Biology Reference
In-Depth Information
Therefore, with or without antivenom therapy, provision of platelets is at the dis-
cretion of the physician and the need for platelet therapy should be determined by
close serial monitoring of platelet counts and other hemostatic variables (see
Table
4.3
) balanced with the clinical status of the patient (especially evidence of active
spontaneous systemic bleeding and consumptive coagulopathy, etc.).
4.6.2.9 Heparin, Antifibrinolytics, Vitamin K, and Adrenocorticotrophic
Hormone
Attempts to inhibit the envenomation-induced DIC from hazard level 1 species have
included administration of heparin, antifibrinolytics (specifically,
-aminocaproic
acid or transexamic acid), or adrenocorticotrophic hormone (ACTH;
Table 4.1
).
Heparin
The strategy of heparinization has been advanced as a means to prevent perpetuation of
the consumptive coagulopathy in a patient treated with replacement therapy (provision
of fibrinogen through FFP, whole blood or isolated fibrinogen, etc.; see section 4.2.6.8).
Hoffmann et al. (1992) suggested that thrombin inhibition with heparin or hirudin would
probably provide the most “logical” means of treating
R. subminiatus
envenoming. Their
view was couched in their proposed coagulopathic mechanism of
R. subminiatus
venom
toxins. This mechanism consisted of potent prothrombin activation along with con-
comitant activation of protein C and, possibly, factor X (Hoffmann et al., 1992). These
authors did not weigh the risks/benefits of heparinization versus the possibility of cross-
neutralization of
R. subminiatus
venom by anti-
R. tigrinus
antivenom, and effectiveness
of heparin assumes that (1) venom-induced thrombin is susceptible to heparin, and (2)
there is adequate circulating antithrombin III to complex with heparin.
Heparin has been included in the treatment strategy of several documented cases
of hazard level 1 colubrid envenomations (
Table 4.1
). For example, in discussing
two published cases of
D. typus
envenomation, Du Toit (1980) observed that heparin
apparently afforded little clinical benefit, while antivenom administration produced
rapid improvement. Similarly, the course of coagulopathy appeared unaffected by
low-dose heparin given to a patient with severe hemorrhagic diathesis from a
R. sub-
miniatus
envenoming (Zotz et al., 1991).
Several clinical trials have assessed heparin therapy for treatment of coagulo-
pathic envenomation (primarily from viperid envenomation; Myint-Lwin et al.,
1989; Paul et al., 2007; Warrell et al., 1976b). Most of these studies have not dem-
onstrated any efficacy of heparin, and some have revealed the dangers of this treat-
ment (Schneemann et al., 2004). However, in a small study of patients envenomed
by
Echis carinatus
(Indian saw-scaled viper), Paul et al. (2007) reported that bleed-
ing and hypotension were reduced in patients receiving low molecular weight hep-
arin (LMWH). AKI was observed more commonly in the test subjects than in the
controls, and mortality was less in the test group. However, none of the differences
were found to be statistically significant, and these investigators called for a larger
trial in order to confirm their results (Paul et al., 2007). The authors opined that the
