What is dialysis disequilibrium syndrome

Dialysis disequilibrium syndrome. West J Med. Arieff AI. More on the dialysis disequilibrium syndrome. Dialysis disequilibrium syndrome: current concepts on pathogenesis and prevention. Kidney Int. Uremic encephalopathies: clinical, biochemical, and experimental features. Am J Kidney Dis. Urea levels in cerebrospinal fluid after haemodialysis. Current concepts of blood—brain barrier development. Int J Dev Biol. The molecular basis of the blood brain barrier differentiation and maintenance.

Is it still a mystery? Pharmacol Res. Abbott NJ. Astrocyte-endothelial interactions and blood—brain barrier permeability. J Anat. Permeability of endothelial and astrocyte cocultures: in vitro blood—brain barrier models for drug delivery studies.

Ann Biomed Eng. Brain swelling after dialysis: old urea or new osmoles? Filtration and reflection coefficients of the rabbit blood—brain barrier. Am J Physiol. Urea transport in the central nervous system. Molecular basis for the dialysis disequilibrium syndrome: altered aquaporin and urea transporter expression in the brain.

Nephrol Dial Transplant. Tight-junctional modification as the basis of osmotic opening of the blood—brain barrier. Ann N Y Acad Sci. Haemodialysis disequilibrium. Br Med J. Verkman AS. Aquaporins: translating bench research to human disease. J Exp Biol. Osmolality of brain tissue and its relation to brain bulk. Dialysis disequilibrium syndrome DDS in the rat: role of the "reverse urea effect". Silver SM. Cerebral edema after rapid dialysis is not caused by an increase in brain organic osmolytes.

J Am Soc Nephrol. Brain water and electrolyte metabolism in uremia: effects of slow and rapid hemodialysis. Dialysis Disequilibrium Syndrome: brain death following hemodialysis for metabolic acidosis and acute renal failure—a case report.

BMC Nephrol. Dialysis disequilibrium: another reversible posterior leukoencephalopathy syndrome? Clin Neurol Neurosurg. Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging. J Clin Invest. A preliminary report of brain edema in patients with uremia at first hemodialysis: evaluation by diffusion-weighted MR imaging.

Central nervous system pH in uremia and the effects of hemodialysis. Dialysis disequilibrium syndrome and other treatment complications of extreme uremia: a rare occurrence yet not vanished. Hemodial Int. Hemodialysis in small children. Superiority of hemofiltration to hemodialysis for treatment of chronic renal failure: comparative studies between hemofiltration and hemodialysis on dialysis disequilibrium syndrome.

Artif Organs. Dialysis disequilibrium syndrome: a narrative review. Semin Dial. Daugirdas JT. Prevention of dialysis disequilibrium syndrome by use of high sodium concentration in the dialysate.

Osmolality changes during hemodialysis. Natural history, clinical correlations, and influence of dialysate glucose and intravenous mannitol. Ann Intern Med. Experimental dialysis disequilibrium syndrome: prevention with glycerol. The pathogenesis and prevention of cerebral dysfunction during dialysis.

Kleeman CR. Metabolic coma. Support Center Support Center. External link. Chest radiograph revealed right middle lobe and lingular patchy opacification. An abdomino-pelvic CT scan demonstrated moderate to severe bilateral hydronephrosis, bladder wall thickening with multiple diverticuli, and retroperitoneal streaking consistent with acute infection.

A provisional diagnosis of severe sepsis was made with multiple potential foci of infection. The patient was given empiric ceftriaxone, metronidazole and vancomycin. Sputum specimen cultured heavy methicillin-sensitive Staphylococcus aureus , blood cultures were positive for S. The patient was admitted to the intensive care unit ICU.

The metabolic acidosis persisted pH 7. The patient had a suprapubic bladder catheter inserted by angiography. However, due to concern the patient remained oliguric following 4 L crystalloid resuscitation, hemodialysis was organized.

Hemodialysis parameters included: F membrane surface area 1. The patient had Although the patient was alert and appropriate Glasgow Coma Scale 15 with tachycardia and stable normal range blood pressure before the initiation of dialysis, he was demonstrating an increased work of breathing and oxygen requirements suggestive of worsening sepsis syndrome. Approximately 2. At completion of HD and over the subsequent 4 hours the patient's neurologic status deteriorated with evidence of loss of all brainstem reflexes.

