Cases reported "Subarachnoid Hemorrhage"

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1/14. diagnosis of subarachnoid hemorrhage indicated by transthoracic echocardiography.

    We report the case of a 63-year-old woman who presented to her local emergency department unresponsive and in a state of cardiogenic shock 4 hours after the sudden onset of a severe headache. Her electrocardiogram revealed nonprogressive 1-mm S-T elevation in leads V(5) to V(6) and a prolonged QTc. A transthoracic echocardiogram performed at the time of her resuscitation revealed regional wall-motion abnormalities not consistent with any known coronary artery territory but consistent with a diagnosis of acute subarachnoid hemorrhage. This diagnosis was subsequently confirmed on computed tomography brain imaging. Although subarachnoid hemorrhage is known to be associated with cardiopulmonary dysfunction, and electrocardiogram and echocardiogram abnormalities, the diagnosis of subarachnoid hemorrhage suspected by echocardiography before brain imaging has not previously been described.
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2/14. Homicidal cerebral artery aneurysm rupture.

    When a normally natural mechanism of death is induced by physical injury or intense emotional stress, it is appropriate to rule the manner of death as something other than natural. When the case-specific circumstances are such that the death occurs as a result of the criminal activity of another person, it is acceptable to rule such deaths as homicides. Presented herein is a case of homicidal cerebral artery aneurysm rupture occuring in an intoxicated, 46-year-old man who was punched in the face by another individual. The details of the case are presented, followed by a discussion of the controversies that exist when dealing with such cases. Guidelines for investigating similar deaths are presented, with emphasis on the timing of the trauma in relation to onset of symptoms due to aneurysm rupture.
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3/14. Multiprofessional follow up of patients after subarachnoid haemorrhage.

    Subarachnoid haemorrhage (SAH) is a life-threatening illness that affects people suddenly and without warning. Previous research has estimated that only 7% of SAH survivors suffer physical deficits (Stegan and Freckmann, 1991), whereas two-thirds of those classed as having made a good recovery actually experience a range of debilitating cognitive or emotional difficulties (Bindschaedler et al, 1997); Buchanan et al, 2000). At hope hospitals, a structures system was set up to help support the survivors of SAH through follow-up via the neurovascular team providing patients with information, guidance and early intervention including screening for potential cognitive and emotional difficulties and fast-track referral to neuropsychology services. Behavioural indices demonstrated that patients experienced a range of difficulties in everyday functioning such as problems that prevent a return to work and excessive fatigue, among others. Although this innovative system does address follow-up need, improvements could be made to ensure that all patients receive an equitable service.
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4/14. Delayed cardiogenic shock and acute lung injury after aneurysmal subarachnoid hemorrhage.

    Both cardiac and lung injury after aneurysmal subarachnoid hemorrhage has been attributed to an adrenergic surge. Cardiogenic shock is very uncommon. We describe a 55-yr-old woman with a delayed cardiogenic shock emerging within hours after aneurysmal rupture. Cardiac damage was documented by increased serum troponin t, CPK-mb fraction, and severe wall motion abnormality, which included an akinetic apex on echocardiography (ejection fraction of 33%). Her coronary angiogram was normal. Decreased cardiac index, increased systemic and pulmonary vascular resistance indices, and persistent oxygen desaturation despite improving ventricular contractility documented both cardiac and pulmonary injury. After treatment with dobutamine and milrinone all manifestations resolved.
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5/14. Neurogenic pulmonary edema during intracranial endovascular therapy.

    Neurogenic pulmonary edema (NPE) is a well-known complication of acute brain injury. Neurogenic stunned myocardium (NSM) occurs clinically in a significant subset of patients with NPE. A 49-year-old woman developed refractory cerebral vasospasm requiring angioplasty following a subarachnoid hemorrhage. During angioplasty, NPE with NSM manifested as acute pulmonary edema associated with elevated pulmonary artery occlusion pressure and reduced cardiac output. Evaluations disclosed a right insular infarction, cardiac wall motion abnormalities, and electrocardiographic characteristics of NSM. The NSM completely resolved, and the neurological outcome was good. A 56-year-old woman developed NPE during complicated coil embolization of an internal carotid artery aneurysm. Cardiac function was normal, and the NPE resolved with a brief period of mechanical ventilation and diuresis. The delayed appearance of NSM and NPE during endovascular therapy in these patients implies a degree of risk for sympathetically mediated cardiopulmonary dysfunction during complex intracranial endovascular procedures.
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6/14. Cardiac function in aneurysmal subarachnoid haemorrhage: a study of electrocardiographic and echocardiographic abnormalities.

    Electrocardiographic (ECG) changes are reported frequently after subarachnoid haemorrhage (SAH). The aim of this study was to investigate the functional significance of ECG changes by echocardiographic assessment of cardiac function. Forty-five patients with intracranial aneurysms were studied. All patients had a 12-lead ECG and a two-dimensional echocardiogram. After patients with an history of chronic cardiac disease (n = 4) were excluded, only four patients were found to have wall motion abnormalities. These patients had only minor ECG abnormalities, but severe neurological dysfunction. Conversely, patients with other ECG abnormalities including the deep inverted T waves associated usually with SAH, had normal echocardiograms. We conclude that the ECG is not an accurate predictor of myocardial function after SAH and that myocardial dysfunction is related more closely to severity of neurological condition.
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7/14. A case of subarachnoid hemorrhage with electrocardiographic and echocardiographic changes simulating transmural myocardial infarction.

    A patient with subarachnoid hemorrhage who exhibited changes suggestive of myocardial infarction by electro- and echocardiography and underwent coronary angiography is reported. echocardiography demonstrated marked hypokinesis in the left ventricular anterior wall to the septum. Since the possibility of concomitant myocardial infarction could not be excluded, coronary angiography was performed with cerebral angiography. No abnormalities were observed in the coronary arteries, and the myocardial damage was considered to be due to subarachnoid hemorrhage. Echocardiograms showed improvements in left ventricular wall motion within a short time after operation of the intracranial lesion.
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8/14. Emotionalism following brain damage: a complex phenomenon.

    Emotionalism is a common and distressing consequence of many forms of brain damage. There is uncertainty about its classification, aetiology and treatment. A commonly used typology is difficult to apply in practice as illustrated by three clinical examples. We describe the various components of emotionalism and highlight their range and variability. In future research each component should be examined in detail using a standardized form of assessment.
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9/14. Case report.

    The nursing care of a patient following subarachnoid hemorrhage (SAH) is challenging and multifaceted. Physical and emotional support through the acute period following the insult and preparation for the rehabilitative process are among the early goals of care. This case report provides a detailed interpretation of the physical and behavioral responses experienced by a patient following SAH. Included are nursing interventions formulated by the interpretation of these responses.
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10/14. pulmonary edema associated with subarachnoid hemorrhage. Evidence for a cardiogenic origin.

    A 56-year-old woman with no history of cardiac disease developed acute pulmonary edema following a subarachnoid hemorrhage. A constellation of findings, including elevated creatine kinase MB isoenzyme activity in the absence of electrocardiographic or scintigraphic evidence of acute myocardial infarction, elevated pulmonary artery wedge pressure, segmental wall motion abnormalities, and depressed ejection fraction of the left ventricle demonstrated by two-dimensional echocardiography and radionuclear ventriculography, pointed to a direct myocardial injury leading to cardiac failure. The evidence for cardiogenic origin of pulmonary edema provided by this case is in contrast to the belief that "neurogenic" pulmonary edema is of noncardiac origin.
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