Transcranial doppler monitoring compared with invasive monitoring of intracranial pressure during acute intracranial hypertension

• Published in: Journal of clinical monitoring and computing Vol. 15; no. 3-4; pp. 185 - 195
• Main Authors: SIDI, A, MESSINGER, G, MAHLA, M. E
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer 01.05.1999; Springer Nature B.V
• Subjects: Acute Disease; Animals; Biological and medical sciences; Blood; Blood Flow Velocity; Blood vessels; Catheters; Epinephrine; Hemodynamics; Intracranial Hypertension - diagnosis; Intracranial Hypertension - diagnostic imaging; Intracranial Pressure - physiology; Investigative techniques, diagnostic techniques (general aspects); Medical sciences; Nervous system; Oxygen; Patient monitoring; Pressure; Pulsatile Flow; Sensitivity and Specificity; Swine; Ultrasonic investigative techniques; Ultrasonic velocity measurement; Ultrasonography, Doppler, Transcranial; Sonography; Human; Nervous system diseases; Intracranial hypertension; Exploration; Intracranial pressure; Duplex ultrasonography; Cerebral disorder; Blood flow; Transcranial route; Surveillance; Central nervous system disease; Medical imagery; Monitoring
• ISSN: 1387-1307; 1573-2614
• DOI: 10.1023/A:1009993232534

To determine whether a simple transcanial Doppler waveform variable-pulsatility difference (systolic - diastolic blood flow velocity) can serve as a measure of critical changes in cerebral perfusion. Thirteen pigs were anesthetized (anesthesia maintained with halothane) and ventilated to maintain normoxia and normocarbia. To measure mean arterial pressure, hemoglobin, and blood gases, the right carotid artery was cannulated. The right intracranial lateral ventricle was cannulated to measure and increase intracranial pressure; the right internal jugular vein was cannulated in 8 of 13 pigs to measure jugular venous oxygen saturation and to calculate cerebral arteriovenous oxygen content difference. Intracranial pressure was also monitored continuously with a subdural bolt in the contralateral frontal region, and blood flow velocity in the middle cerebral artery was measured with a transcranial Doppler probe on the right orbital region. Intracranial pressure was increased in increments of 10 to 20 mmHg by infusing saline through the ventriculostomy catheter until the transcranial Doppler indicated that blood flow velocity had ceased, at which point all variables were allowed to return to baseline. If mean arterial pressure failed to return to baseline, epinephrine, 0.01 to 0.1 microg/kg/min, was infused. Useful data were obtained from 8 pigs and were analyzed separately for pigs that received epinephrine (n = 4) and those that did not (n = 4). Transcranial Doppler measurements correlated more closely with cerebral perfusion pressure = (mean arterial pressure - intracranial pressure) than with intracranial pressure. In the range of 30 to 60 mmHg, cerebral perfusion pressure correlated linearly with the pulsatility difference. The closest nonlinear correlation (third order polynomial relationship) was noted between cerebral perfusion pressure and pulsatility difference (r = 0.8, P < 0.001, n = 217), for the animals that did not receive epinephrine. When a cerebral perfusion pressure < 60 mmHg and a cerebral arteriovenous oxygen content difference > 6.5 vol% were used to define limits of abnormal, pulsatility difference was a sensitive and specific indicator of abnormality in either variable. Pulsatility difference of > 70 cm/sec had > 77.1% and 86.7% positive accuracy rate, and < 0% and 14.3% negative accuracy rate for abnormal cerebral perfusion pressure (CPP) and cerebral arterio-venous O2 (C[a-v]O2), respectively. In pigs with induced diffuse intracranial hypertension, noninvasive transcranial Doppler waveform monitoring of pulsatility difference can identify increased cerebral oxygen extraction and dangerously decreased cerebral perfusion pressure.