Head CT-scan is shown in Figure 1. Computerized Tomography CT head showing diffuse cerebral edema with effacement of basal cisterns and generalized loss of gray-white differentiation.

Repeat laboratory investigations immediately following hemodialysis revealed a pH 7. The patient rapidly progressed to refractory shock and multi-organ dysfunction Diagnosis of brain death was declared independently by an intensivist and a neurologist.

At autopsy, the brain showed evidence of diffuse cerebral edema. Cardiac assessment showed left ventricular enlargement consistent with systemic hypertension likely as a result of chronic kidney disease.

Both lungs showed patchy acute bronchopneumonia with edema and congestion. Both kidneys appeared grossly pyonephrotic with dilated, thickened ureters and suggested the presence of acute on chronic pyelonephritis. The meatal aperture was scarred and stenosed. The immediate indication for renal replacement therapy was correction of refractory metabolic acidosis in the setting of oliguria; however, following initiation of HD this patient developed irreversible symptoms consistent with DDS.

DDS occurs most commonly following initiation of chronic HD for patients with end-stage renal disease[ 2 ]. Patients with pre-existing neurologic disease, such as head trauma, stroke or malignant hypertension, may be at greater risk for developing DDS[ 5 , 6 ]. The precise epidemiology of DDS is poorly defined and may be under-reported due to the wide spectrum of clinical manifestations.

Mild symptoms such as headache, nausea, blurred vision, muscle cramps, disorientation, anorexia, restlessness, hypertension and dizziness are common during or following HD and may be attributed to DDS[ 2 ]. More severe symptoms consistent with central nervous system dysfunction such as seizures, central pontine myelinolysis, coma and death are rare[ 7 ]. The temporal profile for DDS is not well described. DDS has been credited for acute electroencephalographic EEG abnormalities and structural changes on diagnostic imaging following rapid hemodialysis [ 8 — 10 ].

Likewise, brain MRI studies immediately following hemodialysis in chronic dialysis patients have shown quantitative increases in brain volume consistent with cerebral edema[ 11 ].

The pathogenesis remains debated and incompletely understood; however, two central hypotheses have emerged. First, acute urea removal occurs more slowly across the blood-brain barrier than from plasma, generating a 'reverse osmotic gradient' promoting water movement into the brain and cerebral edema[ 12 ]. Absolute increases in brain water content have been demonstrated in a rat model of uremia undergoing rapid hemodialysis that was accounted for by an increase in the ratio of brain to plasma urea[ 13 , 14 ].

Down-regulation of central nervous system urea transporters have been proposed as a mechanism contributing to the delay in urea clearance from the brain[ 15 ]. The second hypothesis states that the increased osmolality of the extracellular fluid in uremia stimulates an adaptive accumulation of intracellular organic osmolytes to limit cerebral cell dehydration[ 16 ].

During hemodialysis, retention of these organic osmolytes contributes to a paradoxical reduction in intracellular pH resulting in increased brain osmolality and cerebral edema[ 17 , 18 ]. The patient in this case unfortunately may have been susceptible to both proposed pathophysiologic mechanisms. Arieff AI, Dialysis disequilibrium syndrome: current concepts on pathogenesis and prevention. Kidney international. Clinical kidney journal. BMC nephrology. Pediatric nephrology Berlin, Germany. Journal of neurosurgery.

Archives of internal medicine. Seminars in dialysis. Arieff AI, More on the dialysis disequilibrium syndrome.

The Western journal of medicine. American journal of kidney diseases : the official journal of the National Kidney Foundation. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Silver SM, Cerebral edema after rapid dialysis is not caused by an increase in brain organic osmolytes.

The Journal of clinical investigation. Natural history, clinical correlations, and influence of dialysate glucose and intravenous mannitol. Annals of internal medicine. Clinical nephrology.

Doorenbos CJ,Bosma RJ,Lamberts PJ, Use of urea containing dialysate to avoid disequilibrium syndrome, enabling intensive dialysis treatment of a diabetic patient with renal failure and severe metformin induced lactic acidosis.

Proceedings of the European Dialysis and Transplant Association. European Dialysis and Transplant Association. Dialysis Disequilibrium Syndrome. The Royal Children's Hospital Melbourne. In this section About Nephrology Resources Contact us.

Plasma becomes hypotonic compared to brain cells and water shifts from the plasma into the brain tissue Systemic and neurological symptoms are associated with disequilibrium syndrome.