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O-032 Role of bedside multi-modality monitoring in detection of cerebral vasospasm following subarachnoid hemorrhage
  1. K Khatibi1,
  2. V Szeder2,
  3. G Korbakis1,
  4. M Buitrago Blanco1,
  5. S Tateshima2,
  6. R Jahan1,
  7. G Duckwiler1,
  8. P Vespa1
  1. 1Neurosurgery, UCLA, Los Angeles, CA
  2. 2Radiology, UCLA, Los Angeles, CA


Introduction/Purpose After aneurysmal subarachnoid hemorrhage (SAH) patients are at risk for delayed ischemic neurologic deficits (DIND), that is thought to be secondary to vasospasm. DIND is suspected in the setting of depressed arousal or focal neurologic deficits and confirmed radiographically. Implanted brain monitors facilitate the detection of DIND and the assessment of treatment effectiveness when unable to follow neurologic examination. In this study we evaluated the efficacy of (1) continuous brain tissue oxygenation (PBTO2) monitoring, (2) glucose, and (3) lactate to pyruvate ratio (LPR) in detecting local vasospasm when confirmed by digital subtraction angiography (DSA).

Materials and methods This retrospective observational study that includes 10 patients with high grade SAH, assessed over multiple time points. The extent of angiographic vasospasm for each vessel was subjectively graded by 5 different neuro-interventionalists. The grading then was quantified as 0 (no spasm) to 6 (severe spasm). The intracranial probes were placed at the Kochers point which lies at the watershed area between the anterior cerebral artery (ACA) and middle cerebral artery (MCA) on corresponding side closest focus to the pathology. The extent of vasospasm was estimated by the weighted average of (1 × ACA +2 × MCA+3 × internal carotid artery (ICA))/6. Presence of clinically significant spasm was defined to be equal or greater than 2 (mild spasms). PBTO2, glucose, and LPR measurements were averaged over the 24 hour period prior to each DSA. The bedside measurements from all patients were divided in the two groups with and without spasm and were compared in between patients using a two-tailed non-paired student T-test.

Results Sixteen time intervals were evaluated for PBTO2 and 18 intervals for glucose and LPR. The average PBTO2 during spasm was significantly lower (17.6+/-5.5 versus 23.8+/-3.73, p=0.003). Glucose was non-significantly lower during spasm: 0.6 versus 1.1, p=0.15). LPR was also non-significantly higher in spasm (34.5 versus 28.6, p=0.24). In the subjects with multiple time intervals PbtO2 negatively correlates with degree of vasospasm (r=−0.97±0.05).

Conclusion Multi-modality monitoring (MMM) of comatose patients with SAH yields potentially useful but difficult to interpret information in the setting of vasospasm, and clear diagnostic thresholds have yet to be determined. Quantitative comparison of MMM and DSA in the setting of vasospasm would be more reliable with more accurate approach to quantifying cerebral blood flow from angiography.

Disclosures K. Khatibi: None. V. Szeder: None. G. Korbakis: None. M. Buitrago Blanco: None. S. Tateshima: None. R. Jahan: None. G. Duckwiler: None. P. Vespa: None.

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