Snake Bite

Snake Bite (Snake Envenomation) 

India accounts for one of the highest snakebite burdens globally.

Important venomous snakes:

“Big Four” of India

Other important species:

• King cobra
• Hump-nosed pit viper
• Bamboo pit viper
• Sea snakes

Clinical Features

Dry Bite

• A venomous snake does not always inject venom.
• This is called a:Dry Bite
• Reported frequency:10–80% depending upon species.

Why Does Dry Bite Occur?

Possible reasons:

• Defensive bite
• Empty venom glands
• Incomplete strike
• Mechanical failure of venom delivery

Clinical Importance of Dry Bite

Patients may develop:

• Tachycardia
• Sweating—Tremors
• Hyperventilation—Tingling sensations

from anxiety alone. These symptoms may mimic early envenomation.Therefore:Never diagnose venomous envenomation based solely upon anxiety symptoms.

Local Manifestations

• Fang marks—May be:Single—Double—Absent
• Pain—Severe in viper bites.,Minimal in krait bites.
• Blistering—Especially viper bites.
• Tissue Necrosis—Cobra,Pit viper

Classic Krait Presentation/Occult Snakebite

Minimal local signs.Krait bite often presents as:

• No fang marks—No swelling
• Abdominal pain—Vomiting
• Progressive paralysis

leading to frequent misdiagnosis

Patient sleeps after bite and awakens with:

• Ptosis
• Ophthalmoplegia
• Respiratory failure

Although overlap is common, snake venom syndromes are classically divided into four major groups.

Neurotoxic Envenomation

Common Snakes:Cobra—Krait—Sea snake

• Presynaptic toxins
• Examples—Krait,Sea snake
• Mechanism—Destroy acetylcholine vesicles.

Characteristics

• Antivenom may stop progression
• Recovery slow (days-weeks)

Postsynaptic toxins

• Examples—Cobra
• Mechanism—Competitive blockade of nicotinic receptors.
• Characteristics Better response to ASV
• Better response to neostigmine

Result:Progressive descending paralysis.

Earliest Signs

• Forehead muscle weakness
• Ptosis-Ptosis is often the first objective sign of neurotoxicity. 

Classical “5 Ds and 2 Ps”

• 5 Ds—Dyspnea—Dysphonia—Dysarthria—Diplopia—Dysphagia
• 2 Ps—Ptosis—Paralysis

Progression

Typical order:Forehead weakness—Ptosis—Diplopia—Dysarthria—Dysphonia—Dyspnea—Dysphagia—Respiratory paralysis 

Vasculotoxic / Hemotoxic Envenomation

Russell’s viper—Saw-scaled viper

Local Features

• Swelling—Blistering—Necrosis—Ecchymosis
• Pain 

Systemic Features

• Gum bleeding—Epistaxis—Hematuria—GI bleeding
• Intracranial hemorrhage—Shock 

Hallmark Laboratory Finding

Venom-Induced Consumption Coagulopathy (VICC)

Characterized by:

• Low fibrinogen—Elevated FDP—Elevated D-dimer
• Prolonged PT—Prolonged aPTT
• Incoagulable blood

Detected bedside using:20-Minute Whole Blood Clotting Test (20WBCT)

Myotoxic Envenomation

Sea snakes—Some kraits

Clinical Features

• Severe muscle pain—Muscle swelling
• Fasciculations
• Dark urine—Hyperkalemia—AKI 

Mechanism

Massive rhabdomyolysis leading to:

• Myoglobin release—Tubular injury—Acute kidney injury

Painful Progressive Swelling Syndrome (PPS)

• Progressive painful swelling indicates significant local venom toxicity. 
• Typical snakes:Russell’s viper—Saw-scaled viper—Cobra
• Features:

• Rapid swelling
• Ecchymosis
• Necrosis
• Blistering
• Lymphadenopathy
• Possible compartment syndrome 

Important Guideline Pearl

• Purely localized swelling alone is NOT necessarily an indication for ASV.
• Rapidly progressive swelling is the key concern. 
• (Controversy: Some international toxicology protocols recommend ASV for extensive swelling crossing major joints even before systemic toxicity develops.)

CAPILLARY LEAK SYNDROME (CLS)

Massive endothelial dysfunction causing:

• Plasma leakage
• Hypotension
• Edema
• Hemoconcentration without overt hemorrhage.

Most Common Snake—Russell’s Viper

Pathophysiology—Venom damages: Vascular Endothelium

Result: Plasma escapes into interstitial tissues.

