Case Presentation:

A 29–year–old woman with a history of HIV nephropathy and end–stage renal disease presented one day of headaches, nausea, and vomiting. She noted no trauma, and no new neurologic abnormalities. She did note that she had not taken her anti–hypertensive medications, and that she had missed her last two dialysis appointments. Upon arrival to the hospital, she was afebrile, with a blood pressure of 215/132 mmHg. She was somnolent and partially responsive to verbal and physical stimulation. The remainder of her neurologic exam was normal; there was no papilledema. She was admitted to the hospital with a diagnosis of hypertensive urgency. Shortly after admission, she was witnessed to have a tonic–clonic seizure. A lumbar puncture was performed, revealing a normal protein and glucose; the Gram stain was negative and there were no white blood cells. CSF cultures were negative. Her serum white blood cell count was 400 cells/mm³ with 38% neutrophils. Her electrolytes wee normal; the blood urea nitrogen was 31 mg/dL and the creatinine was 12.1 g/dL. A cranial T2–weighted MRI showed multiple large areas of edema in the pareitooccipital lobe, with the right greater than left. The patient was treated with labetalol, lorazepam, and phenytoin, and two days later the neurologic findings abated.

Discussion:

The management of hypertensive urgency is a common occurence for the hospitalist. Typically, the initiation of anti–hypertensive therapy in conjunction with resuming dialysis, where indicated, resolves the problem. The hospitalist should be aware, however, of secondary complications of hypertensive urgency. PRES, or posterior reversible encephalopathy syndrome, is one such complication. Posterior reversible encephalopathy syndrome (PRES) is defined by reversible cerebral edema due to dysfunction of the cerebrovascular blood–brain barrier unit. The pathophysiology of PRES is thought to result from abnormalities in the transmembrane flow of intravascular fluid and proteins caused by cerebral autoregulatory failure and loss of integrity of the blood brain barrier. A sudden rise of blood pressure, which exceeds the autoregulatory capability of the brain, causes regions of vasodilation and vasoconstriction to develop. The endothelial dysfunction causes a breakdown of the blood–brain barrier allowing for focal transudation of fluid and edema formation. Both HIV and ESRD appear to further compromise the blood brain barrier.

Conclusions:

The development of PRES appears to be multifactorial and hospitalists should be aware not only of the entity itself, but of the conditions that may predispose to its development in the setting of hypertensive urgency.