Laboratory criteria of brain death

1973 ◽  
Vol 39 (4) ◽  
pp. 429-433 ◽  
Author(s):  
Georges Ouaknine ◽  
Isaac Z. Kosary ◽  
Jackson Braham ◽  
Pinhas Czerniak ◽  
Hillel Nathan
Keyword(s):  
Brain Death ◽  
Laboratory Tests ◽  
Brain Temperature ◽  
Clinical Signs ◽  
Content Type ◽  
Bedside Tests ◽  
New Procedures ◽  
Fine Print

✓ Thirty patients with the clinical signs of brain death were subjected to a series of laboratory tests reputed to be capable of confirming this state. Three new procedures, electronystagmography, RISA intrathecal studies, and brain temperature tests, are described. The authors conclude that certain bedside tests, namely, electroencephalography, echoencephalography, electronystagmography, and electrocardiographic response to atropine, have been shown to be entirely adequate for a confident diagnosis.

Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: a randomized trial

2004 ◽  
Vol 100 (3) ◽  
pp. 376-383 ◽  
Author(s):  
Julio Cruz ◽  
Giulio Minoja ◽  
Kazuo Okuchi ◽  
Enrico Facco
Keyword(s):  
Brain Death ◽  
Emergency Room ◽  
Clinical Outcomes ◽  
Clinical Signs ◽  
High Dose ◽  
Content Type ◽  
Conventional Dose ◽  
Diffuse Brain Swelling ◽  
Fine Print

Object. The authors evaluated long-term clinical outcomes in selected acutely comatose patients with severe diffuse brain swelling and recent clinical signs of impending brain death who received a novel high-dose mannitol treatment compared with those who received conventional-dose mannitol in the emergency room. Methods. Forty-four adult patients with traumatic, nonmissile-inflicted, acute, severe diffuse brain swelling were prospectively and randomly evaluated. All patients were selected based on the presence of recent clinical signs of impending brain death on the first emergency room evaluation. These signs included bilateral abnormal pupillary widening and lack of motor responses to painful stimulation (Glasgow Coma Scale score of 3). The study group (23 patients) received ultra-early and fast intravenous high-dose mannitol treatment (∼1.4 g/kg), whereas the control group (21 patients) received half that dose (∼0.7 g/kg). Ultra-early improvement of bilateral abnormal pupillary widening was significantly more frequent in the high-dose mannitol group than in the conventional-dose group (p < 0.02). High-dose mannitol treatment in the emergency room was also associated with significantly better 6-month clinical outcomes (p < 0.02); the best rate of favorable outcomes was 43.5%, compared with only 9.5% in the conventional-dose mannitol group. The two groups of patients were well matched with respect to all emergency room and head computerized tomography findings, as well as the timing of initial mannitol treatment (∼80–90 minutes after the first evaluation at the scene of the injury). Comparative evaluation of bilateral pupillary widening between the scene of the injury and the emergency room showed no significant differences between groups, whereas mannitol dose dependence was statistically significant (p < 0.05), insofar as early pupillary improvement in the emergency room was concerned. Conclusions. Ultra-early high-dose mannitol administration in the emergency room is the first known treatment strategy significantly to reverse recent clinical signs of impending brain death, and also to contribute directly to improved long-term clinical outcomes for these patients who have previously been considered unsalvageable.

Craniopharyngioma in adults and children: a study of 122 surgical cases

2002 ◽  
Vol 97 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Rémy Van Effenterre ◽  
Anne-Laure Boch
Keyword(s):  
Patient Survival ◽  
Postoperative Radiotherapy ◽  
Clinical Signs ◽  
Functional Results ◽  
Recurrence Risk ◽  
Tumor Removal ◽  
Content Type ◽  
Adults And Children ◽  
Fine Print

Object. This work is devoted to a 25-year retrospective study of 122 cases of craniopharyngiomas in adults and children treated and followed by the same neurosurgeon (R.V.E.). In this homogeneous series, the aim was total microsurgical removal of the tumor, without postoperative radiotherapy. Methods. The operation was performed via a frontopterional approach in 112 cases and a transsphenoidal approach in 10 cases. The tumor removal was considered total in 59%, subtotal in 29%, and partial in 12%. The surgical mortality rate was 2.5%. Even when tumor removal was not complete, radiotherapy was not systematically administered; it was reserved for cases of recurrence. The authors have studied clinical signs, operative characteristics, and ophthalmological, endocrinological, and functional outcomes, as well as recurrence risk and long-term patient survival. The mean follow-up period was 7 years. The functional results in these patients were excellent in 85%, good in 9%, fair in 5% (usually because of ophthalmological sequelae), and poor in 1%. Tumors recurred in 29 patients, but the salvage treatment, by operation or radiotherapy, was successful in 83%. The actuarial patient survival rate was 92% after 5 years and 85% after 10 years. Conclusions. These results compared favorably with the data reported in the literature, suggesting that radical surgery of craniopharyngiomas allows good outcome in terms of survival, full recovery, and quality of life for both adults and children.

