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.

Intolerance to enteral feeding in the brain-injured patient

1988 ◽  
Vol 68 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Jane A. Norton ◽  
Linda G. Ott ◽  
Craig McClain ◽  
Linas Adams ◽  
Robert J. Dempsey ◽  
...  
Keyword(s):  
Brain Injury ◽  
Hospital Admission ◽  
Enteral Feeding ◽  
Content Type ◽  
Brain Injured ◽  
Enteral Feedings ◽  
The Mean ◽  
Injured Patients ◽  
Feeding Tolerance ◽  
Fine Print

✓ Calorie and protein supplementation improves nutritional status. This support may improve outcome and decrease morbidity and mortality in acutely brain-injured patients. Investigators have observed a poor tolerance to enteral feedings after brain injury and have noted that this persists for approximately 14 days postinjury. This delay has been attributed to increased gastric residuals, prolonged paralytic ileus, abdominal distention, aspiration pneumonitis, and diarrhea. In the present investigation, 23 brain-injured patients with an admission 24-hour peak Glasgow Coma Scale (GCS) score between 4 and 10 were studied for 18 days from hospital admission. The mean duration from injury to initiation of full-strength, full-rate enteral feeding was 11.5 days. Seven of the 23 patients tolerated enteral feedings within the first 7 days following hospital admission (mean 4.3 days), four patients tolerated feedings between 7 and 10 days postadmission (mean 9 days), and 12 patients did not tolerate feedings until after 10 days postinjury (mean 15.9 days). There was a marginally significant relationship between low GCS scores on admission and length of days to enteral feeding tolerance (p = 0.07). A significant inverse relationship was observed between daily peak intracranial pressure (ICP) and time to tolerance of feedings (p = 0.02). There was no significant relationship between feeding tolerance and days to return of bowel sounds (p = 0.12). Serum albumin levels decreased during the investigation (mean ± standard error to the mean: 3.2 ± 0.12 gm/dl on Day 1; 2.7 ± 0.23 gm/dl on Day 16; normal = 3.5 to 5.0 gm/dl), whereas the percentage of patients tolerating feedings increased over the course of the study. The authors conclude that patients with acute severe brain injury do not adequately tolerate feedings via the enteral route in the early postinjury period. Tolerance of enteral feeding is inversely related to increased ICP and severity of brain injury. It is suggested that parenteral nutritional support is required following brain injury until enteral nutrition can be tolerated.

Amyloid β accumulation in axons after traumatic brain injury in humans

2003 ◽  
Vol 98 (5) ◽  
pp. 1072-1077 ◽  
Author(s):  
Douglas H. Smith ◽  
Xiao-han Chen ◽  
Akira Iwata ◽  
David I. Graham
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Β ◽  
Immunohistochemical Analysis ◽  
Plaque Formation ◽  
Large Reservoir ◽  
Content Type ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

Object. Although plaques composed of amyloid β (Aβ) have been found shortly after traumatic brain injury (TBI) in humans, the source for this Aβ has not been identified. In the present study, the authors explored the potential relationship between Aβ accumulation in damaged axons and associated Aβ plaque formation. Methods. The authors performed an immunohistochemical analysis of paraffin-embedded sections of brain from 12 patients who died after TBI and from two control patients by using antibodies selective for Aβ peptides, amyloid precursor protein (APP), and neurofilament (NF) proteins. In nine brain-injured patients, extensive colocalizations of Aβ, APP, and NF protein were found in swollen axons. Many of these immunoreactive axonal profiles were present close to Aβ plaques or were surrounded by Aβ staining, which spread out into the tissue. Immunoreactive profiles were not found in the brains of the control patients. Conclusions. The results of this study indicate that damaged axons can serve as a large reservoir of Aβ, which may contribute to Aβ plaque formation after TBI in humans.

Mannitol dose requirements in brain-injured patients

1978 ◽  
Vol 48 (2) ◽  
pp. 169-172 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Randall W. Smith ◽  
L. Andrew Rauscher ◽  
Harvey M. Shapiro
Keyword(s):  
Time Course ◽  
Osmotic Gradient ◽  
Intracranial Volume ◽  
Severe Dehydration ◽  
Dose Response Relationship ◽  
Content Type ◽  
Acute Head Injury ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

