Snake Bite Poisoning (Envenomation)

Epidemiology

• Sabiston Textbook of Surgery, p. 751-753

Classification of Venomous Snakes

• Sabiston Textbook of Surgery, p. 753-754

Venom Delivery Mechanism

Venom Composition

1. Phospholipase A2 - destroys phospholipids in nervous tissue, alters neuromuscular conduction, causes hemolysis
2. Hyaluronidase - spreads venom rapidly from bite site (present in ALL snake venoms)
3. Proteolytic enzymes / metalloproteinases - tissue destruction, hemorrhage, vascular damage
4. L-amino acid oxidase - splits fibrinogen, contributes to DIC
5. Cholinesterase (mainly Elapid) - hydrolyzes acetylcholine, impairs neuromuscular transmission
6. Hemolysin (mainly Viper) - widespread hemolysis in presence of lecithinase
7. Fibrinolysin / Fibrin ferments - coagulation disorders
8. Cytolysin - lysis of blood and tissue cells
9. Collagenase, Elastase - structural tissue breakdown

• P C Dikshit Textbook of Forensic Medicine and Toxicology, p. 493-495; Sabiston Textbook of Surgery, p. 834-836

Venom Types: Colubrine vs. Viperine

Colubrine Venom (Elapids - cobras, kraits, mambas, sea snakes)

• Predominantly neurotoxic - respiratory and cardiac center paralysis
• Cobra venom causes progressive muscular paralysis: mouth and throat muscles first, then respiratory muscles (curare-like action)
• Krait venom produces muscular paralysis only (no convulsions)
• Components: neurotoxin, cholinesterase, cardiotoxin, phospholipase A
• Local pain and swelling are not usually severe

Viperine Venom (vipers - Russell's viper, Echis, rattlesnakes)

• Predominantly hemolytic/hemotoxic
• Cytolysis of vascular endothelium, hemolysis, severe coagulation disorders
• Severe local: swelling, oozing of blood, spreading cellulitis, necrosis
• Blood fails to clot even with thrombin (depleted fibrinogen)
• Causes DIC, renal tubular necrosis
• P C Dikshit Textbook of Forensic Medicine and Toxicology, p. 494-495

Amounts Injected & Fatal Doses

• P C Dikshit Textbook of Forensic Medicine and Toxicology, p. 495

Clinical Features

Pit Vipers / Crotalids

• Immediate burning pain at bite site
• Swelling within minutes, may progress for days
• Ecchymosis, petechiae, blebs, bullae at bite site (see photo below)
• Systemic: weakness, nausea, vomiting, sweating, perioral paresthesias, metallic taste, muscle fasciculations, hypotension
• Hematotoxicity: thrombocytopenia, hypofibrinogenemia, prolonged PT/PTT - risk of DIC
• Compartment syndrome: rare despite edema (most bites are subcutaneous)
• Some species (Mojave rattlesnake type A, Timber rattlesnake) cause neurotoxicity: cranial nerve dysfunction, paralysis, respiratory failure

Fig. A&B: Northern copperhead bite on right hand showing swelling. C: Hemorrhagic bullae formation on upper extremity - Rosen's Emergency Medicine

Coral Snakes (Elapids)

• Often minimal local pain and swelling
• Neurotoxic effects delayed several hours but progress rapidly
• Ptosis, vertigo, paresthesias, fasciculations, slurred speech, dysphagia, drowsiness, proximal muscle weakness
• Death from respiratory failure

Elapids generally (cobras, mambas)

• Predominantly systemic neurotoxic effects
• Some (e.g., Indian cobra) may also cause extensive local tissue destruction
• Rosen's Emergency Medicine, p. 811-812; Sabiston Textbook of Surgery, p. 834-836

Severity Grading

• Sabiston Textbook of Surgery, p. 919

Diagnosis

• Relies primarily on clinical history and physical examination
• Lab workup after pit viper bite: CBC, PT, PTT, fibrinogen levels
• Monitor for hematotoxicity (may persist 2 weeks post-treatment)
• In Australia/Papua New Guinea: swab the wound for venom identification kit - do NOT wash first

Management

Immediate First Aid

• Remove jewelry and tight clothing from the affected limb
• Immobilize and splint in functional position
• Limit exertion (especially walking for lower extremity bites)
• Get promptly to a medical facility with snakebite experience
• For elapid bites (Australia): apply pressure bandage at 55 mmHg between wound and heart to reduce systemic toxicity

