Bleeding and Coagulopathies in Critical Care


The following are 10 points to remember about bleeding and coagulopathies in critical care:

1. The definition of coagulopathy is ‘a condition in which the blood’s ability to clot is impaired.’

2. A medical history taking and physical examination are vital, since many different conditions can produce similar laboratory abnormalities. For example, end-stage liver failure and disseminated intravascular coagulation produce thrombocytopenia and similar changes in standard tests of coagulation, and yet the management of and prognosis for these conditions are very different.

3. A peripheral-blood smear is a vital investigation tool in most cases to confirm a low platelet count and the presence or absence of other diagnostic features, such as red-cell fragmentation, platelet morphologic abnormalities, or evidence of dysplasia or hematinic deficiency.

4. The first principle of the management of coagulopathies in critical care is to avoid the correction of laboratory abnormalities with blood products unless there is a clinical bleeding problem, a surgical procedure is required, or both.

5. Tranexamic acid should be administered to all patients with major bleeding after trauma.

6. There is no supportive evidence for the prophylactic use of fresh-frozen plasma to correct abnormal results on coagulation screening (for prothrombin time, activated partial-thromboplastin time, and fibrinogen) before an invasive procedure. Despite the lack of high-quality evidence and the inability of vitamin K to correct a coagulopathy caused by liver disease, supplementation of vitamin K1 (at a dose of at least 1 mg orally daily or 10 mg intravenously weekly) for critical care patients at risk seems reasonable.

7. The cornerstone for managing disseminated intravascular coagulation remains the management of the underlying cause (e.g., sepsis). Further management may not be necessary in patients with mild abnormalities in coagulation and no evidence of bleeding. Platelet transfusion is indicated to maintain a platelet level of more than 50,000 per cubic millimeter, along with the administration of fresh-frozen plasma to maintain a prothrombin time and activated partial-thromboplastin time of less than 1.5 times the normal control time and a source of fibrinogen to maintain a fibrinogen level of more than 1.5 g/L.

8. A platelet threshold of 10,000 per cubic millimeter for platelet transfusion in patients who are in stable condition is both hemostatically efficacious and cost-effective in reducing platelet-transfusion requirements. If the patient is actively bleeding, then a platelet count of 50,000 per cubic millimeter should be maintained.

9. Fibrinolytic bleeding should be considered, particularly in patients with liver disease and disseminated cancers. The use of tranexamic acid, either by infusion or orally (depending on the severity of the problem and the state of the patient), is beneficial in controlling bleeding.

10. Studies that have evaluated the reversal of the new oral anticoagulants have been limited to reversal of drug effect with the use of recombinant activated factor VII and prothrombin complex concentrate. Current evidence suggests that prothrombin complex concentrate may be the best option and that it reverses the effects of rivaroxaban better than the effects of dabigatran.

Keywords: Prognosis, Partial Thromboplastin Time, Critical Care, Hemorrhage

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