Abstract Disseminated Intravascular Coagulation (DIC) is a rare and complex life-threatening condition in which the coagulation cascade is overactive, leading to excessive clotting and bleeding due to the consumption of clotting factors and platelets. A 21-year-old male patient without significant past medical history and recent viral illness was admitted to the ICU for further management of new-found portal venous and SVC thrombus, liver failure, and renal failure. The physical exam was notable for agitation, scleral icterus, tachycardia, and bruising over the abdomen and lower extremities. On initial workup, an echocardiogram showed biventricular failure with an ejection fraction of 5% - prompting ECMO cannulation. The initial insult was thought to be viral myocarditis but an endomyocardial biopsy was unrevealing. Hematology followed for workup of hypercoagulability. There were concerns for CAPS (catastrophic anti-phospholipid syndrome) given the patient’s quick decompensation and multi-organ failure. Initial APLS (anti-phospholipid syndrome) labs were negative but later found to be triple-positive at a neighboring hospital despite low titers. Bone marrow biopsy was unrevealing, and the liver biopsy showed no evidence of thrombotic microangiopathy. The patient was maintained on anticoagulation and treated with high-dose methylprednisolone, IVIG, and plasmapheresis. The patient ultimately underwent renal and heart transplantation. DIC in this patient may likely be secondary to a non-infectious inflammatory trigger such as CAPS predisposed by acute liver failure. Work-up for malignancy via cytogenics & biopsies, microangiopathies via bloodwork, and infection via cultures all resulted negative. There was some improvement in hemolysis after the plasmapheresis sessions which blurred the lines between DIC and CAPS. A repeat set of APLS titers 12 weeks out would have been helpful to show persistent positivity given the initial non-specific titers. A kidney biopsy would have helped diagnose CAPS versus DIC but was unable to be performed because of the inability to be off anticoagulation. Unfortunately, the host kidney was not biopsied after transplantation. Given the multiorgan failure, positive triple screen on APLS labs, and DIC-like presentation - treatment was initiated to cover both entities with systemic anticoagulation to counteract the hyper-activation of coagulation factors. The clinical course of DIC ranges from asymptomatic to fatal. It is important to think about DIC in a patient who presents with multiorgan failure and numerous thrombi with associated thrombocytopenia - even in a healthy young patient. It is paramount that the diagnosis be made early to treat the underlying cause and manage the irregularity of the coagulation cascade correctly. This abstract is funded by: None
K Ramos (2026) studied this question.