Is the patient envenomed?
Is it likely that a clinically relevant injection of venom has taken place?
Inquire re:
- time of the bite,
- local pain,
- headache, nausea, vomiting,
- abdominal pain,
- muscle pain.
Assess:
- state of consciousness.
Measure:
- blood pressure/pulse,
- respiratory rate.
Observe/investigate:
- bite marks,
- extent and intensity of local swelling,
- enlargement and painfulness of regional lymph nodes,
- clinical signs of shock,
- bleeding in the region of the swelling,
- bleeding from bite marks and other injuries,
- gingival bleeding,
- blood-stained sputum, vomit ("coffee ground vomitus"), stools (melaena) or urine,
- acute abdomen (intra-abdominal bleeding!),
- focal neurological deficits, meningismus (intracranial bleeding!),
- cranial nerve deficits, such as ptosis, ophthalmoplegia, dysphagia, dysarthria,
- paralysis of the skeletal musculature including the respiratory musculature (→ respiratory insufficiency/respiratory failure),
- myalgia with active and passive movement and upon pressure, pseudotrismus,
- dark-brown/red urine (differential diagnosis haemoglobinuria) (rhabdomyolysis!),
- flank pain and renal bed sensitive to percussion.
Determine:
- cause of the accident by determination of specific venom antigen and venom concentration in the serum using the ELISA method (CSL, Parkville, Australia),
- clotting time (bedside test),
- urinary output.
The symptoms and degree of envenoming depend not only on the amount of venom injected and numerous other variables, but also on the time that has elapsed since the bite. This variable factor must be taken into account when making the following decisions:
- exclusion of envenoming (see below),
- the time interval between clinical examinations (see Therapy phase: Hospital),
- emergency care (see below).
The fact that a patient has been bitten by a known venomous snake and the presence of bite marks do not automatically allow the conclusion that a clinically significant injection of venom has taken place.
With many Australian elapids, local signs, such as pain and swelling at the site of the bite, are not a reliable indicator that injection of venom has taken place.
With Pseudonaja sp. bites there are generally no local signs at all. Cases of Australian elapid bites that have occurred unnoticed have been described, especially in children. Only when the children showed signs of systemic envenoming was a snakebite considered as the differential diagnosis. Detection of venom antigen in the serum and urine or venom residue from the region of the bite confirmed the diagnosis (Gaynor et al. 1977, White et al. 1983–84).
If a significant amount of venom is injected during a bite from an Australian elapid, painful enlargement of regional lymph nodes frequently occurs as a sign of systemic envenoming.
Australian elapids cause early (autopharmacological) symptoms of envenoming, nausea, vomiting, abdominal pain, collapse etc., which represent a reliable indication of systemic envenoming.
Noticeable bleeding is generally absent, even if defibrin(ogen)ation is present to such a degree that the blood is completely incoagulable (clotting time test). For this reason the simple clotting time test should always be performed if a snakebite is suspected. However, not all Australian elapids cause haemostatic defects.
Paralysis and clinical as well as laboratory signs of myolysis are reliable indicators of a systemic effect of the venom; however, again it is the case that not all Australian elapids cause such effects.
A validated immunological test kit is available for Australian elapids (CSL, Parkville, Australia). This kit can be used not only for indirect species identification and thus to choose the appropriate antivenom but also to estimate circulating venom in the serum and eliminated venom in the urine (Sutherland 1992, Sutherland and King 1991). Cross-reactions do occur.
Exclusion of clinically relevant envenoming
Monitoring for signs and symptoms (see above) that would indicate systemic envenoming for at least 24 h (Sutherland and King 1991, White 1987b) (for recommended examinations, see Therapy phase: Hospital).
Preclinical phase of severe autopharmacological effects (collapse): 15 min (median) (Oxyuranus sp.) (Currie et al. 1992b).
Preparalytic phase: 390 min (median) (Oxyuranus sp.) (Currie et al. 1992b).
Preclinical phase of a haemostatic defect (bleeding): 105 min (Oxyuranus sp.) (Currie et al. 1992b).
Even severe haemostatic defects that can be detected on laboratory tests may not become clinically evident for a long period, or even not at all.
A study of over 110 symptomatic Oxyuranus scutellatus canni bites provides information on the preclinical phase of significant effects of envenoming (Currie et al. 1992a).