Case reports

Staley 1929
Grasset 1946
Visser and Carpenter 1977
Edwards et al. 1979
Chippaux et al. 1981
Brown et al. 1989
McNally et al. 1993

Signs & symptoms

Autopharmacological effects

Nausea, vomiting, angioneurotic oedema, tachycardia, arterial hypotension, pulmonary oedema, hypovolaemia and shock due to massive fluid loss into the tissue. From a pathophysiological perspective, a possible cause might be the autopharmacological release of endogenous mediators, e.g. release of bradykinin through kallikrein-like activity of the venom, a direct effect of venom components on vessel walls (haemorrhagins) which leads to increased vascular permeability and fluid sequestration in a region of extensive swelling (Marsh and Whaler 1984, McNally et al. 1993).

Local effects

Local pain, local swelling which spreads quickly and can extend to the trunk (a factor which can contribute to hypovolaemia and shock due to massive fluid loss into the tissue). Blistering in the area of the bite. Extensive ecchymoses in the region of the swelling. Frequently local tissue necrosis that can be severe (Marsh and Whaler 1984, McNally et al. 1993).

Haemostatic effects

Systemic bleeding (haematemesis, haematuria) (Marsh and Whaler 1984, McNally et al. 1993).

Neurological effects

Impaired accommodation, deafness (Edwards et al. 1979) (only indication of a neurological effect of the venom).

Cardiac effects

Tachyarrhythmia, ECG: atrial tachyarrhythmia, prolonged QT interval, T wave inversion (this persisted for >14 days) (primary cardiac effect of the venom?) (Edwards et al. 1979).

Morbidity

Local tissue necrosis may be so severe that it leads to tissue defects or amputation becomes necessary (Marsh and Whaler 1984).

Case fatality rate

Fatalities have been reported, but on the whole bites by this species seem to be quite rare (Marsh and Whaler 1984).

Laboratory and physical investigations

1. Haemostasis
Type of haemostatic defect
Defibrinogenation due to the fibrinogen-coagulating ('thrombin-like' = gabonase) activity of the venom (Gaffney et al. 1973, Pirkle et al. 1986) and the fibrin(ogen)olytic (plasmin-like) activity of the venom (Forbes et al. 1969, Viljoen et al. 1979); factor XIII-activating effect; inhibition of platelet aggregation (Huang and Peng 1991); but also thrombopaenia (Brown et al. 1989, Bodio and Junghanss 1993, pers. comm.); haemorrhagic effect of the venom (haemorrhagin) (Marsh and Whaler 1984).

Haemostatic parameters

The haemostatic defect can recur in its full extent after a period of days (on the 3rd day in a case report from McNally et al. 1993), even after neutralisation of the responsible venom components over a period of 48 hours after the first administration of antivenom. This prolonged effect of the venom is explained by continued absorption of venom from the area around the bite.

2. Leucocytes
Neutrophilic leucocytosis (Edwards et al. 1979, Brown et al. 1989).

Treatment (symptomatic)

1. Intravenous fluid replacement. Treatment for hypovolaemic shock (McNally et al. 1993).
2. Clotting factor and platelet substitution: administration of these blood products was not sufficient to manage the haemostatic defect in one patient (Brown et al. 1989, McNally et al. 1993).

Treatment (specific)

Studies
No controlled clinical studies available. There is a small amount of information on the efficacy of antivenom in case reports (Edwards et al. 1979, Brown et al. 1989, McNally et al. 1993).

Antivenoms
Polyvalent antivenom (McNally et al. 1993).

Dose
100 ml (McNally et al. 1993).

Efficacy

With regard to the haemostatic effect:

• Clinical: cessation of bleeding (haematuria, gastrointestinal) within a very short time (Brown et al. 1989).
• Coagulation defect (laboratory investigations): restoration of haemostasis (increase in fibrinogen, decrease in D-dimers) coinciding with antivenom administration (McNally et al. 1993).
• Thrombopaenia: normalisation within hours of antivenom administration (Brown et al. 1989).