Anaphylactic Reaction To Diphtheria–Tetanus Vaccine
Transkript
Anaphylactic Reaction To Diphtheria–Tetanus Vaccine
The New Journal of Medicine 2008;25: 186-188 Case report Anaphylactic Reaction To Diphtheria–Tetanus Vaccine in A Young Woman Behçet AL ¹, Cuma YILDIRIM 1 ¹ Gaziantep University Faculty of Medicine, Department of Emergency Medicine, GAZİANTEP ABSTRACT Anaphylaxis is a severe systemic hypersensitivity reaction characterized by multisystem involvement, which may include hypotension or airway compromise, it is potentially life-threatening. The present study describes the occurrence of an anaphylactic reaction after the administration of dT (diphtheria-tetanus) vaccine in a twenty-four-years old woman. As it is rarely reported in literatures we treated this anaphylactic reaction with corticosteroid, and antihistamine without using epinephrine. Key Words: Anaphylaxis, bronchospasm, corticosteroid, diphtheria toxoid, tetanus toxoid INTRODUCTION Adverse reactions to vaccines are common and those of an immunological nature, such as anaphylaxis and Arthus type reactions, are of more concern. But data are infrequently reported. The mechanisms proposed are the production of specific IgE antibodies to any of the vaccine components and the formation of immune complexes between IgG antibodies and the vaccine antigens1,2. IgE mediated anaphylactic and local reactions have been observed after immunisation with tetanus (Ttx) and diphtheria toxoids (Dtx) notwithstanding these are showing a very low frequency in the whole population3-6. Since vaccines are composed of several constituents, the identification of the responsible allergens or haptens requires a detailed analysis of all the vaccine components. Components and contaminants of toxoid vaccines, such as gelatine or peptones and preservatives such as thimerosal, have been reported as causal agents in these type of reactions7-9. The present report describes the occurrence of an anaphylactic reaction immediately after a dT booster dose in a woman. CASE A twenty-four year-old woman suffered a severe adverse reaction after the second intra-muscular dose of a dT vaccine that performed to the right deltoid muscle. Ten minutes after administration, the patient developed a large local inflammatory response at the injection site, followed by a 186 generalized systemic reaction with erythema, pruritus, urticaria, palpebral edema, discomfort and nausea. About 45 minutes after administration, she had shortness of breath. We took this information from a witness who was a health official and lived in patient’s village. Before administration of vaccine she was in good health, she did not suffer from any medical condition at that time and she did not received any concomitant medication. The patient did not suffer from the first dose of dT vaccine that performed by the same health team. Two hours after the advers reaction she was brought to our emergency department (ED). At admission time she had anxiety, tremor, minimal cyanosis on lips, shortness of breath, a sense of fullness in the throat, a sensation of chest tightness, respiratory distress, lightheadedness, and decreased level of consciousness. The clinical signs of systemic allergic reactions included cutaneous flushing, diffuse urticaria, angioedema, colicy pain in abdomen, nausea, vomiting, bronchospasm, wheezing, rhinorrhea, conjunctivitis and hypotension. Blood pressure was 90/55 mmHg, pulse 124/min, respiratory rate 17/min, temperature 37ºC and SO2 was 90%. Complete blood count was normal limits. In our management we started with the ABC (airway, breathing, circulation) of resuscitation. Vital signs, intravenous access, oxygen, cardiac monitoring, and pulse oximetry measurements were continuosly monitored. Methylprednisolone 125 mg IV, antihistamine-2 (H2) blockers 100 mg (ranitidine) IV, oxygen 4 L/min with mask, 30 B. Al and C. Yıldırım ml/kg/h 0.9 g NaCL, bronchodilator (continuous nebulized salbutamol sulfate) 5 mg was applied immediatelty. The systemic reaction improved 20–30 min after treatment with corticosteroid and anti-histamines, but the palpebral and local oedema subsided three days later. The patient was observed for 12 hours in ED. All of the symptoms were improved except palpebral and local oedema. Hydroxyzine HCL 25 mg/day (PO) and a short course of methtylprednisolon 32 mg/day (PO) were ordered to prevent the frequency of relapses in patients. A discharge plan was provided for patient that reduce the chance of recurrence and reduce the frequency and severity of future episodes and how to avoid future exposure to the causative agent, if possible. The patient was evaluated ten days after the episode again, no any signs of allergic reactions were found. DISCUSSION Anaphylaxis is the most severe life-threatening form of a systemic allergic reaction10,11. The basic mechanism underlying allergic reactions is mast cell and