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PubMed2005

Anaphylaxis in adults referred to a clinical immunology/allergy centre in Singapore.

INTRODUCTION: To study the clinical features and causes of anaphylaxis in consecutive adult patients referred to a clinical immunology/allergy centre in Singapore. METHODS: A retrospective review of 67 consecutive adults with anaphylaxis who presented from July 1, 1998 to February 28, 2002 was performed. Anaphylaxis was defined as a severe life-threatening systemic IgE-mediated hypersensitivity reaction. Non-steroidal anti-inflammatory drug-induced idiosyncratic reactions and other non-IgE mediated reactions were excluded. Hypotension and bronchospasm were not required to make a diagnosis. The aetiology was determined from clinical history followed by measurement of allergen-specific IgE levels, skin prick test with commercially-available allergen extracts or prick-prick test with the fresh/cooked/canned food products. RESULTS: The mean age of patients was 32.9 +/- 10.9 (range 19-57) years. There were 44 (65.7 percent) males and 23 (34.3 percent) females. The main causes were food (44.8 percent), insect stings (32.8 percent) and idiopathic (22.4 percent). There were no cases due to drugs or natural rubber latex. Seafood (crustaceans and molluscs) comprised 66.7 percent of food-induced anaphylaxis. Honeybee and wasp stings together comprised 45 percent of insect venom anaphylaxis. The most common manifestations were dyspnoea (59.7 percent), urticaria (58.2 percent), angioedema (44.8 percent), and syncope (43.3 percent). Hypotension was documented in only 28.4 percent of cases. CONCLUSION: Food (crustaceans and molluscs) was the most common cause followed by insect stings or bites. The inability to identify the causative insect in 50 percent of cases with insect venom anaphylaxis limited the role of specific immunotherapy. Compared to other reported series, there were no cases of drug or latex anaphylaxis.

Adult↗
PubMed1985

Decreased incidence and mortality of anaphylaxis to chymopapain.

A recognized side effect of chemonucleolysis is life-threatening anaphylaxis to chymopapain. In the clinical trials of chymopapain, 13 cases of anaphylaxis were reported in 1585 administrations (0.82%). Two patients died. Data from a postmarketing survey (48,239 questionnaires) were reviewed to identify factors influencing the incidence and severity of anaphylaxis. The results indicate the incidence of anaphylaxis decreased to 0.44% in the 1983-1984 period (126/23,736), a level significantly (P less than or equal to 0.001) below the incidence of 0.82% observed in initial clinical trials. Only three deaths from complications related to anaphylaxis occurred in approximately 75,000 administrations (producing 252 anaphylactic episodes) reported since December 1982. The prophylactic use of antihistamines and pretreatment with intravenous fluids coincide with the dramatic reduction in mortality due to anaphylaxis. However, overdiagnosis of anaphylaxis in the clinical trials and avoidance of chemonucleolysis in patients with IgE antibodies to chymopapain may account, in part, for the reduction in incidence.

Adult↗
PubMed1993

Mast cells contribute to the changes in heart rate, but not hypotension or death, associated with active anaphylaxis in mice.

The mast cell is widely thought to contribute importantly to the cardiopulmonary changes associated with anaphylaxis, but much of the evidence for this is indirect. We, therefore, performed a detailed assessment of heart rate and pulmonary function during active anaphylaxis in genetically mast cell-deficient W/Wv or S1/S1d mice, the congenic normal (+/+) mice, and W/Wv mice repaired of their mast cell deficiency by transplantation of bone marrow from the congenic +/+ mice (+/+ BM-->W/Wv mice). For all five groups of mice, Ag challenge resulted in the death of more than two-thirds of the sensitized animals, whereas none of the nonsensitized control mice died as a result of Ag infusion. Sensitized normal (WBB6F1(-)+/+ or WCB6F1(-)+/+) mice and +/+BM-->W/Wv mice developed increases in heart rate that were significantly greater than those of nonsensitized +/+ mice or those of sensitized mast cell-deficient mice, indicating that mast cells contribute to the tachycardia observed in this form of active anaphylaxis. By contrast, even though some of the pulmonary changes associated with active anaphylaxis were more severe in +/+ than in mast cell-deficient mice, it was not clear to what extent this difference was mast cell dependent. W/Wv mice undergoing active anaphylaxis developed decreases in systemic arterial blood pressure that occurred more rapidly and were more severe than those observed in the congenic +/+ mice, indicating that the hypotension associated with this model of anaphylaxis also can occur by mast cell-independent mechanisms. We conclude that in this model of anaphylaxis mast cells: 1) are required for the development of the tachycardia response; 2) may contribute to, but are not essential for, production of decreases in lung function; and 3) are not necessary for the development of hypotension or death.

