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Lewis  Ariane 《Neurocritical care》2019,31(2):411-418
Neurocritical Care - (1) Determine the pervasiveness of the belief that brain death/death by neurologic criteria (BD/DNC) is not death among rabbis. (2) Examine rabbinic beliefs about management...  相似文献   

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The genuine prevalence and intensity of grief reactions among physicians in response to patient death is unknown. However, a number of authorities and studies indicate that such experiences are fairly commonplace among physicians practicing in the clinical arena. In addition, it appears that the grief response of physicians may be tempered by a number of personal and environmental/contextual factors. A number of authors have proffered various approaches to resolving grief responses in these unique circumstances and many emphasize the importance of doing so in an effort to stave off burnout.  相似文献   

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Advances in psychopharmacology raise the prospects of enhancing neurocognitive functions of humans by improving attention, memory, or mood. While general ethical reflections on psychopharmacological enhancement have been increasingly published in the last years, ethical criteria characterizing physicians’ role in neurocognitive enhancement and guiding their decision-making still remain highly unclear. Here it will be argued that also in the medical domain the use of cognition-enhancing drugs is not intrinsically unethical and that, in fact, physicians should assume an important role in gating their usage. For finding normative orientation, concepts of disease, normality or medicine will not be helpful since—due to their cryptonormative nature—they rather hamper than allow targeted discussion and decision-making. As an alternative, the common and widely accepted bioethical criteria of beneficence, non-maleficence, autonomy and distributive justice allow a clinically applicable, highly differentiated context- and case-sensitive approach. By embedding decision-making in a participative physician–patient relationship extrinsic objections against neurocognitive enhancement (e.g. invalid perceptions about efficacy, benefit or risk; questionable voluntariness; restrained decision-making capacity) can be curtailed.
Matthis SynofzikEmail:
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Neurologic complications due to catheterization   总被引:1,自引:0,他引:1  
In our university cardiac center, the incidence of a cohort of children with acute neurologic complications resulting from cardiac catheterization performed for acyanotic or cyanotic congenital heart disease is 0.38% (14 children of a total of 3,648 catheterization procedures). Neurologic complications consisted of convulsion (n = 10), stroke (n = 6), intracranial hemorrhage (n = 2), extrapyramidal features (n = 1), paraplegia (n = 1), visual impairment (n = 1), hearing impairment (n = 1), and brachial plexus injury (n = 1). The main risk factors included prolonged duration of catheterization procedure and interventional manipulation in addition to cardiac catheterization. The possible mechanisms causing brain injury included cerebral embolism from local clots and hypoxia resulting from complications during the procedure. Other complications included intracranial hemorrhage secondary to anticoagulation and peripheral plexopathy because of prolonged fixed posture during anesthesia. The prognosis for the majority of patients with stroke is good. Neurologic sequelae, such as global developmental delay or epilepsy, occurred in those with hypoxic-ischemic encephalopathy.  相似文献   

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Neurologic complications related to cardiac surgery.   总被引:1,自引:0,他引:1  
Neurologic complications are a major cause of morbidity, complicating open heart surgery, cardiac catheterization, and interventional techniques. Global or focal brain ischemia related to embolism or hypoperfusion predominates. Breakthrough cerebral hemorrhage and infection can complicate cardiac transplantation. Identifying individuals at risk for cerebrovascular complications may lead to more effective preventative and treatment measures.  相似文献   

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We examined 126 patients, of whom 54 had suffered brain hemorrhage, 33 subdural hematoma, 18 subarachnoid bleeding, nine spinal hemorrhage and twelve hematoma with peripheral deficits. Neurologic disorders were seen in patients subject to therapy with coumarins 2-4 years after initiating therapy, whereas hemorrhages under heparine and streptokinase regimes were observed after only a few days. Clotting values were below a therapeutic range in only some of the cases. A clinical diagnosis should be verified by CT scanning. Blood clotting normally recovers after discontinuation of anticoagulation or fibrinolysis. Surgery will improve the prognosis in many cases of subdural hematoma or spinal hemorrhage; conservative treatment in cases of intracerebral, subarachnoid, and peripheral hemorrhage. A 70-percent lethality was recorded for patients suffering a cerebral hemorrhage. More than a third of patients with subarachnoid bleeding and less than a third of cases with subdural hematoma died. While peripheral lesions tended to improve, spinal hemorrhage often resulted in irreversible paraplegia. By respecting contra-indications for anticoagulation therapy and limiting the duration of such regimes the risk of hemorrhage within the CNS and other nerve structures may be reduced. Interactions with other drugs precipitating clotting disorders should also be taken into account.  相似文献   

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OBJECTIVE: To review the literature on the permanent neurological sequelae resulting from acute lithium poisoning. METHOD: Sixty-six articles were reviewed in English and in French. They were accessed through Medline and cover the period from 1968 to 1997. RESULTS: Fifty-nine case studies were broken down into 3 groups: lithium intoxications without a neuroleptic that has provoked a cerebellar syndrome; those in which there was a neuroleptic; and those with diverse neurological consequences, with or without a neuroleptic. CONCLUSIONS: Lithium has an intrinsic toxicity for the central nervous system and provokes a tropism specific to the cerebellum. The association with neuroleptics appears to increase toxicity as well as some associated factors, including infections and the rapid correction of the lithium level in the blood. We discuss the psychopathological mechanisms invoked to explain lithium's neurotoxicity.  相似文献   

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