Demonstration of massive traumatic brain swelling within 20 minutes after injury

1977 ◽  
Vol 46 (2) ◽  
pp. 256-258 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Eugene Timmins ◽  
Rodwan K. Rajjoub ◽  
Hugo V. Rizzoli ◽  
David O. Davis
Keyword(s):  
Head Injury ◽  
Closed Head Injury ◽  
Brain Swelling ◽  
Axial Tomography ◽  
Content Type ◽  
Closed Head ◽  
Vascular Dilatation ◽  
Computerized Axial Tomography ◽  
The Brain ◽  
Fine Print

✓ The authors documented by computerized axial tomography a case of massive brain swelling occurring within 20 minutes of a closed head injury. It is suggested that the cause of the brain swelling is acute vascular dilatation.

The use of moderate therapeutic hypothermia for patients with severe head injuries: a preliminary report

1993 ◽  
Vol 79 (3) ◽  
pp. 354-362 ◽  
Author(s):  
Donald W. Marion ◽  
Walter D. Obrist ◽  
Patricia M. Earlier ◽  
Louis E. Penrod ◽  
Joseph M. Darby
Keyword(s):  
Head Injury ◽  
Therapeutic Hypothermia ◽  
Closed Head Injury ◽  
Metabolic Effects ◽  
Secondary Brain Injury ◽  
Content Type ◽  
Closed Head ◽  
Hypothermia Group ◽  
Rebound Increase ◽  
Fine Print

✓ Animal research suggests that moderate therapeutic hypothermia may improve outcome after a severe head injury, but its efficacy has not been established in humans. The authors randomly assigned 40 consecutively treated patients with a severe closed head injury (Glasgow Coma Scale score 3 to 7) to either a hypothermia or a normothermia group. Using cooling blankets and cold saline gastric lavage, patients in the hypothermia group were cooled to 32° to 33°C (brain temperature) within a mean of 10 hours after injury, maintained at that temperature for 24 hours, and rewarmed to 37° to 38°C over 12 hours. Patients in the normothermia group were maintained at 37° to 38°C during this time. Deep-brain temperatures were monitored directly and used for all temperature determinations. Intracranial pressure (ICP), cerebral blood flow (CBF), and cerebral metabolic rate for oxygen (CMRO2) were measured serially for all patients. Hypothermia significantly reduced ICP (40%) and CBF (26%) during the cooling period, and neither parameter showed a significant rebound increase after patients were rewarmed. Compared to the normothermia group, the mean CMRO2 in the hypothermia group was lower during cooling and higher 5 days after injury. Three months after injury, 12 of the 20 patients in the hypothermia group had moderate, mild, or no disabilities; eight of the 20 patients in the normothermia group had improved to the same degree. Both groups had a similar incidence of systemic complications, including cardiac arrhythmias, coagulopathies, and pulmonary complications. It is concluded that therapeutic moderate hypothermia is safe and has sustained favorable effects on acute derangements of cerebral physiology and metabolism caused by severe closed head injury. The trend toward better outcome with hypothermia may indicate that its beneficial physiological and metabolic effects limit secondary brain injury.

Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion

2001 ◽  
Vol 95 (6) ◽  
pp. 1053-1056 ◽  
Author(s):  
Michael L. Cannon ◽  
Steven S. Glazier ◽  
Loren A. Bauman
Keyword(s):  
Metabolic Acidosis ◽  
Head Injury ◽  
Myocardial Dysfunction ◽  
Closed Head Injury ◽  
Pediatric Intensive Care ◽  
Cardiovascular Collapse ◽  
Severe Metabolic Acidosis ◽  
Content Type ◽  
Closed Head ◽  
Fine Print

✓ The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 µg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's Glasgow Coma Scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.

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.

Changes in cerebral blood flow during PaCO2 variations in patients with severe closed head injury: comparison between the Fick and transcranial Doppler methods

1998 ◽  
Vol 88 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
Aram Ter Minassian ◽  
Eliane Melon ◽  
Caroline Leguerinel ◽  
Carlo Alberto Lodi ◽  
Françis Bonnet ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Transcranial Doppler ◽  
Closed Head Injury ◽  
High Group ◽  
Content Type ◽  
Closed Head ◽  
Fine Print ◽  
Group 1

Object. The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. Methods. The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, “high” and “low,” with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (Δ)AVDO2 and ΔMCAv was not different from identity in the low group (1/ΔAVDO2 = 1.08 × ΔMCAv − 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/ΔAVDO2 = 1.46 × ΔMCAv − 0.4, r = 0.83, p < 0.001). Conclusions. In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.

