Acute pancreatitis induced thrombotic thrombocytopenic purpura
A 43-yrs-old Indian male was admitted to the hospital with abdominal pain of one-day duration. The pain was mainly in the epigastrium, was severe in intensity and radiating to the back, and associated with nausea and vomiting.\nHis past medical history was insignificant except for alcoholism. His physical examination was normal apart from tenderness over the epigastrium.\nLaboratory findings showed an elevated serum amylase of 878 μ/L. His urea was 6.7 mmol/L, creatinine being 87 mmol/L. Total bilirubin was 29 μmol/L with a direct component of 6 μmol/L and indirect bilirubin of 23 umol/L. His aspartate aminotransferase (AST) was 45 IU/L, blood glucose of 7.3 mmol/L, and Lactate dehydrogenase (LDH) was 190 IU/L. His white blood count was elevated to 12,000 cells/mm3. Hematocrit was 42%, with a hemoglobin of 14 g/dL and platelets were 1,97,000/mm3. Ultrasound abdomen showed gallstones and a bulky hypo echoic pancreatic tail representing the area of pancreas. Computed tomography abdomen also showed the tail of pancreas to be edematous with fat stranding and a calculus at the neck of the gall bladder []. Bilateral pleural effusions were also noted which was mild to moderate, more on the left than the right. The patient was diagnosed as acute pancreatitis secondary to gallstones. He was started on the standard treatment for acute pancreatitis.\nOn the 4th day of admission, his platelets dropped to 14,000/mm3, along with a fall in hemoglobin to 8.7 g/dL. LDH rose to 2,037 IU/L, associated with an increase in indirect hyperbilirubinemia. The urea and creatinine increased to 17 and 169 mmol/L, respectively. Peripheral smear showed significant schistocytes of 4%. The fibrinogen levels and the coagulation profile remained normal. ADAMTS 13 enzyme assay was not done as the test was not available in our hospital. Based on these typical lab values, a diagnosis of TTP was made as the patient was having thrombocytopenia, MAHA, and renal impairment. The only other differential diagnosis is hemolytic uremic syndrome (HUS). The severe thrombocytopenia with mild renal impairment went in favor of TTP rather than HUS, which is expected to have severe renal impairment with mild thrombocytopenia. The patient underwent pan CT, which ruled out malignancy anywhere else as a triggering factor for TTP. The patient was commenced on plasmapheresis in addition to methylprednisolone, which is an established treatment for both TTP and HUS.\nPatient's platelet counts, urea, creatinine along with hemoglobin started to improve after the second session of plasmapheresis. His recovery was complicated by the progression of bilateral pleural effusion, which resulted in respiratory compromise, requiring intubation and mechanical ventilation. Bilateral intercostal drains were inserted and the patient was weaned off the ventilator by the 7th day. He had a total of eight sessions of plasmapheresis and the laboratory parameters were back to normal and the patient was discharged from the hospital on the 20th day of admission. Follow up of the patient a month after discharge from hospital found him to be doing well.