Child, male, 1 year old. Head trauma, left limb immobility for 3 days on April 9, 2012, transferred from an outside hospital. At 19:00 on April 6, 2012, the child fell in place and landed on the ground with his head and left upper limb, crying and screaming at that time. He was rushed to the local hospital after 5 minutes without any response to the call, and regained consciousness half an hour later, and his pupils were equal in size. Head CT examination showed: right temporal parietal subdural hematoma (Figure 1), the family refused to operate, so conservative treatment, April 9, the child was unresponsive, no crying, left limb activities become less, repeat CT showed: right frontal, temporal, occipital large low-density shadows (Figure 2), then transferred to our hospital. Examination: hazy consciousness, little crying, poor spirit, skin abrasion on the left frontal-temporal region, bilateral pupils were equal in size and 3mm in diameter, light reflex was sensitive, muscle strength of the right limb was grade 5, proximal upper limb of the left limb was grade 2, distal upper limb was grade 0; lower limb was grade 3, muscle tone of the left upper limb was decreased, and the pathology signs were positive. MRI of the head: T1-weighted image showed right frontotemporal parietal subdural thin layer high signal, right hemisphere brain tissue was full, and the sulcus structure was not clear (Figure 3); T2 image showed right hemisphere swelling, and bilateral frontal subdural effusion, which was obvious on the left side (Figure 4); DWI image showed right hemisphere obvious high signal manifestation. The midline structure was slightly left deviated (Figure 5). Diagnosis: 1. traumatic right hemisphere cerebral infarction, 2. right frontotemporal subdural hematoma, 3. bilateral frontal subdural effusion. After admission, he was given conservative treatment of dehydration, antispasmodic (popovine injection 10mg), vasodilator (danshen chuanxiongzine injection 2ml) and antacid (pantoprazole sodium 10mg). On April 11th, the muscle strength of the left lower limb was restored to grade 4. On April 12, the muscle strength of the left upper limb was restored to grade 3, with occasional twitching of the limb, and antiepileptic treatment with sodium valproate oral solution was added. on April 14, the muscle strength of the left upper limb was restored to close to grade 4, and the muscle tone was restored compared with the previous one. on April 17, the muscle strength of the left upper limb was close to grade 4, and the muscle tone increased compared with the previous one, while the muscle strength of the left lower limb was grade 4 with normal muscle tone. on April 18, the MRI of the head was repeated. On April 18, the MRI of the head was repeated: the DWI image showed that the original high signal of the right cerebral hemisphere had turned to normal (Figure 6), and the subdural effusion of the right hemisphere was normal. On April 23rd, the muscle strength of left upper limb was grade 4, the grip of distal hand was poor, the muscle tone was higher than before, the muscle strength of left lower limb was grade 5, the muscle tone was normal, and the CT: the subdural effusion of right frontal-temporal parietal and left frontal-temporal area was higher than before (Fig. 7). on April 24th, the drilling and drainage of subdural fluid was carried out under the basic anesthesia, and the CT: the subdural effusion of right frontal area was increased after drilling and drainage of fluid. On April 26, the head CT: the right frontal subdural effusion drilling and drainage of effusion disappeared (Figure 8), and the drainage tube was removed.May 5, discharge: the left upper limb is close to grade 5, can grasp things, slightly worse than the right hand, the left lower limb muscle strength is grade 5, a little worse than the right side, the parents can walk on the ground with the help of the. Discussion The diagnosis and treatment process of this case involves the characteristics of traumatic brain injury in young children, the development of subdural hematoma, the diagnosis and treatment of traumatic massive cerebral infarction and the evolution of subdural effusion, and other aspects of the problem. In-depth discussion of each issue can help to improve the treatment effect of traumatic brain injury in young children and reduce and prevent the occurrence of serious complications.1. Surgical indications The case had consciousness disorder within one hour of the trauma, and the CT showed a right subdural hematoma with a left shift of the midline, although the pupils were equal in size, and brain hernia had not been formed yet, but the indications for surgery were clear, and the family refused to have surgery due to the fear of surgical risk and