Early immunological defects in comatose patients after acute brain injury

2001 ◽  
Vol 94 (5) ◽  
pp. 706-711 ◽  
Author(s):  
Baruch Wolach ◽  
Leon Sazbon ◽  
Ronit Gavrieli ◽  
Arieh Broda ◽  
Menachem Schlesinger
Keyword(s):  
Immune System ◽  
Brain Injury ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Acute Brain Injury ◽  
High Rate ◽  
Mechanical Trauma ◽  
Severe Brain Injury ◽  
Content Type ◽  
Fine Print

Object. The aim of this prospective study was to evaluate the phagocytic, humoral, and cellular arms of the immune system in comatose patients shortly after severe brain injury and to compare the findings with those reported earlier in patients in a persistent vegetative state. The study was conducted in intensive care units and immunology laboratories of university-affiliated hospitals in central Israel. Methods. The study group consisted of 14 men aged 16 to 65 years who were comatose as a result of acute brain injury due to mechanical trauma. All were studied within 72 hours of injury. Brain damage was severe in all cases (Glasgow Coma Scale score < 8). Healthy age- and sex-matched volunteers served as simultaneous controls. Infections arose in nine (75%) of the 12 patients in whom data were available; the cumulative mortality rate was 38% (five of 13 patients in whom outcome data were available). Every patient exhibited one or more defects in at least one arm of the immune system. Significant deficiencies were noted in neutrophil superoxide release, immunoglobulin (Ig)G, IgG1, IgM, C1q, C2, properdin, alternate C pathway, T cells, T helper cells, T suppressor cells, and natural killer cells. In an earlier series of patients examined by the authors months after the primary insult, these impairments were absent in most of the patients in the vegetative state. Conclusions. Significant deficiencies of the immune system, particularly the cellular arm, are precipitated by severe brain injury within 72 hours of the event. These impairments probably play a role in the high rate of complicating infections and multiple organ failure. Together with earlier findings, the results of this study indicate that if brain-injured patients survive these hazards, their immune system will eventually recover.

Cerebral acid—base homeostasis after severe traumatic brain injury

2005 ◽  
Vol 103 (4) ◽  
pp. 597-607 ◽  
Author(s):  
Tobias Clausen ◽  
Ahmad Khaldi ◽  
Alois Zauner ◽  
Michael Reinert ◽  
Egon Doppenberg ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Acid Base ◽  
Content Type ◽  
Time Points ◽  
Tissue Acidosis ◽  
Fine Print

Object. Brain tissue acidosis is known to mediate neuronal death. Therefore the authors measured the main parameters of cerebral acid—base homeostasis, as well as their interrelations, shortly after severe traumatic brain injury (TBI) in humans. Methods. Brain tissue pH, PCO2, PO2, and/or lactate were measured in 151 patients with severe head injuries, by using a Neurotrend sensor and/or a microdialysis probe. Monitoring was started as soon as possible after the injury and continued for up to 4 days. During the 1st day following the trauma, the brain tissue pH was significantly lower, compared with later time points, in patients who died or remained in a persistent vegetative state. Six hours after the injury, brain tissue PCO2 was significantly higher in patients with a poor outcome compared with patients with a good outcome. Furthermore, significant elevations in cerebral concentrations of lactate were found during the 1st day after the injury, compared with later time points. These increases in lactate were typically more pronounced in patients with a poor outcome. Similar biochemical changes were observed during later hypoxic events. Conclusions. Severe human TBI profoundly disturbs cerebral acid—base homeostasis. The observed pH changes persist for the first 24 hours after the trauma. Brain tissue acidosis is associated with increased tissue PCO2 and lactate concentration; these pathobiochemical changes are more severe in patients who remain in a persistent vegetative state or die. Furthermore, increased brain tissue PCO2 (> 60 mm Hg) appears to be a useful clinical indicator of critical cerebral ischemia, especially when accompanied by increased lactate concentrations.

