Page 12 - Journal of Special Operations Medicine - Winter 2014
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Table 1  National Institute of Allergy and Infectious Disease/  cardiac arrest and can be triggered by inappropriately
          Food Allergy and Anaphylaxis Network (NIAID/FAAN)   placing the patient in an upright or semi-upright (sit-
          Consensus Clinical Definition of Anaphylaxis 1     ting) position. 4

           Anaphylaxis is highly likely when any one of the following
           three criteria are fulfilled:
                                                             Causes
           1. Acute onset of an illness (minutes to several hours)
             with involvement of the skin, mucosal tissue, or both   Overall, the causes of anaphylaxis are roughly equally
             (e.g., generalized hives, pruritus or flushing, swollen   distributed among drugs, stinging insect (hymenoptera)
             lips-tongue-uvula), AND AT LEAST ONE OF THE     venoms,  foods,  and  unidentified  causes,  although  the
             FOLLOWING:                                      relative proportions vary between geographical areas
             a.  Respiratory compromise (e.g., dyspnea, wheeze-  and populations. In urban settings, severe reactions in
               bronchospasm, stridor, reduced peak expiratory    adults are usually due to drugs.  In rural and outdoor
                                                                                         5
               flow, hypoxemia);
             b.  Reduced blood pressure (BP) or associated symptoms   settings, severe reactions are predominantly due to hy-
               of end-organ dysfunction (e.g.,  hypotonia [collapse],   menoptera stings (venoms), as well as other insect bites
               syncope, incontinence).                       (e.g., March or “horse” flies), leech bites, snakebites,
           2. Two or more of the following that occur rapidly after   and marine venoms (e.g., jellyfish stings). Exercise may
             exposure to a likely allergen for that patient (minutes    be a cofactor in some cases, leading to “summative ana-
             to several hours):                              phylaxis,” in which a stimulus (usually a physical one
             a.  Involvement of the skin-mucosal tissue (e.g.,    such as exertion, but heat, cold, and alcohol have been
               generalized hives, itch-flush, swollen lips-tongue-uvula);  suggested)  appears  to  increase  the  sensitivity  of  mast
             b.  Respiratory compromise (e.g., dyspnea, wheeze-  cells to an IgE-mediated trigger in susceptible people.
               bronchospasm, stridor, reduced PEF, hypoxemia);  The main form of summative anaphylaxis is food-
             c.  Reduced BP or associated symptoms (e.g., hypotonia
               [collapse], syncope, incontinence);           dependent, exercise-induced anaphylaxis, where the
             d.  Persistent gastrointestinal symptoms (e.g., crampy   combination of exercise plus ingestion of the food (usu-
               abdominal pain, vomiting).                    ally within 2 hours but sometimes as long as 5 hours)
           3. Reduced BP after exposure to known allergen for that   leads  to  sudden  anaphylaxis  with  cardiovascular  col-
             patient (minutes to several hours):             lapse during or soon after exercise. The food, despite
             a.  Infants and children: low systolic BP (age specific) or   presence of specific IgE antibodies, is normally tolerated
                                                                                    6
               greater than 30% decrease in systolic BP;     in the absence of exercise.  As well as exercise being a
             b  Adults: systolic BP of less than 90mmHg or greater   potential cofactor in triggering some reactions, reduced
               than 30% decrease from that person’s baseline  physiological reserve and lactic acidosis from strenuous
                                                             exercise may significantly reduce physiological reserve
          It is important to note that skin features may be ab-
          sent in about 20% of cases.  Therefore, if an otherwise   and thus increase the severity of any reaction and make
                                  2
          young and healthy patient presents with sudden cardio-  it resistant to treatment.
          vascular collapse or severe bronchospasm, initial treat-
          ment for anaphylaxis is warranted even if the typical   Biochemical Mediators
          skin features are absent. A simple pragmatic approach   Allergen exposure results in activation of local mast
          to diagnosis that clinicians can use to trigger the admin-  cells. These respond with degranulation and release of
          istration of epinephrine is as follows:            preformed and newly synthesized mediators. More gen-
                                                             eralized mediator release by other inflammatory cells
                                                             and possibly also mast cells in areas remote from the al-
            Any acute onset illness with typical skin features   lergen exposure then may occur, although the amplifica-
            (urticarial rash or erythema/flushing, and/or angio­  tion mechanism for this process is poorly understood.  5,7
            edema), PLUS involvement of respiratory and/or
            cardiovascular systems and/or persistent severe   Historically, we have focused on histamine as the main
            gastrointestinal symptoms.                       mediator involved in anaphylaxis. We now know that
                                 OR                          a wider spectrum of mediators are involved, including
            Any acute onset of hypotension or bronchospasm   histamine, mast cell tryptase, tumor necrosis factor, a
            or upper airway obstruction where anaphylaxis is   number of interleukins (ILs) (especially IL-6, IL-10, and
            considered possible, even if typical skin features are   tumor necrosis factor receptor inhibitor), leukotrienes,
            not present.                                     and complement breakdown products.  Therefore, any
                                                                                               8
                                                             attempt at specific mediator antagonism is likely to be fu-
          It is also important to note that bradycardia typically   tile, and treatment relies on more general “ physiological
                                                3
          accompanies hypotension in awake patients,  not tachy-    antagonism” with epinephrine and fluids to address:
          cardia as seen in this case. Indeed, a sudden fall in heart   (i) dilation of blood vessels; (ii) extravasation of fluid
          rate after an initial tachycardia may herald impending   into the tissues; (iii) impaired cardiac   function; and



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