Treatment of head injuries in the American Civil War

1993 ◽  
Vol 78 (5) ◽  
pp. 838-845 ◽  
Author(s):  
Howard H. Kaufman
Keyword(s):  
Civil War ◽  
Head Injury ◽  
Head Injuries ◽  
Closed Head Injury ◽  
Gunshot Wounds ◽  
American Civil War ◽  
Content Type ◽  
Severity Of Injury ◽  
Surgical History ◽  
Fine Print

✓ At the time of the American Civil War (1861–1865), a great deal was known about closed head injury and gunshot wounds to the head. Compression was differentiated from concussion, but localization of lesions was not precise. Ether and especially chloroform were used to provide anesthesia. Failure to understand how to prevent infection discouraged physicians from aggressive surgery. Manuals written to educate inexperienced doctors at the onset of the war provide an overview of the advice given by senior surgeons. The Union experiences in the treatment of head injury in the Civil War were discussed in the three surgical volumes of The Medical and Surgical History of the War of the Rebellion. Wounds were divided into incised and puncture wounds, blunt injuries, and gunshot wounds, which were analyzed separately. Because the patients were not stratified by severity of injury and because there was no neuroimaging, it is difficult to understand the clinical problems and the effectiveness of surgery. Almost immediately after the war, increased knowledge about cerebral localization and the development of antisepsis (and then asepsis) permitted the development of modern neurosurgery.

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.

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.

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.

Prophylactic phenytoin in severe head injuries

1979 ◽  
Vol 51 (4) ◽  
pp. 507-509 ◽  
Author(s):  
Richard N. W. Wohns ◽  
Allen R. Wyler
Keyword(s):  
Retrospective Study ◽  
Head Injury ◽  
High Probability ◽  
Late Onset ◽  
Head Injuries ◽  
Content Type ◽  
Posttraumatic Epilepsy ◽  
Fine Print

✓ We are reporting a retrospective study of 62 patients whose head injury was sufficiently severe to cause a high probability of posttraumatic epilepsy. Of 50 patients treated with phenytoin, 10% developed epilepsy of late onset. Twelve patients not treated with phenytoin but who had head injuries of equal magnitude had a 50% incidence of epilepsy. These data from a highly selected group of patients with severe head injuries confirm the bias that treatment with phenytoin decreases the incidence of posttraumatic epilepsy.

Moderate hypothermia in patients with severe head injury: cerebral and extracerebral effects

1996 ◽  
Vol 85 (4) ◽  
pp. 533-541 ◽  
Author(s):  
Christoph Metz ◽  
Matthias Holzschuh ◽  
Thomas Bein ◽  
Christian Woertgen ◽  
Anton Frey ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Head Injury ◽  
Elevated Serum ◽  
Closed Head Injury ◽  
University Hospital ◽  
Moderate Hypothermia ◽  
Serum Lipase ◽  
Content Type ◽  
Coagulation Tests ◽  
Fine Print

✓ Cerebral and extracerebral effects of moderate hypothermia (core temperature 32.5°C–33.0°C) were prospectively studied in 10 patients with severe closed head injury (Glasgow Coma Scale score, < 7) in the intensive care unit of a university hospital. Hypothermia was induced by cooling the patient's body surface with water-circulating blankets. Before cooling, a conventional intracranial pressure (ICP) reduction therapy was applied, which remained unchanged throughout the study. Cerebral blood flow (CBF), cerebral metabolic rates for oxygen (CMRO2) and lactate (CMRL), and ICP were simultaneously measured prior to inducing hypothermia, after obtaining hypothermia, after 24 hours of hypothermia, and after rewarming. With respect to extracerebral effects, supplemental investigations were conducted 24 and 72 hours after rewarming. The median delay between injury and induction of hypothermia was 16 hours. Hypothermia reduced CMRO2 by 45% (p < 0.01), whereas CBF did not change significantly. Before cooling, six patients had elevated CMRL indicating cerebral ischemia. Cooling normalized CMRL in all patients (p < 0.01). The intracranial hypertension present prior to cooling declined markedly during hypothermia (p < 0.01) without significant rebound effects after rewarming. Cardiac index decreased by 18% after hypothermia was reached (p < 0.05), recovered at 24 hours of hypothermia, and surpassed baseline values after rewarming. Platelet counts dropped continuously up to 24 hours after rewarming (p < 0.01). Plasma coagulation tests did not show significant worsening. Creatinine clearance decreased during cooling (p < 0.01) and recovered by 24 hours after rewarming. Twenty-four hours after cooling had begun, eight patients had elevated serum lipase activity (p < 0.01) and four of them acquired pancreatitis. Rewarming normalized both pancreatic alterations. Seven patients made a good recovery; one survived severely disabled; and two patients died. Moderate hypothermia is effective in preventing secondary brain damage while reducing cerebral ischemia. However, there are potentially hazardous side effects that require additional monitoring.