Creatine kinase isoenzymes in acute brain injury

1981 ◽  
Vol 55 (4) ◽  
pp. 511-515 ◽  
Author(s):  
Markku Kaste ◽  
Juha Hernesniemi ◽  
Hannu Somer ◽  
Matti Hillbom ◽  
Aarne Konttinen
Keyword(s):  
Creatine Kinase ◽  
Brain Injury ◽  
Prognostic Significance ◽  
Myocardial Damage ◽  
Gunshot Wounds ◽  
Acute Brain Injury ◽  
Peak Activity ◽  
Content Type ◽  
T Wave ◽  
Fine Print

✓ Brain-type creatine kinase (CK) isoenzyme (CK-BB) was detected in the serum in 13 out of 26 patients with acute brain injury (50%). The peak of CK-BB activity ranged from 5 to 188 U/liter, constituting, on average, 10.5% of the total CK activity. The highest activities were seen in patients with gunshot wounds. High CK-BB activity was associated with poor prognosis, but minimal CK-BB elevations did not have prognostic significance. Heart-type creatine kinase isoenzyme (CK-MB) was detected in the serum in 17 out of 26 patients (65%). The peak activity ranged from 5 to 115 U/liter, constituting, on average, 6.6% of total CK activity. Electrocardiograms taken from 20 patients revealed transient T-wave inversions in the precordial leads in four patients; three of them also showed serum CK-MB activity. Subendocardial hemorrhage was detected at autopsy in three of the five CK-MB-positive patients, but in none of the four CK-MB-negative cases. Present findings suggest that acute brain injury may secondarily cause myocardial damage.

Long-term follow-up review of 31 children with severe closed head trauma

1990 ◽  
Vol 73 (5) ◽  
pp. 684-687 ◽  
Author(s):  
Hanan Costeff ◽  
Zeev Groswasser ◽  
Ruth Goldstein
Keyword(s):  
Head Trauma ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Acute Stage ◽  
Ct Scans ◽  
Permanent Disability ◽  
Content Type ◽  
Closed Head ◽  
Closed Head Trauma ◽  
Fine Print

✓ Thirty-one children aged 3 to 15 years were followed for 5 to 11 years after suffering severe closed head trauma which caused coma for 1 week or more (median duration of coma 3 weeks). One patient remained in a persistent vegetative state until his death 9 years later. The other 30 recovered consciousness and were discharged. All suffered diminution of their abilities, and 24 of them had major permanent disability. The most common motor disabilities were pure spastic hemiparesis (seven cases), basal ganglia syndromes (four cases), ataxia (three cases), and a combination of hemiparesis and ataxia (five cases). Of the 30 patients, 26 regained independent ambulation, seven were epileptic, and 14 were dysarthric in various degrees. Only 10 had the cognitive ability to profit from the normal educational system, and none had attempted postsecondary education. Social problems were common. The worst outcomes were associated with intracranial bleeding and/or brain contusion seen on computerized tomography (CT) scans at the acute stage; the best were associated with normal CT scans. The degree of residual disability in these children seems no less than that of adults with trauma of similar severity.

Intercenter variance in clinical trials of head trauma—experience of the National Acute Brain Injury Study: Hypothermia

2001 ◽  
Vol 95 (5) ◽  
pp. 751-755 ◽  
Author(s):  
Guy L. Clifton ◽  
Sung C. Choi ◽  
Emmy R. Miller ◽  
Harvey S. Levin ◽  
Kenneth R. Smith ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Brain Injury ◽  
Phase Iii ◽  
Severe Brain Injury ◽  
Quality Of Data ◽  
Content Type ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Present On Admission ◽  
Fine Print

