subarachnoid hemorrhage/edema

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The role of p53 in brain edema after 24 h of experimental subarachnoid hemorrhage in a rat model.

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Our previous study demonstrated that p53 plays an orchestrating role in the vasospasm and apoptotic cell death after subarachnoid hemorrhage (SAH). We now hypothesize that p53 also plays an important role in brain edema by up-regulating the expression of MMP-9 via the NF-kappaB molecular signaling

Endovascular Treatment for Aneurysmal Subarachnoid Hemorrhage with Neurogenic Pulmonary Edema in the Acute Stage.

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OBJECTIVE Severe neurogenic pulmonary edema (NPE) can occur in a variety of brain insults, including subarachnoid hemorrhage (SAH), and severe case of NPE can cause devastating consequences. But the literature on the treatment strategy about aneurysmal SAH with NPE is very scant. We present that SAH

Could cardiac biomarkers predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?

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Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after a significant central nervous system (CNS) insult. NPE occurs as a result of release of catecholamines into the blood immediately after aneurysm rupture. The aim of this study is to

Impact of clipping versus coiling on postoperative hemodynamics and pulmonary edema after subarachnoid hemorrhage.

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Volume management is critical for assessment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). This multicenter prospective cohort study compared the impact of surgical clipping versus endovascular coiling on postoperative hemodynamics and pulmonary edema in patients with SAH.

[Cerebral edema following experimental subarachnoid hemorrhage (author's transl)].

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Despite the fact that cerebral edema appears to be a common complication of subarachnoid hemorrhage (SAH) due to a ruptured cerebral aneurysm, measurements of brain tissue water content have not been carried out in this entity. For this reason, the development of cerebral edema has been analized in

Neurogenic Pulmonary Edema in Aneurysmal Subarachnoid Hemorrhage.

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Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and

Severe subarachnoid hemorrhage with pulmonary edema successfully treated by intra-aneurysmal embolization using Guglielmi detachable coils--Two case reports.

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A 48-year-old male and a 39-year-old female presented with subarachnoid hemorrhage (SAH) due to ruptured anterior communicating artery aneurysms. Both patients were comatose on admission. Chest radiography disclosed pulmonary edema. They were conservatively treated under controlled ventilation, but

Subarachnoid hemorrhage causes pulmonary endothelial cell apoptosis and neurogenic pulmonary edema in mice.

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OBJECTIVE Neurogenic pulmonary edema (NPE) is a well-known complication of subarachnoid hemorrhage (SAH), which potentially causes a poor outcome. The aim of this study was to examine if NPE occurs in the endovascular perforation model of SAH in mice and if apoptosis contributes to NPE development

Association between serum lactate levels and early neurogenic pulmonary edema after nontraumatic subarachnoid hemorrhage.

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OBJECTIVE Few studies have described the risk factors associated with the development of neurological pulmonary edema (NPE) after subarachnoid hemorrhage (SAH). We have hypothesized that acute-phase increases in serum lactate levels are associated with the early development of NPE following SAH. The

Endovascular Therapy for Aneurysmal Subarachnoid Hemorrhage Complicated by Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy: A Report of Ten Cases.

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Patients sustaining aneurysmal subarachnoid hemorrhage (aSAH) can be further complicated by neurogenic pulmonary edema (NPE) and Takotsubo-like cardiomyopathy (TCM) with dismal outcomes. The present study aimed to validate the efficacy of endovascular therapy for patients with aSAH

Neurogenic pulmonary edema following intracranial coil embolization for subarachnoid hemorrhage -A case report-.

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Neurogenic pulmonary edema (NPE) is a well-known complication of acute central neurologic injury, particularly aneurysmal subarachnoid hemorrhage. Both increased intracranial pressure and severe over-activation of the sympathetic nervous system seem to be pathogenetic for the onset of NPE. Although

Focal brain edema and natriuretic peptides in patients with subarachnoid hemorrhage.

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Central salt wasting syndrome may be caused by pathological increases in serum natriuretic peptides after subarachnoid hemorrhage (SAH). However, it is unclear as to why the serum concentration of atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) increases in the subacute phase of

Vascular Endothelial Growth Factor in Brain Edema Formation After Subarachnoid Hemorrhage.

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Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of brain edema formation after experimental subarachnoid hemorrhage (SAH). In this study, we evaluated the effect of anti-VEGF antibody neutralization on brain edema formation after experimental SAH in mice. Mice

Pulmonary Edema and Stunned Myocardium in Subarachnoid Hemorrhage

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Aneurysmal subarachnoid hemorrhage is a life-threatening event that can cause permanent disability. This life-threatening event can be further complicated by subsequent cardiac and pulmonary disability. The presence of a neurogenic cardiomyopathy and pulmonary edema increases the morbidity and

Neurogenic pulmonary edema and large negative T waves associated with subarachnoid hemorrhage.

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We describe a 72-year-old woman with hypertension who developed acute neurogenic pulmonary edema and giant negative T waves on electrocardiography (ECG) due to subarachnoid hemorrhage. The patient was alert and complained of precordial chest discomfort, dyspnea and shoulder stiffness.

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