• Do NOT incise the wound - historical incision-and-suction has been contraindicated since 1980; risks vessel, tendon, nerve damage and removes only a tiny amount of venom
• Do NOT apply ice or heat
• Do NOT apply tourniquets (especially for crotalid bites - concentrates venom, increases necrosis)
• Do NOT massage the wound
• Do NOT use electric shock (TASER, car battery, outboard motor) - historically attempted, no scientific basis
• Do NOT try to catch the snake (risk of second bite; dead snakes can still bite reflexively)
• Sabiston Textbook of Surgery, p. 872-893

Hospital Treatment

1. Identify the species if possible - most important step in management
2. Document puncture site location, fang mark distance (indicates snake size), local and systemic symptoms
3. Cleanse wound gently (unless venom ID kit available)
4. Serial vital signs guided by clinical response
5. Labs: CBC, coagulation studies, fibrinogen, metabolic panel
6. Antivenom is the mainstay of treatment

Antivenom

North American Crotalid antivenoms:

• CroFab (Crotalidae polyvalent immune Fab, ovine): ~$3,198/vial; 4-12 vials typical dose; half-life ~15 hours; requires refrigeration
• ANAVIP (Crotalidae immune F[ab']2, equine): ~$1,220/vial; starting dose 10 vials; half-life ~133 hours; room-temperature storage; less expensive

Adverse reactions:

• Immediate reactions (anaphylaxis): 6-14% with CroFab (much lower than older equine antivenom which caused ~50% anaphylaxis)
• Serum sickness (type III hypersensitivity): 13-16% with CroFab; treat with corticosteroids tapered over 7-14 days
• If anaphylaxis: stop infusion, give diphenhydramine + epinephrine + steroids, secure airway, volume resuscitation

Special populations:

• Can be used in children as young as 14 months
• Pregnancy: antivenom generally recommended when indicated - fetal loss rate up to 20% reported with snakebites globally, improved with antivenom
• Sabiston Textbook of Surgery, p. 952-960

Medico-Legal / Forensic Notes

• Snake venom is toxic only when injected, not when ingested (not absorbed by gastric mucosa)
• However, blood of a bitten animal is poisonous if injected into a human
• Venom retains potency for years in dried state
• Snakes emerging from hibernation in early spring give the most dangerous bites
• Nocturnal bites are more serious than daytime bites
• Cobras and other "spitting snakes" can project venom 4-8 feet; if it reaches the eye, causes severe corneal and conjunctival inflammation (snake venom ophthalmia)
• P C Dikshit Textbook of Forensic Medicine and Toxicology, p. 493-495

Liver Abscess

• Bailey and Love's Short Practice of Surgery 28th Edition, p. 2669
• Yamada's Textbook of Gastroenterology 7e

Types and Etiology

1. Pyogenic Liver Abscess (PLA)

• Biliary origin: E. coli, Klebsiella spp., Enterococcus
• Enteric origin: Bacteroides fragilis, other anaerobes
• Cryptogenic: Klebsiella pneumoniae (monomicrobial) - associated with colon cancer; consider colonoscopy to rule out occult malignancy
• In USA: Streptococcus spp. are actually the most common isolated pathogens (population-based studies)
• Most PLAs are polymicrobial

• Current Surgical Therapy 14e, p. 103-111; Yamada's Textbook of Gastroenterology 7e

2. Amebic Liver Abscess (ALA)

• Ingestion of E. histolytica cysts/trophozoites via fecally contaminated food or water
• Intestinal mucosal invasion → trophozoites seed the liver via the portal venous system
• Typically occurs 2-4 months after colonic amebiasis
• Abscess contains necrotic hepatocytes in a characteristic thick brown fluid: "anchovy paste"
• Current Surgical Therapy 14e, p. 191-196

3. Fungal Hepatic Abscess

Clinical Features

• Rupture into peritoneum → purulent peritonitis (high mortality without surgery)
• Rupture into right pleural space
• Rare rupture into pericardium
• Portal vein / hepatic vein thrombosis from local inflammation
• Ipsilateral pleural effusion (>50% if abscess >10 cm)
• Yamada's Textbook of Gastroenterology 7e; Current Surgical Therapy 14e

Laboratory Findings

Imaging

Ultrasound

• First-line imaging in pediatrics and initial assessment
• Abscesses appear hypoechoic, often with internal echoes
• Can identify multiloculated cystic mass
• Less sensitive than CT overall