prognosis, and the physician should patiently explain the situation and fully explain the advantages and disadvantages to strive for the best outcome for young children. The physician should patiently explain the situation, fully explain the advantages and disadvantages, and strive for the consent of the family. Had the hematoma been removed surgically, it would have been possible to prevent the occurrence of large cerebral infarction and subdural effusion in the later stages of the disease. It is controversial whether to remove the bone flap or not [1]. While it is well recognized that adults should have a large bone flap for decompression, young children are susceptible to complications such as subcutaneous effusion, incisional leakage, and cerebral pontine outgrowth due to the large proportion of the brain volume, the underdevelopment of temporalis muscle, and the thin and easy stretching of the scalp after removing the bone flap. The child was 1 year old, fell on the ground, no coma at the time of injury, brain contusion is not serious, the bone flap must be careful, we think that after removing the hematoma intraoperatively and observing the cerebral cortex, if the contusion is light and the tension is low, you can close the dura mater and replace the bone flap back. 2. traumatic large cerebral infarction Traumatic cerebral infarction in children is not common, but it has been reported in the literature [2,3], and most of them are small cerebral infarctions in basal ganglia. In this case, left hemiparesis appeared on the third day of trauma, and CT showed hypodensity in the right hemisphere, and infarction of the whole right hemisphere occurred, which is relatively rare. Chen Deng et al [4] reported 60 cases of traumatic cerebral infarction in children, including 4 cases of large-area infarction, and concluded that most of these children died due to the severity of their injuries, and even if they survived, they were left with severe disabilities. The pathogenesis of traumatic cerebral infarction in children has been widely reported: 1) After head trauma. The vessel wall is subjected to direct mechanical damage caused by organic stenosis or occlusion, resulting in the interruption of its blood supply. ② Vascular wall damage caused local vasospasm, blood microcirculation disorders, resulting in insufficient blood supply to brain tissue. ③ Vascular endothelial injury activates endogenous and exogenous coagulation system, prompting thrombus formation. ④ After trauma, vascular spasm and blood rheology change, cerebrovascular reactivity decreases, cerebral blood flow decreases, causing free radicals in the blood to enhance the reaction, resulting in intracellular environmental disorders, thus aggravating cerebral tissue hypoxia, necrosis, and dissolution leading to cerebral infarction. ⑤ Cerebral contusion, subarachnoid hemorrhage and cerebral edema can make cerebral blood vessels twist, spasm and contract, aggravating the original ischemia and hypoxia leading to cerebral infarction. Cerebral infarction refers to the destruction of the corresponding part of brain tissue after arterial obstruction, and the pathogenesis is thrombosis or embolism. The child was hemiplegic 3 days after the injury, CT showed a large area of low density on the right side, large area of brain tissue destruction, the diagnosis of cerebral infarction is certain, MRI diffusion imaging of the right hemisphere obvious high signal is also sufficient to prove that the early infarction occurs, whether thrombosis or embolism occurs? Our answer was negative. Considering the cause of intracranial hematoma, we did not use thrombolytic therapy, and after 5 days of vasodilator and antispasmodic therapy, the hemiplegic limbs recovered significantly, indicating that the infarction was not due to thrombosis or embolism. We believe that the cause of large infarction of the child is mainly cerebral contusion, subdural hematoma, local occupation and high cranial pressure so that the right hemisphere cerebral vascular pressure, distortion, spasm, contraction, resulting in the right hemisphere cerebral tissue hypoperfusion, hypoperfusion state more than a certain threshold and time, large cerebral infarction. 10 August MRI diffusion imaging right hemisphere was significantly high signal, indicating that the brain tissue water diffusion obstacles, it is the ultra early stage of the On August 10, MRI diffusion imaging of the right hemisphere showed obvious high signal, indicating that the water diffusion disorder of brain tissue was a typical manifestation of cerebral infarction, which was the cause of hypoperfusion rather than embolism. This proves that the child’s cerebral infarction is caused by hypoperfusion. For the treatment of this type of cerebral infarction, early removal of hematoma, relieve the cerebral vascular compression, distortion and displacement, can fundamentally prevent the occurrence of cerebral hypoperfusion and infarction, a certain course of vasodilatation, antispasmodic, dilatation therapy is also effective.3. Subdural effusion Bilateral subdural effusion appeared in the late stage of the child, after unilateral drainage and postoperative dilatation, albumin and gangliosides, to obtain a satisfactory outcome. 