Diagnosis & Treatment — General practitioner / health post
see also Warrell (2004) Snakebites in Central and South America: Epidemiology, Clinical Features, and Clinical Management. In: Venom Poisoning by North American Reptiles. In: J. A. Campbell and W. W. Lamar: The Venomous Reptiles of the Northern Hemisphere. Comstock; Ithaca, London S. 709-761
General problems
At particular risk are: children, elderly people, patients with pre-existing conditions, such as coronary heart disease, arterial hypertension, lung disease, kidney disease, allergies (sensitisation), patients with predilection sites for bleeding such as gastrointestinal ulcers, kidney stones, pulmonary cavities (tuberculous), and patients taking particular drugs, such as coumarin derivatives, platelet aggregation inhibitors and beta-blockers.
Patient presents with a tourniquet on the affected extremity
Check venous and arterial blood supply in the extremity.
If a tourniquet has been applied, it should not be removed until antivenom is at hand and the means for treating complications, including possible complications caused by the antivenom, are available.
If these requirements cannot be met within a suitable period of time, it is necessary to weigh the risk of the systemic effects of the venom that could occur after removing the tourniquet against the risk of progressive local tissue damage that may arise if the bandage is left in place.
Is it likely that a clinically relevant injection of venom has taken place?
Inquire re:
- time of the bite,
- local pain,
- 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,
- swelling in the facial region, including the larynx/pharynx (angio-oedema),
- clinical signs of shock,
- bleeding from bite marks and other injuries,
- subcutaneous bleeding in the region of the swelling,
- 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),
- muscle pain with active and passive movement and upon pressure (rhabdomyolysis!),
- dark-brown/red urine (differential diagnosis haemoglobinuria) (rhabdomyolysis!),
- flank pain and renal bed sensitive to percussion
- severe headache, shock, refractory arterial hypotension, signs of hypoglycaemia and loss of consciousness (acute pituitary insufficiency!).
Determine:
- cause of the accident by determination of specific venom antigen and venom concentration in the serum using the ELISA method (if clinically proven and standardised test kits are commercially available),
- clotting time (bedside test),
- blood sugar,
- 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 relevant injection of venom has taken place.
Following Bothrops sp. and Lachesis sp. bites, local signs, such as swelling at the site of the bite, can very quickly indicate that a significant injection of venom has occurred. This does not apply to bites from Crotalus durissus ssp. in the southern regions of the distribution area of this species. Likewise, following Micrurus sp. bites, local swelling is minimal or absent.
Noticeable bleeding may be absent during the initial phase or the entire course of envenoming following crotalid bites, even though defibrin(ogen)ation may be present to such a degree that the blood is completely incoagulable (clotting time test). This is true in particular for C. durissus and Lachesis sp. bites, as the venoms of these species primarily contain components that have direct fibrinogen-coagulating activity ("thrombin-like" activity).
The simple clotting time test should always be performed if a crotalid or colubrid bite is suspected.
To date, acute pituitary insufficiency has been reported once in South America as a complication of a B. jararacussu bite (Wolff 1958). This complication is probably the result of ischaemia of the hypophysis through bleeding or thrombosis. The symptoms may occur after some delay. A simple rapid diagnostic test for blood sugar and monitoring of the treatment-resistant hypotensive state are helpful for the purposes of differential diagnosis (see the Biomedical database entry for B. jararaca).
Exclusion of clinically relevant envenoming
Monitoring for signs and symptoms (see above) that would indicate systemic envenoming for at least 24 h (recommended examinations, see Therapy phase: Hospital).
Preparalytic phase:
Elapids (Micrurus sp.) and C. durissus terrificus as well as other C. durissus ssp. that cause symptoms of paralysis: from 30–60 min.
Preclinical phase of haemostatic defects:
Crotalids and colubrids: systemic bleeding can occur within the first hour after the bite. 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. However, on laboratory investigations (clotting time), haemostatic defects can become apparent as early as <1 h after the bite (Rosenfeld 1971), although they may also appear after a delay of >12 h (Cardoso et al. 1993).
