2026 Southeastern Residency Conference

Background:  
A common complication of traumatic and non-traumatic neurological injuries is elevated intracranial pressure (ICP). Preventing elevated ICP is critical for minimizing secondary neurologic injuries. First line pharmacologic therapies include hyperosmolar agents, such as hypertonic saline and mannitol. In the 2020 Neurocritical Care Society (NCS) Guidelines for Acute Treatment of Cerebral Edema, hypertonic saline and mannitol are both considered viable options, and there is little data to support one therapy over another, with many patients receiving both in clinical practice. Hypertonic saline is a plasma volume expander and may lead to hypernatremia; while mannitol is an osmotic diuretic and may not be preferred in patients due to risk of acute kidney injury (AKI). 
Increased serum concentrations of mannitol may be associated with AKI due to renal vasoconstriction. While most hospitals do not directly measure mannitol serum concentrations, osmolar gap monitoring has emerged as a surrogate marker for serum levels of mannitol. The NCS Guidelines recommend monitoring osmolar gap over serum osmolarity to assess the risk of AKI; however, the osmolar gap value at which to withhold mannitol remains unclear. The aim of this study is to determine risk factors for AKI among patients who receive mannitol for elevated ICP.  
 
Methods:  
This was a multi-center, retrospective, observational cohort study to identify the risk factors for AKI in patients who receive mannitol to manage elevated ICP. Patients were included if admitted to the Neurocritical Care or Trauma ICU between March 1st, 2024, and November 1st, 2025, received at least 1 g/kg of mannitol, and at least 2 doses of mannitol during admission. Patients were excluded if they had end-stage renal disease or have a baseline dependence on renal replacement therapy.  The primary outcome was identification of risk factors associated with AKI. Univariate logistic regression analysis was used to determine which variables are associated with AKI. We included variables such as peak osmolar gap, total mannitol dose administered, age, comorbid conditions, and number of nephrotoxic medications.  The secondary outcome was to compare characteristics of patients with AKI to those without AKI. Other statistical analyses were descriptive and inferential in nature.  
 
Results:   
A total of 230 patients who received mannitol between March 1st, 2024, and November 1st, 2025, were screened for inclusion. Of these, 102 patients met inclusion criteria and were included in the study cohort. The most common reason patients were not included was receiving less than 1 g/kg of mannitol and/or fewer than two doses of mannitol during admission. 
Baseline characteristics included patients that were predominantly male (56%) and White (53%), with a median age of 58 years. Most patients were admitted with a nontraumatic neurologic injury (94%) and were managed in the Neurocritical ICU (95%). Baseline serum creatinine was higher in patients who developed AKI compared to those who did not (1.02 mg/dL vs 0.79 mg/dL (p = 0.001). 
Among the 102 included patients, 28 developed AKI as defined by the Stage 1 AKI KDIGO Criteria. A univariate logistic regression analysis was conducted to evaluate differences between patients with and without AKI. Baseline serum creatinine (p = 0.010) and APACHE-II score (p = 0.032) were significantly associated with AKI. The median [IQR] peak serum creatinine among patients with AKI was 1.66 [1.41 - 2.46] mg/dL. 

Conclusions: 
In a univariate logistic regression analysis, higher baseline serum creatinine and APACHE II scores were associated with an increased risk of AKI. Factors associated with administration of mannitol, such as peak osmolar gap and total mannitol dose administered, were not associated with an increased risk of AKI.