Page 13 - Journal of Special Operations Medicine - Winter 2014

(iv) smooth muscle contraction in the lungs (bronchi) Glucocorticoid Steroids
and gut. There is no evidence to support the routine use of ste-
roids. There are similarities with asthma (where there
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is clear evidence of benefit from steroid treatment), and
Clinical Presentation
it has been proposed that they have a role in attempting
The individual mediators cause specific physiological ef- to shorten the duration of symptoms and reduce the in-
fects, which, in turn, cause the signs and symptoms of cidence and severity of the biphasic response sometimes
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anaphylaxis that we see clinically. Table 1 summarizes seen in anaphylaxis. There is no evidence to suggest
these clinical features. that steroids do either. We also do not know if there are
any long-term effects on allergic reactivity from steroids
Anaphylaxis is unique in how it produces the pattern of given around the time of antigen exposure.
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poor perfusion and shock seen clinically. Anaphylaxis has
been (and still is, in most teaching material) classified as
distributive shock; however, it probably encompasses vary- Field Management
ing degrees of the four main types of shock mechanisms: The focus on the treatment of anaphylaxis in a field en-
vironment must be the placement of the patient in a su-
• Cardiogenic – from a direct myocardial depressive ef- pine position, the administration of epinephrine, and, if
fect from the mediators required, IV fluid resuscitation.
• Hypovolemic – from the loss of circulating volume
into the tissues due to leaky blood vessels General Measures
• Distributive – from the vasodilation of vessels result- It has been demonstrated that rapid changes in posture
ing in pooling of the circulating volume may precipitate cardiac arrest, and those who remain in
• Obstructive – from vasoconstriction of the pulmo- a sitting position once they have lost consciousness are
nary arteries at greater risk of cardiac arrest. A relative bradycardia
is also seen in some patients following venom-mediated
Bradycardia may occur suddenly as a reflex response to anaphylaxis associated with the onset of hypotension;
poor venous return to the heart and a dramatic reduc- although the exact mechanism is not known, this may
tion in ventricular filling. There may be a reflex com- in part explain the positional cardiac arrest that is some-
4,9
ponent to this, perhaps accentuated by anaphylactic times seen. Therefore, all patients displaying evidence
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mediators. The degree to which one factor contributes of anaphylaxis should be laid supine early as a basic first
to the shock pattern seen varies depending on the aller- aid measure and should not be propped in a sitting or
gen and the route of exposure. semi-reclined position.
Epinephrine and IV Fluids
Management
Although there is no high-level evidence for the efficacy
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The evidence on which management is based is extremely of epinephrine, pathophysiological considerations,
sparse, consisting of anecdotes, some observational animal studies, large case series, and a prospective
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studies, animal studies, pathophysiological principles, epinephrine infusion study, in which reaction features
and expert opinion. The cornerstones of recommended stopped with epinephrine and returned when the infu-
3
management are epinephrine and, in presence of shock, sion was halted, provide support for its likely usefulness.
intravenous (IV) fluid therapy.
The quickest and often effective route of initial admin-
Antihistamines istration for epinephrine is via IM administration. Ab-
There is no evidence to support the routine use of anti- sorption via this route has been shown to be superior
histamines in anaphylaxis. There have been no random- to subcutaneous administration. In most patients, a
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ized or good observational human studies supporting single dose is all that is required; however, in about 30%
10
the use of H1 or H2 receptor blocking drugs. There of severe reactions, repeated doses can be required. 5
is also animal evidence of harm. 11,12 H1 antihistamines,
when administered parenterally, have also been associ- A small number of patients will not respond to IM admin-
ated with hypotension. 13 istration—this may be due to poor circulation and hence
poor absorption from muscle beds, or a need for higher
The administration of oral H1 antihistamines has a role systemic concentrations to reverse the cardiovascular
in the treatment of symptomatic itch associated with effects of anaphylaxis. This is not infrequently seen in
urticarial rashes seen in hypersensitivity reactions (of both hospital and pre-hospital practice and has been
which anaphylaxis is a subgroup) but none as a front- demonstrated in an animal model of severe anaphylaxis
line treatment agent. with cardiovascular collapse. This response has been
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Anaphylaxis in an Austere or Operational Environment 3