Dialysis disequilibrium syndrome (DDS) is a clinical syndrome of neurologic deterioration resulting from cerebral edema seen in patients undergoing dialysis [1,2,3,4,5]. DDS is most prevalent during or immediately after initial hemodialysis, but may also occur during maintenance hemodialysis, especially in those with preexisting neurological disease [1, 6,7,8]. Risk factors include initial dialysis, resuming dialysis after missing multiple sessions, markedly elevated blood urea concentration pre-dialysis, severe metabolic acidosis, and preexisting neurologic disease including any condition that increases blood–brain barrier permeability [1, 4, 9,10,11]. Symptoms are nonspecific, but similar to those of increased intracranial pressure (ICP), including headaches, mental confusion, and coma .
The etiology of DDS is unknown, but two prevailing theories of its pathophysiology are the reverse urea effect, in which shifts of urea concentrations create an osmotic gradient promoting cerebral edema [12, 13] and transient intracerebral metabolic acidosis after hemodialysis, which displaces sodium and potassium from organic anions making them osmotically active and resulting in cerebral edema [1, 13]. If left unmanaged, DDS can lead to severe clinical sequelae from highly uncontrolled ICPs, resulting in global anoxic brain injury, seizures, coma, and death.
Traditionally, DDS has been managed with preventative measures aimed at reducing ICP, including manipulation of hemodialysis parameters, use of osmotically active substances, and continuous renal replacement therapy [1, 9, 14]. In this case, we describe the successful treatment of refractory intracranial hypertension during DDS with a lumbar drain and the use of invasive cerebrospinal fluid (CSF) diversion as a novel method of managing ICP crises secondary to DDS in the neurocritical care setting.