✓ There is little information as to the optimal use of mannitol. To determine the dose-response relationship, the osmotic gradient required, and the time course of intracranial pressure (ICP) reduction produced by mannitol, eight patients with acute head injury were studied in whom ICP was monitored with a ventriculostomy and found to be elevated. Ventilation was controlled to a pCO2 of 25 ± 3 mm Hg and all were paralyzed with Pavulon. None had received barbiturates. Before mannitol administration the intracranial volume-pressure response was determined. Mannitol was administered as a bolus of 0.25 gm/kg, 0.5 gm/kg, and in six patients, 1 gm/kg, separated by at least 8 hours. In all patients the ICP reduction with 0.25 gm/kg (41.3 ± 10.2 mm Hg→16.4 ± 5.6, p < 0.01) was equivalent to that achieved with the larger doses. Serum osmolality rises of 10 mOsm or more were associated with a reduction in ICP. Much smaller doses than those previously recommended were effective in reducing the ICP acutely, although at 5 hours there was a trend toward persistent reduction when the larger dose is used. This trend was small and indicates that smaller and more frequent doses are as effective in reducing the ICP while avoiding the risk of osmotic disequilibrium and severe dehydration.

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.

Proton magnetic resonance spectroscopy for detection of axonal injury in the splenium of the corpus callosum of brain-injured patients

1998 ◽  
Vol 88 (5) ◽  
pp. 795-801 ◽  
Author(s):  
Kim M. Cecil ◽  
Everett C. Hills ◽  
M. Elizabeth Sandel ◽  
Douglas H. Smith ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
White Matter ◽  
Proton Magnetic Resonance ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Resonance Spectroscopy ◽  
Proton Mrs ◽  
Content Type ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

Object. This study was conducted to determine whether proton magnetic resonance spectroscopy (MRS) is a sensitive method for detecting diffuse axonal injury, which is a primary sequela of traumatic brain injury (TBI). Diffuse axonal injury is characterized by selective damage to white matter tracts that is caused in part by the severe inertial strain created by rotational acceleration and deceleration, which is often associated with motor vehicle accidents. This axonal injury is typically difficult to detect by using conventional imaging techniques because it is microscopic in nature. The splenium was selected because it is a site vulnerable to shearing forces that produce diffuse axonal injury. Methods. The authors used proton MRS to evaluate the splenium, the posterior commissure of the corpus callosum, in normal control volunteers and in patients with TBI. Proton MRS provided an index of neuronal and axonal viability by measuring levels of N-acetyl aspartate (NAA). Conclusions. A majority of mildly brain injured patients, as well as those more severely injured, showed diminished NAA/creatine (Cr) levels in the splenium compared with normal control volunteers. The patients displaying lowered NAA/Cr in the splenium were also likely to exhibit lowered NAA/Cr in lobar white matter. Also, the levels of NAA/Cr in the splenium of normal volunteers were higher compared with those found in lobar white matter. Decreases in NAA/Cr levels in the splenium may be a marker for diffuse injury. A proton MRS examination may be particularly useful in evaluating mildly injured patients with unexplained neurological and cognitive deficits. It is concluded that MRS is a sensitive tool in detecting axonal injury.

The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury

1992 ◽  
Vol 77 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Kwan-Hon Chan ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
Peter J. D. Andrews ◽  
Susan Midgley
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Perfusion Pressure ◽  
Jugular Bulb ◽  
Artery Blood Flow ◽  
Content Type ◽  
Brain Injured ◽  
Venous Oxygen Saturation ◽  
Injured Patients ◽  
Fine Print

✓ Middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation (SJO2) were measured by transcranial Doppler (TCD) ultrasonography and continuous venous oximetry, respectively, in 41 severely brain-injured patients. The purpose of the study was to examine the relationships between TCD flow velocity, SJO2, and alterations in blood pressure (BP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). In these patients, CPP was reduced either by rising ICP or by falling BP. Both forms of reduction of CPP resulted in a greater fall in diastolic flow velocity than other flow parameters. As CPP decreased below a critical value of 70 mm Hg, a progressive increase in TCD pulsatility index (PI) was observed (r = −0.942, p < 0.0001), accompanied by a fall in SJO2 (r = 0.78, p < 0.0001). At pressures above 70 mm Hg, there was no correlation of either PI or SJO2 with CPP. The relationship between PI and CPP held true in patients with both focal and diffuse pathologies and was the same whether changes in CPP resulted from alterations in ICP or BP. The PI and SJO2 correlated better with CPP than with ICP or BP. Transcranial Doppler ultrasonography can identify states of reduced CPP. Decreases in SJO2 with falling CPP suggested progressive failure of cerebral blood flow to meet metabolic demands. Monitoring of TCD and SJO2 may be used to define the optimum CPP level for management of severely brain-injured patients.

