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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute pulmonary edema after subarachnoid hemorrhage is presented. A supra and infratentorial arteriovenous malformation was revealed by serial cerebral angiography. Sequential chest films documented regression of both, pulmonary edema and cardiac enlargment. The literature is reviewed and a possible physiopathology is discussed.
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PMID:[Acute neurogenic pulmonary edema]. 16 44

A case of neurogenic pulmonary edema (NPE) associated with a ruptured spinal cord arteriovenous malformation (AVM) is presented. The mechanisms involved in the development of NPE are discussed briefly. The possible role of preganglionic sympathetic fibers in the spinal cord in the etiology of NPE is suggested.
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PMID:Neurogenic pulmonary edema associated with ruptured spinal cord arteriovenous malformation. 687 52

The case of a 12-year-old girl who suffered a severe intracranial bleed secondary to a large arteriovenous malformation (AVM) is described. Following investigation the appropriate treatment was considered to be embolization of the AVM, under general anaesthesia, using N-butyl cyanoacrylate (NBCA). During the procedure acute desaturation and pulmonary oedema occurred secondary to accidental pulmonary embolization with NBCA. The management of the procedure and subsequent clinical course is reported and available literature reviewed.
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PMID:Pulmonary embolism following embolization of an arteriovenous malformation. 893 49

The neurogenic pulmonary edema is a rare clinical situation caused by an imbalance characterized by an excessive sympathetic outflow. It is observed mostly in young patients, is associated with brain or spinal cord haemorrhage, trauma, tumours or infections and is usually fatal. A case of neurogenic pulmonary edema in a 27-year-old woman is presented, caused by a cerebellar haemorrhage due to a vermian and paravermian arteriovenous malformation rupture. The vermian and hemispheric haemorrhage injuring the sub-lobule IX-b of the uvula induced a disruption of both carotid baroreceptor and chemoreceptor reflexes control mechanisms. Medical treatment with controlled ventilation, PEEP, diuretics and morphine reverted the pulmonary edema. After surgical treatment of the haemorrhage and cerebellar AVM the patient recovered to an almost normal social and professional life. The cerebellar lesion induced a temporary vermian sub lobule IX-b dysfunction that was responsible for the sympathetic storm that evoked the neurogenic pulmonary edema.
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PMID:Cerebellar haemorrhage as a cause of neurogenic pulmonary edema - case report. 1632 80

Acute respiratory distress syndrome (ARDS) is characterized by sudden onset of respiratory distress, infiltrates on radiographs consistent with pulmonary oedema, hypoxaemia and increased work in breathing. Infiltrates on radiographs are bilateral, but may be patchy or diffuse and fluffy or dense. It is associated with absence of left heart failure and a PaO2/FiO2 ratio of < or =200. Ethylene vinyl alcohol copolymer dissolved in dimethyl sulfoxide (DMSO), which was approved by the US FDA in July 2005, is used as an embolic agent for cerebral arteriovenous malformation (AVM). It is a biocompatible liquid polymer that precipitates and solidifies on contact with blood, thus forming a soft and spongy embolus. We report a case of ARDS following therapeutic embolization with ethylene vinyl alcohol copolymer for cerebral AVM under general anaesthesia. Experienced perioperative physicians adopted standard anaesthetic technique and monitoring for this procedure. Acute respiratory distress and hypoxaemia developed in the patient following extubation of the trachea. Infiltrates seen on postprocedural chest radiographs were consistent with pulmonary oedema. DMSO, the solvent for the ethylene vinyl alcohol copolymer, is excreted via the lungs after administration and we postulate that DMSO was the possible cause of ARDS in this patient. Monitoring of haemodynamic parameters (invasive blood pressure, electrocardiography) and ventilatory parameters (ETCO2, SpO2, airway pressure monitoring) are important in the recognition of this possible event. One should be vigilant and anticipate this complication following therapeutic embolization with ethylene vinyl alcohol polymer for the treatment of cerebral AVM.
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PMID:Severe pulmonary oedema following therapeutic embolization with Onyx for cerebral arteriovenous malformation. 1817 30

