Can CT Scan Findings Predict Intracranial Pressure in Closed Head Injury Patients?

1980 ◽  
pp. 48-53 ◽  
Author(s):  
F. L. Haar ◽  
V. K. Sadhu ◽  
R. S. Pinto ◽  
P. L. Gildenberg ◽  
J. M. Sampson
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Ct Scan ◽  
Closed Head Injury ◽  
Closed Head

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.

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

1998 ◽  
Vol 89 (5) ◽  
pp. 796-806 ◽  
Author(s):  
Koen Engelborghs ◽  
Jan Verlooy ◽  
Jos Van Reempts ◽  
Bruno Van Deuren ◽  
Mies Van de Ven ◽  
...  
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Experimental Model ◽  
Closed Head Injury ◽  
Content Type ◽  
Closed Head ◽  
Impact Acceleration ◽  
The Moment ◽  
The Impact ◽  
Fine Print

Object. The authors describe an experimental model of closed head injury in rodents that was modified from one developed by Marmarou and colleagues. This modification allows dual control of the dynamic process of impact compared with impulse loading that occurs at the moment of primary brain injury. The principal element in this weight-drop model is an adjustable table that supports the rat at the moment of impact from weights positioned at different heights (accelerations). The aim was to obtain reproducible pathological intracranial pressure (ICPs) while maximally reducing the incidence of mortality and skull fractures. Methods. Intracranial pressure was investigated in different experimental settings, including two different rat strains and various impact-acceleration conditions and posttrauma survival times. Identical impact-acceleration injuries produced a considerably higher mortality rate in Wistar rats than in Sprague—Dawley rats (50% and 0%, respectively). Gradually increasing severity of impact-acceleration conditions resulted in findings of a significant correlation between the degree of traumatic challenge and increased ICP at 4 hours (p < 0.001, R2 = 0.73). When the impact-acceleration ratio was changed to result in a more severe head injury, the ICP at 4, 24, and 72 hours was significantly elevated in comparison with that seen in sham-injured rats (4 hours: 19.7 ± 2.8 mm Hg, p = 0.004; 24 hours: 21.8 ± 1.1 mm Hg, p = 0.002; 72 hours: 11.9 ± 2.5 mm Hg, p = 0.009). Comparison of the rise in ICP between moderate and severe impact-acceleration injury at 4 and 24 hours revealed a significantly higher value after severe injury (4 hours: p = 0.008; 24 hours: p = 0.004). Continuous recordings showed that ICP mounted very rapidly to peak values, which declined gradually toward a pathological level dependent on the severity of the primary insult. Histological examination after severe trauma revealed evidence of irreversible neuronal necrosis, diffuse axonal injury, petechial bleeding, glial swelling, and perivascular edema. Conclusions. This modified closed head injury model mimics several clinical features of traumatic injury and produces reliable, predictable, and reproducible ICP elevations with concomitant morphological alterations.

Increased intracranial pressure is associated with elevated cerebrospinal fluid ADH levels in closed-head injury

2010 ◽  
Vol 32 (10) ◽  
pp. 1021-1026 ◽  
Author(s):  
Marsha A. Widmayer ◽  
Jeffrey L. Browning ◽  
Shankar P. Gopinath ◽  
Claudia S. Robertson ◽  
David S. Baskin
Keyword(s):  
Cerebrospinal Fluid ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Closed Head Injury ◽  
Increased Intracranial Pressure ◽  
Closed Head

scholarly journals Temporal changes in intracranial pressure in a modified experimental model of closed head injury

2001 ◽  
Vol 11 (4) ◽  
pp. 796-806
Author(s):  
Koen Engelborghs ◽  
Jan Verlooy ◽  
Jos Van Reempts ◽  
Bruno Van Deuren ◽  
Mies Van de Ven ◽  
...  
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Experimental Model ◽  
Diffuse Axonal Injury ◽  
Closed Head Injury ◽  
Neuronal Necrosis ◽  
Closed Head ◽  
Impact Acceleration ◽  
The Moment ◽  
The Impact