Vertebral artery rupture associated with closed head injury

1985 ◽  
Vol 62 (1) ◽  
pp. 135-138 ◽  
Author(s):  
John M. McLean ◽  
Robert M. Wright ◽  
John P. Henderson ◽  
J. Richard Lister
Keyword(s):  
Head Injury ◽  
Vertebral Artery ◽  
Closed Head Injury ◽  
Mechanism Of Injury ◽  
Content Type ◽  
The Third ◽  
Closed Head ◽  
Angiographic Evidence ◽  
Head And Neck Injury ◽  
Fine Print

✓ The authors report two patients with closed head injury who suffered laceration with rupture of the third portion of the vertebral artery. One patient died suddenly, with angiographic evidence of bilateral vertebral artery rupture. The mechanism of injury to the C1–2 segment of the vertebral artery relating to head and neck injury is discussed.

Improving the prediction of outcome in severe acute closed head injury by using discriminant function analysis of normal auditory brainstem response latencies and amplitudes

2002 ◽  
Vol 97 (5) ◽  
pp. 1062-1069 ◽  
Author(s):  
Wayne J. Wilson ◽  
Claire Penn ◽  
David Saffer ◽  
Farzin Aghdasi
Keyword(s):  
Head Injury ◽  
Confidence Level ◽  
Auditory Brainstem Response ◽  
Function Analysis ◽  
Closed Head Injury ◽  
Auditory Brainstem ◽  
Content Type ◽  
Closed Head ◽  
Brainstem Response ◽  
Fine Print

Object. The auditory brainstem response (ABR) is a useful addition to standard medical measures for predicting outcome in patients with severe acute closed head injury (ACHI). Limiting this success, however, is the poor predictive value of a so-called “normal” ABR. In this study the authors used discriminant function analysis (DFA) of ABR Wave I, III, and V latencies and amplitudes to improve the predictive accuracy of the normal ABR, both as a single measure and in combination with other standard medical measures. Methods. The DFAs were conducted using the ABR and medical results in 68 patients with severe ACHI (30 who died [ACHI-died], and 38 who survived [ACHI-lived]) who presented with normal ABR responses in the neurosurgical intensive care unit of the authors' hospital in Johannesburg. All patients had undergone surgery to remove an intracranial hematoma. Correct predictions of outcome by ABR DFA measures were 83% for the ACHI-died group (48% at ≥ 90% confidence level) and 87% for the ACHI-lived group (71% at ≥ 90% confidence level); by medical DFA measures the correct predictions were 83% for the ACHI-died group (96% at ≥ 90% confidence level) and 95% for the ACHI-lived group (94% at ≥ 90% confidence level); and by combined ABR and medical DFA measures correct predictions were 100% for the ACHI-died group (100% at ≥ 90% confidence level) and 97% for the ACHI-lived group (100% at ≥ 90% confidence level). Conclusions. The DFA of ABR Wave I, III, and V latencies and amplitudes improved the predictive ability of normal ABR results to rates similar to those obtained using DFA for the medical measures, although at lower confidence levels. The DFA of the combined ABR and medical measures improved correct predictions to rates significantly higher than for either of the measures on its own.

Ventriculo-orbital fistula in closed head injury

1975 ◽  
Vol 43 (6) ◽  
pp. 754-756 ◽  
Author(s):  
Hideo Terao ◽  
Seitaro Sato
Keyword(s):  
Head Injury ◽  
Closed Head Injury ◽  
Percutaneous Injection ◽  
Content Type ◽  
Closed Head ◽  
Downward Deviation ◽  
Fine Print

✓ A ventriculo-orbital fistula developing as a result of closed head injury produced intraorbital compression symptoms including downward deviation of the globe and inability of upward gaze. Percutaneous injection of Conray clearly demonstrated the fistula, which was successfully closed by frontal craniotomy.

Acute subdural hematomas

1975 ◽  
Vol 42 (1) ◽  
pp. 37-42 ◽  
Author(s):  
David A. Fell ◽  
Sean Fitzgerald ◽  
Richard H. Moiel ◽  
Pedro Caram
Keyword(s):  
Nursing Home ◽  
Head Injury ◽  
Mortality Rate ◽  
Closed Head Injury ◽  
Nursing Home Care ◽  
Content Type ◽  
Subdural Hematomas ◽  
Closed Head ◽  
Burr Holes ◽  
Fine Print

✓ The authors report 144 cases in which acute subdural hematomas resulting from closed head injury were surgically treated. The mortality rate was 48% for those treated within 24 hours of injury and 45% for those treated within 72 hours. Patients under 10 years of age had a 33% mortality, while 69% of those over 60 years died. In the first 6 years of the series, 75% of the patients were treated by multiple burr holes and a subtemporal craniectomy, with a mortality of 41%; in the last 6 years, 92% of the patients had large craniotomies with a 45% mortality. Of the 32 survivors among the last 60 patients treated, nine require full nursing home care, eight have returned to their own homes, 12 are able to care for themselves but not work, and three have returned to work.

