From Pirates to Patients: Errors in Omission in Obtaining Dietary Histories in Children With Behavioral Disorders.

Abstract

One week before presenting to the hospital, a 20-year-old man with Landau–Kleffner Syndrome, a disorder characterized by loss of higher cortical functioning similar to autism spectrum disorder, developed acute onset skin changes, pallor, and fatigue. His primary care doctor noted bruising and petechiae overlying his bilateral upper and lower extremities. Laboratories were drawn, including a complete cell count prothrombin time and international normalized ratio (INR), all of which returned unremarkable (white blood cells 6.7 k/mm3, platelets 283 mg/dL, INR 1.1, hematocrit 33.7%). Over the next several days, the patient developed gross hematuria and stopped walking, subsequently presenting to the emergency department for further evaluation. There, he was found to have persistent skin findings along with gum bleeding. He underwent an extensive laboratory evaluation notable for a hematocrit of 25.3% with a mean corpuscular volume of 83.5 fL per cell, an elevated C-reactive protein of 7 mg/L and erythrocyte sedimentation rate of 75 mm/hour, an elevated unconjugated bilirubin at 2.7 mg/dL, and a slightly decreased albumin at 3.6 g/dL. Raw absolute reticulocyte count was 0.142 M/mm3, and hematocrit-corrected reticulocyte count was 2.5%. Peripheral smear was notable for hypochromasia, polychromasia, Dohle bodies, and giant platelets. Haptoglobin was 264 mg/dL, and platelet count was 301 000 per μL. D-Dimer was elevated at 4.1 μg/mL, whereas prothrombin time, INR, partial thromboplastin time, and lactate dehydrogenase were within normal limits. Direct antiglobulin test was negative. Urine microscopy demonstrated 0 to 2 red blood cells per high powered field with positive urobilinogen despite no gross hematuria. The patient was admitted with a presumptive diagnosis of hemolytic anemia of unknown etiology. During the first 24 hours of admission, he …