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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dialysis Disequilibrium Syndrome (DDS) is characterized by neurological symptoms caused by rapid removal of urea during hemodialysis. It develops primarily from an osmotic gradient that develops between the brain and the plasma as a result of rapid hemodialysis. This results in brain edema that manifests as neurological symptoms such as headache, nausea, vomiting, muscle cramps, tremors, disturbed consciousness, and convulsions. In severe cases, patients can die from advanced cerebral edema. Recent advancements in cell biology implicate the role of urea disequilibrium (with a smaller contribution from organic osmolytes) as the pathophysiological mechanism responsible for this syndrome. In this review, we discuss the pathogenesis, clinical features and prevention of DDS.
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PMID:Dialysis disequilibrium syndrome: a narrative review. 1876 99

Brain metastases usually occur secondary to lung, breast, unknown primary, melanoma, and colon cancers. A growing tumor in the brain is commonly associated with edema and increased intracranial pressure (ICP). Common signs and symptoms due to increased ICP or brain edema include headache, nausea, and vomiting. One of the main treatment modalities in the management of brain metastases is whole-brain radiation. However, increased ICP may lead to acute deterioration of the neurologic status due to development of radiation-induced edema. Therefore, alternative management options should be considered for these patients to avoid complications from whole-brain radiation treatment. We discuss the case of a brain metastases patient who presented with bradycardia induced by brain edema.
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PMID:Neurosurgical rescue of bradycardia induced by intracerebral hypertension: a case report and review of the literature. 1950 46

A 77-year-old woman was admitted to a local hospital with a 7-day history of vertigo and nausea, followed by gait disturbance. Magnetic resonance imaging showed extensive brain edema with a hemorrhagic component in the right cerebellum. The lesion was heterogeneously enhanced after administration of contrast medium. The presumptive diagnosis was malignant glioma based on these findings, as well as the presence of mass effect and abnormal enhancement. She was referred to our hospital. However, cerebral angiography did not reveal tumor stain or arterial occlusion, but confirmed corkscrew-like venous collaterals and absence of opacification of the superior petrosal vein (SPV) and superior petrosal sinus. Topography of the brain edema was consistent with the drainage territory of the SPV. These findings suggested that the lesion was vasogenic edema caused by thrombosis of the SPV. The patient was conservatively treated without anticoagulation therapy, and the neurological and imaging abnormalities resolved spontaneously. To avoid unnecessary biopsy, thrombosis of the SPV should be considered in the differential diagnosis of infratentorial lesion mimicking brain tumors. Knowledge of the posterior fossa venous anatomy is essential to achieve the correct diagnosis.
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PMID:Thrombosis of the superior petrosal vein mimicking brain tumor. Case report. 1970 2

This study describes the clinical and neuroimaging features of five patients with 1, 2-Dichloroethane (DCE) toxic encephalopathy. From January 1st 1998 to June 30th 2009, five patients who were subsequently diagnosed with DCE toxic encephalopathy were admitted to our hospital. All were female workers who had been in contact with DCE and subsequently had had seizures or symptoms of intracranial hypertension, including headache, nausea, and vomiting. The cranial MRI showed extensive brain edema in either the subcortical white matter, bilateral globus pallidus, and cerebellar nucleus dendatus, or the cortices. Of the five patients in the study, three had vasogenic edema, one had cytotoxic edema, and one had both types of edema. Following treatment with steroids and mannitol for 3 to 10 weeks, all patients made either a partial or complete recovery. The imaging findings were resolved on a follow-up MRI. It is clear that occupational exposure to DCE can cause severe toxic encephalopathy. Moreover, extensive brain edema, secondary to blood-brain barrier damage or neuronal injury, is the major neuroimaging feature and the cause of clinical manifestations. Early diagnosis and prompt treatment leads to a good outcome.
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PMID:Toxic encephalopathy caused by occupational exposure to 1, 2-Dichloroethane. 2016 7

