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Dialysis disequilibrium syndrome is a disorder of the central nervous system in patients on dialysis. The underlying etiology is thought to be primarily due to cerebral edema; however, neuroradiologic findings have not been described previously. We describe a patient who presented with new onset headaches and status epilepticus after beginning hemodialysis. Her neuroimaging studies revealed white matter changes in the posterior parietal and occipital lobes similar to those seen in patients with reversible posterior leukoencephalopathy syndrome (RPLS). This case suggests that dialysis disequilibrium syndrome and RPLS may represent a spectrum of disorders in which the underlying mechanism is vasogenic edema.
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PMID:Dialysis disequilibrium: another reversible posterior leukoencephalopathy syndrome? 1295 40

The purpose of this paper is to report a case of dialysis disequilibrium syndrome as an unusual cause of papilledema. A 38-year-old woman with type 1 diabetes mellitus presented with decreased visual acuity and bilateral optic nerve swelling associated with systemic signs and symptoms of dialysis disequilibrium syndrome. Repeated lumbar punctures revealed elevated intracranial pressures. She was placed on acetazolamide with some improvement in symptoms. After renal transplantation, the patient had complete resolution of headaches, nausea and the papilledema. Our conclusion is that patients with visual disturbance and focal neurological symptoms during and after hemodialysis should be suspected of having dialysis disequilibrium syndrome (DDS). DDS is thought to occur as a result of a rapid reduction in plasma osmolality during dialysis. As the shift of urea from cerebral spinal fluid (CSF) is delayed, the relative increase in CSF osmolality draws fluid into the brain. The ensuing cerebral edema is responsible for the characteristic neurological symptoms. We report the association of papilledema with this syndrome, and caution as to the possible concurrent risk of permanent visual impairment.
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PMID:Papilledema associated with dialysis disequilibrium syndrome. 1776 31

Spontaneous spinal CSF leaks are best known as a cause of orthostatic headache, but may also be the cause of coma. The authors encountered a unique case of a spontaneous spinal CSF leak causing coma 2 days after craniotomy for clipping of an unruptured aneurysm. This 44-year-old woman with autosomal dominant polycystic kidney disease underwent an uneventful craniotomy for an incidental anterior choroidal artery aneurysm. No intraoperative spinal CSF drainage was used. Two days after surgery the patient became comatose with a left oculomotor nerve palsy. Computed tomography scanning revealed a right extraceberal hematoma and loss of gray-white matter differentiation. The hematoma was evacuated and a diagnosis of hemodialysis disequilibrium syndrome was made. Continuous hemodialysis and hyperosmolar therapy were instituted without any improvement. The CT scans were then reinterpreted as showing sagging of the brain, and the patient was placed in the Trendelenburg position which resulted in prompt improvement in her level of consciousness. A CT myelogram demonstrated an upper thoracic CSF leak that eventually required surgical correction. The patient made a complete neurological recovery. Neurological deterioration after craniotomy may be caused by brain sagging caused by a spontaneous spinal CSF leak, similar to intracranial hypotension due to intraoperative lumbar CSF drainage.
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PMID:Spontaneous spinal cerebrospinal fluid leak as a cause of coma after craniotomy for clipping of an unruptured intracranial aneurysm. 1901 77

A 42-year-old female end-stage renal disease (ESRD) patient with reversible posterior leukoencephalopathy syndrome (RPLS) post-transfusion during initiation of hemodialysis is reported. Eleven days after the onset of illness, we diagnosed encephalopathy as a grand mal seizure resulting from diffuse cerebral edema. One reason for the delayed diagnosis was that her symptom, a throbbing headache that occurred during her first dialysis, indicated dialysis disequilibrium syndrome. We must bear in mind that a small amount of transfusion could cause RPLS even during the first dialysis. To our knowledge, this is the first case report on RPLS after blood transfusion in an ESRD patient.
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PMID:Reversible posterior leukoencephalopathy syndrome after blood transfusion in a patient with end-stage renal disease. 2189 31

The dialysis disequilibrium syndrome is a rare but serious complication of hemodialysis. Despite the fact that maintenance hemodialysis has been a routine procedure for over 50 years, this syndrome remains poorly understood. The signs and symptoms vary widely from restlessness and headache to coma and death. While cerebral edema and increased intracranial pressure are the primary contributing factors to this syndrome and are the target of therapy, the precise mechanisms for their development remain elusive. Treatment of this syndrome once it has developed is rarely successful. Thus, measures to avoid its development are crucial. In this review, we will examine the pathophysiology of this syndrome and discuss the factors to consider in avoiding its development.
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PMID:Dialysis disequilibrium syndrome. 2271 Jun 92

A 20-year-old woman with a functioning ventriculoperitoneal (VP) shunt consistently reported unbearable vertex headaches and nausea during the last hour of her haemodialysis (HD) sessions. After one particularly severe episode, which was associated with vomiting, restlessness and blurred vision, her team suspected that she was developing dialysis disequilibrium syndrome. She improved fully on cessation of HD, requiring simple analgaesia only, and continued dialysis three times per week. Several more distressing episodes of nausea and headaches compelled us to give intravenous mannitol during HD, resulting in temporary improvement. Subsequently, shorter and more frequent dialysis sessions along with intravenous mannitol resulted in satisfactory clinical response.
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PMID:Headache during haemodialysis in a patient with shunt: a cause for concern? 2585 63

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

We present the case of a 25-year-old female with End-Stage Renal Disease (ESRD) and Idiopathic Intracranial Hypertension (IIH) who developed severe headaches during haemodialysis (HD). The headaches resolved several hours after each HD session. We were able to diagnose dialysis disequilibrium syndrome (DDS) following intracranial pressure (ICP) monitoring and use a novel strategy to treat her symptoms.
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PMID:Intra-dialytic intracranial pressure monitoring in a patient with lumbo-peritoneal shunt for idiopathic intracranial hypertension. 3251 91


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