Objective To describe a case of emphysematous hepatitis which is a rare clinical entity, characterized by a fatal, rapidly progressive infection of the liver with a radiological appearance simulating emphysematous pyelonephritis and to help provide more data about the causative organisms and precipitating factors of this pathology. Data Sources and Synthesis Relevant literature was reviewed and, to the best of our knowledge, there is limited data regarding the pathogenesis, causative organisms, and management of this condition. Conclusion Emphysematous hepatitis is a rapidly progressive infection that can be fatal in the absence of appropriate therapeutic intervention. Initial clinical manifestations are usually subtle and thus high clinical suspicion is required for early diagnosis and management of this condition to help decrease the mortality rates.
Patient: Female, 34Final Diagnosis: Refractory thrombotic thrombocytopenic purpuraSymptoms: FatigueMedication: —Clinical Procedure: Plasma exchangeSpecialty: Rheumatology • Hematology and Critical CareObjective:Rare co-existance of disease or pathologyBackground:Thrombotic thrombocytopenic purpura (TTP) is one of the thrombotic microangiopathic (TMA) syndromes, caused by severely reduced activity of the vWF-cleaving protease ADAMTS13. Systemic lupus erythematosus (SLE), on the other hand, is an autoimmune disease that affects various organs in the body, including the hematopoietic system. SLE can present with TMA, and differentiating between SLE and TTP in those cases can be very challenging, particularly in patients with no prior history of SLE. Furthermore, an association between these 2 diseases has been described in the literature, with most of the TTP cases occurring after the diagnosis of SLE. In rare cases, TTP may precede the diagnosis of SLE or occur concurrently.Case Report:We present a case of a previously healthy 34-year-old female who presented with dizziness and flu-like symptoms and was found to have thrombocytopenia, hemolytic anemia, and schistocytes in the peripheral smear. She was subsequently diagnosed with TTP and started on plasmapheresis and high-dose steroids, but without a sustained response. A diagnosis of refractory TTP was made, and she was transferred to our facility for further management. Initially, the patient was started on rituximab, but her condition continued to deteriorate, with worsening thrombocytopenia. Later, she also fulfilled the Systemic Lupus International Collaborating Clinics (SLICC) criteria for diagnosis of SLE. Treatment of TTP in SLE patients is generally similar to that in the general population, but in refractory cases there are few reports in the literature that show the efficacy of cyclophosphamide. We started our patient on cyclophosphamide and noticed a sustained improvement in the platelet count in the following weeks.Conclusions:Thrombotic thrombocytopenic purpura is a life-threatening hematological emergency which must be diagnosed and treated in a timely manner. Refractory cases of TTP have been described in the literature, but without clear evidence-based guidelines for its management, and is solely based on expert opinion and previous case reports. Further studies are needed to establish guidelines for its management. We present this case to highlight the role that cyclophosphamide might carry in those cases and to be a foundation for these future studies.
Introduction Hemothorax is usually related to chest or iatrogenic trauma from procedures such as central lines and thoracentesis. Spontaneous hemothorax is defined as pleural fluid hematocrit greater than 50% of serum hematocrit in absence of natural or iatrogenic trauma affecting the lung or pleural space. Coagulopathy secondary to anticoagulant use has been associated with spontaneous hemothorax. We present a case of spontaneous hemothorax in a patient taking apixaban for venous thromboembolism disease. To our knowledge, this is the first case report of apixaban as a cause of spontaneous hemothorax. Case Presentation A 56-year-old woman with end-stage renal disease (ESRD) was diagnosed with upper extremity deep vein thrombosis (DVT) one month prior to presentation and was started on apixaban presented with dyspnea and left-sided pleuritic chest pain for two weeks. She was found to have left-sided large pleural effusion which was diagnosed as hemothorax. Other etiologies for spontaneous hemothorax were excluded and drainage by 12-French pigtail catheter achieved total resolution of hemothorax in three days. Discussion Apixaban is a DOAC used to prevent stroke or thromboembolic events in patients with nonvalvular atrial fibrillation and to prevent recurrent venous thromboembolic disease. Events such as gastrointestinal, intracranial, and soft tissue bleeding have been well-documented. However, bleeding manifestation as hemothorax is seldom reported. Our patient presented with isolated left-sided large pleural effusion which was diagnosed as spontaneous hemothorax. 12-Fr pigtail catheter drainage was effective in the management of our patient and provided total resolution in three days. Conclusion Spontaneous hemothorax is a rare complication of anticoagulant therapy and might not exhibit the usual radiological signs of traumatic hemothorax. Health care providers should have high index of suspicion for spontaneous hemothorax when evaluating new pleural effusion in patients receiving DOACs therapy. Drainage by small bore pigtail catheter might be as effective as larger chest tubes.
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