Biology Reference
In-Depth Information
provided that antivenom had been administered. Further confirmation of these find-
ings is essential.
Therefore, the role of FFP and cryoprecipitate in the treatment of coagulopathic
envenoming remains unclear. Although current data suggest similar mechanisms of
coagulopathy induced by elapid, viperid, and hazard level 1 colubrid snakes, there
is insufficient evidence regarding the utility and safety of FFP/cryoprecipitate ther-
apy in serious coagulopathic envenomations. Thus, caution should be exercised as
prodigious volumes of plasma products may comprise replacement therapy in these
cases. For example, during an admission for severe
R. subminiatus
venom-induced
consumptive coagulopathy/DIC, a patient was given 2 units of PRBCs, 59 units of
FFP, and 76 bags of cryoprecipitate (Seow et al., 2000).
In sepsis-related DIC (see Appendix C), replacement therapy is rarely helpful and
seems likely to aggravate microvascular thrombosis (Marino, 2009). The primary goal
of management is to treat the specific cause of the DIC. This is crucial as advanced
cases of DIC may exhibit a mortality rate exceeding 80% (DeLoughery, 2005; Marino,
2009). It is important to note that some investigators are questioning whether snake
venom-induced coagulopathic effects and DIC are truly comparable. Isbister (2010)
has suggested that as the coagulopathy overlaps with thrombotic microangiopathy, the
combined effects are mistakenly interpreted as DIC. Although this definition remains
to be fully settled, optimal management for envenomation-related DIC as currently
defined is provision of specific antivenom if available. In cases of severe bleeding,
replacement treatments may have a role at the discretion of the attending physician as
determined by individual patient characteristics and the clinical course of the venom
disease. The role of FFP/cryoprecipitate in less severe cases requires further study in
order to evaluate its effectiveness as well as potential risks (e.g., perpetuation of micro-
thrombi formation) associated with this therapy.
Platelets
Thrombocytopenia is a common feature of coagulopathic envenomation (Warrell,
2004; White, 2005; White and Dart, 2008) including from hazard level 1 colubrids
(
Table 4.1
). In a review of several
D. typus
envenomations, Du Toit (1980) remarked
that although thrombocytopenia was not ubiquitous in these cases, it could be severe.
Four vials of anti-
D. typus
antivenom did not have any effect on the development
of venom-induced thrombocytopenia in a patient with consumptive coagulopa-
thy from a
D. typus
envenomation. It took 1 week for platelet counts to be restored
from 10,000/cu. mm to 300,000/cu. mm (Lakier et al., 1969). Atkinson et al. (1980)
reported that platelet levels returned to “near-normal values” over a 7-day period
following a
T. capensis
envenoming in a pediatric patient treated with only limited
replacement therapy. In a case of
T. c. oatesii
envenoming, thrombocytopenia devel-
oped over 4-5 days followed by a gradual rise in platelets from 6 days postenven-
oming (Muguti and Dube, 1998). The patient was treated with PRBCs, platelets,
vitamin K, and hydrocortisone (Muguti and Dube, 1998).
It is possible that hazard level 1 colubrid envenomations may cause MAHA
(see pg. 243). This may contribute to the profound and prolonged thrombocytope-
nia as well as the anemia that occurs in some envenomations by these species. The
