Correct!
4. Platelet transfusion to restore platelet function in patients with normal platelet counts, but platelet dysfunction due to aspirin or other antiplatelet drugs.

Hypertension control to a goal systolic blood pressure of 140 mmHg should ideally be achieved within the first hour of presentation with hemorrhagic stroke. The effects of antithrombotic therapies such as warfarin, heparin, and oral Xa inhibitors and dabigatran should be rapidly reversed and platelets transfused if needed to achieve >100 x103/uL. These therapies may limit hemorrhagic extension – an independent predictor of mortality and poor outcome. Clinical trial data suggests that platelet transfusions in patients receiving antiplatelet drugs, but without thrombocytopenia, may be hazardous and should be avoided. Neurosurgical consultation should be emergently pursued for management of intracranial hypertension. 

Clinical trial data suggests that platelet transfusions in patients receiving antiplatelet drugs, but without thrombocytopenia, may be hazardous and should be avoided. Neurosurgical consultation should be emergently pursued for management of intracranial hypertension. 

Emergent neurosurgical consultation was obtained and a nicardipine infusion was administered to maintain SBP <140 mmHg. Fresh frozen plasma (FFP), cryoprecipitate and platelets were administered with a goal of achieving a platelet count >100 x103/uL and fibrinogen >150 mg/dL. Four-factor prothrombin complex concentrate (50u/kg) was administered in a further attempt to reverse coagulopathy given the life-threatening nature of the hemorrhage. A ROS focused on symptoms of infection was negative. A chest radiograph was clear and a urinalysis showed no pyuria. The procalcitonin was 0.12. Blood cultures were draw and cefepime and vancomycin started empirically for a presumptive diagnosis of sepsis-related DIC.

Which of the following is true  of disseminated intravascular coagulation? (Click on the correct answer to be directed to the third of six pages)

1. Pathogenesis involves abnormal simultaneous activation of coagulation and fibrinolysis, potentially leading to bleeding and clotting complications.
2. Causes include sepsis, solid tumors (typically associated with chronic DIC), obstetrical catastrophes such as placental abruption, and acute hemolytic transfusion reactions.
3. Differential diagnosis includes acute liver failure, heparin-induced thrombocytopenia, HELLP syndrome, TTP/HUS and COVID-19 coagulopathy.
4. The diagnosis is made based on clinical and laboratory data; there is not a single pathognomonic diagnostic laboratory test for DIC.
5. Many patients, such as those with sepsis-related DIC, do not require specific therapy of DIC except for aggressive treatment of the underlying cause.
6. All the above.

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