摘要:

Adverse neurological events during hypoxic episodes in high-risk patients or in patients not thought to be at risk while undergoing procedures increase morbidity and mortality. The ability to reliably monitor cerebral oxygenation could serve as an indicator for the need of therapeutic intervention and it's overall effect. This study was designed to verify the reliability of the only commercially available continuous noninvasive monitor, the INVOS 3100 (Somanetics Corp., Troy, MI), in subjects with varying levels of hypoxemia. Six adult volunteer subjects were enrolled. After placement of electrocardiogram (EKG), noninvasive blood pressure (NIBP), pulse oximeter (SpO2), cerebral oximeter (rSO2), a 20 g radial artery catheter, and a 4 F oximetric jugular bulb catheter, the subjects were given hypoxic mixtures to breathe to varying levels of desaturation. Arterial and mixed venous blood was drawn for blood-gas analysis at each level of O2saturation. The cerebral hemoglobin saturation value from the cerebral oximeter was compared to the combined brain saturation using the formula: estimated field saturation between the light source and the detector (fSO2) = 0.25 × the arterial oxygen saturation (SaO2) + 0.75 × the jugular bulb venous oxygen saturation (SjvO2), (fSO2= 0.25 SaO2+ 0.75 SjvO2). Statistical analysis demonstrated a correlation of 0.67 between rSO2and fSO2and a bias of -3.1% with a precision of 12.1%. Minimal bias of 0.38% and precision of 6.22% were calculated for transitional error. We concluded from the study that rSO2may serve as a reliable indicator of changes in brain oxygenation induced by hypoxemia.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Cerebral perfusion pressure is commonly calculated from the difference between mean arterial pressure and intracranial pressure because intracranial pressure is known to represent the effective downstream pressure of the cerebral circulation. Studies of other organs, however, have shown that effective downstream pressure is determined by a critical closing pressure located at the arteriolar level. This study was designed to investigate the effects of PCO2-induced variations in cerebrovascular tone on the effective downstream pressure of the cerebral circulation. Sixteen patients recovering from head injury were studied. Intracranial pressure was assessed by epidural pressure transducers. Blood flow velocity in the middle cerebral artery was monitored by transcranial Doppler sonography. Effective downstream pressure was derived from the zero flow pressure as extrapolated by regression analysis of instantaneous arterial pressure/middle cerebral artery flow velocity relationships. PaCO2was varied between 30 and 47 mm Hg in randomized sequence. Intracranial pressure decreased from 18.5 ± 5.2 mm Hg during hypercapnia to 9.9 ± 3.1 mm Hg during hypocapnia. In contrast, effective downstream pressure increased from 13.7 ± 9.6 mm Hg to 23.4 ± 8.6 mm Hg and exceeded intracranial pressure at hypocapnic PaCO2levels. Our results demonstrate that, in the absence of intracranial hypertension, intracranial pressure does not necessarily represent the effective downstream pressure of the cerebral circulation. Instead, the tone of cerebral resistance vessels seems to determine effective downstream pressure. This suggests a modified model of the cerebral circulation based on the existence of two Starling resistors in a series connection.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

We report a case of a 35-year-old man with achondroplasia who previously had thoracolumbar decompressive laminectomies, who developed recurrence of spinal stenosis at the thoracolumbar junction. The patient underwent standard repeat thoracolumbar decompression, removal of a disc, and spinal fusion with instrumentation in the prone position. Postoperatively the patient was confused. Computed tomography (CT) revealed hemorrhages in both cerebellar hemispheres with surrounding edema and mild mass effect. These were interpreted as venous hemorrhages. Conservative therapy was successful. This is the first case report of perioperative venous intracranial hemorrhage in the context of spinal surgery for achondroplasia. Distinctive anatomic characteristics of achondroplasia, combined with several potentially modifiable aspects of his management, may have predisposed the patient to this complication.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Fat embolism syndrome is a dire complication of long bone trauma. It is usually associated with neurological, hematological and respiratory involvement, the latter being the major cause of death. We present a case of severe fat embolism syndrome occurring 3 hours after a long bone injury, leading to permanent vegetative state and death without any respiratory signs. The diagnosis was confirmed by cytology of the bronchoalveolar lavage fluid. Clinical presentation of the puzzling fat embolism syndrome and diagnostic tests in suspected fat embolism syndrome are reviewed.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

A 51-year-old female patient, with an adrenocorticotrophic hormone-secreting pituitary tumor, was scheduled for transphenoidal hypophysectomy. She had a history of recent onset diabetes mellitus and a 2-year history of arterial hypertension. Despite ongoing medical therapy, preoperative blood pressure was 150–160/90–120 mm Hg. During general anesthesia, in response to perinasal infiltration with 10 ml of a solution containing lidocaine 200 mg and epinephrine 100 &mgr;g, blood pressure increased from 144/80 mm Hg to 317/175 over 3 minutes, as assessed by direct blood pressure monitoring. At the completion of the anesthetic, as the patient awakened and coughed and moved, blood pressure again increased dramatically, this time from 154/87 mm Hg to 285/170 over 3 minutes. Five months postoperatively, the patient's serum cortisol concentrations had normalized and her cuff blood pressure was 126/82, despite a reduction in her antihypertensive medications. The dramatic intraoperative blood pressure changes in this patient were attributed to the effects of hypercortisolemia on the normal physiologic responses to epinephrine and patient movement.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Cerebral amyloid angiopathy frequently causes recurrent intracerebral hemorrhages in elderly patients who do not have systemic hypertension. Surgery should be reserved for conditions which cannot be controlled by medical treatment. When surgery is needed, potential complications (such as bleeding near the operation site or remote area) should be kept in mind. A case study of a 66-year-old woman with cerebral amyloid angiopathy and recurrent intracerebral hemorrhages is presented.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