Object. In a recently conducted trial of hypothermia in patients with severe brain injury, differences were found in the effects of hypothermia treatment among various centers. This analysis explores the reasons for such differences. Methods. The authors reviewed data obtained in 392 patients treated for severe brain injury. Prerandomization variables, critical physiological variables, treatment variables, and accrual methodologies were investigated among various centers. Hypothermia was found to be detrimental in patients older than the age of 45 years, beneficial in patients younger than 45 years of age in whom hypothermia was present on admission, and without effect in those in whom normothermia was documented on admission. Marginally significant differences (p < 0.054) in the intercenter outcomes of hypothermia-treated patients were likely the result of wide differences in the percentage of patients older than 45 years of age and in the percentage of patients in whom hypothermia was present on admission among centers. The trial sensitivity was likely diminished by significant differences in the incidence of mean arterial blood pressure (MABP) less than 70 mm Hg (p < 0.001) and cerebral perfusion pressure (CPP) less than 50 mm Hg (p < 0.05) but not intracranial pressure (ICP) greater than 25 mm Hg (not significant) among patients in the various centers. Hours of vasopressor usage (p < 0.03) and morphine dose (p < 0.001) and the percentage of dehydrated patients varied significantly among centers (p < 0.001). The participation of small centers increased intercenter variance and diminished the quality of data. Conclusions. For Phase III clinical trials we recommend: 1) a detailed protocol specifying fluid and MABP, ICP, and CPP management; 2) continuous monitoring of protocol compliance; 3) a run-in period for new centers to test accrual and protocol adherence; and 4) inclusion of only centers in which patients are regularly randomized.

Cerebellar hemorrhage caused by dural arteriovenous fistula: a review of five cases

2001 ◽  
Vol 94 (3) ◽  
pp. 422-426 ◽  
Author(s):  
Koichi Satoh ◽  
Junichiro Satomi ◽  
Norio Nakajima ◽  
Shunji Matsubara ◽  
Shinji Nagahiro
Keyword(s):  
Fourth Ventricle ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Vascular Anomaly ◽  
Venous Drainage ◽  
Massive Hemorrhage ◽  
Cerebellar Hemorrhage ◽  
Content Type ◽  
The Right ◽  
Fine Print

Object. In this study the authors performed a retrospective analysis of five cases in which the patients (three women and two men) were treated for intracranial dural arteriovenous fistulas (AVFs) associated with cerebellar hemorrhage. On the basis of their findings, the authors evaluated the characteristics of this unusual symptom. Methods. The dural AVFs were located in the right cavernous sinus in one patient, the left transverse—sigmoid sinus in three patients, and the right superior petrosal sinus (SPS) in one patient. All patients presented with severe headache and/or loss of consciousness. Computerized tomography scans revealed a small cerebellar hemorrhage near the fourth ventricle and hydrocephalus in four cases, and a massive hemispheric cerebellar hemorrhage in the remaining case. The four patients with small hemorrhages underwent ventriculostomy and endovascular treatment; all recovered. The patient suffering from a massive hemorrhage because of a dural AVF in the SPS was treated by suboccipital craniectomy, hematoma evacuation, and removal of the vascular anomaly. This patient remains in a persistent vegetative state. In four cases, results of angiography demonstrated retrograde leptomeningeal venous drainage through the SPS to the anastomotic lateral mesencephalic vein (ALMV) and/or to the vein of the lateral recess of the fourth ventricle (VLR4V). Retrograde leptomeningeal venous drainage to the ALMV and/or VLR4V was responsible for cerebellar hemorrhage in these cases. Conclusions. Thus, it is important to consider dural AVF in cases in which there is even a small hemorrhage near the fourth ventricle accompanied by intraventricular perforation and a decreased level of consciousness.

Early induction of hypothermia for evacuated intracranial hematomas: a post hoc analysis of two clinical trials

2012 ◽  
Vol 117 (4) ◽  
pp. 714-720 ◽  
Author(s):  
Guy L. Clifton ◽  
Christopher S. Coffey ◽  
Sierra Fourwinds ◽  
David Zygun ◽  
Alex Valadka ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Relative Risk ◽  
Brain Injury ◽  
Vegetative State ◽  
Acute Brain Injury ◽  
Multicenter Clinical Trial ◽  
Severe Brain Injury ◽  
Start Time ◽  
Clinical Trial Registration ◽  
Intracranial Hematomas

