Cjem | 2021
Severe hypocalcaemia and hypomagnesemia presenting with severe neurologic and gastro-intestinal symptoms: a case report and review of literature
Abstract
A 65-year old male patient presented to the ED with general weakness, vomiting and diffuse abdominal pain for several days. There was a history of pulmonary embolism and recent repeated autologous stem cell transplantation due to recurrent multiple myeloma 2 months ago. His medication included rivaroxaban, esomeprazole and fluconazole. The latter was prescribed during the latest visit to the outpatient clinic for an oropharyngeal infection that was presumably caused by Candida spp. On arrival conversation was not possible. Medical history taken from his wife revealed that the epigastric pain started 5 days ago with subsequent vomiting for 2 days. Fever, chills or abnormal stools were not reported. On examination patient appeared moderately ill, was disoriented and unable to communicate. Further physical examination revealed normal heart and lung sounds, active bowel sounds and mild diffuse abdominal tenderness to deep palpation without involuntary guarding or rebound tenderness. Neurological examination revealed a tremor without other neurological deficits apart from aphasia and confusion. Electrocardiography (ECG) showed a sinus rhythm (76 bpm) with a right bundle branch block (RBBB) and a prolonged QT-interval (QTc 511 ms). Our differential diagnosis was delirium due to ileus or abdominal sepsis, primary cerebral pathology (including intracerebral hemorrhage, tumor or ischemia) or electrolyte disorder (e.g. hypercalcemia, hyponatremia). Point-of-care blood gas analysis revealed a metabolic alkalosis (pH 7.59, pCO2 3.4 kPa [25.51 mmHg], HCO3 24 mmol/L), hypocalcaemia (1.63 mmol/L; corrected for albumin; ionized 0.77 mmol/L) and hypokalemia (2.9 mmol/L, while additional blood analysis revealed a hypomagnesemia (0.13 mmol/L). A computed tomography (CT) scan of the brain was made that showed no abnormalities. Based on a working diagnosis of severe hypocalcaemia with major neurologic and gastro-intestinal symptoms, we administered one ampule of calcium gluconate (10 ml, which contains 1 g [2.25 mmol] of calcium) intravenously over 10 min. His aphasia, confusion and nausea recovered within minutes after calcium supplementation and the QT-interval normalized. Additional laboratory analysis revealed no increase in inflammatory parameters. Urinary magnesium excretion was low (0.56 mmol/L) and potassium excretion was high (74 mmol/L). We concluded severe hypomagnesemia with secondary hypocalcaemia and hypokalemia in our patient to be due to a drug-drug interaction between the fluconazole that was initiated 10 days prior to presentation and esomeprazole, leading to increased plasma levels of the latter. Previous measurements of magnesium, potassium and calcium, as was performed 1 month before presentation, had been within the normal range. Profuse vomiting likely aggravated the electrolyte disturbances. The patient was admitted to the ward for further supplementation of calcium, magnesium and potassium, while esomeprazole was discontinued. He could be discharged in good condition 3 days later. * H. R. Bouma [email protected]