Transsphenoidal surgery in Cushing disease: 10 years of experience in 34 consecutive cases

2004 ◽  
Vol 100 (4) ◽  
pp. 634-638 ◽  
Author(s):  
Charlotte Höybye ◽  
Eva GrenbäcK ◽  
Marja Thorén ◽  
Anna-Lena Hulting ◽  
Lars Lundblad ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Transsphenoidal Surgery ◽  
Cushing Syndrome ◽  
Preoperative Evaluation ◽  
Clinical Signs ◽  
Pituitary Hormone ◽  
Years Of Experience ◽  
Cushing Disease ◽  
Content Type ◽  
Fine Print

Object. Cushing disease is a rare disorder. Because of their small size the adrenocorticotropic hormone (ACTH)—producing tumors are often not detectable on neuroimaging studies. To obtain a cure with transsphenoidal surgery (TSS) may therefore be difficult. In this report the authors present 10 years of experience in the treatment of patients with Cushing disease who were followed up with the same protocol and treated by the same surgeon. Methods. Thirty-four patients, 26 of them female and eight of them male (mean age 40 years, range 13–74 years) were studied. All had obvious clinical signs and symptoms of Cushing syndrome. Magnetic resonance (MR) imaging was performed in all patients, and inferior petrosal sinus (IPS) sampling was done in 14. In 12 patients MR imaging indicated a pituitary tumor; 10 were microadenomas and two were macroadenomas. In six patients with no visible tumor, the results of IPS sampling supported the diagnosis. All patients underwent TSS; the mean follow-up duration was 6 ± 0.5 years. Selective adenomectomy was performed in 32 and hemihypophysectomy in the other two patients. A cure was obtained in 31 patients (91%) after one TSS and in two more patients after further TSS; one patient was not cured despite two TSSs and one underwent bilateral adrenalectomy. Disease recurrence was seen in two patients after 3 years, and they were successfully treated with stereotactic gamma knife surgery. Half of the patients had an ACTH deficiency postoperatively, whereas one third had other pituitary hormone insufficiencies. There were no serious complications attributable to the surgical intervention. Conclusions. Transsphenoidal surgery with selective adenomectomy is an effective and safe treatment for Cushing disease. In the patients presented in this study, the surgical outcome seemed to depend on careful preoperative evaluation and the surgeon's experience. For optimal results in this rare disease the authors therefore suggest that the endocrinological, radiological, and surgical procedures be coordinated in a specialized center.

Families, brain death, and traditional medical excellence

1984 ◽  
Vol 60 (6) ◽  
pp. 1192-1194 ◽  
Author(s):  
Rosa Lynn Pinkus
Keyword(s):  
Brain Death ◽  
Tertiary Care Hospital ◽  
Tertiary Care ◽  
Care Hospital ◽  
Personal Beliefs ◽  
Content Type ◽  
The Past ◽  
Transplant Center ◽  
Fine Print

✓ Staff neurosurgeons and residents at a tertiary care hospital designated as a transplant center were surveyed regarding personal opinions concerning brain death and family conferences. Compared to an extensive survey done in 1976, the responses indicated that, while a professional consensus regarding the definition and meaning of brain death has emerged in the past 10 years, a range of personal beliefs and opinions regarding the concept still exists. In spite of the professional consensus, it is still difficult for the physician to communicate gently, yet firmly, to families both the scientific groundwork that validates the determination of brain death, the concept, and the finality of the information.

