Search Results (2)

Background/Objectives: Spontaneous chest wall hematomas are rare but potentially life-threatening complications, particularly in patients with multiple comorbidities such as those undergoing hemodialysis. This case report aims to highlight the significance of early diagnosis and appropriate management in preventing complications associated with this condition. Methods: We report the case of a 79-year-old man with end-stage renal disease on hemodialysis, presenting with a large spontaneous hematoma (18.7 × 13.1 × 9.6 cm) in the right upper chest wall. Initial interventions, including diagnostic imaging and transarterial angiography, did not detect active bleeding. Surgical exploration revealed bleeding from a branch of the lateral thoracic artery, which was managed through vessel ligation and hematoma drainage. Results: The hematoma was successfully managed through surgical intervention, with no postoperative complications such as infection, recurrent bleeding, or wound issues. The patient’s recovery was uneventful, and he was discharged in stable condition. This case underscores the role of microvascular fragility and uremic coagulopathy in the development of spontaneous bleeding in hemodialysis patients. Conclusions: This case emphasizes the importance of timely recognition and individualized management of spontaneous soft tissue bleeding in hemodialysis patients. Surgical intervention is necessary for large hematomas or cases of hemodynamic instability to ensure hemostasis and mitigate complications. Full article

Hemolytic uremic syndrome (HUS) is defined by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (AKI). Atypical HUS (aHUS), distinguished by its etiology, is caused by uncontrolled overactivation of the alternative complement pathway. The correct diagnosis of aHUS is complex and involves various gene mutations. Severe combined immunodeficiency (SCID), characterized by severe T-cell lymphocytopenia and a lack of antigen-specific T-cell and B-cell immune responses, is of seldom occurrence. In 10–15% of pediatric patients, SCID is caused by adenosine deaminase (ADA) deficiency. The authors describe the case of a boy who suffered from both aHUS and ADA-deficient SCID. At the age of 9 months, the patient presented acute kidney injury with anuria and coagulopathy. The diagnosis of aHUS was established on the basis of alternative complement pathway deregulation and disease-associated gene mutations. Further examination revealed immune system failure and, at the age of 13 months, the ADA deficiency was confirmed by genetic tests and the boy was diagnosed with ADA-SCID. ADA SCID has recently been described as a possible triggering factor of aHUS development and progression. However, more research is required in this field. Nevertheless, it is crucial in clinical practice to be aware of these two co-existing life-threatening diseases. Full article