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.

The repair of dural venous sinus wounds by autogenous venorrhaphy

1971 ◽  
Vol 35 (4) ◽  
pp. 392-395 ◽  
Author(s):  
Berkley L. Rish
Keyword(s):  
Venous Sinus ◽  
New Technique ◽  
Surgical Experience ◽  
Content Type ◽  
Venous Sinuses ◽  
Dural Venous Sinus ◽  
A New Technique ◽  
Combat Casualties ◽  
Fine Print ◽  
Dural Venous Sinuses

✓ Military surgical experience with acute wounds of the dural venous sinuses is reviewed. A new technique, autogenous venorrhaphy, is described and reported as the method used in 10 Vietnam combat casualties.

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 internal shunt for use in the reconstruction of dural venous sinuses

1971 ◽  
Vol 35 (3) ◽  
pp. 351-354 ◽  
Author(s):  
John P. Kapp ◽  
Isaac Gielchinsky ◽  
Clayton Petty ◽  
Claude McClure
Keyword(s):  
Blood Flow ◽  
Illustrative Case ◽  
Content Type ◽  
Venous Sinuses ◽  
Flow Through ◽  
Fine Print ◽  
Dural Venous Sinuses

✓ A technique is described for construction and use of an internal shunt which provides hemostasis and permits blood flow through the injured sinus during the period of repair. An illustrative case is presented.

Isotope sinograms

1976 ◽  
Vol 44 (3) ◽  
pp. 393-394 ◽  
Author(s):  
John P. Kapp ◽  
Harry C. Alfred ◽  
Terri Jones
Keyword(s):  
Content Type ◽  
Venous Sinuses ◽  
Fine Print ◽  
Dural Venous Sinuses

✓ A technique is described for examination of the dural venous sinuses using isotope angiography.

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.

Pseudotumor cerebri syndrome: venous sinus obstruction and its treatment with stent placement

2003 ◽  
Vol 98 (5) ◽  
pp. 1045-1055 ◽  
Author(s):  
Brian K. Owler ◽  
Geoffrey Parker ◽  
G. Michael Halmagyi ◽  
Victoria G. Dunne ◽  
Verity Grinnell ◽  
...  
Keyword(s):  
Stent Placement ◽  
Pseudotumor Cerebri ◽  
Venous Sinus ◽  
Stent Insertion ◽  
Benign Intracranial Hypertension ◽  
Content Type ◽  
Venous Sinuses ◽  
Pseudotumor Cerebri Syndrome ◽  
New Treatment ◽  
Fine Print

Object. Pseudotumor cerebri, or benign intracranial hypertension, is a condition of raised intracranial pressure in the absence of a mass lesion or cerebral edema. It is characterized by headache and visual deterioration that may culminate in blindness. Pseudotumor cerebri is caused by venous sinus obstruction in an unknown percentage of cases. The purpose of this study was to investigate the role of cerebral venous sinus disease in pseudotumor cerebri and the potential of endoluminal venous sinus stent placement as a new treatment. Methods. Nine consecutive patients in whom diagnoses of pseudotumor cerebri had been made underwent examination with direct retrograde cerebral venography (DRCV) and manometry to characterize the morphological features and venous pressures in their cerebral venous sinuses. The cerebrospinal fluid (CSF) pressure was measured simultaneously in two patients. If patients had an amenable lesion they were treated using an endoluminal venous sinus stent. Five patients demonstrated morphological obstruction of the venous transverse sinuses (TSs). All lesions were associated with a distinct pressure gradient and raised proximal venous sinus pressures. Four patients underwent stent insertion in the venous sinuses and reported that their headaches improved immediately after the procedure and remained so at 6 months. Vision was improved in three patients, whereas it remained poor in one despite normalized CSF pressures. Conclusions. Patients with pseudotumor cerebri should be evaluated with DRCV and manometry because venous TS obstruction is probably more common than is currently appreciated. In patients with a lesion of the venous sinuses, treatment with an endoluminal venous sinus stent is a viable alternative for amenable lesions.

Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas

2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  
Keyword(s):  
Contrast Agent ◽  
Brain Edema ◽  
Brain Tissue ◽  
Magnetic Resonance Images ◽  
Content Type ◽  
Extracellular Contrast Agent ◽  
Peritumoral Brain Edema ◽  
Hydrodynamic Processes ◽  
Fine Print

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.

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.

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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