Is the patient envenomed?
Is it likely that a clinically relevant injection of venom has taken place?
- time of the bite,
- local pain,
- nausea, vomiting, abdominal pain,
- paraesthesias of the extremities and around the mouth,
- muscle pain.
- state of consciousness.
- blood pressure/pulse,
- respiratory rate.
- 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),
- flank pain and renal bed sensitive to percussion.
- 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),
- 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.
It is estimated that in 75% of North American crotalid bites no clinically relevant envenoming occurs (Minton 1987a); in contrast, in only 40–75% of Micrurus fulvius bites does envenoming not take place (Russell 1983, Kitchens and van Mierop 1987).
Following North American crotalid bites, strong local pain, swelling, discolouration of the skin and occasionally hyposensitivity in the region of the bite are early signs of a relevant injection of venom. If these do not occur within 15–30 min after the bite, it is highly likely that no venom was injected. Important exceptions to this rule are some populations of Crotalus scutulatus ("type A"), C. mitchelli, C. lepidus and C. tigris, which can cause systemic envenoming without significant local effects (Minton 1987a). Local symptoms may also be relatively insignificant following bites by C. adamanteus, even if systemic effects, including incoagulability of the blood, are present (Kitchens and Van Mierop 1987). The same applies to all bites in which direct intravenous injection of venom occurs (Minton 1987a). Within an hour after an effective crotalid bite the regional lymph nodes are generally swollen and painful. Nausea, vomiting and diarrhoea develop. Paraesthesias of the extremities and perioral as well as muscle fasciculations are characteristic for rattlesnake bites (Minton 1987a, Russell 1983) (see Biomedical database entry for C. horridus). Haemorrhagic blisters usually develop within less than 2 h after a rattlesnake bite, but can also occur after a long delay (Minton 1987a).
Progressive arterial hypotension, leading to loss of consciousness and cardiovascular failure, is one of the most significant complications of North American rattlesnake bites and is a certain sign of severe envenoming (Minton 1987a).
Apart from ecchymoses in the region of the swelling, bleeding, in particular life-threatening bleeding, is very uncommon with North American crotalid bites. This is so despite the fact that marked defibrinogenation and thrombopaenia can occur and although the venoms contain haemorrhagins. However, the haemorrhagins appear to be primarily locally active. In particular following bites by crotalids, whose venoms possess only direct fibrinogen-coagulating activity ("thrombin-like" activity), the haemostatic defect usually only manifests itself in the form of abnormal clotting test results and not clinically (Kitchens 1991, pers. comm.). For this reason coagulation should always be monitored if a crotalid bite has taken place or is suspected.
North American elapid bites (Micrurus fulvius) cause only minor local signs of envenoming. Bite marks may be so small as to be invisible. These bites are not particularly painful, there is no discolouration of the skin, and swelling, if it occurs at all, is insignificant. Moreover, systemic signs of envenoming, such as progressive paralysis that may ultimately lead to respiratory insufficiency and respiratory failure, may only appear several hours after the bite (Minton 1987a, Micrurus fulvius).
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: Monitoring of the patient).
Elapids (Micrurus fulvius): generally several hours up to >12 h in some cases.
Preclinical phase of systemic signs of envenoming:
Crotalids: minutes to hours, up to >8 h (Hurlburt et al. 1988).
Preclinical phase of haemostatic defects:
Crotalids: 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, in laboratory investigations (clotting time), haemostatic defects can become apparent as early as <1 h after the bite, although they may also appear after a delay of >8 h (Kitchens and Van Mierop 1983), in exceptional cases even later (Hurlburt et al. 1988).
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.
Following crotalid bites, whose venom is known to cause defibrinogenation, there may be a delay of several hours before this condition is detectable on laboratory tests. Also, the absence of local signs of envenoming does not exclude the later development of a haemostatic defect (Van Mierop and Kitchens 1980, Kitchens and Van Mierop 1983). The same is true for other systemic signs of envenoming, including arterial hypotension. Several patients developed cardiovascular failure following progressive arterial hypotension that first occurred hours after the bite (Hurlburt et al. 1988).
In a group of 45 patients, initially none or only one had minimal swelling and no other local or systemic signs of envenoming such as nausea, vomiting, perioral paraesthesia, alteration of consciousness, ecchymosis, blistering or marked pain. 24 (53%) later developed significant signs of envenoming such as moderate to marked swelling, thrombocytopaenia or cardiovascular failure. Of these 24 patients, 11 (46%) deteriorated within 4 h, 5 (21%) within 4–8 h and 6 (25%) within >8 h (no data for 2 patients) (Hurlburt et al. 1988).
Following Micrurus sp. bites the problem of assessing the risk of a clinically relevant envenoming is even greater. Minimal or no local signs of envenoming are the rule, and systemic signs of envenoming only develop after a long delay.