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

PEDIATRICS ◽  
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.

Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

1993 ◽  
Vol 265 (5) ◽  
pp. H1557-H1563 ◽  
Author(s):  
M. L. Kearney ◽  
J. E. Backofen ◽  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Fetal Sheep ◽  
Peripheral Vasoconstriction ◽  
Significant Difference

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.

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

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
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.

Management of raised intracranial pressure

2020 ◽  
pp. 3892-3897
Author(s):  
David K. Menon
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Brain Oedema ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Brain Perfusion ◽  
Normal Brain ◽  
Intracranial Volume ◽  
Nervous System Diseases

Normal intracranial pressure is between 5 and 15 mm Hg in supine subjects. Intracranial hypertension (ICP >20 mm Hg) is common in many central nervous system diseases and in fatal cases is often the immediate cause of death. Increases in intracranial volume and hence—given the rigid skull—intracranial pressure may be the consequence of brain oedema, increased cerebral blood volume, hydrocephalus, and space-occupying lesions. Brain perfusion depends on the cerebral perfusion pressure which is mean arterial pressure minus intracranial pressure. The normal brain autoregulates cerebral blood flow down to a lower limit of cerebral perfusion pressure of about 50 mm Hg in healthy subjects, and perhaps 60–70 mm Hg in disease. Cerebral perfusion pressure reduction to below these values results in cerebral ischaemia.

Effect of Early Physiotherapy on Intracranial Pressure and Cerebral Perfusion Pressure

2012 ◽  
Vol 18 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Christian Roth ◽  
Hubertus Stitz ◽  
Anas Kalhout ◽  
Jens Kleffmann ◽  
Wolfgang Deinsberger ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure
Sign in / Sign up

Export Citation Format

Share Document