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.

Cerebral blood flow and metabolism in severely head-injured children

1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cerebral Blood Volume ◽  
Closed Head Injury ◽  
Volume Index ◽  
Content Type ◽  
Gcs Score ◽  
Fine Print

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.

Head injuries due to falls caused by seizures: a group at high risk for traumatic intracranial hematomas

1997 ◽  
Vol 86 (3) ◽  
pp. 433-437 ◽  
Author(s):  
Thomas J. Zwimpfer ◽  
Jennifer Brown ◽  
Irene Sullivan ◽  
Richard J. Moulton
Keyword(s):  
Head Injury ◽  
Alcohol Intoxication ◽  
Head Injuries ◽  
Chi Square ◽  
Focal Neurological Deficit ◽  
Content Type ◽  
Intracranial Hematomas ◽  
Chi Square Analysis ◽  
Mass Lesions ◽  
Fine Print

✓ This prospective review of adult patients with head injuries examines the incidence of head injuries due to falls caused by seizures, the incidence and severity of intracranial hematomas, and the morbidity and mortality rates in this patient population. A head injury was attributed to a fall caused by a seizure if the seizure was witnessed to have caused the fall, or the patient had a known seizure history, appeared postictal or was found convulsing after the fall, and no other cause for the fall was evident. A total of 1760 adult head-injured patients were consecutively admitted to the authors' service between 1986 and 1993. Five hundred eighty-two head injuries (33.1%) were due to falls and 22 (3.8%) of these were caused by seizures. Based on the prevalence rates for epilepsy in the general population of 0.5 to 2%, these results indicate that epileptics are several times more likely to suffer a head injury due to a fall. Mass lesions were found in 20 (90.9%) of these 22 patients and the remaining two patients suffered mild diffuse head injuries. There was a high incidence of extraaxial mass lesions: 17 (85%) of the 20 intracranial hematomas were either epidural (five cases) or acute subdural (12 cases) hematomas. Eighteen (81.8%) of the 22 patients required evacuation of a hematoma. Both the incidence of intracranial hematomas (90.9% vs. 39.8%; p < 0.001, chi-square analysis) and the rate of hematoma evacuation (81.8% vs. 32.3%; p < 0.001) was significantly greater in patients injured in falls due to seizures (22 cases) than in the group injured in falls from all other causes (560 cases). The higher incidence of hematomas and the need for evacuation were not explained by differences in age, severity of head injury, or incidence of alcohol intoxication. Despite the greater incidence of mass lesions and the need for operative treatment in patients injured because of seizures, their mortality rate was similar to that of patients injured in falls from other causes. On the basis of their review of patients admitted to a neurosurgical center with complaints of head injury, the authors conclude that patients with head injuries due to a fall caused by a seizure should undergo computerized tomography scanning early in their management. Until a mass lesion has been excluded, any decrease in level of consciousness or focal neurological deficit should not be attributed to the seizure itself.

Cause of decline in head-injury mortality rate in San Diego County, California

1985 ◽  
Vol 62 (4) ◽  
pp. 528-531 ◽  
Author(s):  
Melville R. Klauber ◽  
Lawrence F. Marshall ◽  
Belinda M. Toole ◽  
Sharen L. Knowlton ◽  
Sharon A. Bowers
Keyword(s):  
Head Injury ◽  
San Diego ◽  
Head Injuries ◽  
Mortality Rates ◽  
San Diego County ◽  
Content Type ◽  
Severity Of Injury ◽  
Prehospital Emergency ◽  
Injured Patients ◽  
Number Of Individuals

✓ Even with an increasing population, there were 100 fewer deaths due to head injury in San Diego County, California, in 1982 compared to 1980. During the 5 years from 1976 to 1980 there was nearly a constant death rate from head injuries, followed in the next 2 years by a decline of 24%. The number of deaths at the scene of injury declined 28%, and the number of individuals listed as dead on arrival at the hospital declined 68%. Mortality rates in the emergency room increased slightly and later death rates declined slightly. Mortality rates of hospitalized patients, adjusted for severity of injury, did not vary materially by year. This decline in deaths due to head injury followed a marked improvement in the county's emergency ground and prehospital air evacuation services. The data strongly suggest that advanced prehospital emergency medical services can substantially reduce mortality rates in head-injured patients. The authors postulate that some patients who ordinarily “would die now talk” because of early airway and circulatory management by highly trained paramedical personnel and airborne trauma specialists. Despite a search for other factors that might explain these observations, no satisfactory alternatives could be identified.

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.

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