RESUMO
Several mechanisms have been postulated as potentially involved in life-threatening complications during cemented surgery. In this study, we evaluated the role of anaphylaxis and pulmonary fat embolism in the pathophysiology of bone cement implantation syndrome in a series of fatal cases that underwent medicolegal investigations. Postmortem findings in these cases were compared with those obtained from individuals who died after other injuries and/or interventions and in which activated mast cells and pulmonary fat embolism were involved in the pathogenesis of death. Fifty subjects were selected including 6 individuals who had undergone cemented total hip arthroplasty and died intraoperatively, 32 subjects who died shortly after being involved in traffic accidents, 8 individuals who died shortly after the injection of contrast material, and 4 subjects who had undergone orthopedic surgery and died postoperatively. Massive pulmonary fat embolism was determined to be the cause of death in all the 6 subjects who died intraoperatively as well as the main cause of death in traffic-road victims with rapid respiratory function deterioration. Mast cell activation was identified exclusively in the group of subjects who died shortly after contrast material administration. Massive pulmonary fat embolism appears to be the most important factor responsible for severe cardiorespiratory function deterioration during cemented arthroplasty. Cardiac comorbidities can also significantly influence the severity of intraoperative complications, thus corroborating the hypothesis of a multifactorial model in the pathogenesis of bone cement implantation syndrome.
Assuntos
Cimentos Ósseos/efeitos adversos , Embolia Gordurosa/patologia , Embolia Pulmonar/patologia , Acidentes de Trânsito , Anafilaxia/induzido quimicamente , Anafilaxia/patologia , Artroplastia de Quadril/efeitos adversos , Meios de Contraste/efeitos adversos , Feminino , Fraturas Ósseas/cirurgia , Humanos , Laminectomia/efeitos adversos , Masculino , Mastócitos/enzimologia , Pessoa de Meia-Idade , Complicações Pós-Operatórias , Triptases/metabolismoRESUMO
Catheter-induced pulmonary artery rupture is an infrequent complication that may occur during invasive cardiopulmonary monitoring. Fatal cases are uncommon and result from hemoptysis and flooding of the opposite lung with resulting hypoyxia. Alpha-1-antitrypsin deficiency is a rare genetic disorder characterised by low serum levels of alpha-1-antitrypsin, critical in maintaining connective tissue integrity. Besides pulmonary emphysema, recent observations suggest that alpha-1-antitrypsin deficiency may also be involved in vascular wall weakening, thereby predisposing arteries to dissection and aneurysm formation. In this article, we describe an autopsy case of pulmonary artery iatrogenic rupture due to insertion of a Swan-Ganz catheter in an 82-year-old woman suffering from pulmonary hypertension and alpha-1-antitrypsin deficiency. The exact source of bleeding could not be precisely identified during autopsy due to the extent of tissue hemorrhage, though postmortem angiography revealed a contrast medium extravasation from a branch of the left pulmonary lower lobar artery. The case herein emphasises the importance of postmortem angiography in facilitating the detection of vascular injuries, the importance of familiarity with intensive care techniques and procedures on behalf of forensic pathologists as well as in-depth knowledge of all possible contributing conditions and predisposing disorders in the pathogenesis of death.
Assuntos
Cateterismo de Swan-Ganz/efeitos adversos , Artéria Pulmonar/lesões , Idoso de 80 Anos ou mais , Evolução Fatal , Feminino , Hemoptise/etiologia , Humanos , Hipertensão Pulmonar/complicações , Pulmão/patologia , Artéria Pulmonar/diagnóstico por imagem , Artéria Pulmonar/patologia , Radiografia , Aspiração Respiratória/etiologia , Ruptura/etiologia , Choque Hemorrágico/etiologia , Deficiência de alfa 1-Antitripsina/complicaçõesRESUMO
Light chain deposit disease (LCDD) is a rare condition caused by deposition of overproduced monoclonal light chains and has been frequently related to multiple myeloma or lymphocytic disorders. LCDD in association with human immunodeficiency virus (HIV) has only been described twice in the literature and is thought to result from HIV direct/indirect effects on B and T-cell populations, leading to chronic immune activation with paraprotein production. We report a renal LCDD case diagnosed at autopsy in a severely immunodepressed HIV patient and analyse renal histopathology of 18 HIV patients who had an autopsy in our department between 2000 and 2010.