When a Forensic Pathologist and/or Neuropathologist evaluates a brain that has been subjected to traumatic brain injury (TBI), they tend to focus on the anatomic injuries, i.e., fractures of the calvarium or base of the skull; presents of epidural, subdural or subarachnoid hemorrhage; acute contusions, whether they be coup, contracoup or gliding; the presence of intraparenchymal hemorrhage; the presence of edema; and evidence of herniation to name a few of the anatomic injuries.
Following noting the anatomic changes, they then attempt to relate the injuries to the circumstances that led to the TBI. In this process, they will note whether the patient was under the influence of alcohol and or other drugs, however, they typically do not explore the role alcohol and or other drugs had on the pathophysiologic process that occurs at the molecular level in a TBI.
This is a case in which I was asked, as a forensic pathologist, to examine two TBIs a patient sustained, separated by approximately two months. I was also asked to look at whether the patient’s acute and chronic alcoholism played a role in the pathophysiologic process of these TBIs, and his subsequent precipitous death following the second TBI due to an assault.
First Traumatic Brain Injury
A 44-year-old male was found lying on the side of a road. He was initially unresponsive according to bystanders. Upon arrival of the EMTs he was noted to be awake but had an altered level of consciousness. The patient admitted to being intoxicated, stating he had “a lot to drink tonight.” He did not know what had happened to him or where he was. He had injuries to his face and the back of his head.
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