A 29-year-old man presented to the emergency department (ED) after a motorcycle accident. Upon arrival to the ED he was found to have suffered a crush injury to his left temple. He was intubated and underwent urgent evacuation of an epidural hematoma. The next day he developed progressive hypotension and spiking fevers. Oozing from multiple line and venipuncture sites was noted. His hemoglobin and platelet count began to decline and his prothrombin time (PT) and partial thromboplastin time (PTT), which were initially normal, started to rise. His liver function test showed a rise in transaminases.
What is the differential diagnosis?
The differential diagnosis includes the following: thrombotic thrombocytopenic purpura, idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, and heparin-induced thrombocytopenia.
The most likely diagnosis in this clinical setting is disseminated intravascular coagulation (DIC). DIC is a syndrome, not a diagnosis. It is an acquired state that occurs as a result of a number of underlying conditions (Table 51-1). For the purpose of this chapter, we will focus on acute DIC. In the setting of DIC, there is global activation of the coagulation system with formation of fibrin within the circulation. Fibrin deposition leads to thrombosis and occlusion of small vessels, with subsequent end-organ damage. At the same time, depletion of platelets and clotting factors can also lead to bleeding.1
Table 51-1.Etiology of Disseminated Intravascular Coagulation ||Download (.pdf) Table 51-1. Etiology of Disseminated Intravascular Coagulation
|CNS injury |
|Cancer: solid tumors, myeloproliferative disorders, lymphoproliferative disorders, leukemia |
|Obstetric complications: abruptio placentae, amniotic fluid embolism |
|Vascular disorders: large aneurysms, Kasabach-Merritt syndrome, atherosclerosis |
|Severe toxic reactions |
|Severe immunologic reactions |
|Transplant rejection |
|Severe trauma |
In the clinical scenario described above, DIC may be due to his traumatic brain injury (TBI) as well as his sepsis. The brain has a high concentration of tissue thromboplastin, which has a tendency to become prothrombotic when released into systemic circulation.2 DIC has been described in a signification proportion of patients with TBI and is associated with increased morbidity and mortality. He is also bacteremic. Sepsis may cause marked activity of the inflammatory system, and inflammation-induced activation of coagulation is a well-recognized phenomenon.3 Severe sepsis may be complicated by DIC in about 35% of cases.4
What are the clinical manifestations of DIC?
DIC is a clinical diagnosis of a syndrome. Clinical manifestations include:5
On physical examination one may note cool, mottled extremities; petechiae; ecchymoses; or hemorrhages at the site of invasive procedures. From a laboratory standpoint, there is not one single laboratory test in isolation that can determine the diagnosis of DIC. Instead, DIC is a clinical syndrome, and laboratory data help support clinical suspicion (Table 51-2).