Post-Traumatic Cerebral Infarction Following Low-Energy Penetrating Craniocerebral Injury Caused by a Nail

Post-traumatic cerebral infarction (PTCI) is a secondary insult which causes global cerebral hypoxia or hypoperfusion after traumatic brain injury, and carries a remarkable high mortality rate. PTCI is usually caused by blunt brain injury with gross hematoma and/or brain herniation. Herein, we present the case of a 91-year-old male who had sustained PTCI following a low-energy penetrating craniocerebral injury due to a nail without evidence of hematoma. The patient survived after a decompressive craniectomy, but permanent neurological damage occurred. This is the first case of profound PTCI following a low-energy penetrating craniocerebral nail injury and reminds clinicians of possibility this rare dreadful complication for care of head-injured patients.

Post-Traumatic Cerebral Infarction

We report a series of 19 consecutive patients with post-traumatic cerebral infarction. Post-traumatic cerebral infarction(PTCI) was diagnosed by CT within 24 hours of admission in 6 cases and up to 14 days after admission in 13 cases of 1092 patients who required cranial CT for trauma during the period. The frequency, vaascular territories, cause, and mortality rate of post traumatic cerebral infarction were discussed.

Morphologic study of the post-traumatic cerebral infarction / 中国法医学杂志

Objective To observe the morphologic characteristics of the post-traumatic cerebral infarction and discriminate it from brain contusion. Methods From 81 severe brain injury samples 15 were selected which met the criteria of the secondary necrosis and hemorrhage of brain. Another 15 simple brain contusion samples were selected as control. They were cut according to various requirements either coronary or saggittally or horizontally and observed grossly and histologically. Results The post-traumatic cerebral infarctions were found mainly in 5 localities: basal ganglia (3 cases), cingulate gyrus (2 cases), both cuneus of the occipital lobes (2 cases), lateral occipito-temporal gyrus (6 cases, 5 of them complicated with hemorrhage in the midbrain and pons), and occipital gyrus (2 cases). All of the infarctions were located not at the point of coup or contrecoup. They were localized and had clear boundaries. All of the lesions could be traced back to be related to brain hernia. Microscopically, there were extravasation of blood, and necrosis in the infarction, and usually severe congestion and edema with white blood cells infiltration and glia cell reaction. If the lesion was in the cerebrum, it was usually located at the junction of cortex and medulla, in severe cases extended to whole thickness of the cortex and the subarachnoid space, but the pia mater was not ruptured. There were marked ischemic and hypoxia changes in the neurons. The lesions of brain contusion, on the contrary, were always ruptured. The contused brain tissue may be necrotic. Conclusion The Post-traumatic cerebral infarction is synonymous with secondary necrosis and hemorrhage of the brain. The mechanism of the infarction is compression of intra-cerebral blood vessels due to cerebral hernia. It could be differentiated from cerebral contusion by the relation with cerebral hernia, the location of the lesion, the in-tactness of the pia mater, as well as other related histological changes.