Post-Mortem CT Delivers Fast and Accurate Injury Identification in Trauma Patients.

BACKGROUND: Accurate and timely injury identification is critical but difficult to achieve in trauma patients who die shortly after arrival to the hospital. Autopsy has historically been used to detect injuries, but few undergo formal autopsy. This study investigates the utility of post-mortem computed tomography (PMCT) for injury identification in a diverse trauma population. METHODS: Cross-sectional study of adult trauma patients who died within 24 hours of arrival to a Level I trauma center were included. Among patients with PMCT, injury severity score (ISS) and number of injuries (NOI) were calculated either from physical exam alone (pre-PMCT) or exam and imaging (post-PMCT). ISS and NOI before and after PMCT were compared. A cause of death analysis was performed for patients who underwent comprehensive (ie, head, neck, and torso) PMCT. Non-parametric repeated measures tests were used, as appropriate. RESULTS: 7.3% (N = 28) of patients received PMCT. Compared to pre-PMCT, median ISS (21 vs 3.5) and NOI (5 vs 2) were greater post-PMCT (P < .001, respectively). Autopsy rate was 13.2% overall; 82.5% of autopsies were due to a penetrating mechanism, and median time to autopsy reporting was 38.5 days. Among 17 patients who received comprehensive PMCT, 64.7% had a single cause of death identified, and the remaining were classified as either multiple potential contributors or unknown. DISCUSSION: PMCT is a readily available method to identify injuries in trauma patients who expire shortly upon presentation. Given the low autopsy rate for blunt trauma and delay in reporting, PMCT is an important adjunct for trauma providers.

A 66-Year-Old Woman with a Progressive, Longitudinally Extensive, Tract Specific, Myelopathy.

A 66-year-old woman presented with progressive lancinating pain and sensory deficits attributable to a myelopathy of unclear etiology. Spinal cord magnetic resonance imaging showed a longitudinally extensive T2-hyperintense lesion of the dorsal columns. Comprehensive serum, urine, and cerebrospinal fluid analyses failed to identify an etiology. Empiric intravenous methylprednisolone and intravenous immunoglobulin were of no benefit and serial screens for an occult malignancy were negative. She developed dysesthesias and allodynia affecting her entire body and lost the use of her arms and legs due to severe sensory ataxia that was steadily progressive from onset. She opted against additional aggressive medical management of her condition and passed away on hospice eleven months after symptom onset. Autopsy revealed findings most consistent with polyphasic spinal cord ischemia affecting the dorsal and lateral white matter tracts and, to a lesser extent, adjacent gray matter. The underlying etiology for the progressive vasculopathy remains unknown. Spinal cord ischemia affecting the posterior spinal cord is rare and to our knowledge this case represents the only instance of a progressive spinal cord tractopathy attributable to chronic spinal cord ischemia.