Clinical Features

• Parotid Swelling—Highly characteristic.
• Conjunctival Chemosis
• Periorbital Edema
• Hypotension
• Pleural Effusion
• ARDS
• Refractory Shock

Laboratory Markers

• Elevated Hematocrit
• Leukocytosis
• Hypoalbuminemia
• Pleural Effusions

DIFFERENTIAL DIAGNOSIS

WHO Severity Classification

Diagnosis

Snakebite is primarily a clinical diagnosis.

History

Ask:Species?

• Time of bite?—Site?
• First aid given?—Progression?

Investigations

Note: Avoid arterial puncture for ABG in patients with severe coagulopathy because of the risk of uncontrolled bleeding or hematoma formation.

20-Minute Whole Blood Clotting Test (20WBCT)

Most useful bedside test in resource-limited settings.

Method

• 2 mL fresh venous blood
• Clean dry glass tube
• Leave undisturbed 20 min

Interpretation

• Clotted = normal
• Liquid blood = coagulopathy
• Highly useful for viper bites.

False Positive

• Plastic tube used
• Wet tube used
• Dirty tube used

Repeat Testing

Repeat:if initial test is normal. 

• Hourly × 3 hours
• Then every 6 hours × 24 hours

Blood Grouping and Cross-Matching-the first blood sample should be typed and cross-matched because both venom and ASV may later interfere with compatibility testing.

Pre hospital Management

DO Reassure,Most bites are nonfatal.

Anxiety itself may cause:

• Tachycardia
• Hyperventilation
• Sweating—Tremors
• Paraesthesia

Immobilize Limb

The bitten limb should be treated exactly like a fractured limb.Splint entire limb

• Immobilize all joints
• Minimize muscle movement
• Prevent lymphatic spread of venom 

Why Immobilization Works?

• Venom spreads mainly through Lymphatics and not initially through veins.
• Muscle contraction pumps lymphatic flow.
• Movement accelerates venom dissemination.

Remove Constricting Objects before swelling develops. 

• Rings—Watches
• Bracelets—Tight clothing
• Shoes

Recovery Position to reduce aspiration risk

Unconscious patients should be transported in:

• Left lateral
• Airway protected

DO NOT

❌ Cut wound

❌ Suck venom

❌ Apply ice

❌ Electric shocks

❌ Herbal remedies

❌ Tight arterial tourniquets

Pressure Immobilization Technique—controversial areas

Recommended mainly for:Neurotoxic snakes,Australian elapids

Less useful for viper bites.

If transport delay is:30 minutes and <3 hours

a crepe bandage may be applied ONLY by trained personnel.

Controversy

(Pressure immobilization is standard in Australian elapid envenomation. Many Indian toxicologists avoid routine use because most Indian bites are associated with significant local tissue toxicity.)

Hospital management

• Never start by looking at the bite wound.
• Airway—Neuroparalysis?
• Breathing—Respiratory failure?
• Circulation—Shock?
• Local signs
• Extent of swelling?
• Mark edge every 30 min.

Bedside Respiratory Assessment

Child Assessment

A child whose cry becomes:Weak—Husky—Soft may be developing respiratory failure. 

DISABILITY ASSESSMENT

• Assess:Consciousness—Cranial nerves—Pupils—Motor power
• The Glasgow Coma Scale is unreliable in severe neurotoxic snakebite because:
• Patient may be:Fully conscious,Completely paralyzed
• This resembles coma but is actually preserved consciousness. 

LOCKED-IN SYNDROME

Defined as:

• Conscious patient
• Quadriplegic
• Unable to speak
• but aware of surroundings. 

Why Is It Important?

Patients may be incorrectly diagnosed as:

• Brain dead
• Comatose
• when they are actually alive and recoverable. 

Bilateral Dilated Pupils ≠ Brain Death

Can occur in severe neurotoxic snakebite. 

EXPOSURE ASSESSMENT

Examine entire body for:

• Bite marks—Swelling
• Bleeding—Ecchymosis
• Necrosis—Blisters
• Lymphadenopathy

Antisnake Venom (ASV)

Cornerstone of therapy.

ASV DOES NOT:

• Reverse established necrosis
• Reverse established tissue destruction
• Immediately reverse established paralysis

Indian Polyvalent ASV Covers

• Cobra
• Krait
• Russell’s viper
• Saw-scaled viper

Specific antivenom for:

• Sea snakes
• Pit vipers is not routinely available in India.,Cross-neutralization may provide some benefit. 

Indications for ASV

• Neurotoxicity features
• Hemotoxicity features
• Cardiovascular Toxicity—Hypotension,Shock
• AKI Due to Envenomation
• Progressive Local swelling
• Rapid swelling crossing joints.

