Disseminated intravascular coagulation associated with massive brain injury

1973 ◽  
Vol 39 (2) ◽  
pp. 178-180 ◽  
Author(s):  
Rudolph M. Keimowitz ◽  
Byron L. Annis
Keyword(s):  
Brain Injury ◽  
Disseminated Intravascular Coagulation ◽  
Brain Trauma ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Diagnostic Studies ◽  
Fine Print

✓ The authors report a case of disseminated intravascular coagulation in a patient with massive brain trauma. It is suggested that the condition was caused by the liberation of thromboplastin. The detailed diagnostic studies and related theories are discussed.

An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake

1995 ◽  
Vol 82 (3) ◽  
pp. 379-385 ◽  
Author(s):  
Julio Cruz
Keyword(s):  
Brain Injury ◽  
Intracranial Pressure ◽  
Glucose Uptake ◽  
Therapeutic Effect ◽  
Brain Trauma ◽  
Metabolic Effect ◽  
Normal Range ◽  
Content Type ◽  
Cerebral Extraction Of Oxygen ◽  
Fine Print

✓ In a total of 309 frequent serial studies, arteriojugular differences in glucose and oxygen levels were concurrently evaluated in 33 adult patients who were experiencing the most acute phase of severe brain trauma. Hyperventilation therapy was optimized to maintain both normalized intracranial pressure and cerebral extraction of oxygen. Under these circumstances, global cerebral glucose extraction was found to be closest to normal during profound optimized hyperventilation, with PaCO2 levels below 25 mm Hg. In contrast, during normocapnia global cerebral glucose extraction dropped below normal range, indicating impairment of cerebral glucose uptake. Findings from this study show that in severe acute brain injury, optimized hyperventilation exerts an additional metabolic effect with respect to cerebral glucose uptake.

Disseminated intravascular coagulation following cranial trauma

1980 ◽  
Vol 52 (2) ◽  
pp. 266-269 ◽  
Author(s):  
Jerrold A. Clark ◽  
Robert E. Finelli ◽  
Martin G. Netsky
Keyword(s):  
Brain Tissue ◽  
Disseminated Intravascular Coagulation ◽  
Spinal Trauma ◽  
Clotting System ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Cranial Trauma ◽  
Venous Sinuses ◽  
Fine Print ◽  
Dural Venous Sinuses

✓ Cranial and spinal trauma resulted in disseminated intravascular coagulation (DIC) in a 78-year-oldman, causing widespread bleeding and incoagulable blood. Traumatized brain tissue was found in the lumina of dural venous sinuses. The mechanisms of DIC are reviewed. It is suggested that intravascular release ofpotent cerebral thromboplastin contributed to the severity of DIC in this patient, by causing activation of the extrinsic clotting system. Intrasinus brain tissue in cases of human trauma has not previously been reported.

Low clinical ischemic threshold for cerebral blood flow in severe acute brain trauma

1994 ◽  
Vol 80 (1) ◽  
pp. 143-147 ◽  
Author(s):  
Julio Cruz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Marked Reduction ◽  
Critical Level ◽  
Brain Trauma ◽  
Cerebral Hypoperfusion ◽  
Content Type ◽  
Satisfactory Recovery ◽  
Fine Print

✓ A case of severe acute brain trauma is presented in which the patient made a satisfactory recovery after suffering a marked reduction in cerebral blood flow, to a level previously reported in association with impending brain death (10 ml/100 gm/min). This is believed to be the first report of a patient with severe acute brain injury in whom serial clinical and physiological assessments allowed documentation of the reversibility of such a critical level of cerebral hypoperfusion.

Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury

2002 ◽  
Vol 97 (6) ◽  
pp. 1373-1377 ◽  
Author(s):  
Sherman C. Stein ◽  
Xiao-Han Chen ◽  
Grant P. Sinson ◽  
Douglas H. Smith
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Strong Association ◽  
Focal Lesions ◽  
Severe Injuries ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Secondary Insult ◽  
Time Courses ◽  
Fine Print

