Early changes of intracranial pressure, perfusion pressure, and blood flow after acute head injury

1989 ◽  
Vol 70 (5) ◽  
pp. 774-779 ◽  
Author(s):  
Ernst G. Pfenninger ◽  
Andreas Reith ◽  
Dieter Breitig ◽  
Ad Grünert ◽  
Friedrich W. Ahnefeld
Keyword(s):  
Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Cerebral Circulation ◽  
Perfusion Pressure ◽  
Control Group ◽  
Sudden Increase ◽  
Subsequent Increase ◽  
Systemic Hemodynamic ◽  
The Impact

✓ The present study examines intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral circulation immediately after experimental head injury in an animal model. The underlying systemic hemodynamic changes were also observed. To produce a standardized head injury, a fluid-percussion device was applied to the dura at the midline of 10 piglets. Seven other nontraumatized animals served as a control group. Hemodynamic parameters as well as ICP and CPP were recorded on-line, one value every 1.4 seconds. Cerebral blood flow (CBF) and cerebral vascular resistance (CVR) were measured three times using a microsphere technique. Immediately after head injury, the traumatized animals showed a sudden increase in ICP, with a maximum of 40 torr at 3 to 5 minutes, while there was a pronounced decrease in CPP from 85 to 40 torr. The CBF in the various brain areas fell from 55 to 22 ml/min/100 gm within 5 minutes after the impact, and CVR increased to 300% of control values within 90 minutes. The findings of this study demonstrated that cerebral circulation is critically jeopardized within a few minutes after trauma. This, in combination with a subsequent increase in CVR, makes the early development of ischemic brain damage very likely. In traumatized patients, treatment prior to hospital admission must therefore be directed at prevention of this fatal course.

Detection of Brain Death in Barbiturate Coma: The Dilemma of an Intracranial Pulse

Neurosurgery ◽  
1989 ◽  
Vol 25 (2) ◽  
pp. 275-278 ◽  
Author(s):  
Howard H. Kaufman ◽  
Fred H. Geisler ◽  
Thomas Kopitnik ◽  
William Higgins ◽  
Dan Stewart
Keyword(s):  
Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Brain Death ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Elevated Intracranial Pressure ◽  
Barbiturate Coma ◽  
The Face

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.

scholarly journals EFFECT OF 30° HEAD-UP POSITION ON INTRACRANIAL PRESSURE CHANGE IN PATIENTS WITH HEAD INJURY IN SURGICAL WARD OF GENERAL HOSPITAL OF Dr. R. SOEDARSONO PASURUAN

2017 ◽  
Vol 3 (3) ◽  
pp. 89-95 ◽  
Author(s):  
Sumirah Budi Pertami ◽  
Sulastyawati Sulastyawati ◽  
Puthut Anami
Keyword(s):  
Mean Arterial Pressure ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Control Group ◽  
P Value ◽  
Increased Intracranial Pressure ◽  
Head Injured ◽  
Injured Patients ◽  
The Impact

Background: Head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the 15 degrees head-up position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of 30 and 15 degrees on intracranial pressure change.Methods: This was a quasi-experimental study with posttest only control time series time design.  There were 30 head-injured patients was selected using consecutive sampling, with 15 assigned in the treatment (30° head-up position) and control group (15° head-up position). Intracranial pressure variable was identified using the level of consciousness and mean arterial pressure parameters. Wilcoxon signed rank test was used for data analysisResults: Findings showed p-value 0.010 (0.05) on awareness level and p-value 0.031 (0.05) on mean arterial pressure, which indicated that there was a statistically significant effect of the 30° head-up position on level of awareness and mean arterial pressure.Conclusion: There was a significant effect of the 30° head-up position on intracranial pressure changes, particularly in the level of awareness and mean arterial pressure in patients with head injury. It is recommended that for health workers to provide knowledge regarding this intervention to prevent increased intracranial pressure.