Delayed presentation does not automatically exclude ASV therapy.

NOT Indications

❌ Fang marks only

❌ Mild pain only

❌ Fear of poisoning

Stable Local Swelling Without Progression

Purely localized swelling with or without bite marks is not an indication for ASV. 

Controversy

Some international toxicology groups advocate ASV if:

• Swelling crosses major joints
• Swelling involves >50% of limb

even without systemic toxicity.

Current Indian practice generally follows the more conservative approach.

ASV Dose—Adults = Children Same dose.

• Because ASV dose depends on: Amount of Venom not body weight.
• A child receives the same venom load as an adult.
• Pregnancy is NOT a contraindication.

Initial Dose

• Neurotoxic—8–10 vials IV
• Hemotoxic—8–10 vials IV
• Many Indian centers use:10 vials initially.

Administration

• Dilute in:200–500 mL NS and Infuse over: 1 hour
• Continuous monitoring required for:Pulse,BP,Respiratory status,Anaphylaxis

Reassessment Typically: 6 Hours after initial dose.

Neurotoxic Bite

Repeat ASV if:

• Paralysis progresses
• Ptosis worsens
• Respiratory weakness progresses

after initial dose.

Hemotoxic Bite

Repeat ASV if:

• 20WBCT remains abnormal
• Ongoing bleeding persists
• Coagulopathy continues

Repeat Dose

• Persistent Neurotoxicity—Repeat 10 vials.
• Persistent Coagulopathy—Repeat 10 vials.
• Maximum Dose—No universally fixed maximum.
• Traditional practice:—20–30 vials.

ASV Reactions

Early Anaphylaxis

Occurs in 10–50%.Non-IgE Mediated Therefore: Patients may react during first exposure.

Symptoms:

• Urticaria
• Wheeze
• Hypotension
• Bronchospasm

Treatment

• If any reaction occurs:STOP ASV TEMPORARILY
• Treat reaction immediately.
• After stabilization:Restart ASV
• because venom neutralization remains essential.

Adrenaline First

• 0.5 mg IM (0.5 mL of 1:1000)
• Repeat every 5–10 min if needed.

Pediatric Dose

• 0.01 mg/kg IM
• Maximum: 0.5 mg

Additional

• Oxygen
• IV fluids
• H1 antihistamines
• Steroids

Premedication

Routine premedication not universally recommended.(WHO)

Some Indian centers use:

• Low-dose adrenaline prophylaxis 0.25 mg SC or IM

PYROGENIC REACTION

Occurs:1–2 hours after infusion.

Features

• Fever
• Chills
• Rigors

Cause-Usually contamination during manufacturing or storage.

Treatment

• Stop infusion temporarily
• Antipyretics
• Fluids
• Restart after stabilization

SERUM SICKNESS

Occurs:5–14 days later.

Mechanism—Immune complex disease.

Clinical Features

• Fever
• Arthralgia
• Rash
• Lymphadenopathy

Treatment

• Antihistamines
• Prednisolone

Neostigmine Test

• Useful mainly for: Postsynaptic neurotoxicity (Cobra)
• Protocol:Atropine 0.6 mg IV then Neostigmine 1.5–2.5 mg IV
• Evaluate:Ptosis within 1 hour.
• Positive response: ≥50% improvement of ptosis

Maintenance Regimen

• Repeat: Neostigmine 0.5 mg plus atropine every 30 minutes
• for five doses.
• Then taper at:1 hour2 hours—6 hours—12 hours

When To Stop?

No improvement after: Three doses ,Stop AN therapy.

Pediatric Dose

Atropine:0.05 mg/kg then Neostigmine: 0.04 mg/kg

Signs of Impending Respiratory Failure

• Single breath count <15
• FVC <15 mL/kg
• Neck weakness
• Poor cough
• Breath Holding Time <20 seconds concerning
• Head Lift Test Unable to lift head for:5 seconds
• Paradoxical Respiration

Intubation

• Early rather than late.
• Duration of Ventilation—Depends on toxin type.
• Cobra Bite: 24–72 hours
• Krait Bite May require: Several days Occasionally: 1 week because presynaptic recovery is slow.

Hemotoxicity Management

ASV is primary treatment.

Do NOT give FFP before ASV.

Reason: Venom consumes clotting factors.

After ASV If bleeding persists:FFP,Cryoprecipitate,Platelets may be indicated.

Massive Bleeding-Treat like major hemorrhage:PRBC+FFP+Platelets

AKI Management

Common after Russell’s viper bite.

