Biology Reference
In-Depth Information
antivenom were provided 86 h postenvenoming. Reversal was dramatic and immediate.
The patient showed almost full clinical recovery 30 h after antivenom administration (Du
Toit, 1980; see also sections 4.1.1.6 and 4.13).
As demonstrated by these representative cases, although additional therapies
directed at correction of anemia and afibrinogenemia have been used (see later and
Table 4.1
), antivenom is the only evidence-based effective treatment for life-threat-
ening
D. typus
envenoming. Clearly, delayed presentation (even up to approximately
5 days postenvenoming) is not a contraindication to administering this antivenom,
if available, provided that there is persisting evidence of systemic envenomation
(WHO AFRO, 2010). Availability is a significant issue, but delay to provision of
antivenom should not influence any effort to procure at least two ampoules for use in
serious cases.
Table 4.3
outlines a recommended approach to administering antive-
nom for treatment of
D. typus
envenoming.
Reactions to SAVP (SAIMR) Anti-
D. typus
Antivenom
Authors of several case studies of
D. typus
envenoming treated with monospecific anti-
venom have raised concerns regarding reportedly frequent hypersensitivity reactions,
including anaphylaxis associated with this antivenom (Du Toit, 1980). A limited ret-
rospective review reported that treatment for anaphylaxis was required in three out of
five patients who received anti-
D. typus
antivenom (Du Toit, 1980). However, like all
antivenoms, SAVP equine F(ab
)
2
monospecific boomslang antivenom has occasion-
ally caused early anaphylactic reactions, but the danger of these reactions must not be
exaggerated. Although they may, on rare occasions, be life threatening, there have been
very few reported deaths and even the most severe reactions are eminently controlla-
ble by the early use of i.m. epinephrine. The terminology and perceived mechanism of
early antivenom reactions have been plagued by confusing and incorrect terminology,
made worse by a consensus review of definitions of allergic phenomena (Johansson
et al., 2004). The use of terms, such as “allergic,” “sensitization,” or “hypersensitiza-
tion,” implying that early anaphylactic reactions to antivenoms were the result of prior
sensitization to animal serum proteins ignored abundant published evidence of lack of
specific IgE as a basis for these reactions. According to the classic Gell and Coombs
(1963) classification, Type I immediate hypersensitivity reactions are IgE-mediated.
However, skin tests, the most sensitive means of detecting specific IgE hypersensitiza-
tion, are negative in the vast majority of patients who suffer early antivenom reactions
(Cupo et al., 1991; Malasit et al., 1986), hence the futility of skin (or conjunctival)
testing with antivenom before therapeutic use as these tests have no predictive value.
Early antivenom reactions usually consist of pruritus and/or urticaria, but in about
10% of cases more severe features of anaphylaxis develop. They were formerly des-
ignated “anaphylactoid” reactions to distinguish them from cross-linked IgE-mediated
anaphylaxis, but nomenclatural revisions now include them in the term “anaphylactic
reactions” (Johansson et al., 2004). Reactions to any particular antivenom are dose
dependent (Reid, 1980) in a positively monotonic fashion, like reactions to macromol-
ecules and
N
-acetylcysteine that occur in patients not previously exposed and lacking
detectable specific IgE. Comparison of the low reactogenicity of single vial treatment
with antivenom that is sufficient for most cases of envenoming by scorpions, spiders,