Age Factors↗
PubMed1998

An epidemiologic study of severe anaphylactic and anaphylactoid reactions among hospital patients: methods and overall risks. The International Collaborative Study of Severe Anaphylaxis.

To quantify the risk of severe anaphylaxis due to drugs and other exposures in hospital patients, a study of incident cases has been in progress since 1992, with data collection in Hungary, Spain, India, and Sweden. All cases of anaphylaxis that develop after admission to participating hospitals are enrolled. To confirm the diagnosis, clinical information for potential cases is reviewed by two physicians without knowledge of exposures, according to an algorithm developed for the study. Confirmed cases are classified as definite, probable, or possible anaphylaxis. As of March 1995, 123 cases were enrolled in Budapest, Barcelona, and Bombay/Pune (the study began in January 1996 in Sweden): 99 were classified as definite or probable anaphylaxis, and 24 as possible. Two of the 123 cases were fatal (2%). Based on teh definite and probable cases and a denominator of 481,752 individuals in the nine participating institutions for which the age and sex distribution was known, we estimated the overall risk of severe anaphylaxis to be 154 per million hospital admissions; when the possible cases were included, the risk was 196 per million. The risk was higher among women, and it varied, although not linearly, according to age. A major problem in the epidemiologic evaluation of anaphylaxis has been resolved in the present study with the development of a case definition that, contrary to usual clinical practice, is independent of exposure. The results thus far indicate that severe anaphylaxis occurs infrequently among hospitalized patients and is rarely fatal.

Adolescent↗
PubMed1996

Anaphylaxis and Anaphylactoid Reactions: Diagnosis and Management.

Anaphylaxis is an acute fatal or potentially fatal hypersensitivity reaction. Anaphylaxis represent a clinical diagnosis based on history and physical examination and includes symptoms of airway obstruction, generalized skin reactions, particularly flushing, itching, urticaria, angioedema cardiovascular symptoms including hypotension and gastrointestinal symptoms. These symptoms result from the action of mast cell mediators, especially histamine and lipid mediators such as leukotrienes and platelet activating factor on shock tissue. The shock tissue includes blood vessels, mucous glands, smooth muscle, and nerve endings. Anaphylaxis follows the typical immediate hypersensitivity time course, with a reaction beginning within minutes of antigen exposure. A late-phase reaction hours after the initial reaction may occur. Mast cell mediator release can be triggered by both IgE and non--IgE-mediated factors. Therefore, anaphylaxis may be termed anaphylaxis (IgE mediated) or anaphylactoid (non--IgE mediated). The most common IgE-mediated triggers are drugs, typically penicillin or other beta-lactam antibiotics, foods, most commonly nuts, peanuts, fish and shellfish, or hymenoptera stings. Non-IgE-mediated causes include factors causing marked complement activation such as plasma proteins or compounds which act directly on the mast cell membrane, such as vancomycin, quinolone antibiotics, or radiographic contrast media. The pathophysiology of some trigger factors, such as aspirin, remains unclear. Therapy of anaphylaxis revolves around patient education, avoidance, desensitization or pharmacologic pretreatment when agents causing anaphylaxis need to be readministered, and early recognition and prompt therapy of reactions should they occur.

