Clinic
Case reports
Campbell 1977: 1 Notechis sp. bite.
Frost 1980: 2 Notechis sp. bites; identification: bite in a child; the snake that caused the bite was not seen by any adults; rapid improvement of respiratory symptoms and reversal of the haemostatic defect (DIC) coinciding with administration of Tiger snake antivenom, CSL; ELISA (wound swab). Bite in an adult: identification of the snake by the patient; rapid reversal of the symptoms of envenoming coinciding with administration of Tiger snake antivenom, CSL; ELISA (wound swab).
Frost 1981: 1 Notechis sp. bite; identification: the snake that caused the bite was identified as a tiger snake by 2 adults; rapid reversal of the symptoms of envenoming coinciding with administration of Tiger snake antivenom, CSL; ELISA (wound swab).
Gaynor 1977: 1 Notechis sp. bite; identification: RIA (serum).
Harvey et al. 1982: 1 N. ater humphreysi bite; identification: morphological.
Hood and Johnson 1975: 1 Notechis sp. bite; identification: morphological.
Kirkland 1990: 1 N. ater bite; identification: morphological.
Lloyd 1932: 1 Notechis sp. bite; identification: morphological.
Lodge et al. 1988: 1 N. scutatus bite; identification: ELISA (wound swab).
McGarity et al. 1991: 1 Notechis sp. bite; identification: ELISA (wound swab).
Rollison 1928: 1 N. scutatus bite; identification: morphological.
Sutherland and Coulter 1977: 3 Notechis sp. bites (1 case identical to that reported by Gaynor 1977); identification: RIA (serum, urine, venom from the area around the bite).
Sutherland et al. 1975: 1 Notechis sp. bite; identification: RIA (serum).
Tibballs et al. 1991: 1 N. scutatus bite; identification: morphological; ELISA (wound swab).
Wallace 1954: 1 N. scutatus bite; identification: morphological.
White 1992: 16 N. scutatus bites; identification: 13 positive, 3 probable. 3 N. ater bites; identification: positive.
White et al. 1983–84: 1 Notechis sp. bite; identification: ELISA (serum).
Signs & symptoms
Autopharmacological effects
Nausea, vomiting, diarrhoea, abdominal pain, headache, arterial hypotension, loss of consciousness, cerebral seizures. These symptoms develop very rapidly after the bite, sometimes within 15 min (White 1987b and other case reports).
14 cases with systemic envenoming: nausea 10/14, vomiting 7/14, abdominal pain 5/14, headache 3/14, arterial hypotension and loss of consciousness 3/14, cerebral seizures 2/14 (children) (White 1992).
Allergic symptoms (rash, swelling and secretion of the nasal mucosa, bronchospasm, tachycardia, periorbital oedema) within 15 min after the bite. The patient had been repeatedly exposed to tiger snake venom (Kirkland 1990).
Local effects
Local pain, local oedema, enlarged and painful regional lymph nodes, small local necroses, subcutaneous bleeding in the area around the bite (White 1987b and other case reports).
14 cases of systemic envenoming: local pain 13/14, local swelling 10/14, local erythema and bleeding into the skin 8/14, local necrosis 2/14 (White 1992).
Haemostatic effects
Bleeding from skin lesions (e.g. injection sites), ecchymosis, petechial haemorrhages, haematemesis, haematuria, intracranial haemorrhages (White 1987b and other case reports).
Neurological effects
Ptosis within 20 min after the bite, blurred vision, ophthalmoplegia, dysphagia, dysarthria, paralysis of the limb musculature, paralyis of the respiratory musculature (dyspnoea) from 15 min after the bite (White 1987b and other case reports).
14 cases with systemic envenoming: signs of paralysis 6/14, assisted/controlled ventilation 3/6 (White 1992).
Muscular effects
Fasciculation within 20 min after the bite, muscular pain and spasms, pressure sensitivity of the musculature, pseudotrismus, stiff neck, muscular weakness, dark urine colour (myoglobinuria) (White 1987b and other case reports).
14 cases with systemic envenoming: signs of myolysis 3/14 (White 1992).
Renal effects
Acute kidney failure (secondary): in the context of rhabdomyolysis, arterial hypotension, amongst other causes (White 1987b and other case reports).
14 cases with systemic envenoming: impaired kidney function/kidney failure (0/14) (White 1992).
Morbidity
Skin necrosis, 5 × 8 cm (split-thickness skin grafting) (Frost 1981).
Kidney failure (Sutherland and Coulter 1977, Hood and Johnson 1975).
