No abstract

The relative contributions of microvascular inflammation and vasomotor dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been intensely studied. The present observational study was designed to examine the levels of circulating proinflammatory cytokines, anti-inflammatory cytokines, and vasoactive mediators during and after acute painful crisis. In symptomatic sickle cell patients, plasma levels of endothelin-1 and prostaglandin E2 were elevated during crises compared with healthy African-American controls. These levels had decreased, but not normalized, when patients were seen 1 to 3 weeks after discharge from hospital. Other mediators (tumor necrosis factor α [TNFα], interleukin-1β [IL-1β], IL-6, IL-8, and IL-10) were neither elevated in asymptomatic sickle cell disease nor in acute vaso-occlusive crisis. As a potent long-acting mediator of vasoconstriction and inflammation, endothelin-1 may play a key role in the cycle of ischemia and inflammation that initiates and sustains pain of crisis. The downregulatory effects of prostaglandin E2on immune cell function may contribute to the increased susceptibility to infection observed in patients with sickle cell disease.

Endothelin-1 and endothelin-4 may activate leukocytes after shock or gut ischemia, resulting in further injury to reperfused tissues and distant injury to lungs and other organs.

No abstract

Nonoperative management of blunt splenic trauma in adults is controversial despite numerous reports advocating this mode of therapy. Blunt splenic trauma is frequently managed without operation at our institution and, to define criteria that may predict a successful outcome, a retrospective review (1980 to 1988) of all adult splenic injuries was undertaken. Splenic injuries were documented by scintillation studies, CAT scanning, or at laparotomy. Sixty of 252 (24%) splenic injuries were initially treated without operation, which included bed rest, ICU monitoring, frequent physical exams, nasogastric tube, serial hematocrits, and follow-up splenic imaging. Five patients (5 of 60) failed nonoperative management and required interval laparotomy. Reasons for failure included blood loss greater than four units, enlarging splenic defect, or increasing peritoneal signs. Parameters predicting a successful outcome were localized trauma to the left flank or abdomen, hemodynamic stability, transfusion requirements less than four units, rapid return of GI function, age less than 60 years, and early resolution of splenic defects on imaging studies. No morbidity or deaths resulted from delayed operative intervention. In carefully selected adult patients, blunt splenic trauma may be successfully managed without operation.