Journal Article↗
PubMed1999

Action of Sosiho-Tang on systemic and local anaphylaxis by anal administration.

The herbal formulation Soshiho-Tang (SS-Tang) has been used against allergic disease for generations, and still occupies an important place in traditional medicine in Korea. Previously, we reported that SS-Tang potently inhibited mast cell- mediated anaphylaxis when orally administered. In this study, we investigated the effect of SS-Tang by anal administration in anaphylaxis responses. SS-Tang dose-dependently inhibited compound 48/80-induced systemic anaphylaxis with doses of 10(-4) to 1 g/kg 1 h before anally administered. Of special note, SS-Tang inhibited systemic anaphylaxis completely with a dose of 1 g/kg. SS-Tang reduced plasma histamine levels induced by compound 48/80 significantly. However, the mortality was 100% when SS-Tang was administered after compound 48/80 treatment. SS-Tang (10(-1) g/kg) also inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl IgE antibody by 30.9%. These results provide evidence that anal therapy of SS-Tang may be beneficial in the treatment of systemic and local anaphylaxis.

Administration, Rectal↗
PubMed1995

Idiopathic anaphylaxis. An attempt to estimate the incidence in the United States.

BACKGROUND: Idiopathic anaphylaxis has been described and classified, and increasing numbers of cases are being seen in the United States and abroad. Treatment regimens have been shown to be effective in prophylactic management. There is no available information about the number of cases in the United States. METHODS: We attempted to determine the number of cases of idiopathic anaphylaxis in the United States by mailing a questionnaire to all graduates (for the last 31 years) of the Northwestern University Allergy-Immunology Fellowship training program. RESULTS: Response to the questionnaire was 100%, and 633 cases were reported by this survey of 75 allergists. The current total number of identified cases of idiopathic anaphylaxis from all reports of cases in the United States is 1020. CONCLUSIONS: By extrapolation of the cases of idiopathic anaphylaxis reported by the allergists surveyed to the approximately 4000 allergists in the United States, the estimated number of cases in the United States is between 20,592 and 47,024. Idiopathic anaphylaxis is potentially fatal, represents a source of major medical health care costs, causes anxiety to patients and families, occurs in pediatric and adult populations, and is controlled by appropriate regimens. The estimated number of cases emphasizes the need for careful attention to idiopathic anaphylaxis by physicians.

Anaphylaxis↗
PubMed1991

Glafenine-associated anaphylaxis as a cause of hospital admission in The Netherlands.

In 1981 generalized anaphylaxis was registered on 166 occasions in Dutch general and academic hospitals. Clinical details of 120 of those patients revealed that in 107 anaphylaxis was either probable (n = 90) or possible (n = 17), whereas in 13 cases some other reaction than anaphylaxis had occurred. The series of confirmed cases contained 46 men and 61 women, with mean ages of 47 y and 48 y, respectively. There was a complete recovery in 102 patients and two patients died. Hypotension was present in 79 cases (74%), dyspnoea in 34 cases (32%) and a skin reaction, mainly urticaria, erythema or angioedema, was mentioned in 62 cases (58%). Most cases of anaphylaxis were drug-induced (76%), the main causes being the analgesic glafenine and contrast media. Glafenine was mentioned as the cause in 36% of all admissions for drug-induced anaphylaxis. Only 3.7% of cases had been reported to the voluntary reporting scheme of the Netherlands Centre for Monitoring of Adverse Reactions to Drugs. On the basis of reimbursement data, the risk of developing severe anaphylaxis to glafenine was estimated at 11.7-19.3-fold relative to indomethacin, and 13.4-20.2-fold relative to oral penicillins.

Adolescent↗
PubMed1984

Mouse paw anaphylaxis.

