Cases reported "Hypoxia, Brain"

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1/12. The possible role of hypoxia in the formation of axonal bulbs.

    AIMS: To assess the possible role of hypoxia in the formation of axonal bulbs. methods: Study material comprised sections from 28 brains showing evidence of cerebral hypoxia with no history of head injury, four with a history of head trauma but no evidence of hypoxic change, eight with a history of head trauma and hypoxic change, and four from control brains originally described as "diffuse axonal injury." These were subjected to microwave antigen retrieval and immunohistochemistry using monoclonal antibodies to beta amyloid precursor protein (beta APP), glial fibrillary acid protein (GFAP), and CD68-PGM1. RESULTS: Positive staining for beta APP was seen in all four controls, all four cases of head injury only, seven of eight cases of head injury and hypoxic changes, and 12 of 28 cases of hypoxia without history of head injury; 22 of 25 cases who had been ventilated showed positive staining. The majority of cases showed evidence of cerebral swelling. CONCLUSIONS: Axonal bulbs staining positively for beta APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone.
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2/12. Central structure preservation of the reversal sign.

    We report serial changes of central structure preservation of the reversal sign in a case of child abuse. The serial CT images show that the relatively spared attenuation at the basal ganglia, thalami, and posterior fossa develops before the occurrence of transtentorial herniation. This finding makes the theory that central preservation of the reversal sign is due to pressure relief after transtentorial herniation less convincible.
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3/12. Use of cerebral oximetry to detect and manage cerebral desaturation with a rapidly expanding neck hematoma.

    BACKGROUND: We report a case in which cerebral oximetry was used to successfully demonstrate when cerebral oxygen saturation is dangerously low. methods: In a 60-year-old-man with end-stage multiple myeloma and hyperviscosity syndrome, a rapidly expanding hematoma developed after insertion of an internal jugular central venous catheter. As the hematoma expanded, the patient became lethargic and disoriented (Glasgow coma Score of E2/M4-5/V2-ETT). His platelet count was 17,000.mm(-3), hemoglobin was 4.5 g/dl, partial thromboplastin time was 51 s, and his international ratio was 1.7. Although carotid pulses became unpalpable, blood pressure and heart rate remained stable. Cerebral oximeter probes positioned on the patient's forehead showed that cerebral oxygen saturation was 22-26% bilaterally. The surgery team was advised to surgically evacuate the hematoma. RESULTS: The hematoma was evacuated and a small needle hole in the right internal jugular vein adjacent to the central-venous catheter was found and repaired. Cerebral oxygen saturation increased to 56-58% within 1 h and stabilized near 60%. The patient awoke with normal cognitive function. CONCLUSION: This case demonstrates how cerebral oximetry can be used to give quantitative evidence of cerebral hypoxia, thus showing that immediate surgical intervention is necessary.
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4/12. Hypoxic-ischemic leukoencephalopathy in man.

    Three cases of hypoxic-ischemic leukoencephalopathy were studied. In two patients, the neurologic disorder followed drug overdosage; in the third, the apparent precipitating event was a postoperative myocardial infarction complicated by circulatory insufficiency. All patients were deeply unresponsive, with varying reflex patterns. In all three cases, the brain showed extensive symmetrical necrotic lesions of the central white matter, with minimal damage to gray matter structures. The lesions in case 3 showed, in addition, vascular necrosis and ring hemorrhages. Common to all cases was a prolonged period of hypoxemia, hypotension, and elevated venous pressure. acidosis occurred in two. These observations and analysis of previous reports of similar cases suggest that leukoencephalopathy tends to occur when the hypoxemia is prolonged and is associated with periods of hypotension and metabolic imbalance.
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5/12. Successful outcome in severe traumatic brain injury: a case study.

    This case study describes the management of a 54-year-old male who presented to the Hospital of the University of pennsylvania (HUP) with a traumatic brain injury (TBI) after being assaulted. He underwent an emergent bifrontal decompressive hemicraniectomy for multiple, severe frontal contusions. His postoperative course included monitoring of intracranial pressure, cerebral perfusion pressure, partial pressure of brain oxygen, brain temperature, and medical management based on HUP's established TBI algorithm. This case study explores the potential benefit of combining multimodality monitoring and TBI guidelines in the management of severe TBI.
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6/12. Effect of therapy with oxygen under high pressure on regional cerebral blood flow in the interval form of carbon monoxide poisoning: observation from subtraction of technetium-99m HMPAO SPECT brain imaging.

