ABSTRACT
Cerebral venous sinus thrombosis (CVST) is a cerebrovascular condition due to the thrombosis of cerebral venous sinuses, leading to intracranial hemorrhage, increased intracranial pressure, focal deficit, seizure, toxic edema, encephalopathy, and death. The diagnosis and therapeutic approach of CVST remain challenging because of its highly nonspecific clinical presentation including headaches, seizures, focal neurologic deficits, and altered mental status, etc. Anticoagulation is the mainstay of CVST treatment and should be started as soon as the diagnosis is confirmed. Here, we present the case of a 34-year-old male construction worker who presented to the emergency department with a complaint of right chest wall pain and swelling. He was admitted to the hospital following a diagnosis of anterior chest wall abscess and mediastinitis. During hospitalization, his complete blood count revealed pancytopenia with blast cells, and bone marrow biopsy revealed 78.5% lymphoid blasts by aspirate differential count and hypercellular marrow (100%) with decreased hematopoiesis. He developed concurrent CVST and intracranial hemorrhage while receiving CALGB10403 (vincristine, daunorubicin, pegaspargase, prednisone) with intrathecal cytarabine induction chemotherapy for acute lymphoblastic leukemia (ALL). The patient failed two standard chemotherapy for ALL and achieved remission while on third-line chemotherapy with an anti-CD19 monoclonal antibody, blinatumomab. Although this patient had an MRI scan of the brain with multiple follow-up non-contrast CT scans, it was CT angiography that revealed CVST. This showed the diagnostic challenge in CVST, with CT and MRI venography having excellent sensitivity in diagnosing CVST. Risk factors for CVST in our patient were ALL and its intensive induction chemotherapy with pegaspargase.
ABSTRACT
INTRODUCTION: There is a paucity of data on the outcomes of coronavirus disease 2019 (COVID-19) in patients with sickle cell disease (SCD) in the United States. We examined the outcomes of patients with COVID-19 and SCD. METHODS: We utilized the National Inpatient Sample (NIS) to identify the data of patients diagnosed with COVID-19 and SCD in 2020 using the International Classification of Disease, Tenth Revision codes. In-hospital outcomes (invasive mechanical ventilation and mortality) were compared between SCD and non-SCD groups. RESULTS: Of the 1 057 550 COVID-19 hospitalizations, 2870 (0.3%) had SCD. The median age of the SCD group was 42 (IQR: 31) vs. 66 (IQR: 23) in the non-SCD group (p < .0001). Patients with SCD were likely to be females (62.02% vs. 37.98%, p < .0001), Blacks (87.81% vs. 12.19%, p < .0001), and in the lowest income quartile (50.62% vs. 11.15%, p < .0001). There was no difference in the outcomes between the two groups. There were increased odds of invasive mechanical ventilation and in-hospital mortality in COVID-19 in Asians, Hispanics, Native Americans, and Blacks (except for in-hospital mortality) compared to Whites. CONCLUSION: In-hospital mortality and invasive mechanical ventilation outcomes in SCD are comparable to that in non-SCD patients hospitalized with COVID-19.
ABSTRACT
The management of primary immune thrombocytopenia (ITP) is becoming a subject of interest as there appears to be treatment failure and resistance to modern conventional treatment, necessitating a more universal and goal-directed approach to management. Our patient is a 74-year-old male who was diagnosed with ITP six years ago and recently presented to the emergency department (ED) with complaints of melena stools and severe fatigue lasting for two days. Prior to the ED presentation, he had received multiple lines of treatment including splenectomy. On admission, the pathology after splenectomy showed a benign enlarged spleen with a focal area of intraparenchymal hemorrhage/rupture and changes compatible with ITP. He was managed with multiple platelet transfusions, IV methyl prednisone succinate, rituximab, and romiplostim. His platelet counts improved to 47,000, and he was discharged home on oral steroids with outpatient hematology follow-up. However, in a few weeks, his condition deteriorated, and he presented with an increased platelet count and further multiple complaints. Romiplostim was discontinued, and he was continued on prednisone 20 mg daily, after which he improved, and his platelet count reduced to 273,000 on 20 mg prednisone. This case calls attention to the need to review the role of combination therapy in treating refractory ITP and the prevention of complications of thrombocytosis secondary to advanced therapy. Treatment needs to be more streamlined, focused, and goal-directed. Escalation and de-escalation of treatment should be synchronized to prevent adverse complications from overtreating or undertreating.