ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: PUB133

Optimizing Intracranial Pressure Management in AKI: A Novel Approach Using Enhanced Sodium Concentration in Continuous Kidney Replacement Therapy

Session Information

Category: Dialysis

  • 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Abdulrahman, Zeinab A., Jersey Shore University Medical Center, Neptune TWP, New Jersey, United States
  • Dounis, Harry J., Jersey Shore University Medical Center, Neptune TWP, New Jersey, United States
  • Masud, Avais, Jersey Shore University Medical Center, Neptune TWP, New Jersey, United States
  • Kim, Sion, St. Mary Medical Center, Langhorne, Pennsylvania, United States
  • Kaur, Supreet, Jersey Shore University Medical Center, Neptune TWP, New Jersey, United States
  • Mehandru, Sushil, Jersey Shore University Medical Center, Neptune TWP, New Jersey, United States
Introduction

Hypertonic saline treats elevated intracranial pressure (ICP) and cerebral edema by causing osmotic dehydration, avoiding complications like acute kidney injury and pulmonary edema. Maintaining therapeutic hypernatremia in patients needing renal replacement therapy is challenging as dialysis dilutes serum sodium, reducing hypertonic saline efficacy.

Case Description

A 25-year-old male with a history of polysubstance abuse presented in cardiac arrest and was resuscitated after 25 minutes. The patient was comatose with no response to stimuli, non-reactive pupils, and absent corneal and oculocephalic reflexes. A CT scan showed diffuse cerebral edema with potential herniations. Laboratory results revealed acute kidney injury with serum sodium of 142 mmol/L, necessitating continuous venovenous hemodiafiltration (CVVHDF). For cerebral edema, 3% hypertonic saline was administered. To maintain a serum sodium of 150-155 mEq/L, dialysis bath solution adjustments were made. This involved infusing 10 ml of a 23.4% hypertonic saline solution into a 2.5-liter bag of dialysis solution. Each ml of the 23.4% solution contained 4 mEq of sodium, adding a total of 40 mEq to the bag. This resulted in 40 mEq sodium/2.5 liters = 16 mEq/L added to the 140 mEq/L in the dialysis solution, reaching 156 mEq/L. Adjustments maintained serum sodium between 146-153 mEq/L during hospitalization. Despite efforts, the patient's neurological status did not improve, leading to hospice care.

Discussion

This case highlights the complexity of managing patients with anoxic brain injury and cerebral edema undergoing dialysis. Conventional intermittent hemodialysis can exacerbate ICP; thus, CVVHDF is preferable due to its continuous nature and lesser impact on systemic and cerebral hemodynamics. Increasing dialysis bath sodium concentration can effectively maintain a desired hyperosmolar state. For patients with increased ICP undergoing renal replacement therapy, a dialysis bath sodium concentration of 150-160 mEq/L, achieved by augmenting standard solutions with hypertonic saline, is crucial for managing cerebral edema. This strategy stabilizes patients in critical care settings.