ABSTRACT
Aims: Among the antiepileptic drugs (AEDs) applied for secondary prophylaxis of posttraumatic epilepsy (PTE), carbamazepine (CBZ) may cause severe side effects and worsen traumatic brain injury (TBI). Presentation of Case: Two days after a bicycle accident causing severe TBI, a 23yo female developed a questionable seizure and received CBZ. Since then she required substitution of sodium. Six days after the accident she was extubated. Serum sodium was 123mmol/l. One day after transfer to the general ward, she was found comatose with a serum sodium of 114mmol/l. Cerebral CT showed diffuse cerebral edema. Electroencephalography did not record paroxysmal activity. After replacement of CBZ by levetiracetam, her condition markedly improved with a favourable outcome. Discussion and Conclusion: CBZ was made responsible for severe hyponatraemia in the presented case after exclusion of all other possible causes. Hyponatraemia may trigger the recurrence of cerebral edema after TBI. Hyponatraemia from CBZ may favourably respond to slow substitution of sodium with physiologic saline. CBZ for secondary prophylaxis of PTE may cause hyponatraemia, cerebral edema, and deterioration of pre-existing TBI. Replacement of CBZ by levetiracetame may resolve the condition. CBZ should be used with caution for secondary prophylaxis of PTE in TBI.
ABSTRACT
Objective To know the effect of pre-hospital emergency care for patients with acute cranio-cerebral injury. Methods Selected 312 patients with acute cranio-cerebral injury from Jan of 2005 to Jan of 2009 as the emergency group, selected 285 patients with acute cranio-cerebral injury from Jan of 2000 to Dec of 2004 as the control group. Retrospective analized the clinical condition between the two groups to know the effect of pre-hosptial emergency cares. Results There was significant difference of dead rate betweent the two groups, the prognosis of the two groups was also different. Conclusions Effective pre-hospital emergency care is very important for patients with acute eranio-cerebral injury, which can avoid certain complications and reduce dead rate.
ABSTRACT
Objective To study the type, characteristics, common complications of the cranio-cerebral injury and assessment for the body impairment in victims involved in road traffic accidents. Method Data from 862 cases with cranio-cerebral injury in road traffic accidents were collected and were statistically analyzed according to injured body part, complication, the type of complications and the severity of injury. Results Compound cranio-cerebral injuries were sustained in 276 cases, brain contusion in 192 cases, skull fracture in 79 cases, intracranial hemorrhage in 91 cases, and scalp injury in 224 cases. The chief complications were identified as hydrocephalus (19,2.20%), epilepsy (l6,1.86%), hemiplegia (14, 1.62%), decerebrate cortical syndrome (12,1.39%). Conclusion Among the cranio-cerebral injuries sustained in the road traffic accidents, compound injury was the commonest insult, in which serious cerebral contusion was the major type of injury. The complications following cranio-cerebral injury should be diagnosed strictly according to the diagnostic standard and identification time, which should be differentiated from the other related diseases.
ABSTRACT
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.