Object The authors describe an experimental model of closed head injury in rodents that was modified from one developed by Marmarou and colleagues. This modification allows dual control of the dynamic process of impact compared with impulse loading that occurs at the moment of primary brain injury. The principal element in this weight-drop model is an adjustable table that supports the rat at the moment of impact from weights positioned at different heights (accelerations). The aim was to obtain reproducible pathological intracranial pressure (ICPs) while maximally reducing the incidence of mortality and skull fractures. Methods Intracranial pressure was investigated in different experimental settings, including two different rat strains and various impact-acceleration conditions and posttrauma survival times. Identical impact-acceleration injuries produced a considerably higher mortality rate in Wistar rats than in Sprague–Dawley rats (50% and 0%, respectively). Gradually increasing severity of impact-acceleration conditions resulted in findings of a significant correlation between the degree of traumatic challenge and increased ICP at 4 hours (p < 0.001, R2 = 0.73). When the impact-acceleration ratio was changed to result in a more severe head injury, the ICP at 4, 24, and 72 hours was significantly elevated in comparison with that seen in sham-injured rats (4 hours: 19.7 ± 2.8 mm Hg, p = 0.004; 24 hours: 21.8 ± 1.1 mm Hg, p = 0.002; 72 hours: 11.9 ± 2.5 mm Hg, p = 0.009). Comparison of the rise in ICP between moderate and severe impact-acceleration injury at 4 and 24 hours revealed a significantly higher value after severe injury (4 hours: p = 0.008; 24 hours: p = 0.004). Continuous recordings showed that ICP mounted very rapidly to peak values, which declined gradually toward a pathological level dependent on the severity of the primary insult. Histological examination after severe trauma revealed evidence of irreversible neuronal necrosis, diffuse axonal injury, petechial bleeding, glial swelling, and perivascular edema. Conclusions This modified closed head injury model mimics several clinical features of traumatic injury and produces reliable, predictable, and reproducible ICP elevations with concomitant morphological alterations.

Continuous measurement of intracranial pressure in awake rats after experimental closed head injury

2003 ◽  
Vol 131 (1-2) ◽  
pp. 75-81 ◽  
Author(s):  
Servan Rooker ◽  
Philippe G Jorens ◽  
Jos Van Reempts ◽  
Marcel Borgers ◽  
Jan Verlooy
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Continuous Measurement ◽  
Closed Head Injury ◽  
Closed Head ◽  
Awake Rats

Effect of Mannitol on Increased Intracranial Pressure

Neurosurgery ◽  
1983 ◽  
Vol 13 (3) ◽  
pp. 269-271 ◽  
Author(s):  
C. Patrick McGraw ◽  
George Howard
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Closed Head Injury ◽  
Study Analysis ◽  
Long Term Effects ◽  
Increased Intracranial Pressure ◽  
Cumulative Amount ◽  
Closed Head ◽  
Increased Icp

Abstract We studied 61 patients with a closed head injury and increased intracranial pressure (ICP). The ICP was monitored continuously, concomitant with the administration of 20% mannitol. If the ICP remained higher than 25 mm Hg for 10 minutes or more, the patient was included in the study. Analysis of monitoring records delineated four variables that were related to the response of ICP to mannitol: (a) the level of ICP 1 hour before mannitol was administered, (b) the level of ICP when mannitol was administered, (c) the amount of mannitol that was administered immediately before the resulting changes in ICP were measured, and (d) the cumulative amount of mannitol given over the 6 hours before the most recent mannitol dosage was administered. The level of the ICP measurements and the cumulative amount of preceding doses of mannitol influenced the response of ICP to mannitol more than did the size of the dose of mannitol. These findings imply that: (a) the initial administration of more mannitol than is absolutely needed may lead to larger doses being required to control ICP and (b) for that reason, mannitol given on a gram/kilogram, an hourly, or a serum osmolarity basis to control increased ICP has negative long term effects because more mannitol may be required to decrease ICP when an excessive amount of it has been given previously.

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