Case Presentation:

A 36–year–old man presented with acute neurologic changes. He described an inability to see objects in the lower left aspect of his visual field which quickly progressed to numbness in his left arm, leg and trunk. His only past medical history was hypertension which had been poorly treated due to medical noncompliance. His blood pressure was 150/80. He was noted to alternate between agitation and mild somnolence, but he was always arousable and oriented. A left lower quadrant visual field deficit was noted in his left eye. No other abnormal neurologic findings were noted. Labs were significant for a creatinine of 4.9 mg/dl, increased from 1.1 mg/dl just 2 months prior. Hematocrit was 29% from 44% just 2 months prior. Platelets were 112 x 109/L (from 226 x 109/L). Troponin was borderline at 0.47 ng/mL. Reticulocyte count was 3.1%. Haptoglobin was low at 21 mg/dL (normal: 30–200). LDH was elevated at 494 U/L. Three schistocytes were seen per high power field on peripheral blood smear. An MRI confirmed the presence of an acute lacunar infarct in the right thalamus. Given the constellation of neurologic symptoms, microangiopathic hemolytic anemia, mild thrombocytopenia, and renal failure, he was presumptively diagnosed with thrombotic thrombocytopenic purpura (TTP). He was presumed to have platelet thrombi and hemorrhage causing cardiac infarction and stroke. A hematology consultant agreed and recommended transfer to tertiary care for plasmapheresis. In the intervening hours, he was admitted to the floor for stabilization. Once admitted, concerns about the relatively preserved platelet count prompted repeat complete blood count which demonstrated a rising hematocrit and platelet count. Upon further questioning, the patient admitted taking numerous blood pressure agents just prior to presenting to the emergency department, masking his underlying severe hypertension. Reevaluating his presentation with this new information, malignant hypertension causing acute renal failure, cardiac ischemia, mild hemolysis, and stroke seemed more likely than TTP. His blood pressure was carefully managed and his hemolytic anemia improved quickly. His renal function also stabilized and the patient did not require hemodialysis.

Discussion:

Malignant hypertension is most commonly encountered by the hospitalist. It can cause a variety of findings, including those seen in this patient: stroke, renal failure, and cardiac ischemia. Microangiopathic hemolytic anemia is a more rare complication, which can make it difficult to distinguish from TTP, especially if the blood pressure has normalized prior to presentation. Fortunately, the diagnosis of TTP was questioned in this patient and a careful history revealed the correct diagnosis.

Conclusions:

Objective: (1) Recognize that malignant hypertension can cause mild hemolysis. (2) Consider malignant hypertension even in a patient whose blood pressure has been recently normalized with medications.