basophil degranulation and mediator release. The causes of cell degranulation include IgE cross-linking, complement activation, nonimmunologic or direct activation, modulation of arachidonic acid metabolism, exercise or temperature-dependent effects, and idiopathic causes2. Although anaphylactic reactions are extremely rare cases have been reported in individuals immunized with toxoids12. Most of these cases provide just a clinical description and in only a few was the presence of IgE antibodies studied3.4.7.12. The prevalence of anaphylaxis ranges from as high as 5 per 1000 to as low as 2 per 10,000 ED visits13,14. The prevalence of less-severe allergic reactions in the emergency department is much higher, but data are infrequently reported. In the vast majority of patients, signs and symptoms begin within 60 min of exposure. In general, the faster the onset of symptoms, the more severe the reaction, as evidenced by the fact that onehalf of anaphylactic fatalities occur within the first hour. Currently, the most common causes of serious anaphylaxis are drugs (Beta-Lactam antibiotics, Acetylsalicylic acid, Trimethoprim-sulfamethoxazole, Vancomycin, Nonsteroidal anti-inflammatory drugs, virtually any drug antibiotics), foods and addıtıves (Shellfish, Soybeans, Nuts, Wheat, Milk, Eggs, Salicylates, Seeds, Sulfites), and others (Hymenoptera stings insect, parts and molds, radiographic contrast, material Latex)10,15. The clinical signs of systemic allergic reactions include diffuse urticaria and angioedema. As we found in our case; at times these major symptoms are accompanied by any of the following: colic pain in abdomen, nausea, vomiting, diarrhea, bronchospasm, rhinorrhea, conjunctivitis, dysrhythmias, and/or hypotension. The diagnosis of anaphylaxis is made by history and physical examination. The differential diagnosis of anaphylactic reactions is extensive including vasovagal reactions, myocardial ischemia, arrhythmias, status asthmaticus, seizure, epiglottitis, hereditary angioedema, foreignbody airway obstruction, mastocytosis, vocal cord dysfunction, and non-IgE-mediated drug reactions10. It is designated in reports that epinephrine is the cornerstone of treatment for anaphylactic reactions; however, research suggests that epinephrine in anaphylaxis is underused10,14,16. The present report describes the occurrence of an anaphylaxis in a twenty-four year-old woman after the simultaneous administration of the second booster dose of dT vaccine. The symptoms developed within 10 minutes after administration and deteriorated rapidly. As it is designated in Kemp et al. study10, the second-line anaphylaxis treatments are corticosteroids and antihistamines. In our study we began with corticosteroid and antihistamine-2 blocker directly. We were hesitant to give intravenous epinephrine because of the patient’s tachycardia (124/min) and tremor. The shock was not refractory to this treatment, and the systemic reaction improved within 30 min after the treatment applied. Our patient needed only a single dose of corticosteroid and antihistamine for treatment. Treatment in the outpatient setting should include antihistamines and a short course of corticosteroids, although the evidence for this is weak17. Our study demonstrates that, although epinephrine is the first drug for treatment of anaphylaxis, corticosteroids can be useful and can treat anaphylaxis with antihistamines. The treatment of an anaphylaxis may not finish at ED; emergency physicians should provide discharge plans for patients that reduce the chance of recurrence and reduce the frequency and severity of future episodes. A brief limitations section: It was not possible to do a detailed study to establish the causal agent or agents in our hospital. (I saw this case in Batman State Hospital seven months ago. At that time I worked there). Although, we treated our 187 B. Al and C. Yıldırım case with corticosteroid and antihistamine; we don’t propose this treatment for anaphylaxis at first. Epinephrine is the first preference; corticosteroid and antihistamine are alternative treatment. REFERENCES 1. Relyveld EH, Bizzini B and Gupta RK. Rational approaches to reduce adverse reactions in man to vaccines containing tetanus and diphtheria toxoids. Vaccine 1998;16: 1016–23. 2. Ewan PW: ABC of allergies. 5MJ 1998;316: 1442. 3. Brindle MJ, Twyman DG. Allergic reactions to tetanus toxoids. A report of four cases. Br Med J 1962;1: 1116–7. 4. Sisk CW and Lewis CE. Reactions to tetanus–diphtheria toxoid. Arch Environ Health 1965;11: 34–36. 5. Zaloga GP and Chernow B. Life-threatening anaphylactic reaction to tetanus toxoid. Ann Allergy 1982;49: 107–108. 6. Mark AB, Björksten M. 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Correspondence: Behçet AL, M.D. Gaziantep University Faculty of Medicine Gaziantep e-mail:behcetal@hotmail.com Received : 30.06.2008 Acceptance date : 29.07.2008