    Changes in brain images with single photon emission computed tomography (SPECT) using 99mTc hexamethylpropyleneamine oxime (HMPAO) before and after therapy with oxygen under high pressure (OHP) were measured in a 66-year-old man with the interval form of carbon monoxide (CO) poisoning by a new technique, i.e., subtraction of brain images. This study was performed 187 days after acute CO poisoning, in a state of chronic akinetic mutism that followed a lucid interval. A diffuse, but frontal-dominant, hypoperfusion pattern involving both the gray and white matter was observed in the pre-OHP SPECT image. After OHP, regional cerebral blood flow increased in both the gray and white matter and markedly increased in the frontal cortical regions. The present finding suggests that OHP is effective against the chronic state of the interval form of CO poisoning.
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7/12. Judo as a possible cause of anoxic brain damage. A case report.

    The rules of judo provide for strangulation techniques in which the blood supply to the brain is blocked by pressure on the carotid arteries; such techniques produce anoxia and possible unconsciousness if the victim fails to submit. A case is presented of a patient with signs of anoxic brain damage, with psychometric investigation showing memory disturbance consistent with a left temporal lobe lesion. This patient had been frequently strangled during his career as a judo player; it is suggested that such frequent strangulation was the cause of the damage. Such an observation indicates the need for caution in the use of such techniques.
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8/12. Neurochemical monitoring and on-line pH measurements using brain microdialysis in patients in intensive care.

    We will report on our preliminary findings using microdialysis to monitor three patients in intensive care with either severe head injury (SHI) or severe subarachnoid hemorrhage (SAH) for up to 72 hours. In addition, basal levels in uninjured brain were assessed during an extra-intracranial bypass operation. Samples were collected hourly or half-hourly (flow rate 2 microliters/min, perfusion medium 0.9% saline). Parameters measured were the antioxidants ascorbic acid, uric acid, glutathione and cysteine. In 2 patients, the pH of the dialysate (pHD) was also measured on-line with a specially constructed flow-through meter, and glucose and lactate levels were assessed in the dialysate. In patient 1 (SHI), there was practically no cerebral perfusion pressure because of high ICP; cysteine and lactate levels were very high and glucose not measurable. In patient 2 (SAH) a hypoxic episode was accompanied by increased uric acid and decreased glucose. In patient 3 (SHI), the pHD reflected normalisation of blood gases after hyperventilation. Results indicate that parameters are in the range known from experimental studies, and can be correlated with clinical situations. The pHD as valuable indicator of metabolic changes is also feasible bedside.
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9/12. Case report. Delayed death after pressure on the neck: possible causal mechanisms and implications for mode of death in manual strangulation discussed.

    death from hypoxic cerebral damage 1 week after manual strangulation is described, with a discussion of the competing pathophysiological mechanisms responsible for the fatal outcome in this case, and in manual strangulation in general.
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10/12. Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain.

    OBJECTIVE: brain interstitial glycerol was studied as a potential marker for membrane phospholipid degradation in acute human brain injury. methods: glycerol was measured in microdialysis samples from the frontal lobe cortex in four patients in the neurointensive care unit, during the acute phase after severe aneurysmal subarachnoid haemorrhage. microdialysis probes were inserted in conjunction with a ventriculostomy used for routine intracranial pressure monitoring. Clinical events involving hypoxia/ischaemia were diagnosed by neurological signs, neuroimaging (CT and PET), and neurochemical changes of the dialysate-for example, lactate/pyruvate ratios and hypoxanthine concentrations. RESULTS: Altogether 1554 chemical analyses on 518 microdialysis samples were performed. Clinical events involving secondary hypoxia/ischaemia were generally associated with pronounced increases (up to 15-fold) of the dialysate glycerol concentration. In a patient with a stable condition and no signs of secondary hypoxia/ischaemia the glycerol concentration remained low. Simultaneous determination of glycerol in arterial plasma samples showed that the changes in brain interstitial glycerol could not be attributed to systemic changes and an injured blood brain barrier. CONCLUSIONS: This study suggests that membrane phospholipid degradation occurs in human cerebral ischaemia. Interstitial glycerol harvested by microdialysis seems to be a promising tool for monitoring of membrane lipolysis in acute brain injury. The marker may be useful for studies on cell membrane injury mechanisms mediated by for example, Ca2 disturbances, excitatory amino acids, and reactive oxygen species; and in the evaluation of new neuroprotective therapeutic strategies.
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