Therapeutic hypernatremia management during continuous renal replacement therapy with elevated intracranial pressures and respiratory failure

Abstract

Cerebral edema and elevated intracranial pressure (ICP) are common complications of acute brain injury. Hypertonic solutions are routinely used in acute brain injury as effective osmotic agents to lower ICP by increasing the extracellular fluid tonicity. Acute kidney injury in a patient with traumatic brain injury and elevated ICP requiring renal replacement therapy represents a significant therapeutic challenge due to an increased risk of cerebral edema associated with intermittent conventional hemodialysis. Therefore, continuous renal replacement therapy (CRRT) has emerged as the preferred modality of therapy in this patient population. We present our current treatment approach, with demonstrative case vignette illustrations, utilizing hypertonic saline protocols (3% sodium-chloride or, with coexisting severe combined metabolic and respiratory acidosis, with 4.2% sodium-bicarbonate) in conjunction with the CRRT platform, to induce controlled hypernatremia of approximately 155 mEq/L in hemodynamically unstable patients with acute kidney injury and elevated ICP due to acute brain injury. Rationale, mechanism of activation, benefits and potential pitfalls of the therapy are reviewed. The impact of hypertonic citrate solution during regional citrate anticoagulation is specifically discussed. Maintaining plasma hypertonicity in the setting of increased ICP and acute kidney injury could prevent the worsening of ICP during renal replacement therapy by minimizing the osmotic gradient across the blood-brain barrier and maximizing cardiovascular stability.