Marked loss of muscle mass. Physiotherapy necessary. Led to slow (complete) recovery (Hood and Johnson 1975).
Persistent muscle weakness (for a period of weeks). Explained by the insufficient capacity of the antivenom to neutralise the already manifest presynaptic effects of the venom, among other factors (White et al. 1983–84).
Case fatality rate
The mortality rate of untreated cases is estimated to be approx. 40% (Fairley 1929).
Reports of fatalities: Rollison 1928, Sutherland et al. 1975, Sutherland and Coulter 1977, Tibballs et al. 1991 (intracranial haemorrhage), McGarity et al. 1991 (intracranial haemorrhage).
Laboratory and physical investigations
1. Haemostasis
Type of haemostatic defect
Defibrin(ogen)ation through prothrombin activation. Prothrombin activator requires phospholipids, Ca2+ and factor Va as co-factors (Rosing et al. 1988).
Haemostatic parameters
| Overview haemostasis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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A
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B
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B
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D
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H | CT | (FSP) | Tc | PT | aPTT | TT | I | FSP | D | II | V | VIII | X | XIII | PC | ATIII | PI | tPA | α2AP | |||||||||||||||||||||||||||||||||||||||||||
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C
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E
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E
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E
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Essential bed-side tests |
Tests for full clinical assessment | Tests for research purposes | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| A | CT: blood not coagulable (White et al. 1983–84). |
| B |
PT, aPTT: increased (Frost 1980, White et al. 1983–84, McGarity et al. 1991). |
| C |
Fibrinogen: not detectable (4 h after hospitalisation) (Frost 1980), not detectable 2.5 h after the bite (White et al. 1983–84). 14 cases with systemic envenoming: coagulation defect [defibrin(ogen)ation] (10/14) (White 1992). |
| D |
FSP: maximum 5,000 mg/l (White et al. 1983–84), 32–128 mg/l (normal: <0.25 mg/l) (McGarity et al. 1991). |
| E |
Clotting factors: factor II minimum 37%, V minimum 6% , VIII minimum 1% (White et al. 1983–84). |
| F |
Platelets: not decreased (White et al. 1983–84, Tibballs et al. 1991, McGarity et al. 1991). |
2. Leucocytes
Leucocytosis: 20,600/mm3 (Hood and Johnson 1975); 25,800/mm3 (Gaynor 1977).
3. Creatinine phosphokinase
Doubled within 4 h (Frost 1980); 4,640 U (normal <250 U) (Hood and Johnson 1975); >4,000 IU/l (Gaynor 1977); 6,426 U/l (normal <110 U/l) (White et al. 1983–84); 33,200 U/l (normal <80 U/l) (Sutherland and Coulter 1977); >30,000 IU (in the absence of impaired kidney function) (White 1992).
4. CPK isoenzymes
Marked increase in MM and MB in some cases. Discussion of effect of the venom on the myocardium and liver (Sutherland and Coulter 1977).
5. GOT
1,300 U (normal <8 U) (Hood and Johnson 1975).
6. AST (GPT)
1,300 IU/l (normal <30 IU/l) (Sutherland and Coulter 1977).
7. Urine myoglobin
Detectable (Tibballs et al. 1991).
8. ELISA
See above.
9. Muscle biopsy
Focal necrotising myopathy (Hood and Johnson 1975).
10. Kidney biopsy
Acute tubular necrosis (Hood and Johnson 1975).
Treatment (symptomatic)
- Endotracheal intubation and artificial respiration,
- dialysis (Hood and Johnson 1975).
Treatment (specific)
Antivenom
Tiger snake antivenom, CSL, Parkville, Australia.
Efficacy
- With regard to the neurological symptoms (signs of paralysis, including paralysis of the respiratory musculature): rapid reversal coinciding with administration of antivenom (Frost 1980, 1981, Wallace 1954); prevention of progression with the administration of antivenom (White et al. 1983–84).
- With regard to the skeletal musculature symptoms: fasciculation: rapid reversal coinciding with the administration of antivenom (Frost 1981).
- With regard to the haemostatic effect:
- clinical: rapid cessation of bleeding coinciding with the administration of antivenom (Frost 1980),
- coagulation defect (laboratory investigations): reversal of the haemostatic defect coinciding with the administration of antivenom (Frost 1980, White 1987b); clear tendency to normalisation of the coagulation parameters within 5 h (White et al. 1983–84).
Several patients who received antivenom early on due to neurological symptoms did not develop any haemostatic defect detectable on haemostatic tests (e.g. patients described by Hood and Johnson 1975 and Frost 1981).