Object The authors hypothesized that cooling before evacuation of traumatic intracranial hematomas protects the brain from reperfusion injury and, if so, further hypothesized that hypothermia induction before or soon after craniotomy should be associated with improved outcomes. Methods The National Acute Brain Injury Study: Hypothermia I (NABIS:H I) was a randomized multicenter clinical trial of 392 patients with severe brain injury treated using normothermia or hypothermia for 48 hours with patients reaching 33°C at 8.4 ± 3 hours after injury. The National Acute Brain Injury Study: Hypothermia II (NABIS:H II) was a randomized, multicenter clinical trial of 97 patients with severe brain injury treated with normothermia or hypothermia for 48 hours with patients reaching 35°C within 2.6 ± 1.2 hours and 33°C within 4.4 ± 1.5 hours of injury. Entry and exclusion criteria, management, and outcome measures in the 2 trials were similar. Results In NABIS:H II among the patients with evacuated intracranial hematomas, outcome was poor (severe disability, vegetative state, or death) in 5 of 15 patients in the hypothermia group and in 9 of 13 patients in the normothermia group (relative risk 0.44, 95% CI 0.22–0.88; p = 0.02). All patients randomized to hypothermia reached 35°C within 1.5 hours after surgery start and 33°C within 5.55 hours. Applying these criteria to NABIS:H I, 31 of 54 hypothermia-treated patients reached a temperature of 35°C or lower within 1.5 hours after surgery start time, and the remaining 23 patients reached 35°C at later time points. Outcome was poor in 14 (45%) of 31 patients reaching 35°C within 1.5 hours of surgery, in 14 (61%) of 23 patients reaching 35°C more than 1.5 hours of surgery, and in 35 (60%) of 58 patients in the normothermia group (relative risk 0.74, 95%, CI 0.49–1.13; p = 0.16). A meta-analysis of 46 patients with hematomas in both trials who reached 35°C within 1.5 hours of surgery start showed a significantly reduced rate of poor outcomes (41%) compared with 94 patients treated with hypothermia who did not reach 35°C within that time and patients treated at normothermia (62%, p = 0.009). Conclusions Induction of hypothermia to 35°C before or soon after craniotomy with maintenance at 33°C for 48 hours thereafter may improve outcome of patients with hematomas and severe traumatic brain injury. Clinical trial registration no.: NCT00178711.

The persistent vegetative state after closed head injury: clinical and magnetic resonance imaging findings in 42 patients

1998 ◽  
Vol 88 (5) ◽  
pp. 809-816 ◽  
Author(s):  
Andreas Kampfl ◽  
Gerhard Franz ◽  
Franz Aichner ◽  
Bettina Pfausler ◽  
Hans-Peter Haring ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Mr Imaging ◽  
Vegetative State ◽  
Axonal Injury ◽  
Persistent Vegetative State ◽  
Diffuse Axonal Injury ◽  
Resonance Imaging ◽  
Content Type ◽  
Temporal Lobes ◽  
Fine Print

Object. In this retrospective study, the authors analyzed the frequency, anatomical distribution, and appearance of traumatic brain lesions in 42 patients in a posttraumatic persistent vegetative state. Methods. Cerebral magnetic resonance (MR) imaging was used to detect the number of lesions, which ranged from as few as five to as many as 19, with a mean of 11 lesions. In all 42 cases there was evidence on MR imaging of diffuse axonal injury, and injury to the corpus callosum was detected in all patients. The second most common area of diffuse axonal injury involved the dorsolateral aspect of the rostral brainstem (74% of patients). In addition, 65% of these patients exhibited white matter injury in the corona radiata and the frontal and temporal lobes. Lesions to the basal ganglia or thalamus were seen in 52% and 40% of patients, respectively. Magnetic resonance imaging showed some evidence of cortical contusion in 48% of patients in this study; the frontal and temporal lobes were most frequently involved. Injury to the parahippocampal gyrus was detected in 45% of patients; in this subgroup there was an 80% incidence of contralateral peduncular lesions in the midbrain. The most common pattern of injury (74% in this series) was the combination of focal lesions of the corpus callosum and the dorsolateral brainstem. In patients with no evidence of diffuse axonal injury in the upper brainstem (26% in this series), callosal lesions were most often associated with basal ganglia lesions. Lesions of the corona radiata and lobar white matter were equally distributed in patients with or without dorsolateral brainstem injury. Moreover, cortical contusions and thalamic, parahippocampal, and cerebral peduncular lesions were also similarly distributed in both groups. Conclusions. The data indicate that diffuse axonal injury may be the major form of primary brain damage in the posttraumatic persistent vegetative state. In addition, the authors demonstrated in this study that MR imaging, in conjunction with a precise clinical correlation, may provide useful supportive information for the accurate diagnosis of a persistent vegetative state after traumatic brain injury.

Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension

2004 ◽  
Vol 101 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
Michelle J. Smith ◽  
Stephanie Bloom ◽  
Eileen Maloney-Wilensky ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracranial Hypertension ◽  
Brain Tissue ◽  
Medical Management ◽  
Cerebral Oxygenation ◽  
Severe Brain Injury ◽  
Content Type ◽  
Decompressive Hemicraniectomy ◽  
Gcs Score ◽  
Fine Print

Object. Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease. Methods. The study focused on seven patients (mean age 30.6 ± 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management. Conclusions. All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 ± 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 ± 11 mm Hg) and an increase in CPP (81 ± 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 ± 13.8 mm Hg to 45.5 ± 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

Relation of cerebral blood flow to neurological status and outcome in head-injured patients

1979 ◽  
Vol 51 (3) ◽  
pp. 292-300 ◽  
Author(s):  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Hiromu Segawa ◽  
Carol A. Dolinskas ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Low Oxygen ◽  
Content Type ◽  
Head Injured ◽  
Luxury Perfusion ◽  
Injured Patients ◽  
Fine Print

✓ Noninvasive studies of regional cerebral blood flow (CBF) were performed on 36 head-injured patients in varying degrees of coma, using the intravenous xenon-133 method. Serial examinations, averaging four per patient, were begun during the acute phase of illness and continued until death or recovery of normal consciousness. Comparison of the initial and final studies revealed that CBF declined to very low levels in all nine patients who died, and remained subnormal in a patient with persistent vegetative state. In contrast, 25 of 26 patients who recovered consciousness showed increases in blood flow. Because of the presence of both reduced and elevated blood flows on the initial study, CBF was not predictive of outcome. Absolute or relative hyperemia, observed in nine acute cases, was associated with either diffuse cerebral swelling (observed on computerized tomography) or recovery from systemic shock. Cerebral metabolic studies in hyperemic patients yielded a very low oxygen uptake and arteriovenous oxygen difference, indicating that the high blood flow was a true “luxury perfusion.” When instances of presumed luxury perfusion were excluded, CBF was positively correlated with level of consciousness, assessed on a four-point coma scale.

Vascular compression of the duodenum following severe brain injury

1973 ◽  
Vol 39 (3) ◽  
pp. 405-407 ◽  
Author(s):  
William F. Bouzarth ◽  
J. N. Crowley ◽  
Harris R. Clearfield
Keyword(s):  
Weight Loss ◽  
Differential Diagnosis ◽  
Brain Injury ◽  
Vascular Compression ◽  
Severe Brain Injury ◽  
Content Type ◽  
Brain Injured ◽  
Progressive Weight Loss ◽  
Injured Patients ◽  
Fine Print

✓ A patient with severe brain injury began vomiting 12 weeks after admission. This magnified a progressive weight loss of 34 kg. Vascular compression of the duodenum was confirmed as the cause of the vomiting. With hyperalimentation, vomiting stopped and weight gain occurred. This easily reversible syndrome should be considered in the differential diagnosis of vomiting in brain-injured patients with weight loss.

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