Anaphylactic swelling passively transferred to the hind paws of mice with homologous antibodies was investigated. The ascites fluid containing homocytotropic antibodies of the IgG1 class in a high concentration was obtained by repeated injections of bovine serum albumin in complete Freund's adjuvant into the peritoneal cavity of female ICR mice. The standard procedure for mouse paw anaphylaxis defined was as follows: female ICR mice received subcutaneously 25 microliters of a 1:20 diluted ascites in the hind footpad and 2 h later were given intravenously 1.0 mg of the antigen in saline, and subsequently at 5 min intervals paw thickness was assessed by means of a simple thickness gauge. Maximal paw edema occurred invariably 15 min after antigen challenge. Sex difference in response was not observed. Heating at 56 degrees C for 4 h resulted in a reduction of the activity of mouse ascites by approximately 40%. Histological examinations revealed that paw anaphylaxis was accompanied by mast cell degranulation and release of biologically active constituents from mast cell granules. Promethazine, pyrilamine, diphenhydramine, methysergide, cyproheptadine, ketotifen and phenoxybenzamine provided significant protection from the anaphylactic reaction in mice, while bromocriptine, dexamethasone and indomethacin were inactive. Relative drug effectiveness in paw anaphylaxis, passive cutaneous anaphylaxis and active and passive systemic anaphylaxis in mice was compared and discussed. Consequently, it was shown that mouse paw anaphylaxis was not only convenient for quantitative assessment of homocytotropic antibodies, but also useful in the routine work for screening of potential anti-allergic drugs.

Animals↗
PubMed1985

Effect of anaphylaxis on conjunctival goblet cells.

Rats undergoing ocular anaphylaxis induced by systemic or local injection of antigen, topical application of antigen, or topical application of compound 48/80 were evaluated conjunctival goblet cell changes that might be related to anaphylaxis. The number of goblet cells in 1 micron, alkaline Giemsa-stained sections averaged 500/mm2 of epithelium in normal rats; this number was not significantly changed in any of the experimental groups. Goblet cells in control rats occasionally demonstrated evacuation of their contents (less than 1%) or upward displacement of the intracellular bolus of mucus (about 1%); these percentages were not increased in anaphylaxis. Topical application of 2.0 micrograms of histamine induced an intracellular displacement of mucus in both control animals and animals undergoing anaphylaxis. These findings suggest that in ocular anaphylaxis the amount of histamine released may be insufficient to produce such intracellular changes. Our results indicate that in ocular anaphylaxis in the rat, there is no light microscopic evidence of increased mucus discharge from conjunctival goblet cells. Increased mucus in secretions of patients with ocular allergic syndromes may not be attributable to anaphylactic mechanisms alone.

Administration, Topical↗
PubMed1986

Food skin testing in patients with idiopathic anaphylaxis.

Avoidance is the key treatment of anaphylaxis if an allergen exists; thus, we have evaluated 102 patients with the initial diagnosis of idiopathic anaphylaxis with a battery of 79 food-antigen skin prick tests selected to include foods reported or suspected of provoking anaphylaxis. Only those patients whose episodes consisted of at least two of the following were included in the study: angioedema with or without hives, laryngeal edema leading to severe dyspnea, hypotension, or loss of consciousness. Detailed history, physical examination, and conventional laboratory tests ruled out known causes of anaphylaxis. Thirty-two patients (31%) had positive tests to one or more food antigens. In five of these patients, subsequently eating a food that elicited a positive test provoked an anaphylactic reaction. Two patients eliminated the foods completely, stopped having reactions, and refused challenge. In these seven patients, 10 different antigens provoked anaphylaxis: aniseed, cashew nut, celery, flaxseed, hops, mustard, mushroom, shrimp, sunflower, and walnut. We conclude that a battery of selected food-antigen skin prick tests provided a useful method for identifying an offending antigen in these patients and that some (7% in our series) cases of "idiopathic" anaphylaxis by history are not truly idiopathic.

Adolescent↗
PubMed1992

The effect of three novel thromboxane A2 receptor antagonists (S-1452, AA-2414 and ONO-3708) on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs.

