagnosis: Emergent non-contrast head CT scan.
Treatment: Aggressive ASV therapy, fresh frozen plasma transfusions, supportive neurocritical care.
Myotoxicity in Viper Bites
Description: Muscle tissue breakdown caused by specific myotoxins present in certain viper venoms.
Symptoms: Generalized muscle pain, muscle weakness, dark reddish-brown urine (myoglobinuria).
Causes: Direct damage to skeletal muscle membranes by phospholipase A2 enzymes.
Risk Factors: Bites from specific viper subspecies, delayed hospital admission.
Diagnosis: Serum creatine kinase (CK) levels, urine test for myoglobin.
Treatment: IV hydration with urinary alkalinization to protect kidneys, monitoring electrolytes.
Late-Onset Serum Sickness
Description: An immune-mediated reaction occurring days after anti-snake venom therapy.
Symptoms: Fever, joint pain (arthralgia), skin rash, swollen lymph nodes, swelling in face.
Causes: Type III hypersensitivity reaction to circulating horse-serum proteins.
Risk Factors: Large doses of ASV (more than 10-20 vials).
Diagnosis: Clinical history of ASV administration 7-14 days prior, elevated inflammatory markers.
Treatment: Oral corticosteroids (prednisolone), antihistamines, supportive care.
