The potential risk factors for his deterioration are multiple bony traumas; multi-organ injuries and surgeries including lungs, liver, kidneys, and spleen; multiple blood transfusions; and hospital-acquired infection in the high-dependency unit. The provisional diagnosis could be one of acquired coagulopathy that may have resulted due to the above risk factors. The provisional diagnosis could be DIC or disseminated intravascular coagulation since the most common signs of this disorder are petechiae, ecchymosis, and oozing from venipuncture sites and catheter sites, as well as bleeding from surgical incisions (Attar et al., 1969, p. 939-965). In some situations, DIC becomes only evident after laboratory analysis with mild or no clinical symptoms at all. As in this case, these patients become symptomatic after stress situations, such as, surgery, or severe infections. The common denominator of DIC is the pathological generation of thrombin, which leads to widespread intravascular deposition of fibrin and to the consumption of coagulation factors and platelets. DIC is as such not a disease entity, but the consequence of a variety of disorders that diffusely lead to the activation of coagulation mechanisms within the bloodstream (Carey and Rodgers, 1998, 65-73). The formation of thrombi in the microcirculation activates the fibrinolytic process as a compensatory mechanism to lyse the clots. This mechanism generates circulating fibrin degradation products, which in concert with the coagulation deficiencies and thrombocytopenia results in bleeding. DIC occurs in a wide spectrum of diseases. Another mechanism potentially triggering DIC is the widespread endothelial damage occurring in endotoxinaemia, meningococcal septicemia, or following severe burns or hypothermia. Vascular stasis as in circulatory shock and severe pulmonary embolism can also precipitate DIC (Hack and Zeerleder, 2001, s21-s27).
In this patient, this has been an acquired coagulation disorder. The acquired forms usually are associated with multiple coagulation abnormalities, and the disorder often is complicated by thrombocytopenia, deficient platelet function, abnormal inhibitors of coagulation, and vascular abnormalities. Because of the compound nature of the haemostatic defect, the severity of bleeding often correlates poorly with the results of laboratory tests in patients with acquired coagulation disorders, and replacement therapy may be ineffective. The clinical picture is often complicated by signs and symptoms of the underlying disease. In this patient, there is a chance for septicemia due to the facts that the patient had a road traffic accident, had massive trauma, multiple surgeries, and the patient had been put in an intensive care unit. Major risk factors of gram-positive bacteriaemia include vascular catheterization and the presence of indwelling devices. Mechanical ventilation has also a role to play (Baglin T., 1996, p 683-687).