snake venom
- suspension of proteins, lipids and enzymes
- Wide variation in constitution even in same species
clinical features
=>Local Effects
=>Systemic effects:
->General
->Three distinct clinical syndromes
Local effects
=>Local pain, swelling, bruising (e.g. brown snake)
* Enlarged, tender draining lymph nodes
Typically early, usually confined to bite site
* Fang marks present
Systemic effects
->General Systemic Effects
* Nausea, vomiting, abdominal pain, diarrhoea.
* Diaphoresis, headache
->Three distinct syndromes-
* VICC
* Myotoxicity
* Neurotoxicity
Venom-Induced Consumption Coagulopathy (VICC)
* Timing of occurence
* Lab abnoemalities
* Pathophysiology
=>Occurs early (often on presentation)
* Platelets: ↓ (<100 ×10⁹/L)
* INR: markedly ↑ (>3, may be unreportable) APTT: prolonged (>100 sec)
* Fibrinogen: ↓ or undetectable
* D-dimer: markedly ↑
* May evolve into thrombotic microangiopathy (TMA) → MAHA + renal failure
=>Pathophysiology: consumption of fibrinogen & factors due to procoagulant venom enzymes
Neurotoxicity Syndrome
- Onset over hours
- Descending flaccid paralysis
- Early: ptosis, diplopia, blurred vision
- Then bulbar dysfunction (dysphagia, dysarthria)
- Late: respiratory & limb paralysis
Due to presynaptic (irreversible) or postsynaptic (reversible) neurotoxin
Myotoxicity Syndrome
- Develops over hours
- CK normal initially, rises within 24–48 h
- Rhabdomyolysis with myoglobinuria → renal failure
- Myonecrosis (esp. black and tiger snakes)
Caused by direct myotoxins (esp. tiger, black snakes)
Investigations
->CK: myotoxicity / rhabdomyolysis
-> Coags: VICC (INR >3, aPTT >100)
-> Fibrinogen: low
->FBC: thrombocytopenia, schistocytes (TMA) **
->EUC: renal function
->LFTs: hepatic injury
->Snake Venom Detection Kit:** identify species to guide antivenom
Enables diagnosis, grading, and monitoring of envenomation
First Aid / Decontamination
- Apply pressure-immobilisation bandage to bitten limb.
- Immobilise with splint → delay lymphatic spread.
- Do not remove until antivenom ready.
- Do NOT cut, suck, or wash wound.
- Ingestion of venom not toxic (destroyed by gastric secretions
2). Enhanced Elimination
- None effective – venom proteins not dialysable.
- Dialysis only for renal failure, not toxin removal.
4). Choice of Antivenom
->Polyvalent antivenom if:
- Snake unidentified / SVDK unavailable / monovalent unavailable / multiple bites / rapid deterioration.
->Monovalent antivenom if:
* Snake identified or SVDK positive.
* Choice guided by toxidrome or local species knowledge.
* Dose: 1 ampoule usually adequate – further doses rarely useful (neutralises only circulating venom).
3). Indications for Antivenom
- Abnormal coagulation (INR ↑, APTT ↑, fibrinogen ↓).
- CK rising (myotoxicity).
- Neurological deficit (ptosis, bulbar weakness, respiratory failure).
- Cardiac arrest or sudden collapse.
5). Adverse Reactions
6). Monitoring Treatment
->Anaphylaxis: risk 3–5 %; keep adrenaline ready, treat per ALS.
->Routine pre-treatment not required.
->Serum sickness (4–14 days): fever, myalgia, arthralgia, rash.
=>Monitoring Treatment
* No rapid marker of efficacy.
* Do not repeat antivenom unless clear deterioration.
* Coagulation recovery may take time (requires hepatic synthesis).
* Clinical improvement (“feels better”) = informal sign of response.
7). Supportive Care
- Airway & ventilation for neurotoxic paralysis.
- Circulatory support if haemodynamic instability.
- Analgesia & sedation.
- Renal replacement therapy for renal failure / rhabdomyolysis.
- FFP / cryoprecipitate only if bleeding or prolonged coagulopathy after antivenom.
- Delay non-essential invasive procedures until coagulopathy resolves.
- I: Antibiotics not indicated.
Summary line
Key steps — pressure immobilisation, early antivenom for systemic toxicity, anticipate anaphylaxis, and provide full supportive care (airway, renal, circulatory).
Brown Snake Envenomation
Q.Toxic effects
Q. Mechanism of injury
Q. Management
=>Toxic Effects
->Venom-Induced Consumption Coagulopathy (VICC)
* Rapid consumption of all clotting factors → INR markedly ↑, fibrinogen 0.
* Resolves spontaneously in ~24 h.
* FFP (≈ 4 U) ± cryoprecipitate (≈ 8 U) shortens correction time
->Bleeding tendency
* 32 % develop haemorrhage from trivial sites (e.g. cannulas)
->Myotoxicity
* Usually absent in common brown snake; present in king brown (Pseudechis australis) causing local myonecrosis
->Neurotoxicity
* ~1 % incidence: ptosis, diplopia, bulbar weakness (Allen et al, 2012).
* New neuro signs → suspect intracranial haemorrhage (due to coagulopathy) until proven otherwise.
Mx of brown snake poisoning cont..
->Cardiovascular collapse
* Hypotension and ↓ cardiac output; occasionally cardiac arrest.
* Caused by prothrombin-activating component of venom; heparin pre-treatment prevented effects in animal models
-> Thrombotic Microangiopathy (TMA)
* Occurs in ~13 % of cases, usually after VICC resolves (Isbister et al, 2007).
* Features: MAHA, thrombocytopenia (< 20 × 10⁹/L), AKI.
-> Mechanism thought to be direct endothelial injury by toxin rather than DIC sequelae.
Mx of brown snake poisoning cont..
Specific Management
* Urgent antivenom (brown snake or polyvalent if species uncertain).
* FFP ± cryoprecipitate to accelerate correction of coagulopathy.
Supportive management- as above
Causes of Renal failure in snake bite
=>Pre renal:
* Hypovolemia due to dehydration in the outback
* Haemorrhage due to VICC
* Third spacing due to SIRS like response
* Cardiac failure
=>Renal
*Rhabdomyolysis- myoglobin deposition
* ATN -ischemic injury due to hypotension
* Haemolysis
**=> postrenal **
* Haematoma- around urethra/ renal tract
