(464) Atraumatic Spontaneous Splenic Rupture in a Bone Marrow Transplant Recipient on VV ECMO

Introduction: Bone marrow transplantation (BMT) can be lifesaving for patients with acute leukemias. However, a number of hematologic and non-hematologic complications may arise during the recovery process. Spontaneous atraumatic splenic rupture has rarely been reported after BMT, but not while on extracorporeal membrane oxygenation (ECMO).

Description: A 54-year-old male underwent HLA-matched allogeneic BMT for AML. The engraftment was suboptimal but without recurrence of AML. He developed severe ARDS 10 weeks following his transplant from MRSA pneumonia, GVHD, invasive aspergillus infection, and CMV pneumonitis requiring initiation of V-V ECMO. No systemic anticoagulation was used because of profound thrombocytopenia. He received filgrastim for severe neutropenia. On Day 19 of the ECMO run, the patient suddenly developed hypotension and a drop in hemoglobin. An abdominal CT revealed hemoperitoneum. Exploratory laparotomy demonstrated approximately 4 L of blood in the peritoneal cavity, anterior avulsion of the splenic hilum with active bleeding. The patient underwent splenectomy. Unfortunately, the patient continued to have intraabdominal bleeding, and despite return to the OR and aggressive resuscitation, his condition worsened. The family chose not to escalate care further, and the patient died soon after that. The spleen measured 371 gm, measuring 17x11x5cm. Three distinct disruptions of the hilar surface were noted. Histopathology revealed red pulp expansion without any malignancy.

Discussion: Spontaneous splenic rupture has primarily been reported in patients with infection, inflammation and malignancy involving the reticuloendothelial system. Splenic rupture following administration of GM-CSF has also been reported, and the risk is likely higher with filgrastim and pegfilgrastim than with newer medications. Our patient received filgrastim 14 days before the splenic rupture. Both splenomegaly with red pulp expansion and normal-sized spleen have been described in patients with splenic rupture after GM-CSF. Whether aberrations in homeostasis while being on ECMO played an additional role is unclear. Neutropenic patients with worsening hemodynamics and anemia who receive GM-CSF, should be promptly evaluated for spontaneous splenic rupture.