Lateral Ventricle Volume Asymmetry Predicts Midline Shift in Severe Traumatic Brain Injury

Abstract

Midline shift following severe traumatic brain injury (sTBI) detected on computed tomography (CT) scans is an established predictor of poor outcome. We hypothesized that lateral ventricular volume (LVV) asymmetry is an earlier sign of developing asymmetric intracranial pathology than midline shift. This retrospective analysis was performed on data from 84 adults with blunt sTBI requiring a ventriculostomy who presented to a Level I trauma center. Seventy-six patients underwent serial CTs within 3 h and an average of three scans within the first 10 d of sTBI. Left and right LVVs were quantified by computer-assisted manual volumetric measurements. LVV ratios (LVR) were determined on the admission CT to evaluate ventricular asymmetry. The relationship between the admission LVR value and subsequent midline shift development was tested using receiver operating characteristic (ROC) analysis, and odds ratio (OR) and relative risk tests. Sixty patients had no >5 mm midline shift on the initial admission scan. Of these, 15 patients developed it subsequently (16 patients already had >5 mm midline shift on admission scans). For >5 mm midline shift development, admission LVR of >1.67 was shown to have a sensitivity of 73.3% and a specificity of 73.3% (area under the curve=0.782; p<0.0001). LVR of >1.67 as exposure yielded an OR of 7.56 (p<0.01), and a risk ratio of 4.42 (p<0.01) for midline shift development as unfavorable outcome. We propose that LVR captures LVV asymmetry and is not only related to, but also predicts the development of midline shift already at admission CT examination. Lateral ventricles may have a higher "compliance" than midline structures to developing asymmetric brain pathology. LVR analysis is simple, rapidly accomplished and may allow earlier interventions to attenuate midline shift and potentially improve ultimate outcomes.

Keywords: computed tomography; midline shift; traumatic brain injury; ventricle.

FIG. 1.

Illustration of manual lateral ventricle outlining. Left and right lateral ventricles were separately manually outlined based on image anatomy and contrast in each relevant slice. (Present image shows outlining of the left ventricle in one slice.) Then, using outlined areas from each slice and slice thickness information the software performed three-dimensional reconstruction and volume calculation of each lateral ventricle separately.

FIG. 2.

Receiver operating characteristic curve analysis of lateral ventricle volume ratio (LVR) on predicting subsequent midline shift development. Only patients without significant midline shift on admission scan were included. Positive group was formed by patients who developed significant midline shift on follow-up scan, negative group was formed by patients who did not.

FIG. 3.

Admission and follow-up computed tomography scan images of a representative patient with high admission lateral ventricle volume ratio who subsequently developed significant midline shift. Midline shift was measured 1 mm (not significant) on admission scan (<3 h post-injury; left), while it has become 7 mm (significant) on the follow-up scan at 20 h (right). The white line indicates the midline. External ventricular drainage is present on follow-up scan (hyperintense dot near right lateral ventricle).

FIG. 4.

Concept of asymmetric intracranial pathology development. (A) 1. Normal brain. 2. Initiation of asymmetric brain pathology (e.g., bleeding, edema). 3. Pathology propagation, ipsilateral ventricle compression causing lateral ventricular asymmetry. 4. Further propagation causing midline shift. (B) 1. Normal brain 2. Initiation of ventricular entrapment. 3. Pathology propagation, ventricle enlargement causing lateral ventricular asymmetry. 4. Further propagation causing midline shift.