Object. The goal of this study was to determine the frequency with which cerebral intravascular coagulation (IC) complicates traumatic brain injury (TBI). The authors also investigated the incidence of IC in relation to varying mechanisms, time courses, and severities of TBI and in different species. Methods. Tissue was sampled from surgical specimens of human cerebral contusions, from rats with lateral fluid-percussion injuries, and from pigs with head rotational acceleration injuries. Immunohistochemical fluorescent staining for antithrombin III was performed to detect cerebral intravascular microthrombi. Abundant IC was found in all specimens, and microthrombi had formed in arterioles and venules of all sizes, ranging from 10 to 600 µm. Although it was more pronounced in focal lesions and more severe injuries, considerable IC was also observed in mild and diffuse injuries. The authors found a strong association between the severity of coagulopathy and the density of IC. Conclusions. These results strongly support the contention that IC is a universal response to TBI and an important secondary cerebral insult.

Subdural hematoma associated with disseminated intravascular coagulation in patients with advanced cancer

1983 ◽  
Vol 58 (3) ◽  
pp. 398-401 ◽  
Author(s):  
Tomoo Furui ◽  
Kaoru Ichihara ◽  
Akira Ikeda ◽  
Suguru Inao ◽  
Nagatoshi Hirai ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Advanced Cancer ◽  
Disseminated Intravascular Coagulation ◽  
Subdural Hematoma ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Fine Print

✓ Nontraumatic subdural hematoma following disseminated intravascular coagulation (DIC) due to advanced cancer was encountered in four patients. It is suggested that DIC plays an important role in the formation of subdural hematoma in cancer patients.

Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign

2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intraventricular Hemorrhage ◽  
Pneumococcal Meningitis ◽  
Clinical Importance ◽  
Neurological Deterioration ◽  
Content Type ◽  
Transient Nature ◽  
Fine Print

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.

Mobile computerized tomography scanning in the neurosurgery intensive care unit: increase in patient safety and reduction of staff workload

2000 ◽  
Vol 93 (3) ◽  
pp. 432-436 ◽  
Author(s):  
Thorsteinn Gunnarsson ◽  
Annette Theodorsson ◽  
Per Karlsson ◽  
Steen Fridriksson ◽  
Sverre Boström ◽  
...  
Keyword(s):  
Intensive Care ◽  
Brain Injury ◽  
Risk Group ◽  
Ct Scanning ◽  
Secondary Brain Injury ◽  
Content Type ◽  
Medium Risk ◽  
Mobile Ct ◽  
Staff Workload ◽  
Fine Print

Object. Transportation of unstable neurosurgical patients involves risks that may lead to further deterioration and secondary brain injury from perturbations in physiological parameters. Mobile computerized tomography (CT) head scanning in the neurosurgery intensive care (NICU) is a new technique that minimizes the need to transport unstable patients. The authors have been using this device since June 1997 and have developed their own method of scanning such patients.Methods. The scanning procedure and radiation safety measures are described. The complications that occurred in 89 patients during transportation and conventional head CT scanning at the Department of Radiology were studied prospectively. These complications were compared with the ones that occurred during mobile CT scanning in 50 patients in the NICU. The duration of the procedures was recorded, and an estimation of the staff workload was made. Two patient groups, defined as high- and medium-risk cases, were studied. Medical and/or technical complications occurred during conventional CT scanning in 25% and 20% of the patients in the high- and medium-risk groups, respectively. During mobile CT scanning complications occurred in 4.3% of the high-risk group and 0% of the medium-risk group. Mobile CT scanning also took significantly less time, and the estimated personnel cost was reduced.Conclusions. Mobile CT scanning in the NICU is safe. It minimizes the risk of physiological deterioration and technical mishaps linked to intrahospital transport, which may aggravate secondary brain injury. The time that patients have to remain outside the controlled environment of the NICU is minimized, and the staff's workload is decreased.

Measurement of brain tissue oxygenation performed using positron emission tomography scanning to validate a novel monitoring method

2002 ◽  
Vol 96 (2) ◽  
pp. 263-268 ◽  
Author(s):  
Arun K. Gupta ◽  
Peter J. Hutchinson ◽  
Tim Fryer ◽  
Pippa G. Al-Rawi ◽  
Dot A. Parry ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Brain Injury ◽  
Brain Tissue ◽  
Tissue Oxygenation ◽  
Emission Tomography ◽  
Brain Tissue Oxygenation ◽  
Content Type ◽  
Positron Emission ◽  
Pet Scans ◽  
Fine Print