1894, Mayo firstly reported that trauma was the cause of the infarction, and the right hemisphere signal of MRI diffusion imaging was basically restored. , Mayo first reported traumatic subdural effusion with a prevalence of 1.16% to l0% [5]. Traumatic subdural effusion mechanism is controversial, there are four main theories: ① one-way valve theory trauma caused arachnoid tear, CSF through the flap-like breach into the subdural cavity, but can not be refluxed and gradually increase the formation of the ② blood-brain barrier destruction theory that cranio-cerebral injuries are bad after the blood-brain barrier, capillary permeability increased. Plasma components of a large number of exudate the formation of fluid accumulation in the subdural cavity. High osmotic pressure theory: It is believed that the protein content in the effusion is elevated, and the osmotic pressure is also elevated, so that the water of the surrounding brain tissues and the water of the subarachnoid space will be infiltrated into the effusion, and the effusion will keep increasing and be formed. The theory of intracranial pressure imbalance is that trauma causes intracranial pressure imbalance, and CSF accumulates in the pressure-reduced area. At the same time, the arachnoid tear injury formed intradural effusion. In this case, in addition to the right subdural hematoma, low-density subdural fluid can be seen in the hematoma (Figure 1), indicating that the formation of arachnoid unidirectional flap is the reason for the formation of subdural fluid at an early stage.On April 9, CT showed that there was also subdural fluid formation in the contralateral frontal lobe (Figure 2).On the one hand, it may be related to the posterior displacement of brain tissue. On the one hand, it may be related to the posterior downward displacement of brain tissue, relatively low pressure in the left frontal, and overflow of fluid into the contralateral side, and on the other hand, the application of overdose of dehydrating drugs after the injury, which made the left frontal subdural cavity relatively low-pressure causes. It indicates the role of the doctrine of intracranial pressure imbalance in the development of subdural effusion. In later stages, as the hematoma liquefies and hemoglobin dissolves, the protein content within the effusion increases, an envelope forms around the effusion, osmotic pressure increases, and water is drawn into the surrounding area, which may account for the expansion of the subdural effusion in the later stages (Figure 7). The formation of subdural effusion in this child was the result of a combination of factors, which could not be explained by any single theory. We do not agree with the theory of blood-brain barrier disruption. There are three main surgical treatments for subdural effusion in children: external drainage of subdural effusion, arachnoid opening + external drainage of subdural effusion, and subdural cavity-peritoneal shunt. We believe that early drilling for external drainage and postoperative increase of rehydration volume, intravenous albumin and ganglioside can achieve the purpose of lowering the cranial pressure and promoting the reexpansion of brain tissue. The timing of drilling for drainage should be early, and drainage usually does not exceed 1 week. Early adjustment of dehydration medication is also important in this type of childhood trauma; high dosages and long courses can aggravate subdural effusions. Figure 1. 1-hour post-injury CT, crescent-shaped isohyperdense shadow under the right osseous plate, with a low-density crescent-shaped shadow anteriorly and a left shift in the midline. Figure 2. April 9 repeat CT was a large hypodense area in the right hemisphere. Figure 3. April 9 MRI pressurized water image showed swelling of the right hemisphere and a right subdural hematoma. Figure 4. April 9 MRIT2 weighted image shows right hemisphere swelling with bilateral frontal subdural effusions. Figure 5. April 9 MRI DTI image shows right apparent high signal, early cerebral infarction. Figure 6. April 18th review MRI showed right subdural effusion, DTI image right high signal basically returned to normal. Figure 7. April 23, repeat CT showed subdural effusion enlargement. Figure 8. April 26th review CT showed that the effusion had mostly disappeared.