Cases reported "Brain Death"

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1/8. Brainstem death and ventilator trigger settings.

    A patient with cerebral infarction was certified clinically brainstem dead. However, 4 h after the diagnosis of death, while the patient was being ventilated using the biphasic positive airway pressure mode, the 'assist' indicator light on the Drager Evita 2 ventilator illuminated intermittently. There was no evidence of spontaneous breathing. 'Triggering' was probably caused by a decrease in airway pressure in time with cardiac contraction. The trigger flow rate is crucial as factors other than the patient's inspiratory effort can initiate flow from the ventilator with very sensitive settings.
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2/8. Isolated medulla oblongata function after severe traumatic brain injury.

    The objective was to report the first pathologically confirmed case of partly functionally preserved medulla oblongata in a patient with catastrophic traumatic brain injury.A patient is described with epidural haematoma with normal breathing and blood pressure and a retained coughing reflex brought on only by catheter suctioning of the carina. Multiple contusions in the thalami and pons were found but the medulla oblongata was spared at necropsy. In conclusion, medulla oblongata function may persist despite rostrocaudal deterioration. This comatose state ("medulla man") closely mimics brain death.
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3/8. Electrocerebral silence with preserved but reduced cortical brain perfusion.

    Isoelectric electroencephalogram in conformance with clinical findings is strongly suggestive of brain death. In clinical practice, isoelectric electroencephalogram in not-brain-dead patients is rarely seen. We report on a 53-year-old patient who suffered ischaemic encephalopathy after cardiopulmonary arrest. He had residual brainstem function with sufficient spontaneous breathing and evidence of cerebral blood flow on single photon emission computed tomography scan, but his electroencephalogram was isoelectric. He survived this condition for more than 7 weeks. This case demonstrates that isoelectric electroencephalogram can not be equated with brain death, and that in prognostic assessment both clinical findings and supportive technical methods are mandatory.
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4/8. Cardiotocographic and sonographic findings in two cases of antenatally diagnosed intrauterine fetal brain death.

    Intrauterine fetal brain death is a rare cause of a fixed fetal heart rate pattern. Seven cases have been previously reported in the literature, but only two of them were diagnosed prenatally and all the newborns died soon after delivery. Two additional cases of antepartum diagnosis of intrauterine fetal brain death, managed expectantly, are reported. We had the unique opportunity to document progressive sonographic cerebral changes during the follow-up period, following the neurological event, while the fetus continued life and growth in utero. The cardiographic and sonographic findings suggesting intrauterine fetal brain death were a prolonged fixed fetal heart rate, even following a vibroacoustic and contraction stress test; an atonic fetus without breathing and body movement; and the appearance of hydramnios and the development of ventriculomegaly.
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5/8. Loss of brainstem acoustic evoked potentials with spontaneous breathing in a patient with supratentorial lesion.

    The loss of brainstem acoustic evoked potentials (BAEP) is considered as a confirmatory test for the diagnosis of brain death in patients with supratentorial lesions. We report a patient with ischemia in the territory of the left middle and anterior cerebral artery, who showed a loss of BAEP waves III-V as a sign of brainstem compression, but maintained spontaneous breathing and EEG activities. We conclude that occasionally BAEP may provide misleading results in the diagnosis of brain death.
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6/8. The complete apallic syndrome--a case report.

    In six patients with apallic syndrome the EEG was isoelectric, although the patients were breathing spontaneously and vegetative functions remained stable for a long period of time. No cortical somatosensory evoked potentials could be recorded in four of the patients examined. Cranial CT performed in three patients revealed extensive hypodensity of the cortex, whereas the brain stem showed no major damage. This syndrome is labelled a "complete apallic syndrome". None of our patients, and none of the 23 patients described in the literature, recovered.
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7/8. Significance of electrical brain activity in brain-stem death.

    A 46-year-old man was diagnosed clinically brain dead after sustaining head trauma. The patient was in deep coma, brain nerves were unresponsive and spontaneous breathing was absent. However, EEG showed well preserved activity, but no reactivity to external stimuli. EEG activity disappeared within 40 h. BAEP were highly abnormal, flash-VEP as recorded 3 h after the diagnosis of brain stem death was of high amplitude but of simplified form. The neurophysiological findings revealed that the main reason for deep coma was brain stem damage while cortical activity was still present. This condition raises ethical questions when brain death is diagnosed clinically prior to removal of organs for transplantation.
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8/8. Acute presentation of congenital diaphragmatic hernia past the neonatal period: a life threatening emergency.

    PURPOSE: Major gastric distension in the left hemithorax can threaten life in patients with congenital diaphragmatic hernia (CDH) presenting after the neonatal period. After presentation of two pediatric cases, guidelines for the optimal care of these patients are given. CLINICAL FEATURES: Both children had respiratory and cardio-circulatory compromise on arrival. The diagnosis of late presenting CDH was made and the severity of symptoms was related to a voluminous distension of an intrathoracic stomach. Successful placement of an naso-gastric tube in the first patient, lead to a rapid clinical improvement, allowing surgical repair. In the second patient, oro- or naso-gastric decompression was not possible, and while the lungs were mechanically ventilated and the patient was prepared for surgery, a sudden cardiocirculatory arrest was managed by external chest compressions and rescuscitation drugs. Transthoracic percutaneous decompression of the stomach was the sole treatment allowing spontaneous cardiac activity to reappear, and haemodynamic condition to normalize. However, the child died from brain death after this episode. CONCLUSION: Gastric decompression is the key for the treatment of patients with CDH who present respiratory and/or cardiocirculatory distress due to the intrathoracic distension of the stomach. If an oro- or naso-gastric decompression is not possible, then radiologically directed percutaneous decompression under local anesthesia is required. After decompression, the patient is prepared for surgery, with particular emphasis on fluids infusion, in order to correct the frequently associated hypovolaemia.
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