The effects were studied of three novel thromboxane A2 (TXA2) receptor antagonists (S-1452, AA-2414 and ONO-3708) on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs. Three TXA2 antagonists at doses of between 1 and 10 mg/kg administered orally 1 h before the challenge clearly inhibited the pulmonary pressure increase. At a dose of 10 mg/kg, all three antagonists inhibited the pulmonary pressure increase caused by leukotriene D4 (LTD4) and U-46619, but not that caused by histamine. The decrease in peripheral platelet counts caused by Forssman anaphylaxis was also clearly inhibited by the three TXA2 antagonists. However, the decreased peripheral leukocyte counts were unaffected by the three agents. The decrease in serum complement activity (CH50) was inhibited by S-1452 and AA-2414 at a dose of 10 mg/kg. In bronchoalveolar lavage fluid (BALF), significant increases in eosinophils and neutrophils were observed after Forssman anaphylaxis. Three TXA2 antagonists at a dose of 10 mg/kg (except for AA-2414 on eosinophils) did not affect the changes of leukocyte counts in BALF. Moreover, increases in the TXB2 and 6-keto-PGF1 alpha levels of the BALF brought about by Forssman anaphylaxis were unaffected by the three TXA2 receptor antagonists. Histamine and LTD4 were not changed in the BALF after Forssman anaphylaxis. These results indicate the efficacy of TXA2 receptor antagonists on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs by direct antagonism to released TXA2.

6-Ketoprostaglandin F1 alpha↗
PubMed2004

The effects of fexofenadine on eosinophilia and systemic anaphylaxis in mice infected with Trichinella spiralis.

BACKGROUND: The effects of the non-impairing, H(1)-receptor antagonist fexofenadine were investigated in in vivo mouse models of eosinophilia and systemic anaphylaxis. METHODS: Eosinophilia was investigated in C57BL/6 mice (n=5 per group) infected with Trichinella spiralis, with and without administration of fexofenadine HCl (5, 10 and 20 mg/kg/day). Eosinophilia was also studied, with and without fexofenadine administration, in mice with a congenital mast-cell deficiency (W/W(v)) and controls (+/+). The effect of fexofenadine HCl (20 mg/kg/day) on IL-5 and eotaxin blood levels was also investigated in C57BL/6 mice. In a separate model, systemic anaphylaxis was induced in C57BL/6 mice using T. spiralis antigen. Fexofenadine HCl (5, 10 and 20 mg/kg) or vehicle was administered 20 min before antigen challenge (n=5 per group). The effect of fexofenadine on systemic anaphylaxis caused by IgE and anti-IgE was also examined in CBF1 mice injected with serum from NC/Nga mice with high IgE levels. Rectal temperature was measured as an indicator of anaphylaxis. RESULTS: In C57BL/6 mice, repetitive oral administration of fexofenadine HCl (5, 10 and 20 mg/kg/day) resulted in dose-dependent suppression of eosinophilia (p<0.05-0.0001). No suppression was observed in mast-cell deficient W/W(v) mice. In addition, single oral administration of fexofenadine HCl (10 and 20 mg/kg) significantly suppressed the decrease in rectal temperature (p<0.01), a marker for systemic anaphylaxis, in C57BL/6 mice. In CBF1 mice injected with serum from NC/Nga mice with high IgE levels, the decrease in rectal temperature was suppressed by single administration of fexofenadine HCl (10 and 20 mg/kg; p<0.01 and p<0.001, respectively). Fexofenadine had no effect on peripheral IL-5 and eotaxin levels. CONCLUSION: These results indicate that fexofenadine suppresses both eosinophilia and systemic anaphylaxis, both of which are fundamental reactions in allergic diseases.

Anaphylaxis↗
PubMed1999

Participation of histamine H1 and H2 receptors in passive cutaneous anaphylaxis-induced scratching behavior in ICR mice.

