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Clinic

 

Crotalus atrox

Case reports

Budzynski et al. 1984: 1 Crotalus atrox bite; identification: by the companion of the person bitten and by recognition from photographs.

Sivaprasad and Cantini 1982: 1 Crotalus atrox bite; identification: morphological.

Griffen and Donovan 1986: 1 Crotalus atrox bite; identification: morphological.

 

Effects of ontogenetic differences in venom composition on the symptoms of envenoming

The venom of juvenile snakes up to the age of approx. 8 months possesses components with fibrinogen-coagulating ("thrombin-like") activity that are subsequently lost (Reid and Theakston 1978). In contrast, the venom of adult snakes only shows fibrin(ogen)olytic activity. This comes about through the venom-induced release of cellular plasminogen activator (Budzynski et al. 1984, Kirschbaum et al. 1988). This fact could explain the sometimes conflicting reports of the course of C. atrox envenoming. The differences in venom composition between juvenile and adult Crotalus atrox imply that juvenile animals cause more severe envenoming than do adults.

Signs & symptoms

Autopharmacological effects

Nausea, vomiting (Budzynski et al. 1984); recurrent episodes of arterial hypotension and tachycardia; also increased capillary permeability with fluid sequestration in the extravascular space; see below "Treatment (symptomatic)" and direct hypotensive effect of the venom (Mancuso de Mesquita et al. 1991).

Local effects

Local pain. 16 h after the bite swelling of the entire bitten leg; difference in circumference of several centimetres. Petechiae and ecchymosis in the region of the swelling. Haemorrhagic blister with a diameter of 10 cm in the region of the bite (Budzynski et al. 1984).

Haemostatic effects

Bleeding from incisions and both arterial and venous puncture sites (Budzynski et al. 1984; Sivaprasad and Cantini 1982); haematuria (Sivaprasad and Cantini 1982); haematemesis (Sivaprasad and Cantini 1982).

Morbidity

Necrosis; debridement necessary (Budzynski et al. 1984).

Laboratory and physical investigations

1. Haemostasis
Illustrative study
Budzynski et al. 1984: examination of the clinical course in a patient who did not receive antivenom.


Type of haemostatic defect

The venom of juvenile snakes up to the age of approx. 8 months possesses components with fibrinogen-coagulating ("thrombin-like") activity that are subsequently lost (Reid and Theakston 1978). In contrast, the venom of adult snakes only shows fibrin(ogen)olytic activity. This comes about through fibrinogen (Pandya and Budzynski 1984) and the venom-induced release of cellular plasminogen activator (Budzynski et al. 1984, Kirschbaum et al. 1988). Haemorrhagic activity (Bjarnason and Tu 1978). Platelet aggregation (Reid and Theakston 1978).


Haemostatic parameters


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

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

Haemorrhagic activity: minor bleeds from venipuncture sites during the first 7 days after the bite in a patient who did not receive antivenom. Cause probably a combination of afibrinogenaemia, a high FSP concentration and possibly also local haemorrhagic activity (Budzynski et al. 1984). Systemic bleeding, e.g. gastrointestinal, cerebral or renal haemorrhage, is rare (Hardy 1992b).

 

B PT, aPTT, TT: >120 s 16 h after the bite. The patient did not receive antivenom. Spontaneous normalisation of aPTT on day 5, PT on day 8 and TT on day 10 after the bite (Budzynski et al. 1984).
C Fibrinogen: changes in fibrinogen levels in a patient who did not receive antivenom: afibrinogenaemia until day 3, constant improvement of the hypofibrinogenaemia until day 11, fibrinogen in the normal range from day 12 (Budzynski et al. 1984). Fibrinogen frequently <50 mg/dl (normal 150–400 mg/dl) (Hardy 1992b).
D FSP: chiefly composed of non-cross-linked fibrinogen split products (this indicates among other things that coagulation is not induced by a thrombin-generating process) (Budzynski et al. 1984).
E Fibrinolysis: plasminogen decreased, α2-antiplasmin decreased, plasmin-α2-antiplasmin complex increased (Budzynski et al. 1984).
F

Clotting factors, inhibitors: ATIII decreased only slightly, factor VIII in the normal range (this indicates among other things that coagulation is not induced by a thrombin-generating process) (Budzynski et al. 1984).

 

G

Platelets: platelet count 42,000/μl at the time of hospitalisation (approx. 1 h after the bite?), minimum 19,000/μl on the 1st day after hospitalisation after 15 vials of antivenom (Griffen and Donovan 1986).

Platelet count 79,000/μl at the time of hospitalisation, minimum 69,000/μl on the 1st day after hospitalisation after 30 vials of antivenom (Sivaprasad and Cantini 1982).

Platelet counts of <10,000/μl are observed (Hardy 1992b).

 


2. Leucocytes
15,600/mm³ (Sivaprasad and Cantini 1982).

Treatment (specific)


Crotalidae Polyvalent Immune Fab Antivenom, ovine (immunized with Crotalus adamanteus, Crotalus atrox, Crotaus scutulatus ssp. and Agkistrodon piscivorus) / CroFab™, Savage Laboratories, Melville, New York

 

see Crotalus sp.