The Case ∣ Metabolic alkalosis in a patient with cystic fibrosis

Autor: Yelena Rekhtman, Amay Parikh, Abdallah S. Geara, Maya K. Rao
Jazyk: angličtina
Předmět:
Zdroj: Kidney International. (4):421-422
ISSN: 0085-2538
DOI: 10.1038/ki.2011.400
Popis: A 21-year-old woman with cystic fibrosis (CF) with recurrent admissions for CF exacerbations, diabetes mellitus, and allergic bronchopulmonary aspergillosis was hospitalized with shortness of breath and hemoptysis. During her course, she required intubation and was treated with several antibiotics including polymyxin and inhaled tobramycin on admission, then rifampin and intravenous (IV) tobramycin (dose of 7 mg/kg daily) beginning on hospital day 3. The tobramycin troughs ranged between o0.2 and 0.4. Initially, she had a chronic respiratory acidosis with normal serum electrolytes and creatinine. On day 7, she developed profound hypokalemia, hypomagnesemia, hypocalcemia, and metabolic alkalosis (Table 1), which persisted for 2 weeks despite aggressive electrolyte repletion with oral and IV potassium chloride, IV magnesium sulfate (640 mg/h), and IV calcium gluconate (400 mg/h). During the intensive care unit stay, the patient did not receive any loop diuretics and her serum creatinine was stable. The patient serum glucose levels were initially intermittently high but the electrolytes disturbances persisted even after her hyperglycemia was controlled on an IV insulin (mostly below 250 mg/dl). Additional evaluation showed serum parathyroid concentration of 17 pg/ml (10–65 pg/ml), inappropriately low for the level of hypocalcemia. The 24-h urine calcium was 440 mg/24 h. The urinalysis was negative for glucosuria and proteinuria. The fractional excretion of urate was 7.8% (normal: 6–20%); the fractional excretion of phosphorus was 10.25% (normal: 5–20%).
Databáze: OpenAIRE