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      Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure – A case report

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          Abstract

          Background

          Dialysis disequilibrium syndrome (DDS) is the clinical phenomenon of acute neurologic symptoms attributed to cerebral edema that occurs during or following intermittent hemodialysis (HD). We describe a case of DDS-induced cerebral edema that resulted in irreversible brain injury and death following acute HD and review the relevant literature of the association of DDS and HD.

          Case Presentation

          A 22-year-old male with obstructive uropathy presented to hospital with severe sepsis syndrome secondary to pneumonia. Laboratory investigations included a pH of 6.95, PaCO2 10 mmHg, HCO3 2 mmol/L, serum sodium 132 mmol/L, serum osmolality 330 mosmol/kg, and urea 130 mg/dL (46.7 mmol/L). Diagnostic imaging demonstrated multifocal pneumonia, bilateral hydronephrosis and bladder wall thickening. During HD the patient became progressively obtunded. Repeat laboratory investigations showed pH 7.36, HCO3 19 mmol/L, potassium 1.8 mmol/L, and urea 38.4 mg/dL (13.7 mmol/L) (urea-reduction-ratio 71%). Following HD, spontaneous movements were absent with no pupillary or brainstem reflexes. Head CT-scan showed diffuse cerebral edema with effacement of basal cisterns and generalized loss of gray-white differentiation. Brain death was declared.

          Conclusions

          Death is a rare consequence of DDS in adults following HD. Several features may have predisposed this patient to DDS including: central nervous system adaptations from chronic kidney disease with efficient serum urea removal and correction of serum hyperosmolality; severe cerebral intracellular acidosis; relative hypercapnea; and post-HD hemodynamic instability with compounded cerebral ischemia.

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          Most cited references33

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          Blood-brain barrier breakdown in septic encephalopathy and brain tumours.

          D Davies (2002)
          Septic encephalopathy is associated with breakdown of the blood-brain barrier and cerebral oedema. These features are also common properties of brain tumours. Perimicrovessel oedema, disruption of associated astrocyte end feet and neuronal injury occur in a porcine model of acute septic encephalopathy. The adrenergic system has been implicated in the inflammatory response to sepsis and may play a role in controlling blood-brain barrier permeability, since the beta2-adrenoceptor agonist dopexamine inhibits perimicrovessel oedema formation whereas the alpha1-adrenoceptor agonist methoxamine provokes it. Electron microscopy revealed tight junction opening in high-grade astrocytoma microvessels. Expression of the tight junction protein occludin is reduced in these microvessels and this reduction is inversely correlated with the degree of cerebral oedema. Normal astrocytes secrete factors that induce barrier properties in endothelial cells, whereas high-grade astrocytomas secrete vascular endothelial growth factor, which stimulates angiogenesis, down regulates occludin and increases endothelial cell permeability. The water channel protein aquaporin-4 is normally expressed in astrocyte foot processes around cerebral microvessels. Its expression is massively up-regulated in high-grade astrocytoma and around metastatic adenocarcinoma. There is a significant correlation between aquaporin-4 expression and the degree of cerebral oedema, but it is not clear whether increased aquaporin-4 expression enhances oedema formation or clearance. These results suggest that the pathophysiology of brain oedema is multifactorial, but that there may be common processes operating regardless of the aetiology.
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            Epidemiology of acute renal failure: A prospective, multicenter, community-based study

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              Sustained low-efficiency dialysis for critically ill patients requiring renal replacement therapy.

              The replacement of renal function for critically ill patients is procedurally complex and expensive, and none of the available techniques have proven superiority in terms of benefit to patient mortality. In hemodynamically unstable or severely catabolic patients, however, the continuous therapies have practical and theoretical advantages when compared with conventional intermittent hemodialysis (IHD). We present a single center experience accumulated over 18 months since July 1998 with a hybrid technique named sustained low-efficiency dialysis (SLED), in which standard IHD equipment was used with reduced dialysate and blood flow rates. Twelve-hour treatments were performed nocturnally, allowing unrestricted access to the patient for daytime procedures and tests. One hundred forty-five SLED treatments were performed in 37 critically ill patients in whom IHD had failed or been withheld. The overall mean SLED treatment duration was 10.4 hours because 51 SLED treatments were prematurely discontinued. Of these discontinuations, 11 were for intractable hypotension, and the majority of the remainder was for extracorporeal blood circuit clotting. Hemodynamic stability was maintained during most SLED treatments, allowing the achievement of prescribed ultrafiltration goals in most cases with an overall mean shortfall of only 240 mL per treatment. Direct dialysis quantification in nine patients showed a mean delivered double-pool Kt/V of 1.36 per (completed) treatment. Mean phosphate removal was 1.5 g per treatment. Mild hypophosphatemia and/or hypokalemia requiring supplementation were observed in 25 treatments. Observed hospital mortality was 62.2%, which was not significantly different from the expected mortality as determined from the APACHE II illness severity scoring system. SLED is a viable alternative to traditional continuous renal replacement therapies for critically ill patients in whom IHD has failed or been withheld, although prospective studies directly comparing two modalities are required to define the exact role for SLED in this setting.
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                Author and article information

                Journal
                BMC Nephrol
                BMC Nephrology
                BioMed Central (London )
                1471-2369
                2004
                19 August 2004
                : 5
                : 9
                Affiliations
                [1 ]Department of Critical Care Medicine, Calgary Health Region and University of Calgary, Calgary, Alberta, Canada
                [2 ]Department of Community Health Sciences, Calgary Health Region and University of Calgary, Calgary, Alberta, Canada
                [3 ]Department of Surgery, Calgary Health Region and University of Calgary, Calgary, Alberta, Canada
                [4 ]Department of Medicine, Calgary Health Region and University of Calgary, Calgary, Alberta, Canada
                [5 ]Department of Diagnostic and Laboratory Medicine, Calgary Health Region and University of Calgary, Calgary, Alberta, Canada
                Article
                1471-2369-5-9
                10.1186/1471-2369-5-9
                515303
                15318947
                decefcd9-ed33-4dca-bd42-aea2f8d3eb72
                Copyright © 2004 Bagshaw et al; licensee BioMed Central Ltd.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 May 2004
                : 19 August 2004
                Categories
                Case Report

                Nephrology
                Nephrology

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