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 can be a long delay before systemic signs of envenoming develop.
Who requires antivenom?
Antivenom indications (overview)
Systemic signs of envenoming:
- (acute) arterial hypotension,
- (persistent) arterial hypotension,
- haemostatic defects (clinically, laboratory parameters: clotting time or more complex tests),
- cranial nerve deficits (ptosis, ophthalmoplegia, dysphagia, dysarthria),
- paralysis of the limb musculature,
- paralysis of the respiratory musculature (→ respiratory insufficiency/failure),
- rhabdomyolysis: clinical signs; CK, GOT (AST), myoglobinuria,
- acute renal failure.
Local signs of envenoming:
- In the case of (rapidly) progressive or already marked swelling, especially following bites by those species of snakes known to cause necrosis.
How is the appropriate antivenom chosen?
- See Emergency flowchart: South America and the West Indies.
- See the WHO Antivenom list.
- See Biomedical database entries for additional information.
How are antivenoms administered and complications caused by antivenoms treated?
Symptomatic emergency medical treatment and antivenom treatment are complementary strategies.
The aim of antivenom treatment is neutralisation of the venom. The success of antivenom treatment depends on the quality of the antivenom, the specific properties of those venom components relevant to envenoming and the time point at which antivenom is administered.
Symptomatic emergency medical treatment
1. Clinical signs of shock
Early: anaphylactic/anaphylactoid shock (uncommon).
- Treatment of the anaphylactic/anaphylactoid shock,
- possibly antivenom.
Extensive swelling, entire extremity, possibly also involving the trunk (fluid sequestration caused by increased capillary permeability) → hypovolaemic shock.
- Treatment of the hypovolaemia/hypovolaemic shock,
- antivenom.
Usually late (hours to days after the bite): clinical signs of extensive blood loss → haemorrhagic shock (uncommon).
- Treatment of the haemorrhagic shock,
- antivenom.
Symptomatic emergency medical treatment
2. Clinical signs of progressive paralysis; paralysis of the respiratory musculature (→ dyspnoea, respiratory failure)
- Treatment of the respiratory insufficiency/respiratory failure,
- edrophonium (Tensilon®) test/neostigmine,
- antivenom.
Symptomatic emergency medical treatment
3. Clinical signs of focal neurological deficits, meningismus (intracranial bleeding!)
- Treatment of the intracranial bleeding,
- antivenom.
Symptomatic emergency medical treatment
4.Clinical signs of acute pituitary insufficiency
- Treatment of the acute pituitary-adrenocortical insufficiency,
- possibly antivenom.
Symptomatic emergency medical treatment and antivenom treatment are complementary strategies.
The aim of symptomatic emergency medical treatment is the rapid correction of critical parameters (fluid balance, blood pressure, oxygenation etc.) and the maintenance of vital functions (respiratory, cardiovascular).
Symptomatic measures help bridge the gap until specific treatment (antivenom) can be administered and starts being effective. If no antivenom is available or if the required effect is not achieved with antivenom, the goal is to employ symptomatic measures until such time as the venom naturally starts losing its activity.
Local treatment
Bite wound, including the surrounding reaction
- Assessment of the wound according to the usual criteria.
- Swelling: assessment of the extent and increase in magnitude; regional signs of haemorrhage.
- Long-term: observation for the formation of necrosis.
- Cleaning, disinfection and dressing of the wound at regular intervals.
- Immobilisation of the extremity with a splint. Padding and monitoring to prevent pressure necrosis and disturbance of the blood circulation if the oedema increases.
- Possibly also prophylactic antibiotic treatment:
- no interference with the bite wound: penicillin or erythromycin,
- bite wound has been interfered with (incisions etc.): penicillin or erythromycin + aminoglycoside (Warrell 1990b).
Tetanus
Tetanus prophylaxis.