The outcome with aggressive treatment in severe head injuries

1979 ◽  
Vol 50 (1) ◽  
pp. 26-30 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Randall W. Smith ◽  
Harvey M. Shapiro
Keyword(s):  
Intracranial Hypertension ◽  
Head Injuries ◽  
High Rate ◽  
High Dose ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
High Dose Dexamethasone ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

✓ In a series of 100 consecutive patients with severe head injuries, uncontrolled intracranial hypertension, which was defined as occurring when intracranial pressure (ICP) exceeded 40 mm Hg for 15 minutes or more, occurred in 25 patients. This was despite high-dose dexamethasone, hyperventilation, mannitol, normothermia, appropriate surgical evacuation, and cerebrospinal fluid drainage when possible. Persistently elevated ICP occurred in 19 patients with diffuse brain injury, and in six patients uncontrolled intracranial hypertension followed evacuation of a surgical mass. All of these patients received intravenous barbiturates to control the ICP. At the time of initial barbiturate administration, 11 of the 25 had bilaterally unreactive pupils and 12 were decerebrate. The initial pentobarbital loading dose (3 to 5 mg/kg) effectively reduced the ICP in 76% of the patients. Prolonged pentobarbital treatment with blood barbiturate levels from 2.5 to 3.5 mg% was associated with normalization of the ICP (ICP less than 15 mm Hg) in 13 patients. In those patients responding to barbiturates, the daily mannitol requirement was reduced from 4.5 to 0.5 gm/kg/day (p < 0.01). In six nonresponders to barbiturates, mannitol requirements increased to 5.9 gm/kg/day; five of these died and one remains vegetative. Ten of the 19 barbiturate responders have returned to a productive life, two remain moderately disabled, two are severely disabled, one is vegetative, and four are dead. The high rate of good quality survival in this series of severely brain-injured patients indicates that barbiturates are useful in the treatment of uncontrolled intracranial hypertension and that a broader investigation of the clinical application of barbiturates is indicated.

Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

2001 ◽  
Vol 94 (3) ◽  
pp. 403-411 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
Janet M. Vargo ◽  
Carla A. Erickson ◽  
Richard L. Sutton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Hyperbaric Oxygenation ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Brain Injured ◽  
Csf Lactate ◽  
Injured Patients ◽  
Fine Print

Object. Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm. Methods. Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber. Conclusions. The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.

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.

Protective effects of glial cell line—derived neurotrophic factor on hippocampal neurons after traumatic brain injury in rats

2001 ◽  
Vol 95 (4) ◽  
pp. 674-679 ◽  
Author(s):  
Bum-Tae Kim ◽  
Vemuganti L. Raghavendra Rao ◽  
Kurt A. Sailor ◽  
Kellie K. Bowen ◽  
Robert J. Dempsey
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cell Line ◽  
Glial Cell ◽  
Neurotrophic Factor ◽  
Neuronal Loss ◽  
Content Type ◽  
Frontal Horn ◽  
Brain Injured ◽  
Fine Print

Object. The purpose of this study was to evaluate whether glial cell line—derived neurotrophic factor (GDNF) can protect against hippocampal neuronal death after traumatic brain injury (TBI). Methods. Male Sprague—Dawley rats were subjected to moderate TBI with a controlled cortical impact device while in a state of halothane-induced anesthesia. Then, GDNF or artificial cerebrospinal fluid ([aCSF]; vehicle) was infused into the frontal horn of the left lateral ventricle. In eight brain-injured and eight sham-operated rats, GDNF was infused continuously for 7 days (200 ng/day intracerebroventricularly at a rate of 8.35 ng/0.5 µl/hour). An equal volume of vehicle was infused at the same rate into the remaining eight brain-injured and eight sham-operated rats. Seven days post-injury, all rats were killed. Their brains were sectioned and stained with cresyl violet, and the hippocampal neuronal loss was evaluated in the CA2 and CA3 regions with the aid of microscopy. A parallel set of sections from each brain was subjected to immunoreaction with antibodies against glial fibrillary acidic protein (GFAP; astroglia marker). In the aCSF-treated group, TBI resulted in a significant neuronal loss in the CA2 (60%, p < 0.05) and CA3 regions (68%, p < 0.05) compared with the sham-operated control animals. Compared with control rats infused with aCSF, GDNF infusion significantly decreased the TBI-induced neuronal loss in both the CA2 (58%, p < 0.05) and CA3 regions (51%, p < 0.05). There was no difference in the number of GFAP-positive astroglial cells in the GDNF-infused rats in the TBI and sham-operated groups compared with the respective vehicle-treated groups. Conclusions. The authors found that GDNF treatment following TBI is neuroprotective.

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