Object. The benefits of measuring cerebral oxygenation in patients with brain injury are well accepted; however, jugular bulb oximetry, which is currently the most popular monitoring technique used has several shortcomings. The goal of this study was to validate the use of a new multiparameter sensor that measures brain tissue oxygenation and metabolism (Neurotrend) by comparing it with positron emission tomography (PET) scanning. Methods. A Neurotrend sensor was inserted into the frontal region of the brain in 19 patients admitted to the neurointensive care unit. After a period of stabilization, the patients were transferred to the PET scanner suite where C15O, 15O2, and H215O PET scans were obtained to facilitate calculation of regional cerebral blood volume, O2 metabolism, blood flow, and O2 extraction fraction (OEF). Patients were given hyperventilation therapy to decrease arterial CO2 by approximately 1 kPa (7.5 mm Hg) and the same sequence of PET scans was repeated. For each scanning sequence, end-capillary O2 tension (PvO2) was calculated from the OEF and compared with the reading of brain tissue O2 pressure (PbO2) provided by the sensor. In three patients the sensor was inserted into areas of contusion and these patients were eliminated from the analysis. In the subset of 16 patients in whom the sensor was placed in healthy brain, no correlation was found between the absolute values of PbO2 and PvO2 (r = 0.2, p = 0.29); however a significant correlation was obtained between the change in PbO2 (ΔPbO2) and the change in PvO2 (ΔPvO2) produced by hyperventilation in a 20-mm region of interest around the sensor (ρ = 0.78, p = 0.0035). Conclusions. The lack of correlation between the absolute values of PbO2 and PvO2 indicates that PbO2 cannot be used as a substitute for PvO2. Nevertheless, the positive correlation between ΔPbO2 and ΔPvO2 when the sensor had been inserted into healthy brain suggests that tissue PO2 monitoring may provide a useful tool to assess the effect of therapeutic interventions in brain injury.

Intracranial bone marrow transplantation after traumatic brain injury improving functional outcome in adult rats

2001 ◽  
Vol 94 (4) ◽  
pp. 589-595 ◽  
Author(s):  
Asim Mahmood ◽  
Dunyue Lu ◽  
Yi Li ◽  
Jae Li Chen ◽  
Michael Chopp
Keyword(s):  
Traumatic Brain Injury ◽  
Bone Marrow ◽  
Brain Injury ◽  
Motor Function ◽  
Glial Fibrillary Acid Protein ◽  
Protein Markers ◽  
Adult Rats ◽  
Content Type ◽  
The Impact ◽  
Fine Print

Object. The authors tested the hypothesis that intracranial bone marrow (BM) transplantation after traumatic brain injury (TBI) in rats provides therapeutic benefit. Methods. Sixty-six adult Wistar rats, weighing 275 to 350 g each, were used for the experiment. Bone marrow prelabeled with bromodeoxyuridine (BrdU) was harvested from tibias and femurs of healthy adult rats. Other animals were subjected to controlled cortical impact, and BM was injected adjacent to the contusion 24 hours after the impact. The animals were killed at 4, 7, 14, or 28 days after transplantation. Motor function was evaluated both before and after the injury by using the rotarod test. After the animals had been killed, brain sections were examined using hemotoxylin and eosin and immunohistochemical staining methods. Histological examination revealed that, after transplantation, BM cells survived, proliferated, and migrated toward the injury site. Some of the BrdU-labeled BM cells were reactive, with astrocytic (glial fibrillary acid protein) and neuronal (NeuN and microtubule-associated protein) markers. Transplanted BM expressed proteins phenotypical of intrinsic brain cells, that is, neurons and astrocytes. A statistically significant improvement in motor function in rats that underwent BM transplantation, compared with control rats, was detected at 14 and 28 days posttransplantation. Conclusions. On the basis of their findings, the authors assert that BM transplantation improves neurological outcome and that BM cells survive and express nerve cell proteins after TBI.

Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Roberto Imberti ◽  
Guido Bellinzona ◽  
Martin Langer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Cerebral Perfusion ◽  
Content Type ◽  
Secondary Damage ◽  
Tissue Po2 ◽  
Two Parameters ◽  
Fine Print

Object. The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). Methods. Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27–32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score ≤ 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation — posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. Conclusions. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.

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