Magnetic resonance imaging—monitored acute blood-brain barrier changes in experimental traumatic brain injury

1996 ◽  
Vol 85 (6) ◽  
pp. 1113-1121 ◽  
Author(s):  
Pál Barzó ◽  
Anthony Marmarou ◽  
Panos Fatouros ◽  
Frank Corwin ◽  
Jana Dunbar
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Magnetic Resonance ◽  
Mr Imaging ◽  
Blood Brain Barrier ◽  
Closed Head Injury ◽  
Content Type ◽  
Secondary Insult ◽  
Closed Head ◽  
Fine Print

✓ The authors posit that cellular edema is the major contributor to brain swelling in diffuse head injury and that the contribution of vasogenic edema may be overemphasized. The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury and to what extent barrier permeability is affected by the secondary insults of hypoxia and hypotension. The BBB disruption was quantified and visualized using T1-weighted magnetic resonance (MR) imaging following intravenous administration of the MR contrast agent gadolinium—diethylenetriamine pentaacetic acid. To avoid the effect of blood volume changes, the maximum signal intensity (SI) enhancement was used to calculate the difference in BBB disruption. A new impact-acceleration model was used to induce closed head injury. Forty-five adult Sprague—Dawley rats were separated into four groups: Group I, sham operated (four animals), Group II, hypoxia and hypotension (four animals), Group III, trauma only (23 animals), and Group IV, trauma coupled with hypoxia and hypotension (14 animals). After trauma was induced, a 30-minute insult of hypoxia (PaO2 40 mm Hg) and hypotension (mean arterial blood pressure 30 mm Hg) was imposed, after which the animals were resuscitated. In the trauma-induced animals, the SI increased dramatically immediately after impact. By 15 minutes permeability decreased exponentially and by 30 minutes it was equal to that of control animals. When trauma was coupled with secondary insult, the SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically on reperfusion and was equal to that of control by 60 minutes after the combined insult. In conclusion, the authors suggest that closed head injury is associated with a rapid and transient BBB opening that begins at the time of the trauma and lasts no more than 30 minutes. It has also been shown that addition of posttraumatic secondary insult—hypoxia and hypotension—prolongs the time of BBB breakdown after closed head injury. The authors further conclude that MR imaging is an excellent technique to follow (time resolution 1–1.5 minutes) the evolution of trauma-induced BBB damage noninvasively from as early as a few minutes up to hours or even longer after the trauma occurs.

The outcome of severe closed head injury

1991 ◽  
Vol 75 (Supplement) ◽  
pp. S28-S36 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Theresa Gautille ◽  
Melville R. Klauber ◽  
Howard M. Eisenberg ◽  
John A. Jane ◽  
...  
Keyword(s):  
Head Injury ◽  
Mortality Rate ◽  
Severe Head Injury ◽  
Closed Head Injury ◽  
Data Bank ◽  
Content Type ◽  
Severity Of Injury ◽  
Gcs Score ◽  
Fine Print ◽  
Overall Mortality

✓ The outcome of severe head injury was prospectively studied in patients enrolled in the Traumatic Coma Data Bank (TCDB) during the 45-month period from January 1, 1984, through September 30, 1987. Data were collected on 1030 consecutive patients admitted with severe head injury (defined as a Glasgow Coma Scale (GCS) score of 8 or less following nonsurgical resuscitation). Of these, 284 either were brain-dead on admission or had a gunshot wound to the brain. Patients in these two groups were excluded, leaving 746 patients available for this analysis. The overall mortality rate for the 746 patients was 36%, determined at 6 months postinjury. As expected, the mortality rate progressively decreased from 76% in patients with a postresuscitation GCS score of 3 to approximately 18% for patients with a GCS score of 6, 7, or 8. Among the patients with nonsurgical lesions (overall mortality rate, 31%), the mortality rate was higher in those having an increased likelihood of elevated intracranial pressure as assessed by a new classification of head injury based on the computerized tomography findings. In the 276 patients undergoing craniotomy, the mortality rate was 39%. Half of the patients with acute subdural hematomas died — a substantial improvement over results in previous reports. Outcome differences between the four TCDB centers were small and were, in part, explicable by differences in patient age and the type and severity of injury. This study describes head injury outcome in four selected head-injury centers. It indicates that a mortality rate of approximately 35% is to be expected in such patients admitted to experienced neurosurgical units.

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