Mechanisms:

• ATN
• DIC
• Shock
• Pigment nephropathy

Treatment

• Fluid optimization
• Avoid nephrotoxins
• Dialysis when indicated

DIALYSIS IN SNAKEBITE—Indications are Same as standard nephrology indications.

RUSSELL’S VIPER SYNDROME

• Coagulopathy
• AKI
• Shock
• Capillary Leak Syndrome
• Endocrine Sequelae

LONG-TERM SEQUELAE OF RUSSELL’S VIPER BITE

• Pituitary Insufficiency
• Amenorrhea
• Sheehan-like Syndrome
• 
  

SEA SNAKE ENVENOMATION

Sea snake bites are uncommon but extremely dangerous.

The UP guideline specifically includes sea snakes among medically important venomous snakes. 

CHARACTERISTIC CLINICAL TRIAD

• Generalized Myalgia
• Muscle Tenderness
• Dark Urine (Myoglobinuria)

PROGRESSION OF MYOTOXICITY

Stage 1—Muscle pain

Stage 2—Generalized weakness

Stage 3—Rhabdomyolysis CK >5000 IU/L

Stage 4—AKI

Stage 5—Hyperkalemic cardiac arrest

DIFFERENTIATING MYOGLOBINURIA FROM HEMATURIA

Management

Aggressive hydration

Monitor:Potassium,CK,Creatinine

Compartment Syndrome

• True compartment syndrome is uncommon.
• Swelling alone ≠ compartment syndrome.
• Diagnosis—Clinical plus pressure measurement.,Pressure >30–40 mmHg.

Treatment—ASV first.

Fasciotomy only when:

• Proven compartment syndrome
• Coagulopathy corrected

ANTIBIOTICS IN SNAKEBITE

Routine prophylactic antibiotics are not recommended.

WHEN TO GIVE ANTIBIOTICS

Evidence of:

• Cellulitis
• Abscess
• Necrosis
• Secondary Infection
• Surgical Intervention

COMMON PATHOGENS

Snake oral flora may contain:

• Aeromonas
• Morganella
• Proteus
• Klebsiella
• Enterococcus

EMPIRICAL OPTIONS

Depending on local microbiology: Amoxicillin-clavulanate or Piperacillin-tazobactam for severe infections.

TETANUS PROPHYLAXIS

• Fully Immunized—Booster if indicated.
• Unknown Status—Tetanus toxoid ± TIG according to immunization guidelines.

PAIN MANAGEMENT

• Preferred-Paracetamol
• Opioids-If severe pain.
• Avoid NSAIDs Especially in:Coagulopathy,AKI,Bleeding risk

DISCHARGE CRITERIA

Patient may be discharged when:

• Hemodynamically Stable
• No Progressive Neurotoxicity
• No Active Bleeding
• Improving Renal Function
• Stable Coagulation Profile
• Ambulating Safely

FOLLOW-UP

1–2 Weeks Assess:

• Wound healing
• Residual swelling
• Neurological recovery

1–3 Months Assess:

• Renal function
• Functional disability
• Endocrine complications

References 

1. Government of Uttar Pradesh, Department of Medical Health and Family Welfare. Standard Treatment Guidelines: Management of Snake Bite. Lucknow: Government of Uttar Pradesh; April 2024.
2. World Health Organization. WHO Guidelines for the Management of Snakebites. 2nd ed. New Delhi: WHO Regional Office for South-East Asia; 2016.
3. Directorate General of Health Services, Ministry of Health and Family Welfare, Government of India. National Protocol for Prevention and Management of Snakebite Envenoming. New Delhi: MoHFW; 2023.
4. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 22nd ed. New York: McGraw-Hill Education; 2024. Chapter: Snakebite and Envenomation.
5. Rippe JM, Irwin RS, Alhazzani W, editors. Irwin and Rippe’s Intensive Care Medicine. 9th ed. Philadelphia: Wolters Kluwer; 2024. Chapters on Toxicology, Shock, Mechanical Ventilation, Acute Kidney Injury, and Critical Care Emergencies.
6. Vincent JL, Abraham E, Kochanek PM, Moore FA, Fink MP, editors. Textbook of Critical Care. 8th ed. Philadelphia: Elsevier; 2025. Chapters on Envenomation, Shock, Coagulopathy, Respiratory Failure, and Critical Care Toxicology.
7. Alhazzani W, Møller MH, Arabi YM, Loeb M, Gong MN, Fan E, et al. Oh’s Intensive Care Manual. 9th ed. Philadelphia: Elsevier; 2023. Chapters on Poisoning, Mechanical Ventilation, Renal Replacement Therapy, and Critical Care Management.