Transfusion practices in traumatic brain injury.

PURPOSE OF REVIEW: The aim of this review is to summarize the recent studies looking at the effects of anemia and red blood cell transfusion in critically-ill patients with traumatic brain injury (TBI), describe the transfusion practice variations observed worldwide, and outline the ongoing trials evaluating restrictive versus liberal transfusion strategies for TBI. RECENT FINDINGS: Anemia is common among critically-ill patients with TBI, it is also thought to exacerbate secondary brain injury, and is associated with an increased risk of poor outcome. Conversely, allogenic red blood cell transfusion carries its own risks and complications, and has been associated with worse outcomes. Globally, there are large reported differences in the hemoglobin threshold used for transfusion after TBI. Observational studies have shown differential results for improvements in cerebral oxygenation and metabolism after red blood cell transfusion in TBI. SUMMARY: Currently, there is insufficient evidence to make strong recommendations regarding which hemoglobin threshold to use as a transfusion trigger in critically-ill patients with TBI. There is also uncertainty whether the restrictive transfusion strategy used in general critical care can be extrapolated to acutely brain injured patients. Ultimately, the consequences of anemia-induced cerebral injury need to be weighed up against the risks and complications associated with red blood cell transfusion.

Heparin-Induced Thrombocytopenia in the Critically Ill Patient.

Heparin-induced thrombocytopenia (HIT) is associated with clinically significant morbidity and mortality. Patients who are critically ill are commonly thrombocytopenic and exposed to heparin. Although HIT should be considered, it is not usually the cause of thrombocytopenia in the medical-surgical ICU population. A systematic approach to the patient who is critically ill who has thrombocytopenia according to clinical features, complemented by appropriate laboratory confirmation, should lead to a reduction in inappropriate laboratory testing and reduce the use of more expensive and less reliable anticoagulants. If the patient is deemed as being at intermediate or high risk for HIT or if HIT is confirmed by means of the serotonin-release assay, heparin should be stopped, heparin-bonded catheters should be removed, and a direct antithrombin or fondaparinux should be initiated to reduce the risk of thrombosis. Warfarin is absolutely contraindicated in the acute phase of HIT; if administered, its effects must be reversed by using vitamin K.