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4/9/2014

Anaphylaxis Clinical Presentation

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Anaphylaxis Clinical Presentation


Author: S Shahzad Mustafa, MD; Chief Editor: Michael A Kaliner, MD more... Updated: Mar 20, 2014

History
Anaphylaxis is an acute multiorgan system reaction. The most common organ systems involved include the cutaneous, respiratory, cardiovascular, and gastrointestinal (GI) systems. In most studies, the frequency of signs and symptoms of anaphylaxis is grouped by organ system. Anaphylactic reactions almost always involve the skin or mucous membranes. Greater than 90% of patients have some combination of urticaria, erythema, pruritus, or angioedema. In the Memphis study, for example, 87% of patients had urticaria and/or angioedema.[30] Other retrospective studies have reported similar rates of mucocutaneous involvement. Children, however, may be different. An Australian study evaluated 57 children under age 16 years who presented to a pediatric emergency department (ED) over a three-year period. Cutaneous features were noted in 82.5%, whereas 95% had respiratory symptoms. The reasons why a lack of dermal findings would be more common in children than in adults are not well understood. The upper respiratory tract commonly is involved, with complaints of nasal congestion, sneezing, or coryza. Cough, hoarseness, or a sensation of tightness in the throat may presage significant airway obstruction. Eyes may itch and tearing may be noted. Conjunctival injection may occur. Dyspnea is present when patients have bronchospasm or upper airway edema. Hypoxia and hypotension may cause weakness, dizziness, or syncope. Chest pain may occur due to bronchospasm or myocardial ischemia A ds by Keep N ow A d O ptions (secondary to hypotension and hypoxia). GI symptoms of cramplike abdominal pain with nausea, vomiting, or diarrhea also occur but are less common, except in the case of food allergy. The Memphis study reported dyspnea in 59%, syncope or lightheadedness in 33%, and diarrhea or abdominal cramps in 29%.[30] Other studies have reported similar findings. Initially, patients often describe a sense of impending doom, accompanied by pruritus and flushing. This can evolve rapidly into the following symptoms, broken down by organ system: Cutaneous/ocular - Flushing, urticaria, angioedema, cutaneous and/or conjunctival pruritus, warmth, and swelling Respiratory - Nasal congestion, rhinorrhea, throat tightness, wheezing, shortness of breath, cough, hoarseness Cardiovascular - Dizziness, weakness, syncope, chest pain, palpitations Gastrointestinal - Dysphagia, nausea, vomiting, diarrhea, bloating, cramps Neurologic - Headache, dizziness, blurred vision, and seizure (very rare and often associated with hypotension) Other - Metallic taste, feeling of impending doom Symptoms usually begin within 5-30 minutes from the time the culprit antigen is injected but can occur within seconds. If the antigen is ingested, symptoms usually occur within minutes to 2 hours. In rare cases, symptoms
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Anaphylaxis Clinical Presentation

can be delayed in onset for several hours. Parenteral administration of monoclonal antibodies and oral ingestion of mammalian meat (eg, beef, pork, lamb) have recently been reported to be potential causes for anaphylaxis characterized by delayed onset.[53, 54, 55, 56, 57] It must be remembered that anaphylaxis can begin with relatively minor cutaneous symptoms and rapidly progress to life-threatening respiratory or cardiovascular manifestations. In general, the more rapidly anaphylaxis develops after exposure to an offending stimulus, the more likely the reaction is to be severe. A thorough history remains the best test to determine a causative agent. For recurrent idiopathic episodes, a patient diary may be helpful to implicate specific foods or medications, including over-the-counter (OTC) products.

Physical Examination
The first priority in the physical examination should be to assess the patients airway, breathing, circulation, and adequacy of mentation (eg, alertness, orientation, coherence of thought). General appearance and vital signs vary according to the severity of the anaphylactic episode and the organ system(s) affected. Vital signs may be normal or significantly disordered with tachypnea, tachycardia, and/or hypotension. Patients commonly are restless due to severe pruritus from urticaria. Anxiety, tremor, and a sensation of cold may result from compensatory endogenous catecholamine release. Anxiety is common unless hypotension or hypoxia causes obtundation. Frank cardiovascular collapse or respiratory arrest may occur in severe cases.

Respiratory findings
Severe angioedema of the tongue and lips (as may occur with the use of angiotensin-converting enzyme [ACE] inhibitors) may obstruct airflow. Laryngeal edema may manifest as stridor or severe air hunger. Loss of voice, hoarseness, and/or dysphonia may occur. Bronchospasm, airway edema, and mucus hypersecretion may manifest as wheezing. In the surgical setting, increased pressure of ventilation can be the only manifestation of bronchospasm. Complete airway obstruction is the most common cause of death in anaphylaxis.

Cardiovascular findings
Tachycardia is present in one fourth of patients, usually as a compensatory response to reduced intravascular volume or to stress from compensatory catecholamine release. Bradycardia, in contrast, is more suggestive of a vasodepressor (vasovagal) reaction. Although tachycardia is the rule, bradycardia has also been observed in anaphylaxis (see Pathophysiology). Thus, bradycardia may not be as useful for distinguishing anaphylaxis from a vasodepressor reaction as was previously thought. Relative bradycardia (initial tachycardia followed by diminished heart rate despite worsening hypotension) has been reported previously in experimental settings of insect sting anaphylaxis, as well as in trauma patients.[7, 8, 58, 59,
60]

Hypotension (and resultant loss of consciousness) may be observed secondary to capillary leak, vasodilation, and hypoxic myocardial depression. Cardiovascular collapse and shock can occur immediately, without any other findings. This is an especially important consideration in the surgical setting. Because shock may develop without prominent skin manifestations or history of exposure, anaphylaxis is part of the differential diagnosis for patients who present with shock and no obvious cause.

