Biology Reference
In-Depth Information
deposition of fibrin on activated vascular epithelium (possibly damaged by proteo-
lytic rhexic hemorrhagins and other venom components) can alter erythrocyte mor-
phology (e.g., schistocytes or helmet cells) and produce MAHA. This complication
of venom-induced DIC has been reported after envenomations by western brown
snakes (
Pseudonaja nuchalis
), the desert horned viper (
Cerastes cerastes
), the
African lowland or swamp viper (
Proatheris superciliaris
), and others (Keyler, 2008;
Schneemann et al., 2004; Warrell, 2005; White, 2005).
Similar to the case of
D. typus
envenoming reported by Lakier et al. (1969), the
following case of
R. tigrinus
envenoming suggests that antivenom therapy may not
influence venom-induced thrombocytopenia. Akimoto et al. (1991) reported a grad-
ual rise in platelets over a 9-day period following a serious
R. tigrinus
envenoming
treated with anti-
R. tigrinus
antivenom. The rate of recovery of normal platelet levels
reported by those authors is similar to that of a 20-day history reported for a patient
also envenomated by a
R. tigrinus
and treated with exchange blood transfusion and
plasmapheresis (Mori et al., 1983). However, a patient with hemorrhagic diathesis
following a
R. subminiatus
envenoming maintained a normal platelet level through-
out the course of the venom disease (Hoffmann et al., 1992).
Available data indicate that although common, thrombocytopenia is not inevi-
table in envenomation from hazard level 1 colubrids. Therefore, there is no univer-
sal recommendation for platelet replacement in serious envenomation by
D. typus
,
Thelotornis
spp.,
R. tigrinus
, and
R. subminiatus
. Severe thrombocytopenia should
be corrected by platelet infusions as clinically indicated. When available, specific
antivenom is the most effective therapy for reversing the coagulopathy, although
doubts have been expressed regarding efficacy of antivenom in some coagulopathic
envenomings (specifically, envenoming by Australian elapid snakes with types C and
D prothrombin-activators
25
; Isbister et al., 2009). Also, as noted above, thrombocy-
topenia can persist in some coagulopathic envenomings (i.e., from some crotaline
viperids) regardless of provision of antivenom with platelet infusions (Odeleye et al.,
2004).
Analogous to some of the reported cases of envenomation by
Thelotornis
spp.
(
Table 4.1
and previous sections), Mebs et al. (1998) reported that platelet therapy
with fibrinogen infusions appeared to stabilize a patient within 2 days postenvenom-
ation by
Atheris squamiger
(African green bush viper), a species for which no spe-
cific antivenom is available. A patient with coagulopathic envenoming from another
species for which there is no antivenom,
Proatheris superciliaris
, developed throm-
bocytopenia and was successfully managed with platelet infusions, FFP, and hemo-
dialysis (Valenta et al., 2008). It must be noted that these cases may suggest also that
although seriously envenomated, these patients might not have received a potentially
fatal dose of venom.
25
Group C (e.g., pseutarin, from Eastern brownsnake,
P. textilis
venom) and D prothrombin activators
(e.g., notecarin and trocarin, from venoms of the common tiger snake,
Notechis scutatus
and the rough-
scaled snake,
Tropidechis carinatus
, respectively) are structural and functional homologues of factor Xa
and the prothrombinase complex, respectively (see Joseph et al., 2002 and Rao et al., 2003).
