Case Presentation: A 46 year-old man with bipolar disorder and hypertension presented to the emergency department (ED) with total body pain. He had been at the local airport when he had sudden onset total body throbbing sharp pain. He collapsed on the floor and a bystander called EMS who transported him to our ED. His blood pressure was noted to be 227/138. He reported bitemporal headache, but denied any other signs or symptoms of end organ damage. He had been primarily followed at an outside hospital and was prescribed amlodipine, carvedilol, lisinopril, and hydralazine for his hypertension. Cardiac enzymes were negative, EKG was unchanged with nonspecific T-wave changes and evidence of left ventricular hypertrophy. Cardiology was consulted who recommended admission for treatment of hypertension and elective treadmill stress test.
After admission, the patient’s blood pressure was difficult to control. His potassium was repeatedly low on daily laboratory testing. A review of records from the outside hospital stated a full work up of secondary causes had been completed and was negative. However, given continued refractory nature of hypertension, work up of secondary causes was again initiated. A renin and aldosterone level were sent which were 1.0 ng/ml/h and 25 ng/dL respectively. Given the aldosterone to renin ratio, he was suspected of having primary hyperaldosteronism, and endocrine consultation was requested. A saline infusion test confirmed the diagnosis of primary hyperaldosteronism. A CT scan of the adrenals revealed no mass that was resectable. He was initiated on spironolactone with improvement in potassium and blood pressure, and discharged for further care as an outpatient with the endocrine service.
Discussion: Refractory hypertension should prompt consideration of a work up of secondary causes of hypertension. This patient’s persistently low potassium also helped raise the suspicion for his diagnosis of primary hyperaldosteronism, or Conn Syndrome. With appropriate treatment, his blood pressure and hypokalemia improved more so than with other medical interventions that had been previously tried.
In this case, the diagnosis of the underlying cause for this patient’s hypertension was delayed, largely because of the previously documented negative work up for secondary hypertension leading our team to defer repeating the work up. This case highlights the need for us to be comprehensive not only in our review of medical records, but also to approach documentation and prior testing with a skeptical eye, as documentation is not foolproof, nor is medicine as a field. In this case, either the documentation of a full work up was erroneous, or the patient’s own laboratory testing truly revealed normal values in the past.
Conclusions: Primary hyperaldosteronism is a cause of secondary hypertension. Persistent hypokalemia can help suggest this diagnosis. Work up includes the aldosterone to renin ratio, saline infusion testing, and if confirmed, evaluation for resectable adrenal pathology with CT scan is indicated. Diagnostic anchoring based on a patient’s old records should be avoided, and maintaining an open mind to repeating a work up, especially if suggested by the clinical picture, is critical.