We report a case involving a patient undergoing carotid endarterectomy in whom transcranial doppler monitoring demonstrated impaired cerebral blood flow during the initial dissection of the carotid artery, during cross-clamping of the carotid artery, and after the shunt was kinked inadvertently. Only when the carotid artery was cross-clamped were these ischemic changes also seen by electroencephalography. During the other episodes, the electroencephalography tracings demonstrated no detectable changes. This case illustrates the importance of using multiple modalities to determine the adequacy of cerebral blood flow and neuronal integrity.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Glutamate transporters, widely distributed in the brain and spinal cord, maintain extracellular glutamate concentrations below neurotoxic levels. In cerebral ischemia/anoxia, the glutamate transporter runs in reverse and releases glutamate into the extracellular space, causing irreversible neuronal damage. Although hypothermia reduces the elevation of extracellular glutamate concentration during cerebral ischemia/anoxia, little is known about the effect of hypothermia on the glutamate transporter. A human glial glutamate transporter (hGLT-1) cDNA was isolated by screening a human cerebral cortical library, and cloned cDNA was stably transfected in Chinese hamster ovary (CHO) cells. Effects of deep hypothermia (22 to 23°C) on uptake and release of L-glutamate via hGLT-1 were investigated by whole-cell patch-clamp. The control study was performed at 34 to 35°C. The hGLT-1 transporter had the capacity to take up extracellular L-glutamate under essentially physiological ionic conditions, whereas this transporter promoted release of L-glutamate under a nonphysiological condition mimicking complete ischemia. Deep hypothermia decreased a) uptake and b) release of L-glutamate via hGLT-1 to a) 4.8 ± 4.8% (P< .01, n = 7) and b) 19.0 ± 4.5% (P< .01, n = 15) of control values, respectively. The results suggest that deep hypothermia is a potent inhibitor of glutamate uptake by intact glial cells as well as glutamate release from glial cells under certain pathophysiological circumstances. The balance between these antagonistic effects of hypothermia may attenuate the elevation of the extracellular glutamate concentration during ischemia/anoxia.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Previous studies have indicated that prolonging the onset of ischemic depolarization reduces neuronal damage. However, the relationship between the duration of ischemic depolarization and its histological outcome has not been quantitatively evaluated. Rats were anesthetized (with 1% halothane), intubated, and placed in a stereotaxic frame. Direct current (DC)-potential in the 5th layer of the parietal cortex was measured. Changes in cerebral blood flow (CBF) were monitored by a laser-Doppler flow probe placed adjacent to the DC-electrode. Animals were subjected to four-vessel occlusion for 5 minutes, 10 minutes, or 20 minutes. The histological outcome was evaluated at the DC-recorded site 7 days after the insult. Initiation of ischemia reduced CBF to 9%–28% of the preischemic value. Initial DC-deflection (14 ± 3 mV), indicating ischemic depolarization, was observed at 172 ± 112 seconds after the onset of ischemia. Total durations of ischemic depolarization were 6.4 ± 1.5 minutes, 10.6 ± 3.5 minutes and 19.8 ± 4.6 minutes in rats in which ischemia was induced for 5 minutes, 10 minutes, and 20 minutes, respectively. The regression curve showed that there was a close relationship between percentage of damaged neurons and duration of ischemic depolarization (r2= 0.80,P= .001). The durations of ischemic depolarization for neuronal injury in 30%, 50%, and 70% of pyramidal neurons in the parietal cortex were 15.6 minutes (95% confidence interval, 14.2–17.0 minutes), 20.3 minutes (18.5–22.7 minutes) and 25.0 minutes (22.7–28.5 minutes), respectively. It is thought that shortening the duration of ischemic depolarization is a rational approach for reducing the severity of ischemic injury.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Most pharmacologic studies on brain trauma in animals are performed while the animals are under general anesthesia, which can interfere with brain metabolism and modify the experimental results. This study investigates the effects of three anesthetic drugs (halothane 2% and 4%, propofol at 10 mg/kg, and chloral hydrate at 400 mg/kg) on the traumatic brain injury-induced neurologic deficit in mice. Trauma was induced with a weight-drop device. For each drug, animals were divided into four groups; the first did not receive either anesthesia or trauma, the second received anesthesia but no trauma, the third received a trauma without anesthesia, and the fourth received anesthesia before the trauma. A neurologic examination using two different scorings (string and grip test) was performed 1 hour and 24 hours after the trauma. Mortality after trauma was increased for halothane 4% (48% versus 20% in unanesthetized mice), propofol (80% versus 30%), and chloral hydrate (70% versus 44%). Halothane 2% did not increase the mortality in traumatized mice. Halothane 2% or 4% anesthesia did not modify the string score after the trauma. Grip score after the trauma was better in mice anesthetized with halothane at either 2% or 4%. Mice injured under anesthesia with chloral hydrate had worse grip and string scores (P< .05) than unanesthetized mice. These results lead us to question the influence of anesthesia on the results obtained in experimental neuropharmacologic studies, particularly when there are discrepancies between two studies on the same pharmacologic treatment, which differ in their anesthesia protocols.

ISSN:0898-4921    

出版商:OVID    

年代:2000

数据来源: OVID