Brain Metabolism During a Decrease in Cerebral Perfusion Pressure Caused by an Elevated Intracranial Pressure in the Porcine Neocortex

Abstract Patients treated with barbiturate coma for elevated intracranial pressure after head injury may suffer brain death. Since such patients have an iatrogenically induced absence of neurological function, brain death cannot be diagnosed clinically. Furthermore, as demonstrated by two of our patients, monitoring of intracranial pressure, even in the face of brain death, may show a low intracranial pressure and an intracranial pulse, suggesting the presence of adequate cerebral perfusion pressure and, therefore, brain viability. Under these circumstances. however, significant intracranial blood flow may be absent. Therefore, we suggest that a patient in barbiturate coma should undergo serial blood flow studies. even when the intracranial pressure is low and an intracranial pulse is present. to determine whether brain death has occurred.

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Hypertonic Saline Compared to Mannitol for the Management of Elevated Intracranial Pressure in Traumatic Brain Injury: A Meta-Analysis

Frontiers in Surgery ◽

10.3389/fsurg.2021.765784 ◽

2022 ◽

Vol 8 ◽

Author(s):

Chengchen Han ◽

Fan Yang ◽

Shengli Guo ◽

Jianning Zhang

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Perfusion Pressure ◽

Hypertonic Saline ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Meta Analysis ◽

Elevated Intracranial Pressure ◽

Lower Treatment

Background: We performed a meta-analysis to evaluate the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury.Methods: A systematic literature search up to July 2021 was performed and 17 studies included 1,392 subjects with traumatic brain injury at the start of the study; 708 of them were administered hypertonic saline and 684 were given mannitol. They were reporting relationships between the effects of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury. We calculated the odds ratio (OR) and mean difference (MD) with 95% confidence intervals (CIs) to assess the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury using the dichotomous or continuous method with a random or fixed-effect model.Results: Hypertonic saline had significantly lower treatment failure (OR, 0.38; 95% CI, 0.15–0.98, p = 0.04), lower intracranial pressure 30–60 mins after infusion termination (MD, −1.12; 95% CI, −2.11 to −0.12, p = 0.03), and higher cerebral perfusion pressure 30–60 mins after infusion termination (MD, 5.25; 95% CI, 3.59–6.91, p < 0.001) compared to mannitol in subjects with traumatic brain injury.However, hypertonic saline had no significant effect on favorable outcome (OR, 1.61; 95% CI, 1.01–2.58, p = 0.05), mortality (OR, 0.59; 95% CI, 0.34–1.02, p = 0.06), intracranial pressure 90–120 mins after infusion termination (MD, −0.90; 95% CI, −3.21–1.41, p = 0.45), cerebral perfusion pressure 90–120 mins after infusion termination (MD, 4.28; 95% CI, −0.16–8.72, p = 0.06), and duration of elevated intracranial pressure per day (MD, 2.20; 95% CI, −5.44–1.05, p = 0.18) compared to mannitol in subjects with traumatic brain injury.Conclusions: Hypertonic saline had significantly lower treatment failure, lower intracranial pressure 30–60 mins after infusion termination, and higher cerebral perfusion pressure 30–60 mins after infusion termination compared to mannitol in subjects with traumatic brain injury. However, hypertonic saline had no significant effect on the favorable outcome, mortality, intracranial pressure 90–120 mins after infusion termination, cerebral perfusion pressure 90–120 mins after infusion termination, and duration of elevated intracranial pressure per day compared to mannitol in subjects with traumatic brain injury. Further studies are required to validate these findings.

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Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

Journal of Neurosurgery ◽

10.3171/jns.1988.68.5.0745 ◽

1988 ◽

Vol 68 (5) ◽

pp. 745-751 ◽

Cited By ~ 28

Author(s):

Werner Hassler ◽

Helmuth Steinmetz ◽

Jan Gawlowski

Keyword(s):

Intracranial Pressure ◽

Brain Death ◽

Intracranial Hypertension ◽

Cerebral Perfusion Pressure ◽

Transcranial Doppler ◽

Cerebral Perfusion ◽

Doppler Ultrasonography ◽

Perfusion Pressure ◽

Circulatory Arrest ◽

Transcranial Doppler Ultrasonography

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

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Intratracheal Suctioning in Sick Preterm Infants: Prevention of Intracranial Hypertension and Cerebral Hypoperfusion by Muscle Paralysis

PEDIATRICS ◽

10.1542/peds.79.4.538 ◽

1987 ◽

Vol 79 (4) ◽

pp. 538-543

Author(s):

Sergio Fanconi ◽

Gabriel Duc

Keyword(s):

Heart Rate ◽

Intracranial Pressure ◽

Cerebral Perfusion Pressure ◽

Preterm Infants ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Muscle Paralysis ◽

Endotracheal Suctioning ◽

Significant Difference ◽

Transcutaneous Po2

In a prospective nonrandomized study, using each baby as his or her own control, we compared intracranial pressure (anterior fontanel pressure as measured with the Digilab pneumotonometer), cerebral perfusion pressure, BP, heart rate, transcutaneous Po2, and transcutaneous Pco2 before, during, and after endotracheal suctioning, with and without muscle paralysis, in 28 critically ill preterm infants with respiratory distress syndrome. With suctioning, there was a small but significant increase in intracranial pressure in paralyzed patients (from 13.7 [mean] ± 4.4 mm Hg [SD] to 15.8 ± 5.2 mm Hg) but a significantly larger (P < .001) increase when they were not paralyzed (from 12.5 ± 3.6 to 28.5 ± 8.3 mm Hg). Suctioning led to a slight increase in BP with (from 45.3 ± 9.1 to 48.0 ± 8.7 mm Hg) and without muscle paralysis (from 45.1 ± 9.4 to 50.0 ± 11.7 mm Hg); but there was no significant difference between the two groups. The cerebral perfusion pressure in paralyzed infants did not show any significant change before, during, and after suctioning (31.5 ± 9.1 mm Hg before v 32.0 ± 8.7 mm Hg during suctioning), but without muscle paralysis cerebral perfusion pressure decreased (P < .001) from 32.8 ± 9.7 to 21.3 ± 13.1 mm Hg. Suctioning induced a slight decrease in mean heart rate and transcutaneous Po2, but pancuronium did not alter these changes. There was no statistical difference in transcutaneous Pco2, before, during, and after suctioning with and without muscle paralysis. Our data demonstrate that muscle paralysis in sick preterm infants can significantly minimize the increase in intracranial pressure and can stabilize the cerebral perfusion pressure without having any effect on the BP increase during suctioning.

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