Is it an Emergency?
This is relevant for all animals belonging to Terrestrial Snakes in Central and Southern Africa.
Is it likely that the patient is envenomned?
Inquire
- time of the bite,
- local pain,
- nausea, vomiting, abdominal pain.
Assess
- state of consciousness.
Measure
- blood pressure/pulse,
- respiratory rate,
- oxygen saturation (pulse oximeter),
- 20WBCT (bedside test).
Observe/investigate
- bite marks,
- extent and intensity of local swelling,
- eyes: conjunctivitis, corneal lesions, uveitis (spitting cobras!),
- enlargement and painfulness of regional lymph nodes,
- swelling in the facial region, including the larynx/pharynx (angio-oedema),
- conjunctival oedema,
- clinical signs of a pleural effusion, pulmonary oedema,
- 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 including the respiratory musculature (→ respiratory insufficiency/respiratory failure),
- myalgia with active and passive movement and upon pressure,
- dark-brown/red urine (differential diagnosis haemoglobinuria; rhabdomyolysis!),
- flank pain and renal bed sensitive to percussion.
Important clinical features of envenoming in the region
Varibility of symptoms and degree of envenoming
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
- the time interval between clinical examinations
- emergency care (see below)
Bite marks and dry bites
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 relevant injection of venom has taken place.
Autopharmacological signs & symptoms
The venom of vipers in particular can cause clinical symptoms of anaphylaxis in patients within minutes after the bite.
Autopharmacological effects of venom such as arterial hypotension and hypovolaemic shock as a consequence of sequestration of large amounts of fluid in the extravascular space occur with Bitis arientans, Bitis gabonica, Bitis rhinoceros, Bitis atropos (Efrati 1979, Marsh and Whaler 1984, Leviton et al. 1992, McNally et al. 1993, Tianyi et al. 2025, van der Walt and Muller 2019, Warrell 2023, Warrell et al. 1975).
Local signs & symptoms
Bitesite
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 relevant injection of venom has taken place.
Atractaspis sp.: as a rule there is generally at least mild local swelling following injection of venom (Warrell et al. 1976c).
Bitis arietans, Bitis gabonica, Bitis rhinoceros: severe pain, marked local swelling that often extends to the trunk and causes necrosis (Warrell et al. 1975, Marsh and Whaler 1984, Tianyi et al. 2025).
Bitis arietans
“Compartment syndromes may develop, especially involving the anterior tibial compartment after bites on the feet and ankles, leading to ischaemic necrosis of intra-compartmental muscles.” (Amr et al. 2020).
Causus sp.: local swelling generally appears to occur following injection of venom, but is only marked in a small proportion of cases (Warrell et al. 1976c).
Colubrids: local swelling may be very mild and with Dispholidus typus bites may be absent even in cases of severe systemic envenoming (non-clottable blood).
Echis sp.: local swelling always occurs if venom has been injected, but may be only mild (Porath et al. 1992, Warrell et al. 1977).
Mambas (Dendroaspis sp.): local signs of envenoming usually absent or insignificant (Warrell et al. 1976a, Blaylock et al. 1985, Visser and Chapman 1978).
African neurotoxic cobras (Naja sp.): local signs of envenoming usually absent or insignificant (Warrell et al. 1976b, Blaylock et al. 1985, Visser and Chapman 1978).
African spitting cobras (Naja sp.): local swelling may be very extensive, possibly involving the trunk, necrosis (Tilbury 1982, Warrell et al. 1976b).
Compartment syndrome
Even extensive swelling of the extremities is not necessarily an indication of compartment syndrome. The decision to perform a fasciotomy must have a rational basis, see Compartment syndrome.
Eyes (Spitting cobras)
African spitting cobras (Naja sp.) and Hemachatus haemachatus cause eye lesions. Intense local pain; blepharospasm; palpebral oedema; leucorrhoea; photophobia, clouding of vision, temporary blindness (Chu et al. 2010, Tilbury 1982, Warrell 2023, Warrell and Ormerod 1976; WHO 2016a).
Non-clottable blood and bleeding
Even coagulation disorders that are severe according to laboratory tests may only be clinically apparent to a slight degree, or not at all. There is a threat of spontaneous haemorrhage with extensive loss of blood or focal bleeding (e.g. intracranial) as long as the haemostatic defect exists (untreated, i.e. without antivenom treatment, days to weeks).
Atheris sp., Echis sp., Bitis arietans*, Bitis gabonica, Bitis rhinoceros and colubrids (Dispholidus typus, Thelotornis sp.): primarily plasma coagulation disorder with abnormal clotting tests (e.g. 20WBCT).
Bitis arietans and N. nigricollis: thrombocytopaenia.
*Bitis arietans: “There is some regional variation in the pattern of envenoming; spontaneous bleeding, bruising and muco-cutaneous and serosal petechiae associated with thrombocytopenia in West Africa (Warrell et al. 1975), and frank coagulopathy in Uganda (Sezi et al. 1972), South Africa and elsewhere” (Amr et al. 2020, Warrell et al. 1975).
Thrombotic microangiopathy (TMA)
Is observed in the region, e.g. in Echis sp. envenoming.
Descending paralysis / respiratory failure
African neurotoxic cobras (Naja sp.), Mambas (Dendroaspis sp.) and Viperids (Bitis atropos) (van der Walt and Muller 2019).
Neurotic signs & symptoms mostly mild in Hemachatus haemachatus and Aspidelaps sp. envenoming. In the latter two deaths have, however, been described (Barton et al. 2019, Theart et al. 2024).
Autonomic dysfunction (nausea, vomiting, sweating)
Mambas (Dendroaspis sp.)
Acute kidney injury (AKI)
According to the available data, acute renal failure following a snakebite in the region generally appears to be a secondary effect (arterial hypotension, shock, DIC).
For Bitis arietans venom a primary nephrogenic effect is discussed (Warrell et al. 1975).
Exclusion of clinically relevant envenoming
Preclinical phase of autopharmacological effects
Bitis arietans, Bitis gabonica, Bitis rhinoceros: as short as minutes after the bite.
Preparalytic phase
Elapids: as short as 15-30 minutes after the bite.
Preclinical phase of haemostatic defects (coagulopathy and bleeding)
Viperids: 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.
Preclinical phase of thrombotic microangiopathy (TMA)
Within 24 hours of the bite.
Monitoring for signs and symptoms that would indicate systemic envenoming for 24h.
At least hourly
- state of consciousness,
- ptosis,
- heart rate and rhythm,
- blood pressure,
- respiratory rate,
- bleeding,
- local swelling,
- other newly appearing signs and symptoms.
6-hourly (or more frequently if there is cause for suspicion)
- 20WBCT (bedside test),
- labortaory-based clotting tests (see above),
- CK, GOT (AST),
- urine output.
The absence of signs of envenoming in the first hours after the bite does not exclude the possibility that a relevant injection of venom has taken place. There may be a long delay before systemic signs of envenoming develop. Moreover, the continued absorption of venom from the region around the site of the bite can lead to renewed symptoms of systemic envenoming even after successful administration of antivenom (e.g correction of the haemostatic defect).