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Abstract: SA-PO1066

MRI Spatial and Temporal Characterization of Acute and Chronic Hypotonic Brain Edema

Session Information

  • Na+, K+, Cl-
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Fluid, Electrolytes, and Acid-Base

  • 703 Na+, K+, Cl- Basic

Authors

  • Tejedor, Marta, Hospital Infanta Elena, Valdemoro, Madrid, Spain
  • Martín, Giovanna, Universidad Complutense de Madrid, Madrid, Spain
  • Nava, Ángel, Universidad Complutense de Madrid, Madrid, Spain
  • Usón, Clara, Universidad Complutense de Madrid, Madrid, Spain
  • Soto, Javier, Universidad Complutense de Madrid, Madrid, Spain
  • Tejedor jorge, Alberto, Fundación para la Investigación Biomédica del Hospital General Universitario Gregorio Marañón, Madrid, Spain
Background

Hypotonic brain edema has not been studied in depth with imaging techniques such as MRI.
Aims: to assess spatial and temporal responses within different areas of the brain to hypotonicity, and differences between acute and chronic hyponatremia.

Methods

Chronic hyponatremia was induced in Wistar rats by intraperitoneal (ip) injection of desmopressin (0.4 ug/kg/d), hyposodic liquid diet and free access to water for 7 days (G1). A group of control normonatremic animals was fed with pellet based diet (G2). Brain edema was studied with MRI at baseline and after ip injection of either 10% of body weight in water (both G1 and G2) or 2 mL of NaCl3% for every 100 grams of body weight (G1) over 120 minutes. ADC (apparent diffusion coefficient) assessed the degree of brain edema in different regions of interest: cortex, hypothalamus, nervous fibers, extra-pyramidal system.

Results

Baseline [Na] were 147±7mmol/L (G2) and 136±7mmol/L (G1); after acute water load: 112±5mmol/L and 119±5mmol/L respectively. Baseline ADC values were lower in G1, indicating relevant brain edema. After acute water load, a further drop in the ADC levels was observed in both groups. A transient period of cellular defense where water was actively pumped outside the cells was observed, being more efficient in G1, becoming the ADC levels similar in both groups at 60 min, but worsening again at 90 and 120 min. Lateral hypothalamus was the first region to become edematous, followed by the cortex, and then, at different time points, by the extra-pyramidal system and myelinated fibers. Response to edema appeared with different time delays from the maximum degree of edema, but it seemed to follow a structural order: hypothalamus, cortex, extra-pyramidal system and fibers. Treatment of G1 with hypertonic saline (NaCl3%) induced a correction of the edema that was three times faster than the spontaneous one. Sodium concentrations went from 136±7mmol/L to 140±7mmol/L.

Conclusion

Brain response to hypotonicity is not homogeneous, and edema develops at different time points in different regions. The time course of the response to that edema is not homogeneous either. The different speed in the response to brain edema in adjacent areas suggests that damage leading to central pontine myelinolysis could be earlier than observed in clinical practice.