Effects of profound hypothermia and circulatory arrest on cerebral oxygen metabolism and cerebrospinal fluid electrolyte composition in dogs

1974 ◽  
Vol 40 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Edgar A. Bering
Keyword(s):  
Brain Temperature ◽  
Circulatory Arrest ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Profound Hypothermia ◽  
Content Type ◽  
Cerebral Oxygen Metabolism ◽  
Natural Logarithm ◽  
K Concentration ◽  
Fine Print

✓ Cerebral oxygen metabolism was studied in the dog at brain temperatures ranging from 37° to 8°C. As brain temperature decreased, the cerebral oxygen metabolism (CMRO2) decreased following the Arrhenius equation. The natural logarithm of the CMRO2 was a linear function of the reciprocal of the absolute (K) brain temperature. Oxygen metabolism, although much decreased, continued at very low brain temperatures. The CSF composition was unchanged after 1 hour at brain temperatures down to 10°C. Circulatory arrest for tolerable periods and longer caused changes only in the CSF potassium concentration. The interval between the onset of circulatory arrest and the beginning of the CSF K concentration increased with decreasing temperature and the rate of CSF K increase was increasingly slower at lower temperatures. At all temperatures the rate of CSF K changed gradually increased with time. The interval before the CSF K started to increase was dependent upon the amount of O2 available in the brain and the length of this interval was inversely proportional to the CMRO2. The amount of CSF K concentration was not clearly related to the tolerable periods of circulatory arrest, but at normal temperatures an obviously increased CSF K following a period of acute cerebral anoxia without CSF hemorrhage may indicate brain damage.

Experimental chronic compressive cervical myelopathy

1993 ◽  
Vol 79 (4) ◽  
pp. 550-561 ◽  
Author(s):  
Ossama Al-Mefty ◽  
H. Louis Harkey ◽  
Isam Marawi ◽  
Duane E. Haines ◽  
Dudley F. Peeler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Spinal Canal ◽  
Morphological Changes ◽  
Clinical Signs ◽  
Magnetic Resonance Images ◽  
Neurological Deficits ◽  
Cervical Cord ◽  
Flow Measurements ◽  
Content Type ◽  
Fine Print

✓ A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months. Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.

Apnea testing for the determination of brain death: a modified protocol

1992 ◽  
Vol 76 (6) ◽  
pp. 1029-1031 ◽  
Author(s):  
Edward C. Benzel ◽  
Jay P. Mashburn ◽  
Steven Conrad ◽  
Denise Modling
Keyword(s):  
Brain Death ◽  
Apnea Test ◽  
Content Type ◽  
Group I ◽  
The Mean ◽  
Group Ii ◽  
Safe Approach ◽  
Apnea Testing ◽  
Fine Print

✓ The absence of spontaneous respirations at a PaCO2 of 60 mm Hg or above has traditionally been accepted as the respiratory criteria for the determination of brain death. The testing of patients for the presence or absence of apnea has been complicated because the rate of PaCO2 elevation may vary substantially from patient to patient, and a nonlinear relationship exists between the rate of PaCO2 increase and the duration of apnea. In an attempt to refine the apnea test and to further elucidate the physiology of hypercapnia in humans, 11 patients who met all but the respiratory criteria for brain death were evaluated using a modification of a previously utilized apnea testing protocol. All patients were brought to a PaCO2 of 40 mm Hg or above prior to the apnea test. Baseline PaCO2 ranged from 40 to 45 mm Hg in six patients (Group I) and from 46 to 51 mm Hg in five patients (Group II). The mean rate of PaCO2 increase was 5.1 ± 1.4 mm Hg/min in Group I and 6.7 ± 3.1 mm Hg/min in Group II. No problems with cardiovascular instability or hypoxia were encountered during testing in this series. This refinement of the apnea test allows for a streamlined and safe approach to brain death detection.

Serial evaluation of axonal function in patients with brain death by using anisotropic diffusion-weighted magnetic resonance imaging

2004 ◽  
Vol 100 (1) ◽  
pp. 56-60 ◽  
Author(s):  
Toru Watanabe ◽  
Yoshiho Honda ◽  
Yukihiko Fujii ◽  
Miyako Koyama ◽  
Ryuichi Tanaka
Keyword(s):  
Magnetic Resonance ◽  
Brain Death ◽  
Corticospinal Tract ◽  
Imaging System ◽  
Three Dimensional ◽  
Diffusion Anisotropy ◽  
Content Type ◽  
Three Bundles ◽  
Axonal Dysfunction ◽  
Fine Print

