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Benazepril/epinephrine Angioedema and lack of efficacy: case report

A 57-year-old man developed angioedema during treatment with benazepril for hypertension. He also exhibited a lack of efficacy during treatment with epinephrine for angioedema [not all routes stated; dosages not stated]. The man, who had a history of type II diabetes mellitus and hypertension, presented to the emergency department with difficulty in speaking, shortness of breath and worsening of the tongue swelling since morning. In the prehospital setting, he had received multiple doses of IM epinephrine with no improvement in his symptoms. No associated itchiness, pain or rash was reported. He denied vomiting, chest pain, fever, nausea, allergy and cough. He also denied eating other than his regular diet. Approximately 4 months before the presentation, he started receiving benazepril for hypertension. No family or personal history of tongue and facial swelling was reported. At the current presentation, he was normotensive and afebrile with an oxygen saturation of 96% in room air. An examination showed pronounced oedema, which included subcutaneous tissues of the perioral area and lingual mucosa without any pain or pruritus. Cardiac auscultation showed tachycardia, and lung auscultation showed a bilateral decrease in breath sounds with inspiratory effort. No lower limb swelling, urticarial eruption or jugular venous distention was observed. Laboratory test results revealed mild leucocytosis and lymphopenia. He also had elevated levels of high-sensitivity CRP, ferritin and LDH. The chest X-ray revealed bilateral infiltrates in his lung bases, while the CT scan showed multifocal alveolitis in the periphery of both upper lobes. The neck CT scan showed oedema at the submandibular area, submandibular glands, submucosal and prevertebral tissues of the hypopharynx and oropharynx. His nasopharyngeal swab was also taken for COVID-19 assay. Differential diagnosis of anaphylaxis, hereditary or acquired angioedema, lingual abscess, Ludwig’s angina, submandibular space infection, trauma, neoplasm, submental haematoma, Melkersson-Rosenthal syndrome and tongue tuberculosis was made. However, based on his history and recent use of ACE inhibitor (benazepril), a diagnosis of benazepril-associated angioedema was considered. Additionally, his elevated inflammatory markers and pulmonary infiltrates were consistent with COVID-19 infection. Hence, the man was treated with tranexamic acid, and over 3h, his condition improved. However, he had voice hoarseness. Hence, he was admitted for airway monitoring. His treatment with benazepril was stopped, and he started receiving famotidine and diphenhydramine. Within 24h, angioedema was resolved. His oxygen saturation was above 95%. Subsequently, he was discharged from the hospital with famotidine and diphenhydramine as home medication. He was also prescribed with amlodipine for hypertension. After discharge from the hospital, his PCR result showed positive results for COVID-19. Therefore, it was hypothesised that downregu