Dialysis Disequilibrium Syndrome: When Therapy Precipitates Toxicity

Abstract

Dialysis disequilibrium syndrome (DDS) is characterized by a spectrum of neurologic symptoms that can affect patients on hemodialysis. Dialysis naive patients are more prone to this condition but it can also occur in patients who have missed several days of dialysis. Early features may be mild, including headache, nausea, and blurred vision, to severe symptoms such as somnolence, confusion, seizures, coma and death. CASE PRESENTATION: A 35 year old female, history of bipolar disorder and depression, presented to a small community hospital ED with confusion and lethargy. She was found to have an elevated creatinine in the setting of lithium toxicity. She was transferred to our facility for a higher level of care and on arrival was somnolent but hemodynamically stable. Initial laboratory studies were as shown below. CT of the brain showed no intracranial hemorrhage. Given the patient's altered level of consciousness, and renal failure in the setting of lithium toxicity, emergent dialysis was recommended by nephrology. During dialysis, the patient became markedly hypotensive and obtunded. She required intubation for airway protection and vasopressor support. MRI of the brain showed diffuse cortical edema and herniation of the cerebellar tonsils. Brain death was declared independently by an intensivist and a neurologist. DISCUSSION: Our patient required emergent dialysis given her severe altered mental status, and renal failure secondary to lithium toxicity. Unfortunately, she went on to develop DDS. DDS usually affects patients who are undergoing their first dialysis session. The exact incidence is unknown but it is thought to be very rare. The broad nature of the symptoms makes it difficult to identify DDS. Risk factors include extremes of age, severe uremia, hypernatremia, hyperglycemia, preexisting neurologic abnormalities, and first dialysis treatment. DDS remains a clinical diagnosis of exclusion. One must rule out stroke, subdural hematoma, intracerebral hemorrhage, infection, and toxic encephalopathy among others. The cornerstone of treatment is prevention. Prevention entails identifying high-risk patients and utilizing intermittent hemodialysis, or CRRT using slow urea removal. The exact mechanism is not well understood, and there are no guidelines on appropriate dialysis settings. If symptoms are mild, one can consider reducing the blood flow rate, but if patients display severe neurologic abnormalities, one should strongly consider stopping the dialysis session. CONCLUSIONS: DDS is a rare but potentially lethal clinical entity. Early recognition, prompt cardiopulmonary resuscitation, and cessation of the dialysis session are of paramount importance in managing patients with severe DDS.