Biology Reference
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However, the risk/benefit profile for use of these agents in coagulopathic envenoming is
unestablished. Therefore, no evidence-based assessment of these possible therapies for
use in hazard level 1 colubrid envenoming is currently feasible.
4.6.2.11 Plasmapheresis/Exchange Transfusion
Exchange transfusion or plasmapheresis was used to treat several cases of severe
envenoming by
R. tigrinus
(
Table 4.1
). Mori et al. (1983) reported recovery of
“hemostatic function” after exchange transfusion of a pediatric patient with
R. tig-
rinus
venom-induced consumptive coagulopathy/DIC. The authors indicated that
the procedure was used due to lack of antivenom availability. Despite this treatment,
the patient had chronic renal failure for several months (Mori et al., 1983). Another
case of severe
R. tigrinus
envenoming was treated with exchange transfusion due to
unavailability of antivenom (Ogawa and Sawai, 1986). The comatose patient report-
edly exhibited improved coagulation parameters, but the procedure did not alter the
fatal outcome (Ogawa and Sawai, 1986).
Envenomation by
D. typus
,
R. tigrinus
, or
R. subminiatus
should be treated with
antivenom, as noted above. Consumptive coagulopathy from envenomation by spe-
cies without available antivenom (e.g.,
Thelotornis
sp.) should be treated with sup-
portive measures such as conservative replacement therapy as clinically indicated.
There is no clear clinical benefit from exchange transfusion/plasmapheresis in these
cases. This has been similarly noted in management of some consumptive coagulo-
pathic envenomations from Australian elapids (e.g.,
Pseudonaja
spp.; Isbister et al.,
2007).
4.6.2.12 Diuretics and Dialysis: The Causes and Management of Acute
Kidney Injury (AKI) after Bites of Hazard Level 1 Colubrid Species
Venom-induced consumptive coagulopathy/DIC often cause acute and chronic (and,
occasionally, acute on chronic) renal failure and thus are frequent sequelae after enven-
omation by hazard level 1 colubrid snakes (
Table 4.1
; Section 4.3). The AKI observed
in these cases is primarily due to prerenal effects of hypovolemia and shock (hypo-
tension) as well as intrarenal effects (tubulointerstitial disease) due to hemoglobinuric
nephropathy/acute tubular necrosis (
Table 4.1
; Section 4.3 and later). Direct toxin-
induced nephropathy is a possible additional etiology.
Figure 4.4
illustrates some of the
causes of AKI caused by hazard level 1 colubrid envenomations.
Some cases of hazard level 1 colubrid envenomation feature AKI that is poorly
responsive or nonresponsive to diuretics and dialysis (
Table 4.1
; Section 4.3). In
the case reported by Lakier et al. (1969), a patient with
D. typus
venom-induced
consumptive coagulopathy/DIC developed renal failure 4-5 days postevenom-
ing. Hemodialysis was performed four times over a 2-week period (Lakier et al.,
1969). This patient exhibited the triad characteristic of hemolytic-uremic syndrome
(HUS): ARF, thrombocytopenia, and hemolytic anemia with altered erythrocyte
morphology (schistocytes) (Date et al., 1986). However, as noted in Section 4.3,
encompassing these effects under the specific term, HUS, may be misleading. Renal