Cognitive findings
If hypoperfusion or hypoxia occurs, it can cause altered mentation. The patient may exhibit a depressed level of consciousness or may be agitated and/or combative.

Cutaneous findings
The classic skin manifestation is urticaria (ie, hives). Urticaria can occur anywhere on the body, often localizing to the superficial dermal layers of the palms, soles, and inner thighs. Lesions are red and raised, and they sometimes have central blanching. Intense pruritus occurs with the lesions. Lesion borders are usually irregular and sizes vary markedly. Only a few small or large lesions may become confluent, forming giant urticaria. At times, the entire dermis is involved with diffuse erythema and edema.
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In a local reaction, lesions occur near the site of a cutaneous exposure (eg, insect bite). The involved area is erythematous, edematous, and pruritic. If only a local skin reaction (as opposed to generalized urticaria) is present, systemic manifestations (eg, respiratory distress) are less likely. Local reactions, even if severe, are not predictive of systemic anaphylaxis on reexposure. Angioedema (soft-tissue swelling) is also commonly observed. These lesions involve the deeper dermal layers of skin. It is usually nonpruritic and nonpitting. Common areas of involvement are the larynx, lips, eyelids, hands, feet, and genitalia. Generalized (whole-body) erythema (or flushing) without urticaria or angioedema is also occasionally observed. Cutaneous findings may be delayed or absent in rapidly progressive anaphylaxis.

Gastrointestinal findings
Vomiting, diarrhea, and abdominal distension are frequently observed.

Complications
Complications from anaphylaxis are rare, and most patients completely recover. Myocardial ischemia may result from hypotension and hypoxia, particularly when underlying coronary artery disease exists. Ischemia or arrhythmias may result from treatment with pressors. Prolonged hypoxia also may cause brain injury. At times, a fall or other injury may occur when anaphylaxis leads to syncope. Respiratory failure from severe bronchospasm or laryngeal edema can cause hypoxia, which could lead to brain injury if prolonged.

Contributor Information and Disclosures


Author S Shahzad Mustafa, MD Physician in Allergy, Immunology, and Rheumatology, Rochester General Medical Group; Clinical Assistant Professor of Medicine, University of Rochester School of Medicine and Dentistry S Shahzad Mustafa, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology and Finger Lakes Allergy Society, Inc Disclosure: Nothing to disclose. Chief Editor Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Chief, Section of Allergy and Immunology, Washington Hospital Center; Medical Director, Institute for Asthma and Allergy Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, and Association of American Physicians Disclosure: Teva Honoraria Speaking and teaching; Meda Honoraria Speaking and teaching; genentech Honoraria Speaking and teaching; sunovian Consulting fee Consulting Additional Contributors Roy Alson, MD, PhD, FACEP, FAAEM Associate Professor, Department of Emergency Medicine, Wake Forest University School of Medicine; Medical Director, Forsyth County EMS; Deputy Medical Advisor, North Carolina Office of EMS; Associate Medical Director, North Carolina Baptist AirCare Roy Alson, MD, PhD, FACEP, FAAEM is a member of the following medical societies: Air Medical Physician Association, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, North Carolina Medical Society, Society for Academic Emergency Medicine, and World Association for Disaster and Emergency Medicine Disclosure: Nothing to disclose.
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Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and Immunology Practice, University of Colorado Health Sciences Center Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American Association of Immunologists, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, and Joint Council of Allergy, Asthma and Immunology Disclosure: Genentech Consulting fee Consulting; American Health Insurance Plans Consulting fee Consulting; Johns Hopkins School of Public Health Consulting fee Consulting; Array BioPharma Consulting fee Consulting Stephen F Kemp, MD, FACP Professor of Medicine, Associate Professor of Pediatrics, Director of Allergy and Immunology Fellowship Program, Departments of Medicine and Pediatrics, Associate Director of Division of Clinical Immunology and Allergy, Department of Medicine, University of Mississippi Medical Center; Staff Physician and Consultant in Allergy and Immunology, Medical Service, G V (Sonny) Montgomery Veterans Affairs Medical Center Stephen F Kemp, MD, FACP is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Physicians, Association of Subspecialty Professors, Joint Council of Allergy, Asthma and Immunology, Mississippi State Medical Association, and Southern Society for Clinical Investigation Disclosure: Nothing to disclose. Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. G William Palmer, MD Consulting Staff, Shoreline Allergy and Asthma Associates G William Palmer, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology Disclosure: Nothing to disclose. Matthew M Rice, MD, JD, FACEP Senior Vice President, Chief Medical Officer, Northwest Emergency Physicians of TeamHealth; Assistant Clinical Professor of Medicine, University of Washington School of Medicine Matthew M Rice, MD, JD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Washington State Medical Association Disclosure: Team Health Salary Employment Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment

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