Object. The purposes of this study were to evaluate the serial changes in diffusion anisotropy of the brain, probably reflecting axonal function in brain-dead patients, and thus to explore the possibility of quantitatively estimating the risk of brain death. Methods. Ten patients suffering from stroke with or without impending brain death and 10 healthy volunteers were studied using three-dimensional anisotropy contrast (3DAC) magnetic resonance (MR) axonography with the aid of a 1.5-tesla MR imaging system. To detect changes in the diffusion anisotropy of neural bundles, the corticospinal tract was evaluated. Diffusion anisotropy of short axonal fibers decreased immediately after apparent brain death. Whereas the trichromatic coefficients of the corticospinal tract greatly diminished between 6 and 12 hours after apparent brain death, the coefficients of the corpus callosum and the optic radiation decreased in less time, that is, between 1 and 6 hours. The coefficients of these three bundles turned isotropic between 24 and 44 hours after apparent brain death. Conclusions. Results of 3DAC MR axonography revealed that diffusion anisotropy of neural bundles diminished between 1 and 12 hours after the onset of apparent brain death, probably depending on the length of the bundles, and disappeared between 24 and 44 hours after the onset of brain death, which might reflect dynamic changes of axonal structure and indirectly herald axonal dysfunction. These findings seem to be greatly helpful in establishing an appropriate method to estimate the risk of brain death quantitatively and in forming the basis of future definitions of brain death.

Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia

2003 ◽  
Vol 99 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Yoshikazu Nakajima ◽  
Mamoru Taneda ◽  
Osamu Tasaki ◽  
Yoshiaki Inoue ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Mild Hypothermia ◽  
Brain Temperature ◽  
Moderate Hypothermia ◽  
Content Type ◽  
Arterial Blood ◽  
Cell Counts ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. This study was performed to determine whether moderate hypothermia (31°C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34°C). Methods. Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31°C, the volume of intravenous fluid infusion was increased significantly from 1.9 ± 0.9 to 2.6 ± 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 ± 3.1 to 8.2 ± 4.4 µg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 ± 13.1 to 85.1 ± 10.5 mm Hg (p < 0.01) and from 92.2 ± 13.8 to 72.2 ± 14.3 beats/minute at (p < 0.01) at 34 and 31°C, respectively. Arterial base excess was significantly aggravated from −3.3 ± 4 at 34°C to −5.6 ± 5.4 mEq/L (at 31°C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31°C decreased significantly compared with those at 34°C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients, ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. Conclusions. The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.

The effect of brain temperature on hemoglobin extravasation after traumatic brain injury

2002 ◽  
Vol 97 (4) ◽  
pp. 945-953 ◽  
Author(s):  
Kosaku Kinoshita ◽  
Katina Chatzipanteli ◽  
Ofelia F. Alonso ◽  
Mackenzie Howard ◽  
W. Dalton Dietrich
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Injury Severity ◽  
Brain Temperature ◽  
Experimental Studies ◽  
Hemoglobin Concentration ◽  
Contralateral Hemisphere ◽  
Ipsilateral Hemisphere ◽  
Content Type ◽  
Fine Print

Object. Although the benefits of posttraumatic hypothermia have been reported in experimental studies, the potential for therapeutic hypothermia to increase intracerebral hemorrhage remains a clinical concern. The purpose of this study was to quantify the amount of extravasated hemoglobin after traumatic brain injury (TBI) and to assess the changes in intracerebral hemoglobin concentrations under posttraumatic hypothermic and hyperthermic conditions. Methods. Intubated and anesthetized rats were subjected to fluid-percussion injury (FPI). In the first experiment, rats were divided into moderate (1.8–2.2 atm) and severe (2.4–2.7 atm) TBI groups. In the second experiment, the effects of 3 hours of posttraumatic hypothermia (33 or 30°C), hyperthermia (39°C), or normothermia (37°C) on hemoglobin levels following moderate trauma were assessed. The rats were perfused with saline at 24 hours postinjury, and then the traumatized and contralateral hemispheres, including the cerebellum, were dissected from whole brain. The hemoglobin level in each brain was quantified using a spectrophotometric hemoglobin assay. The results of these assays indicate that moderate and severe FPI induce increased levels of hemoglobin in the ipsilateral hemisphere (p < 0.0001). After severe TBI, the hemoglobin concentration was also significantly increased in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Posttraumatic hypothermia (30°C) attenuated hemoglobin levels (p < 0.005) in the ipsilateral hemisphere, whereas hyperthermia had a marked adverse effect on the hemoglobin concentration in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Conclusions. Injury severity is an important determinant of the degree of hemoglobin extravasation after TBI. Posttraumatic hypothermia reduced hemoglobin extravasation, whereas hyperthermia increased hemoglobin levels compared with normothermia. These findings are consistent with previous data reporting that posttraumatic temperature manipulations alter the cerebrovascular and inflammatory consequences of TBI.

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