Abstract SNACC-11

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Positive neurological outcome after acute neurosurgical hemorrhage and sustained hypotension

Zelman V, Ayrian E, O'Barr T
University of Southern California, Los Angeles, California, USA

Introduction

About 75% of cardiac output is directed to vessel-rich tissues. During acute hemorrhage, cardiac output is redistributed to tissues of higher metabolic activity. We describe a case of preserved cardiac output during acute surgical hemorrhage and sustained hypotension.

Case Report

• A 65 year-old male ASA 3 to undergo resection of a meningioma without prior embolization therapy.
• Neurologic exam positive for mild aphasia and memory loss.
• Lasix and mannitol given upon induction.
• Anesthesia maintained with propofol and remifentanil.
• Opening of meningioma capsule resulted in blood loss of 3300 mls over 30 minutes. MAP’s were 25-45 mm Hg for the next 3 hours with HR > 110.
• ETCO2 was 29-36 mm Hg despite sustained hypotension.
• ABG’s consistent with metabolic acidosis from hypovolemia and hypoperfusion, corrected by massive transfusion and vasopressors. Total blood loss was 8000 mls.
• By POD 1, the patient was able to open his eyes and on POD 2 was following commands. No new cognitive or sensorimotor deficits were observed at time of discharge on POD9.

Discussion

Severe hypotension and global cerebral ischemia can lead to poor patient outcomes. Our patient had a positive neurologic outcome despite sustained hypotension, which can be attributed to several mechanisms:

1. The redistribution of the cardiac output to major organ systems as evidenced by a preserved EtCO2. Intra-op hypotension can worsen outcome but studies have proved that a lower SBP during hemorrhage did not affect mortality. Functional or histologic brain damage was not seen in rats following hemorrhagic shock. Despite hypotension, perfusion to vital organs is adequate while decreased in other organ systems such as the splanchnic system.

2. Propofol offers cerebral protective effects through its action on GABA receptors, free radical scavenging, and limiting lipid peroxidation. It also attenuates of the catecholamine surge seen during ischemia.

3. ICP reductions with the use of mannitol and lasix permit adequate CPP during sustained hypotension.


Conclusion

Our patient’s survival and positive neurologic outcome after major blood loss and hypotension can be attributed to a few key cerebral protective mechanisms.
• Preservation of cerebral blood flow by redistribution during times of hypotension.
• Agents that promote cerebral protection by improving CPP and attenuating the cellular effects of ischemia.

References

1) Dutton RP et al: Hypotensive Resuscitation during Active Hemorrhage: Impact on In-Hospital Mortality. J of Trauma-Injury Infection & Crit Care. 06/02

2) Carrillo P et al: Prolonged Severe Hemorrhagic Shock and Resuscitation in Rats Does Not Cause Subtle Brain Damage. J of Trauma-Injury Infection & Crit Care. 08/98

3) Toung T et al: Mesenteric Vasoconstriction in Response to Hemorrhagic Shock. Shock. 04/00

4) Young Y et al: Propofol neuroprotection in a rat model of ischaemia reperfusion injury. Euro J of Anaesthesiology. 1997

5) T. Yamasaka et al: Effects of graded suppression of the EEG with propofol on the neurological 05/99

6) Bratton SL et al: Hyperosmolar therapy. J of Neurotrauma. 05/07


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