Scratching behavior associated with passive cutaneous anaphylaxis was examined and compared to that induced by compound 48/80 or histamine in ICR mice. Elicitation of passive cutaneous anaphylaxis, and intradermal injections of compound 48/80, histamine or serotonin induced both scratching behavior and vascular permeability increase in ICR mice. In mast cell-deficient WBB6F1-W/Wv mice, although histamine induced scratching behavior and vascular permeability increase, passive cutaneous anaphylaxis was not observed. Cetirizine and terfenadine significantly inhibited the scratching behavior and vascular permeability increase caused by passive cutaneous anaphylaxis, compound 48/80 and histamine. The histamine H1 receptor antagonists inhibited the vascular permeability increase almost completely, whereas they failed to abolish the scratching behavior. Famotidine and ranitidine significantly inhibited the scratching behavior caused by histamine. The histamine H2 receptor antagonists did not affect the vascular permeability increase caused by histamine. The combination of cetirizine and ranitidine abolished the histamine-induced scratching behavior. The combination, however, failed to potentiate the inhibition of passive cutaneous anaphylaxis-induced scratching behavior significantly. The results indicated that histamine induces scratching behavior in ICR mice through both histamine H1 and H2 receptors, and that histamine plays a major role in passive cutaneous anaphylaxis-induced scratching behavior. Histamine might also play an important role in compound 48/80-induced scratching behavior.

Animals↗
PubMed2000

Minimum estimated incidence in Japan of anaphylaxis to live virus vaccines including gelatin.

We have previously found that most occurrences of anaphylaxis to live virus vaccines are caused by gelatin present in the vaccines as a stabilizer. After we published the evidence for the role of gelatin in anaphylaxis, vaccine manufacturers in Japan began to eliminate gelatin from live virus vaccines. In the present study, we tried to estimate its incidence before the gelatin elimination was started. Physicians and vaccine manufacturers submitted serum samples from children with anaphylaxis to measles, mumps, rubella or varicella vaccine to National Institute of Infectious Diseases (NIID) for 3 years from April 1994 to March 1997. Specific IgE to gelatin was assayed at NIID or two manufacturers by the CAP and ELISA methods. There were 44 children with life-threatening severe anaphylaxis (airway obstruction or anaphylactic shock) during the 3-year period, 41 of whom had anti-gelatin IgE. There were 64 children with mild anaphylaxis (without airway obstruction); 62 had anti-gelatin IgE. There were 100 children with only systemic cutaneous signs; 81 had anti-gelatin IgE. The estimates for the incidence of the severe anaphylaxis in 1994-1996 are: 6.84, 7.31, 4. 36, and 10.3 cases per million doses of gelatin-containing measles, rubella, mumps, and varicella vaccines, respectively.

Anaphylaxis↗
PubMed2006

Management of anaphylaxis in child care centers: evaluation 6 and 12 months after an intervention program.

BACKGROUND: Many young children with a history of allergic reactions or anaphylaxis spend considerable time in child care centers. We previously reported that a significant knowledge deficit exists in anaphylaxis recognition, evaluation, and treatment and that greater anaphylaxis education is needed among child care providers. OBJECTIVE: To determine whether child care centers can recognize, evaluate, and treat anaphylactic episodes in children aged 1 to 6 years 6 months and 1 year after attending an allergy seminar. METHODS: All 39 child care centers participating in the original study were selected to complete 6-month and 1-year follow-up surveys using a similar questionnaire. Those who did not attend the seminar or complete all the previous surveys were excluded. RESULTS: At 6 months and 1 year, 37 and 29 centers, respectively, completed surveys. There was a significant improvement regarding when to administer intramuscular epinephrine compared with before the allergy seminar. However, only 48% of the centers at 6 months (P = .02) and 31% at 1 year (P = .002) knew how to correctly administer intramuscular epinephrine compared with 77% four weeks after the seminar. With time, there was a significant decline in correctly recognizing typical anaphylaxis symptoms, including abdominal cramping, chest tightness, shortness of breath, low blood pressure, and diarrhea, whereas symptoms such as hives, swelling, and wheezing continued to be identified correctly. CONCLUSIONS: There is a need for renewed anaphylaxis education among child care providers. Initially, this intervention significantly increased the ability of child care center staff to recognize, evaluate, and treat anaphylaxis, but knowledge diminished gradually at 6-month and 1-year follow-up.

