Biology Reference
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of any medical importance. Assakura et al. (1992) reported that hemorrhagic activity of
Duvernoy's gland secretion from
P. olfersii
was neutralized by commercial horse anti-
venoms against
Bothrops
spp., as well as by rabbit antisera specific for hemorrhagic
factors isolated from several
Bothrops
venoms. Notably, no immunoprecipitation was
detected, and this suggested that there were few shared epitopes with
P. olfersii
hemor-
rhagin. In addition, Kamiguti et al. (2000) described a 65-kDa protein from
D. typus
venom that cross-reacted with polyclonal antibody raised against a class P-III snake
venom metalloprotease with hemorrhagic activity from
B. jararaca
venom.
Despite these reports describing antigenic cross-reactivity and limited
in vitro
neutralization of hemorrhagins, there is no current clinical basis for treating any non-
front-fanged colubroid bite with polyvalent antivenoms.
4.6.2.8 Replacement Therapy
Blood Transfusions and PRBCs
As described in detail in Section 4.3, DIC and hemorrhagic diathesis are character-
istic of the clinical effects that occur after hazard level 1 colubrid envenomation.
Prior to the development of antivenom against
D. typus
and
R. tigrinus
, the primary
treatment for envenomation by these species was replacement therapy. This strat-
egy has continued for those species for which there is no antivenom. Due to the
lack of commercial antivenom, treatment of
Thelotornis
spp. envenoming is man-
aged with replacement therapy only, while
R. subminiatus
envenoming has to date
been managed with replacement therapy because antivenom was not available. Anti-
Rhabdophis tigrinus
antivenom now affords a potentially effective cornerstone of
treatment for
R. subminiatus
envenoming.
There is an inherent dilemma in managing consumptive coagulopathic enven-
omation with factor replacement in the absence of antivenom. Some of the venom
toxins that cause coagulation factor consumption, particularly the direct or indirect
consumption of fibrinogen, may have an extended half life. Therefore, as long as
these toxins remain in the circulation, infusion of blood products (including FFP,
cryoprecipitate, and whole blood) that contain toxin-targeted clotting factors pro-
vides more substrate for the toxins, producing ever higher levels of degradation prod-
ucts and the risk of fibrin clot deposition in the microvasculature. Fibrin degradation
products are generally cleared by the kidneys, so that increasing the load may theo-
retically further imperil the increasingly stressed kidneys (see later for a proposed
outlined model of venom coagulopathy-induced renal pathophysiology). Treatment
with clotting factors might therefore increase the severity of the pathophysiology of
coagulopathic envenomation. On the other hand, failure to restore minimal levels of
clotting factors increases the risk of severe or fatal hemorrhage. Similarly, if there is
persisting hemolysis, infusing further RBC (either as whole blood or PRBCs) will
potentially add more substrate for the pathologic process, leading to an increasing
load of hemoglobin and other products of hemolysis that may damage the kidneys.
Yet failure to replace critically depleted RBC carries a clear and lethal risk.
23
The
23
Rapidly developing anemia may cause hypoxia, and in those with preexisting comorbidities (e.g., isch-
emic heart disease, congestive heart failure) this can result in life-threatening decompensation.
