Hydrochlorothiazide
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Systemic capillary leak and non-cardiogenic pulmonary oedema: case report A 50-year-old man developed systemic capillary leak and non-cardiogenic pulmonary oedema following administration of hydrochlorothiazide for elevated BP. The man presented for assessment of possible allergic or immune causes of two previous episodes of pulmonary oedema and hypotension. The first episode was heralded by the onset of progressively worsening difficulty breathing, palpitations, diaphoresis and chills. A few minutes later, he developed nausea, vomiting, crampy abdominal pain, diarrhoea and lightheadedness to the point that he felt he was about to faint. He denied itchy skin, rashes, flushing or angioedema. There were no symptoms of upper airway obstruction. He was given aspirin by the paramedics en-route to the emergency department, intubated and ventilated for respiratory failure and transferred to the ICU because of hypoxaemia. He was treated in the ICU for non-cardiogenic pulmonary oedema and discharged home five days later. When asked about exposures prior to the onset of the symptoms, he reported exposure to a pesticide [details not stated] one day prior to and on the day of onset of symptoms. Because his BP was higher than usual, he took a tablet of hydrochlorothiazide [dosage not stated] shortly before the onset of his symptoms. He had received hydrochlorothiazide in the past with no untoward reactions. Ten months later, when he was getting ready for work in the morning, he took his regular medications comprising levothyroxine-sodium [levothyroxine], olmesartan-medoxomil [olmesartan] and amoxicillin (amoxicillin for a dental abscess). He also took hydrochlorothiazide for elevated BP. He had not received hydrochlorothiazide since his prior hospitalisation for the pulmonary oedema. Forty-five to sixty minutes later, he developed marked diaphoresis, shortness of breath, lightheadedness and feeling that he was about to faint. He then developed nausea, vomiting and lost consciousness. The man was brought to the emergency department where he had a pulseless electrical activity cardiac arrest. Upon resuscitation, he was transferred to the ICU. Abnormal laboratory investigations during his hospital stay included haemoconcentration, with haemoglobin over 200 g/L and haematocrit over 0.6, which improved with unspecified fluids. An echocardiography performed on the 2nd day post admission showed reduced left-ventricular ejection fraction of 20–25% with severe hypokinesis of the distal left ventricular segment. A diagnosis of Takotsubo cardiomyopathy was made. Three days later, his left-ventricular ejection fraction improved to 60–65%. His past medical history included hypertension, hypothyroidism, vitiligo and eczema. He had no allergies. Family history was non-contributory. His medications at the time of the assessment included terazosin, amlodipine, levothyroxinesodium and sennosides [Senokot]. Investigations undertaken included negative prick and intradermal skin tests for hydrochlorothiazide, normal serum tryptase and chromogr
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