We present a 35-year-old healthy male patient who developed pulmonary edema (PE) probably due to venous air embolism during craniotomy in the semi-sitting position for arteriovenous malformation (AVM). Anesthesia was maintained with oxygen, nitrous oxide, propofol and fentanyl. During craniotomy, end-tidal carbon dioxide pressure decreased suddenly from 26 to 9 mmHg. Concurrently, a decrease in oxygen saturation from 99% to 91% occurred. There were no serious changes in blood pressure and heart rate. A "mill-wheel murmur" was confirmed. PE due to venous air embolism was suspected. The operation was discontinued and the patient was transferred to the intensive care unit. In the post-operative period, the patient developed PE and made a full recovery within a week. Four months later, the patient was scheduled again for surgical excision of AVM in the semi-sitting position in the same way as the first time. Anesthesia was maintained with oxygen, air, propofol and fentanyl. Transoesophageal echocardiography and pulmonary artery catheter were used. Saline was filled at the surgical site to prevent aspiration of air bubbles and surgical procedure was performed carefully without large vein injury and uneventfully. During neurosurgical intervention in the sitting position, special attention should be paid to entry of air bubbles into the venous system which may lead to PE.
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PMID:[Pulmonary edema due to venous air embolism during craniotomy: a case report]. 1897 44

Purpose. We report a case of a 60-year-old male who underwent sequential Onyx embolizations of a cerebral arteriovenous malformation (AVM) which we implicate as the most likely etiology of subsequent acute respiratory distress syndrome (ARDS). Methods. Case report and literature review. Results. Shortly after the second Onyx embolization procedure, the patient declined from respiratory failure secondary to pulmonary edema. Clinical entities typically responsible for pulmonary edema including cardiac failure, renal failure, iatrogenic volume overload, negative-pressure pulmonary edema, and infectious etiologies were evaluated and excluded. The patient required mechanical ventilatory support for several days, delaying operative resection. The patient met clinical and radiographic criteria for ARDS. After excluding other etiologies of ARDS, we postulate that ARDS developed as a result of Onyx administration. The Onyx copolymer is dissolved in dimethyl sulfoxide (DMSO), a solvent excreted through the lungs and has been implicated in transient pulmonary side effects. Additionally, a direct toxic effect of the Onyx copolymer is postulated. Conclusion. Onyx embolization and DMSO toxicity are implicated as the etiology of ARDS given the lack of other inciting factors and the close temporal relationship. A strong physiologic rationale provides further support. Clinicians should consider this uncommon but important complication.
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PMID:Acute respiratory distress syndrome after onyx embolization of arteriovenous malformation. 2168 80

Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.
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PMID:Neurogenic pulmonary edema: successful treatment with IV phentolamine. 2294 92

Neurogenic stunned myocardium is a significant complication of subarachnoid hemorrhage. Diagnosis of neurogenic stunned myocardium is complicated by variable presentation. We present a case of a 23-year-old woman admitted with a subarachnoid hemorrhage from an arteriovenous malformation and associated aneurysm. Postoperatively, she developed pulmonary edema and mildly elevated cardiac biomarkers. Echocardiography showed hypokinesis of the basal left ventricular segments and normal contraction of the apical left ventricular segments consistent with a variant form of neurogenic stunned myocardium. We describe characteristics and outcomes of neurogenic stunned myocardium in this young patient with arteriovenous malformation-associated aneurysmal subarachnoid hemorrhage.
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PMID:Variant Neurogenic Stunned Myocardium in a Young Female After Subarachnoid Hemorrhage. 2642 53

Patent foramen ovale (PFO), an embryonic remnant of the fetal circulation, is present in 20-25% of adults. Although recent observational studies and clinical trials have established the link between PFO-mediated right-to-left shunting with cryptogenic stroke and migraine with aura, the role of a PFO in exacerbating hypoxemic medical conditions (ie, sleep apnea, chronic obstructive pulmonary disease, pulmonary hypertension, platypnea-orthodeoxia, pulmonary arteriovenous malformation, high-altitude pulmonary edema, and exercise desaturation) remains less understood. PFO-mediated hypoxemia occurs when deoxygenated venous blood from the right atrium enters and mixes with oxygenated arterial blood in the left atrium. Patients with an intracardiac right-to-left shunt may have profound hypoxemia out of proportion to underlying primary lung disease, even in the presence of normal right-sided pressures. The presence of right-to-left cardiac shunting can exacerbate the degree of hypoxemia in patients with underlying pulmonary disorders. In a subset of these patients, percutaneous PFO closure may result in marked improvement in dyspnea and hypoxemia. This review discusses the association between PFO-mediated right-to-left shunting with medical conditions associated with hypoxemia and explores the role of percutaneous PFO closure in alleviating the hypoxemia.
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PMID:Patent Foramen Ovale and Hypoxemia. 2957 Apr 76


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