Case report

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

Sean M Bagshaw^1,2 , Adam D Peets¹ , Morad Hameed^1,3 , Paul JE Boiteau¹ , Kevin B Laupland^1,4,5 and Christopher J Doig^1,2

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

author email corresponding author email

BMC Nephrology 2004, 5:9doi:10.1186/1471-2369-5-9

Published:	19 August 2004

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.