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Bothrops moojeni


Brazil (São Paulo)

Kouyoumdjian and Polizelli 1988: 37 B. moojeni bites; identification: morphological.


  • No envenoming: no swelling (and no other signs of injection of venom) 3/37.
  • Mild envenoming: swelling in the region of the site of the bite 7/37. Abnormal clotting time 7/7.
  • Moderately severe envenoming: regional swelling that did not, however, involve the whole of the bitten extremity 22/37. In this group 14/22 had an abnormal clotting time, 2/14 had systemic bleeding (haematuria, bleeding from the upper digestive tract).
  • Severe envenoming: swelling involving the whole of the bitten extremity (5/37). In this group 3/5 had an abnormal clotting time.

Case reports

Kouyoumdijan et al. 1991: 1 case; identification morphological.
Nishioka and Silveira 1993: 1 case; stated to be definitely B. moojeni.

Ontogenetic differences in symptoms of envenoming

Patients bitten by juvenile snakes appear to display incoagulability of the blood more frequently (due to very high pro-coagulative activity) (Furtado et al. 1991, Kouyoumdjian and Polizelli 1989). In contrast, in a group of 22 patients, only those who had been bitten by large snakes (80–147 cm) developed necroses. Patients who had been bitten by small snakes generally had minor local effects and no necroses (Kouyoumdjian and Polizelli 1989).

Signs & symptoms

Local effects

Local pain and local swelling 34/34; within 30 min after the bite 32/34, within 2 h after the bite 2/34 (Kouyoumdjian and Polizelli 1988).

Haemostatic effects

Haematuria 1/34, bleeding from the upper digestive tract 1/34 (considering the high rate of patients with incoagulable blood, only a few had systemic bleeding, which was also generally only slight) (Kouyoumdjian and Polizelli 1988).

Extensive frontal subdural haematoma. Neurological signs developed 5 h after the bite and 3 h after administration of antivenom. The clotting time was normal 7 h after administration of antivenom, but had increased again 2 h later. The authors assume that the subdural bleed was primarily haemorrhagin induced (Kouyoumdjian et al. 1991).

Renal effects

Acute renal failure (primary/secondary?) 2/34 (Kouyoumdjian and Polizelli 1988).


In a group of patients treated with antivenom: compartment syndrome (no details concerning how the compartment syndrome was diagnosed) 2/34, 1/2 initially classified as having moderately severe envenoming, 1/2 as having severe envenoming. Necrosis 4/34, all initially classified as having severe envenoming. Infections 5/34, 3/5 initially classified as having moderately severe envenoming, 2/5 as having severe envenoming. Contractures 1/34, initially classified as having moderately severe envenoming; acute renal failure 2/34 (Kouyoumdjian and Polizelli 1988).

Average duration of hospital stay: patients without complications 4.2 ± 1 days, patients with complications 17.6 ± 9.1 days (Kouyoumdjian and Polizelli 1988).

Case fatality rate

1/34 from a group of patients treated with antivenom. The patient died on the 3rd day after the bite. He was initially included in the group with severe envenoming. A fasciotomy was performed on the 2nd day; cause of death unknown (Kouyoumdjian and Polizelli 1988). 1 fatality (cause: extensive subdural haemorrhage) (Kouyoumdjian et al. 1991).

Laboratory and physical investigations

1. Haemostasis
Type of haemostatic defect
Defibrin(ogen)ation ("thrombin-like" activity), factor X activator, prothrombin activator (Nahas et al. 1979).

Haemostatic parameters

Overview haemostasis




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
  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 Clotting time: increased or incoagulable 24/33 (2 ml of blood in a test tube in a water bath at 37°C; ≤10 min: normal, >10 min to ≤30 min: increased, >30 min: incoagulable) (Kouyoumdjian and Polizelli 1988).

2. CK

Maximum CK on the first day after the bite: 1,269 IU/l (normal 10–80 IU/l); the patient had not used a tourniquet and had not received an i.m. injection. The authors argue that increased CK is thus not suitable as a clinical criterion to distinguish between Bothrops and Crotalus bites in Brazil (Nishioka and Silveira 1993). However, this does not prove that this was a systemic rather than a local myotoxic effect, as is seen with a large number of Bothrops species (Gutierrez and Lomonte 1989).

Treatment (specific)

Antibotropico, Instituto Butantan, São Paulo, Brazil.


Kouyoumdjian and Polizelli 1988: 34 patients received antivenom on average 3 h and 24 ± 43 min after the bite (Antibotropico, Instituto Butantan, São Paulo, Brazil).

Initial dose: on average 151 ± 18 mg. Data on the amount of venom that was neutralised by the antivenom administered (corresponds to approx. 60–70 ml of anti-Bothrops antivenom).

A further dose of antivenom of 88 ± 25 mg on average (corresponds to approx. 40 ml of anti-Bothrops antivenom) was administered to 14/34 patients due to a persistently abnormal clotting time or severe deterioration of local signs of envenoming after an average of 16 h 25 min ± 9 h 46 min.

See above for further details of the study design.


  • With regard to necrosis formation: even when large amounts of antivenom were administered 3 h after the bite, no positive effect on necrosis formation was observed (Kouyoumdjian and Polizelli 1988).
  • With regard to the haemostatic effect: clotting time returned to normal on average 17 ± 4 h after the beginning of antivenom treatment (Kouyoumdjian and Polizelli 1988).