Effects of Head Posture on Cerebral Hemodynamics: Its Influences on Intracranial Pressure, Cerebral Perfusion Pressure, and Cerebral Oxygenation

Neurosurgery ◽  
2004 ◽  
Vol 54 (3) ◽  
pp. 593-598 ◽  
Author(s):  
Ivan Ng ◽  
Joyce Lim ◽  
Hwee Bee Wong
Keyword(s):  
Mean Arterial Pressure ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Oxygenation ◽  
Closed Head Injury ◽  
Head Posture ◽  
Head Elevation ◽  
Closed Head

Abstract OBJECTIVE Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 ± 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.

Intracranial pressure monitoring in the ICU

2016 ◽  
Author(s):  
Jonathan K. J. Rhodes ◽  
Peter J. D. Andrews
Keyword(s):  
Brain Injury ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
South American ◽  
Pressure Monitoring ◽  
Recent Trial ◽  
Computed Tomographic ◽  
The Central Nervous System ◽  
Monitoring Modality ◽  
The Impact

Intracranial pressure (ICP) measurement is an established monitoring modality in the ICU and can aid prognostication after acute brain injury. ICP monitoring is recommended in all patients with severe traumatic brain injury (TBI), and an abnormal cranial computed tomographic (CT) scan and the ability to control ICP is associated with improved outcome after TBI. The lessons from TBI studies can also be applied to other acute pathologies of the central nervous system where ICP can be increased. ICP measurement can warn of impending disaster and allow intervention. Furthermore, measurement of ICP allows the calculation of cerebral perfusion pressure (CPP) and maintenance of CPP may help to ensure adequate cerebral oxygen delivery. Various systems exist to monitor ICP. A recent trial in two South American countries suggested that ICP-guided management and management guided by clinical examination and repeated imaging produced equivalent outcomes. Although this trial currently provides the best evidence regarding the impact of monitoring ICP on outcome following TBI, but because of the inadequate power and questionable external validity, the generalizability of the results remain to be confirmed.

ATP-sensitive K+ channel blockade impairs O2 extraction during progressive ischemia in pig hindlimb

1995 ◽  
Vol 79 (6) ◽  
pp. 2035-2042 ◽  
Author(s):  
B. Vallet ◽  
S. E. Curtis ◽  
B. Guery ◽  
J. Mangalaboyi ◽  
P. Menager ◽  
...  
Keyword(s):  
Blood Flow ◽  
Redox State ◽  
Perfusion Pressure ◽  
Glucose Solution ◽  
K Channel ◽  
Control Group ◽  
Cytochrome Aa3 ◽  
K Channels ◽  
O2 Extraction ◽  
O2 Delivery

Tissues maintain O2 consumption (VO2) when blood flow and O2 delivery (DO2) are decreased by better matching of blood flow to meet local cellular O2 demand, a process that increases extraction of available O2. This study tested the hypothesis that ATP-sensitive K+ channels play a significant role in the response of pig hindlimb to ischemia. We pump perfused the vascularly isolated but innervated right hindlimb of 14 anesthetized pigs with normoxic blood while measuring hindlimb DO2, VO2, perfusion pressure, and cytochrome aa3 redox state. In one-half of the pigs, the pump-perfused hindlimb was also infused with 10 micrograms.min-1.kg-1 of glibenclamide, a potent blocker of ATP-sensitive K+ channels. Control animals were infused with 5% glucose solution alone. Blood flow was then progressively reduced in both groups in 10 steps at 10-min intervals. Glibenclamide had no effect on any preischemic hindlimb or systemic measurements. Hindlimb VO2 and cytochrome aa3 redox state began to decrease at a significantly higher DO2 in glibenclamide-treated compared with control pigs. At this critical DO2, the O2 extraction ratio (VO2/DO2) was 53 +/- 4% in the glibenclamide group and 73 +/- 5% in the control group (P < 0.05). Hindlimb vascular resistance increased significantly with ischemia in the glibenclamide group but did not change in the control group. We conclude that ATP-sensitive K+ channels may be importantly involved in the vascular recruitment response that tried to meet tissue O2 needs as blood flow was progressively reduced in the pig hindlimb.

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