CT (with IV contrast) - Most sensitive

• Abscesses appear as hypoattenuating (low-density) lesions
• Peripheral rim enhancement - uncommon but specific
• May show loculations, air-fluid levels
• Identifies extrahepatic causes (appendicitis, diverticulitis)
• Multiple abscesses on imaging favor pyogenic over amebic etiology

CT scan of liver abscess - air-fluid level with rim enhancement (open arrow). The second lesion is a hemangioma (closed arrow). - Bailey and Love's Surgery

CT abdomen: Liver abscess with characteristic rim enhancement - Current Surgical Therapy 14e

Differential Diagnosis

• Hepatic malignancy with necrotic center
• Cholangitis / cholecystitis
• Right lower lobe pneumonia
• Hydatid (echinococcal) cyst
• Non-infected hematoma
• Perforated peptic ulcer

Distinguishing PLA vs. ALA

Note: ALA and PLA cannot be reliably differentiated on imaging alone. Travel history and serology are key.

Treatment

Pyogenic Liver Abscess

Antibiotics

• Blood cultures and abscess cultures are essential (positive >50%)
• Empiric coverage must cover: streptococci, gram-negative enteric organisms, anaerobes
  • Typical regimens: beta-lactam/beta-lactamase inhibitor combination, or 3rd-generation cephalosporin + metronidazole
  • If liver transplant or risk of ESBL: consider carbapenems
  • Metronidazole and clindamycin: excellent anaerobic coverage and abscess penetration
  • 3rd-gen cephalosporins and aminoglycosides: effective against gram-negatives
• Duration: guided by clinical response and imaging resolution at 4-6 weeks

Percutaneous Drainage (standard of care)

• Recommended for all PLAs without evidence of rupture or concurrent intra-abdominal abscess
• Abscess >5 cm: percutaneous catheter drainage (superior to needle aspiration alone)
• Abscess >10 cm: may require multiple catheters
• Abscess <3 cm: aspiration alone (if technically feasible) to guide antibiotics
• Catheters remain until output is low and clear for several days
• Watch for bile in drains - indicates biliary communication → investigate with HIDA or MRCP/ERCP → may need sphincterotomy or percutaneous biliary drain

Surgical Drainage or Resection

• Required in 10-20% of cases (failure of percutaneous approach)
• Indications: large multiloculated abscesses, biliary tree communication, concurrent intra-abdominal abscess
• Laparoscopy preferred; laparotomy for complex cases (e.g., simultaneous diverticulitis)
• No evidence that partial hepatectomy is superior to simple surgical drainage + irrigation
• Current Surgical Therapy 14e, p. 124-176

Amebic Liver Abscess

Antibiotics

• Oral metronidazole 500-750 mg TDS x 7-10 days - highly effective; >90% clinical improvement
• Must also treat intestinal reservoir to prevent recurrence:
  • Oral paromomycin 10 mg/kg TDS x 7 days, OR
  • Oral diiodohydroxyquin 650 mg TDS x 20 days
• Treatment duration is standardized (unlike PLA); imaging resolution may take months but is not needed to stop antibiotics

Drainage

• NOT routinely recommended for ALA - prospective studies show no benefit from early drainage
• Indicated only if no clinical response to antibiotics
• If failing standard ALA therapy: broaden antibiotics (cover for PLA), pursue percutaneous catheter drainage (consider bacterial superinfection)

Fungal Liver Abscess

• Same paradigm: antifungals + percutaneous drainage
• Empiric: Amphotericin B or an echinocandin (caspofungin or micafungin)
• Guided by culture data; duration determined by resolution on imaging
• Antifungal prophylaxis in transplant patients reduces risk

Recurrent / Refractory Abscess

• Recurrence rates: 12-38% depending on organism identification and whether diabetes is controlled
• More common when initial lesion was large, multiple, or with biliary communication
• Management: repeat aspiration → catheter drain → surgical drainage (laparoscopy preferred over laparotomy)

Outcomes / Prognosis

• Mortality has improved dramatically with early diagnosis, antibiotics, and percutaneous drainage
• Current mortality: 4-10%
• Poor prognostic factors: diabetes mellitus, underlying malignancy, cirrhosis, abscess size >10 cm
• Fungal abscess: highest mortality (~20-50%)
• Current Surgical Therapy 14e, p. 179-181