Page 1806 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 128: Anaphylactic and Anaphylactoid Reactions 1275

DIFFERENTIAL DIAGNOSIS organs dysfunction. The absence of cutaneous features may help distin-
guish these forms of shock from the majority of episodes of anaphylaxis.
The differential diagnosis of anaphylaxis is summarized in Table 128-6. There are a number of miscellaneous conditions that can present with
A common condition frequently confused with anaphylaxis is the vasode- signs that may mimic anaphylactic episodes. These include hereditary
pressor reaction (vasovagal syncope), which presents with hypotension, angioedema, “progesterone” anaphylaxis, pheochromocytoma, neuro-
pallor, nausea, vomiting, weakness, and sweating. In severe reactions, loss logic disorders such as seizure and stroke, the “red man syndrome” due
of consciousness can occur. The characteristic bradycardia associated with to vancomycin, and the capillary leak syndrome. For example, some
vasodepressor reactions could be used as a differential diagnostic feature patients with hereditary angioedema exhibit an erythematous, ser-
to distinguish them from anaphylaxis. However, for reasons noted above, piginous rash, which can resemble urticaria. This rash accompanied by
it may be insufficient alone to distinguish vasodepressor reactions from upper airway obstruction can be confused with an anaphylactic episode.
anaphylactic events. Thus, perhaps the most important distinguishing The capillary leak syndrome can present with angioedema, gastrointesti-
features between the two types of events are pale skin and cold sweat in nal symptoms, shock, and hemoconcentration. Recurrent episodes have
vasovagal reactions versus urticaria, flushing, and itching in anaphylaxis. mimicked idiopathic anaphylaxis.
Other forms of shock including hypovolemic, cardiogenic and septic Nonorganic problems, which are “psychologically” based, have also
have to be considered in the differential diagnosis of anaphylaxis, espe- been confused with episodes of anaphylaxis. These include panic
cially in the ICU setting. Some of these other forms of shock may have attacks, vocal cord dysfunction syndrome, Munchausen stridor, and
similar hemodynamic abnormalities, pulmonary edema, and a variety of undifferentiated somatoform anaphylaxis. Panic attacks, except for
flushing and sweating, are usually devoid of cutaneous manifestations,
but can be characterized by tachycardia, gastrointestinal symptoms, and
TABLE 128-6 Differential Diagnosis of Anaphylaxis shortness of breath. There is no pruritus or true airway obstruction, and
Other forms of shock the absence of urticaria and angioedema is usually a telltale sign.
Since flushing occurs relatively frequently in anaphylactic episodes,
Hemorrhagic
other flushing syndromes should be considered. These include carcinoid
Hypoglycemic syndrome; postmenopausal flush; alcohol, drug, and niacin-induced
Cardiogenic flush; and vasoactive polypeptide secreting tumors. Flushing can occur in
Endotoxic both a “wet” and a “dry” form. The wet form is characterized by sweating
mediated by sympathetic cholinergic nerves that innervate sweat glands in
Vasodepressor (vasovagal) reactions the skin. This is the case of postmenopausal flushing which typically lasts
Reactions caused by the excess endogenous production of histamine 3 to 5 minutes, occurs several times a day, and can be aggravated by stress
Systemic mastocytosis and alcohol ingestion. Wet flushing can also occur after the ingestion of
spicy foods containing capsaicin. Direct vasodilatation without stimula-
Urticaria pigmentosa
tion of the sweat glands produces a dry flush as is seen in the carcinoid
Basophilic leukemia syndrome. Other forms of dry flush include those due to niacin, nicotine,
Acute promyelocytic leukemia with retinoic acid treatment catecholamines, and angiotensin-converting enzyme inhibitors. A dry
Hydatid cyst flush can also be seen in vasoactive polypeptide secreting tumors from the
pancreas, gastrointestinal tract, and thyroid gland (medullary carcinoma).
Flushing disorders Flushing can also occur due to pheochromocytoma, rosacea, hypogly-
Rosacea cemia, and niacin ingestion. Flush is also characteristic of mastocytosis.
Alcohol-induced flush is particularly common. It causes a macular
Carcinoid rash more frequently distributed across the trunk, neck, and face, occur-
Red man syndrome as a result of vancomycin ring minutes after the ingestion of alcohol. Symptoms usually peak 30
Postmenopausal to 40 minutes after ingestion, and usually subside within 2 hours. There
Alcohol induced are two forms. One form occurs when alcohol is taken simultaneously
with certain drugs and in patients with certain illnesses. Such drugs
Unrelated to drug ingestion include griseofulvin, cephalosporins, and niacin. Conditions predispos-
Related to drug ingestion ing to alcohol-induced flush include lymphoreticular neoplasms, the
Medullary carcinoma thyroid hypereosinophilic syndrome, and mastocytosis. The second form of
alcohol-induced flush is due to a deficiency in acetaldehyde dehydroge-
Autonomic epilepsy nase-2. This enzyme metabolizes acetaldehyde, a metabolite of alcohol.
Vasointestinal peptide and other vasoactive peptide–secreting In patients with a deficiency of this enzyme, there is accumulation of
gastrointestinal tumors acetaldehyde which results in mast cell degranulation.
A group of “restaurant syndromes” can cause symptoms similar to
Ingestant-related reactions mimicking anaphylaxis (restaurant syndromes)
mastocytosis. Perhaps the most common and similar to anaphylaxis is
Monosodium glutamate histamine poisoning. This condition, referred to as scombroidosis,
Sulfites is produced by the ingestion of histamine contained in spoiled fish.
Scombroidosis Histamine is the major chemical involved in this syndrome but other
chemicals are also involved. The most likely is cis-urocanic acid, an
Miscellaneous imidazole compound similar to histamine. Cis-urocanic acid can also
C1 esterase deficiency syndromes (acquired and hereditary angioedema) cause mast cell degranulation, thus perhaps to some extent augmenting
the response. Histamine in spoiled fish is produced by histidine-decar-
Pheochromocytoma boxylating bacteria that cleave histamine from histidine. This histamine
Neurologic (seizure, stroke) production occurs shortly after the death of the fish and therefore can
Capillary leak syndrome occur on the fishing vessel, at the processing plant, in the distribution
Panic attacks system, or in the restaurant or home. Such contaminated fish cannot
be distinguished by their appearance or smell, and cooking does not
Vocal cord dysfunction syndrome destroy the histamine.

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