Anaphylaxis↗
PubMed2005

Recognition, evaluation, and treatment of anaphylaxis in the child care setting.

BACKGROUND: Anaphylaxis can occur anywhere. Many young children with a history of allergic reactions or anaphylaxis spend considerable time in child care centers. However, little is known about the centers' knowledge of, experience with, and capability to manage anaphylaxis. OBJECTIVE: To evaluate the ability of child care centers to recognize, evaluate, and treat anaphylactic episodes in children aged 1 to 6 years. METHODS: Eighty-five child care centers in the suburbs of Chicago were randomly selected. They were contacted by telephone and asked to participate in a study by completing an initial questionnaire. Center directors and teachers were then offered an allergy seminar addressing anaphylaxis avoidance, recognition, evaluation, and treatment. Center directors completed a questionnaire after the seminar. RESULTS: Forty-four of the 85 centers contacted agreed to participate. Forty-two surveys were completed before the seminar and 39 after the seminar. On average, each center has up to 7 children with an identifiable food allergy. Information provided by the parents was the most commonly reported source of education concerning allergies. Before seminar completion, only 24% of child care centers would administer intramuscular epinephrine for a severe allergic reaction. After the seminar, 77% of centers stated that they would administer intramuscular epinephrine (P < .001). Also, center staff significantly improved their knowledge of typical allergy symptoms and of the correct method of intramuscular epinephrine administration. CONCLUSIONS: There is a need for greater anaphylaxis education among child care providers. Our intervention significantly increased the ability of child care staff to recognize, evaluate, and treat anaphylaxis.

Anaphylaxis↗
PubMed2004

Anaphylaxis during surgical and interventional procedures.

OBJECTIVE: To describe the current evidence-based knowledge of the causes, diagnostic evaluation, and treatment of patients with anaphylaxis associated with surgical and interventional procedures. DATA SOURCES: Articles published between 1966 and 2003 were identified in MEDLINE using the keywords anaphylactoid, anaphylaxis, anesthetics, antibiotics, cephalosporins, contrast media, colloids, flow cytometry, hypersensitivity, latex, neuromuscular depolarizing agents, neuromuscular nondepolarizing agents, penicillins, radioallergosorbent test, skin test, and vancomycin. Additional studies were identified from article reference lists. STUDY SELECTION: Relevant, peer-reviewed original research articles and reviews. RESULTS: Neuromuscular blocking agents, natural rubber latex, antibiotics, and induction agents are the most common causes of anaphylaxis during surgical and interventional procedures. Colloids, opioids, and radiocontrast media probably account for less than 10% of all reactions. Newer agents implicated in anaphylaxis include isosulphan blue and chlorhexidine. Skin tests are useful for evaluating allergic reactions to anesthetic agents and penicillins and for selecting alternative agents. Skin testing and specific IgE measurements for latex vary in allergen standardization and sensitivity and specificity, respectively. Flow cytometric allergen stimulation tests show promise in differentiating allergic from idiosyncratic ("pseudoallergic") reactions. Drug desensitization has been shown to be useful for penicillin anaphylaxis. Premedication with histamine receptor antagonists and corticosteroids helps prevent or attenuate radiocontrast media reactions. CONCLUSIONS: Anaphylaxis during surgical and interventional procedures may be difficult to evaluate because of the rapid, successive use of multiple drugs or diagnostic agents. Careful analysis of anesthetic records and diagnostic tests for all the putative agents are necessary to ensure a complete evaluation.

Anaphylaxis↗