Go to start page
V1.6.6 (T325, R32e7b7a99)
Disclaimer & Information
Search
Show Mindmap
 
Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
Venomous fish
 
Scorpions
 
Spiders
 
Hymenopterans (Bees, Wasps and Ants)
 
Sea snakes
 
Terrestrial snakes
 
Miscellaneous animals
 
North America
 
Mexico and Central America
 
South America and the West Indies
 
Europe
 
North Africa, Near and Middle East
 
Central and Southern Africa
 
The Far East
 
Indian Subcontinent and Southeast Asia
 
Australia and the Pacific Islands
 
 
 
 
 
 
 
 

Clinic

 

Bitis gabonica/B. rhinoceros

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


Overview haemostasis
         
A
 
A
 
B
 
 
D
 
D
 
 
F
F
     
F
     
 
H CT (FSP) Tc PT aPTT TT I FSP D II V VIII X XIII PC ATIII PI tPA α2AP
       
 
E
     
 
C
           
 
F
         
 

Essential

bed-side

tests

Tests for full clinical assessment Tests for research purposes
H haemorhagic effects
+ definite evidence in
human envenoming
CT full blood clotting test
(FSP)  FSP rapid test
Tc platlets
PT prothrombin time
aPTT partial thromboplastin time
TT thrombin time
I fibrinogen
FSP  fibrinogen split products
D D-dimer
II, V, VII, X, XIII
  clotting factors
PC protein C
ATIII antithrombin III
PI plasminogen
tPA tissue plasmin activator
α2AP α2-antiplasmin
 
In this overview, the deviations from normal
are recorded for those haemostasis para-
meters only, for which good evidence is
documented in the literature.

 

A PT, aPTT: increased (Brown et al. 1989).
B

TT: increased.

C

Fibrinogen: decreased (PT was still within the range of normal with a minimum fibrinogen level of approx. 40 g/l) (McNally et al. 1993).

D

FSP, D-dimers: FSPs ↑, D-dimers ↑ (McNally et al. 1993).

E

Platelets: minimum 101,000/mm3 (McNally et al. 1993); minimum platelets 15,000/mm3 1–2 h after the bite (Brown et al. 1989); minimum platelets 34,000/mm3 approx. 5 h after the bite (Bodio and Junghanss, pers. comm. 1993).

F

Clotting factors and inhibitors: FXIII ↓, FV, VII, VII, protein C, ATIII no noticeable decrease (McNally et al. 1993).


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).