Cerebral hyperperfusion syndrome is a rare but well-described complication following carotid endarterectomy or stenting. Clinical signs are ipsilateral, throbbing, unilateral headache with nausea or vomiting, seizures, and neurological deficits, with or without intracerebral abnormalities on CT scan, such as brain edema or intracerebral hemorrhage. Subarachnoidal hemorrhage is rarely described especially if it occurs isolated. We describe a 74-year-old man with a history of high blood pressure, hypercholesterolemia, atrioventricular block with pacemaker, and ischemic cardiopathy with coronary bypass. He underwent right carotid endarterectomy for a 90% NASCET asymptomatic stenosis. Four days after surgery, he complained of unusual headaches with right, throbbing hemicrania. Nine days after surgery, he presented with left hemiplegia and a partial motor seizure. He had fluctuant altered consciousness, left hemiplegia, and left visual and sensory neglect. Brain CT showed right frontal subarachnoidal hemorrhage without parenchymal bleeding. Cerebral angiography found no cerebral aneurysm, no vascular malformation, but a vasospasm of the left middle cerebral artery. Transcranial Doppler confirmed this vasospasm. Evolution was favorable with no recurrence of seizures but with an improvement of the neurological deficits and vasospasm. Physicians should bear in mind this very rare complication of endarterectomy and immediately perform neuroimaging in case of unusual headache following endarterectomy or angioplasty.
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PMID:Isolated Subarachnoidal Hemorrhage following Carotid Endarterectomy. 2067 62

Postoperative delirium is one of the most spectacular, frightening and misdiagnosed postoperative complications of surgery. We describe the case of a caucasian 77-year-old male patient, who developed a severe postoperative delirium after combined transurethral resection of the prostate and cystolithotripsy. This systemic and unpredictable complication of endoscopic surgery is caused by excessive absorption of electrolyte-free irrigation fluids, leading to brain edema and metabolic encephalopathy. The clinical spectrum ranges from asymptomatic hyponatraemia, to electrocardiographic (ECG) changes, nausea, vomiting, convulsions, coma, pulmonary edema, cardiovascular compromise and death. Because of the heterogeneous clinical presentation diagnosis can be difficult. In a patient who develops alterations of consciousness with evidence of hypervolemia and hyponatremia after endoscopic surgery, transurethral resection syndrome must be considered.
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PMID:Post operative delirium with hyponatriemia after transurethral resection of the prostate: a case of transurethral resection syndrome? 2174 38

Dialysis disequilibrium syndrome (DDS) is a central nervous system disorder that occurs during or after hemodialysis. This is caused by brain edema that manifests as neurological symptoms that include headache, emesis, nausea, blurring of vision, disturbed consciousness, tremors and seizures, and in severe cases, death. The incidence of DDS is very high among patients with preexisting neurological diseases. There has been much debate about the origin of DDS. We report a case of DDS, as presenting syndrome of a medulloblastoma in a child aged 5 years, and discuss the pathogenesis and the possible role of DDS for an earlier detection of occult brain lesions in dialyzed patients.
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PMID:Medulloblastoma presenting as dialysis disequilibrium syndrome. 2209 4

An aggressive dialysis in a grossly azotemic patient, especially one with severe metabolic acidosis, can lead to dialysis disequilibrium syndrome (DDS). Mild forms present as nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma, and even death. This clinical picture is caused by cerebral edema induced by one or more of the following mechanisms: "Reverse urea effect" - Dialysis removes urea faster from the blood than from the brain; consequently, water enters the brain. "Cerebrospinal fluid acidosis" - Correction of systemic acidosis engenders the condition due to a lowering of brain pH. "Idiogenic osmoles" - As a response to blood hyperosmolar state, osmoles are produced in the brain. As blood osmolality decreases under relatively quick dialysis, idiogenic osmoles tend to induce brain edema. Because the symptoms of DDS can be life-threatening, preventive measures in patients with severe uremia are important. The first strategy relies on raising blood osmolality by introducing solutes (osmoles) into the blood. The second approach, which is the most common, decreases the efficiency of the dialysis treatment by shortening the duration of a dialysis run to 25% - 30% of normal, by lowering dialyzer blood flow or dialysate flow rate, by using a less efficient dialyzer, or by a combination of these maneuvers. Dialysis frequency is increased instead. Anticonvulsant drugs are needed in cases where the preventive measures have not been used or have been unsuccessful.
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PMID:Dialysis Disequilibrium Syndrome Revisited. 2845 40


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