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Hypertensive Havoc: When Malignant Hypertension Mimics Thrombotic Thrombocytopenic Purpura
Sarah Kim1, Amogh Pathak2, Marjan Koch2
1Anesthesiology, Cooper Medical School of Rowan University, Camden, USA.
Malignant hypertension (HTN) is defined by a rapid rise in blood pressure exceeding 200/130 mmHg, leading to acute end-organ damage. Although relatively uncommon, malignant HTN can cause thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, thrombocytopenia, and elevated serum lactate dehydrogenase (LDH). This presentation can mimic thrombotic thrombocytopenic purpura (TTP), a hematologic emergency characterized by thrombocytopenia, hemolytic anemia, renal and neurologic dysfunction, and fever. We present the case of a 28-year-old male patient who presented with seizures and hypertensive emergency. Imaging showed posterior reversible encephalopathy syndrome (PRES), and labs revealed anemia, thrombocytopenia, low haptoglobin, elevated LDH, and schistocytes. A PLASMIC (platelets, lysis, active cancer, stem cell/solid organ transplant, mean corpuscular volume, international normalized ratio, and creatinine) score of 5 indicated intermediate risk for TTP, prompting empiric treatment with corticosteroids and therapeutic plasma exchange (TPE). Platelets normalized, but hemolysis persisted. When clinical reassessment revealed that lab trends correlated with blood pressure fluctuations, TPE and steroids were discontinued, and aggressive antihypertensive therapy led to the resolution of hemolysis. A normal ADAMTS13 level confirmed the diagnosis of malignant HTN-induced TMA. This case underscores the importance of distinguishing malignant HTN from TTP, as their management differs significantly. This case highlights the diagnostic challenge in distinguishing TTP from malignant HTN-induced TMA and underscores the importance of recognizing this rare manifestation of hypertensive crisis to avoid unnecessary therapies and guide appropriate treatment.
Malignant hypertension (HTN) is defined by a rapid rise in blood pressure exceeding 200/130 mmHg, leading to acute end-organ damage. Although relatively uncommon, malignant HTN can cause thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, thrombocytopenia, and elevated serum lactate dehydrogenase (LDH). This presentation can mimic thrombotic thrombocytopenic purpura (TTP), a hematologic emergency characterized by thrombocytopenia, hemolytic anemia, renal and neurologic dysfunction, and fever. We present the case of a 28-year-old male patient who presented with seizures and hypertensive emergency. Imaging showed posterior reversible encephalopathy syndrome (PRES), and labs revealed anemia, thrombocytopenia, low haptoglobin, elevated LDH, and schistocytes. A PLASMIC (platelets, lysis, active cancer, stem cell/solid organ transplant, mean corpuscular volume, international normalized ratio, and creatinine) score of 5 indicated intermediate risk for TTP, prompting empiric treatment with corticosteroids and therapeutic plasma exchange (TPE). Platelets normalized, but hemolysis persisted. When clinical reassessment revealed that lab trends correlated with blood pressure fluctuations, TPE and steroids were discontinued, and aggressive antihypertensive therapy led to the resolution of hemolysis. A normal ADAMTS13 level confirmed the diagnosis of malignant HTN-induced TMA. This case underscores the importance of distinguishing malignant HTN from TTP, as their management differs significantly. This case highlights the diagnostic challenge in distinguishing TTP from malignant HTN-induced TMA and underscores the importance of recognizing this rare manifestation of hypertensive crisis to avoid unnecessary therapies and guide appropriate treatment.
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