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• W2015216165 abstract "A 77-year-old woman presented with a 2-h history of tongue swelling, throat tightness postprandially (1–5). She had recently been prescribed perindopril for hypertension. No previous history of allergies was elicited. Medical history included hypertension, hypercholesterolaemia and chronic obstructive airways disease. Medications included atorvastatin 10 mg daily, theophylline 225 mg daily and fluticasone/salmeterol 500 mcg bid. On examination, blood pressure was 195/98 mmHg, with normal respiratory rate. Diffuse bilateral wheeze and swollen tongue were noted. Neither rash nor stridor was present. Admission ECG and chest X-ray were normal. The clinical impression was of angio-oedema secondary to the angiotensin-converting enzyme inhibitor. Intramuscular (i.m.) adrenaline 0.5 mg (one in 1000 strength 1 mg/1 ml), i.v. hydrocortisone 100 mg and chlorpheniramine 8 mg were administered. Four hours later, she developed chest pain with new ischaemic ECG changes with anterior lead deep T-wave inversion with a corresponding raised troponin t of 0.218 (NR 0.000–0.050 ng/ml) denoting myocardial damage. Coronary angiography revealed tortuous but normal coronary arteries. Recovery postinfarction was uneventful. An 81-year-old woman presented with a 5-h history of tongue and throat swelling with accompanying dysphagia. She reported her dentures ‘getting tight’ in her mouth. This was her third presentation with identical symptoms in the previous 3 months. She was allergic to morphine. Medical history included ischaemic heart disease, hypertension and hypercholesterolaemia. Medications included aspirin 75 mg, atenolol 100 mg, bendroflumethazide 2.5 mg, atorvastatin 20 mg and omeprazole 20 mg daily. On examination, she was hypertensive (204/96 mmHg) with normal respiratory rate (16/minute) and O2 saturation at room air. Adrenaline 0.5 mg i.m. (one in 1000 strength 1 mg/1 ml), hydrocortisone 100 mg intravenously, oral chlorpheniramine 4 mg were administered. After 1 h, she developed chest tightness at rest with sinus tachycardia (106/min). ECG revealed rate-related ischaemia in the lateral leads. Troponin t increased from normal on admission to 0.473 ng/ml (NR 0.000–0.050 ng/ml). Coronary angiogram revealed three vessel disease (80% stenoses of left anterior descending, left circumflex and complete occlusion of the right coronary artery) requiring percutaneous coronary stenting. At follow-up she remained asymptomatic. Acute systemic anaphylaxis results from mast cell degranulation, with released mediators manifesting clinically as bronchoconstriction, hypotension, angio-oedema and urticaria. Adenaline via α and β adrenoceptors reverses the immediate symptoms of anaphylaxis. α stimulation increases peripheral resistance thereby improving blood pressure and coronary perfusion and reduces peripheral vasodilation and angio-oedema. β1 stimulation causes positive inotropic and chronotropic cardiac effects. β2 stimulation induces bronchodilation and inhibits further mediator release (6). Therefore, adrenaline is the cornerstone in managing of true systemic anaphylaxis. Its role, if any, in mild-to-moderate allergic reactions is less clear. Generalised (or localised) angio-oedema and urticaria without airway involvement, in accordance with current guidelines, would not warrant adrenaline treatment by any route (1,2). Therefore, the decision to administer adrenaline is dependent on an accurate clinical risk/benefit analysis. Our two cases highlight the dangers of inappropriate adrenaline administration for mild anaphylaxis or angio-oedema without cardiac or respiratory compromise. Case 1, without known ischaemic heart disease, developed chest pain after adrenaline treatment. Whilst coronary angiography was normal and non-specific troponin i rises were widely reported (7,8), the troponin rise, in the clinical context, is highly suggestive of myocardial damage. In case 2, with prior ischaemic heart disease, the combined ECG changes and corresponding troponin rise are more conclusive of further myocardial damage. Presenting symptoms in both cases developed over a few hours – any possibility of a biphasic reaction is prevented by chlorpheniramine stat and maintenance. An audit performed by Gompels et al. (9) shows the confusion associated with treating lesser allergic reactions without evidence of cardiac or respiratory compromise. We urge caution in using any adrenaline in elderly patients in the absence of severe anaphylactic features. In mild-to-moderate anaphylaxis, any potential adrenaline benefit must be balanced against the potential risks of coexistent cardiac disease (known or unknown) in this age group with limited ability to recover from an acute cardiac insult. Risks far outweighed any potential benefit of adrenaline in the cases outlined. Treatment with steroids and chlorpheniramine would have sufficed in both cases. When administering adrenaline in elderly patients, follow the rule ‘start low and go slow’. Elderly patients have limited cardiac reserve and adrenaline may contribute to both ischaemia and frank myocardial infarction. Where there is no clinical evidence of cardiac or respiratory compromise, adrenaline is not necessary." @default.
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• W2015216165 date "2009-09-01" @default.
• W2015216165 modified "2023-09-23" @default.
• W2015216165 title "Adrenaline-induced cardiac ischaemia: treating anaphylaxis in two elderly patients" @default.
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• W2015216165 doi "https://doi.org/10.1111/j.1742-1241.2009.02039.x" @default.
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