scholarly journals Intracranial Pressure/Cerebral Perfusion Pressure—Targeted Management of Life-Threatening Intracranial Hypertension Complicating Diabetic Ketoacidosis—Associated Cerebral Edema

2012 ◽  
Vol 28 (8) ◽  
pp. 763
Author(s):  
&NA;
1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski

✓ 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.


1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).


1981 ◽  
Vol 55 (5) ◽  
pp. 704-707 ◽  
Author(s):  
Jon S. Huseby ◽  
John M. Luce ◽  
Jeffrey M. Cary ◽  
Edward G. Pavlin ◽  
John Butler

✓ Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in its absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.


1990 ◽  
Vol 73 (5) ◽  
pp. 725-730 ◽  
Author(s):  
Julio Cruz ◽  
Michael E. Miner ◽  
Steven J. Allen ◽  
Wayne M. Alves ◽  
Thomas A. Gennarelli

✓ Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.


1975 ◽  
Vol 43 (3) ◽  
pp. 318-322 ◽  
Author(s):  
Lawrence F. Marshall ◽  
David I. Graham ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
Frank Welsh ◽  
...  

✓ The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.


PEDIATRICS ◽  
1987 ◽  
Vol 79 (4) ◽  
pp. 538-543
Author(s):  
Sergio Fanconi ◽  
Gabriel Duc

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.


Sign in / Sign up

Export Citation Format

Share Document