Packed red blood cell transfusion increases local cerebral oxygenation*

Objective:To determine a) whether packed red blood cell transfusion (RBCT) increases local brain tissue oxygen partial pressure (Pbto2) in a neurocritical care population; and b) what (if any) demographic, clinical, or physiologic variables mediate the assumed change. Design:Prospective observational study. Setting:A neurosurgical intensive care unit at a university-based level I trauma center and tertiary care hospital. Patients:Thirty-five consecutive volume-resuscitated patients with subarachnoid hemorrhage or traumatic brain injury, without cardiac disease, requiring Pbto2 monitoring and receiving RBCT were studied between October 2001 and December 2003. Interventions:None. Measurements and Main Results:The following physiologic variables were measured and compared 1 hr before and after RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturation (Sao2), Fio2, hemoglobin, and hematocrit. An increase in Pbto2 was observed in 26 of the 35 patients (74%). In nine patients, Pbto2 decreased after RBCT. The mean (±sd) increase in Pbto2 for all patients was 3.2 ± 8.8 mm Hg (p = .02), a 15% change from baseline (1 hr before RCBT). This Pbto2 increase was associated with a significant mean increase in hemoglobin and hematocrit after RBCT (1.4 ± 1.1 g/dL and 4.2% ± 3.3%, respectively; both p < .001). Cerebral perfusion pressure, Sao2, and Fio2 were similar before and after RBCT. Among the 26 patients whose Pbto2 increased, the mean increase in Pbto2 was 5.1 ± 9.4 mm Hg or a 49% mean increase (p < .01). Conclusions:RBCT is associated with an increase in Pbto2 in most patients with subarachnoid hemorrhage or traumatic brain injury. This mean increase appears to be independent of cerebral perfusion pressure, Sao2, and Fio2. Further study is required to determine why Pbto2 decreases in some patients after RBCT.

[1]  W. Sibbald,et al.  Transfusing red blood cells stored in citrate phosphate dextrose adenine-1 for 28 days fails to improve tissue oxygenation in rats. , 1997, Critical care medicine.

[2]  E. Moore,et al.  Age of transfused blood is an independent risk factor for postinjury multiple organ failure. , 1999, American journal of surgery.

[3]  S. Kleinman,et al.  A Multicenter, Randomized, Controlled Clinical Trial of Transfusion Requirements in Critical Care , 1999 .

[4]  P. Barie,et al.  Failure of red blood cell transfusion to increase oxygen transport or mixed venous PO2 in injured patients. , 1982, The Journal of trauma.

[5]  G. Schneider,et al.  Influence of hyperventilation on brain tissue-PO2, PCO2, and pH in patients with intracranial hypertension. , 1998, Acta neurochirurgica. Supplement.

[6]  H. Winn,et al.  Management of the ruptured aneurysm. , 1998, Neurosurgery clinics of North America.

[7]  S. Conrad,et al.  Effect of red cell transfusion on oxygen consumption following fluid resuscitation in septic shock. , 1990, Circulatory shock.

[8]  T. Clemmer,et al.  Descriptive analysis of critical care units in the United States , 1992, Critical care medicine.

[9]  J. P. Elliott,et al.  Blood Transfusion during Aneurysm Surgery , 2001, Neurosurgery.

[10]  W J Sibbald,et al.  Effect of stored-blood transfusion on oxygen delivery in patients with sepsis. , 1993, JAMA.

[11]  R. Bullock,et al.  Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. , 1999, Journal of neurosurgery.

[12]  J. Povlishock,et al.  The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Critical pathway for the treatment of established intracranial hypertension. , 2000, Journal of neurotrauma.

[13]  H. Cowell Perioperative red blood-cell transfusion. , 1989, The Journal of bone and joint surgery. American volume.

[14]  P. Mintz,et al.  Blood Use in Cerebrovascular Neurosurgery , 2002, Stroke.

[15]  H. Corwin,et al.  RBC transfusion in the ICU. Is there a reason? , 1995, Chest.

[16]  David F Wilson,et al.  Effect of Hemorrhagic Hypotension on Cortical Oxygen Pressure and Striatal Extracellular Dopamine in Cat Brain , 1997, Neurochemical Research.

[17]  P. Kirkpatrick On guidelines for the management of the severe head injury. , 1997, Journal of neurology, neurosurgery, and psychiatry.

[18]  M. Poca,et al.  Does an increase in cerebral perfusion pressure always mean a better oxygenated brain? A study in head-injured patients. , 2000, Acta neurochirurgica. Supplement.

[19]  A. Perneczky,et al.  Brain tissue pO2 related to SjvO2, ICP, and CPP in severe brain injury , 2000, Neurosurgical Review.

[20]  G. Manley,et al.  Brain tissue oxygenation during hemorrhagic shock, resuscitation, and alterations in ventilation. , 1999, The Journal of trauma.

[21]  F. Cerra,et al.  Descriptive analysis of critical care units in the United States: Patient characteristics and intensive care unit utilization , 1993, Critical care medicine.

[22]  Consensus conference. Perioperative red blood cell transfusion. , 1988, JAMA.

[23]  G. Manley,et al.  Carbon Dioxide Reactivity and Pressure Autoregulation of Brain Tissue Oxygen , 2001, Neurosurgery.

[24]  H. Winn,et al.  Blood transfusion and increased risk for vasospasm and poor outcome after subarachnoid hemorrhage. , 2004, Journal of neurosurgery.

[25]  N. Laird,et al.  Perioperative red blood cell transfusion , 1988 .

[26]  S. Gross,et al.  Hemoglobin as a chariot for NO bioactivity , 2002, Nature Medicine.

[27]  E. Steyerberg,et al.  CO2 reactivity and brain oxygen pressure monitoring in severe head injury , 2000, Critical care medicine.

[28]  J. Vincent,et al.  Anemia and blood transfusion in critically ill patients. , 2002, JAMA.

[29]  G. Tomei,et al.  Guidelines for the treatment of adults with severe head trauma (part II). Criteria for medical treatment. , 2000, Journal of neurosurgical sciences.