Cranial hematoma ossification is a rare disease that occurs mainly in children, and its onset, clinical manifestations and management principles have not been reported in the literature. In this study, we retrospectively analyzed the clinical characteristics and data methods of 8 cases of cranial hematoma ossification in children treated surgically from January 2000 to December 2006, with the aim of providing reference for the prevention and treatment plan of cranial hematoma ossification in children. Subjects and methods General data There were 8 cases in this group, 6 males and 2 females, with an average age of 16.7±23.3 months. Among them, 6 cases were within 1 year of age, 1 case was 4 years old, and 1 case was 5 years old. Birth history: 1 case was born by cesarean section with difficulty, and the remaining 7 cases were delivered via vagina; 4 cases had a history of obstructed labor (including 1 case of cesarean section), 3 cases were born normal, and 1 case developed after hitting the corner of the table with the head. The site of hematoma was right parietal in one case, right parietal occipital in one case, right occipital in one case, and left parietal in the remaining five cases. The hematoma formed after the trauma was small in scope, about 3*2*2 cm, while the hematoma that appeared after birth was larger in scope, with a minimum of 5*4*3 cm and a maximum of 10*8*6 cm. Clinical manifestations All children had a local soft mass as the first symptom, which did not exceed the bone suture, and then the mass gradually became hard, and the examination showed a bony head elevation (Figure 1). Ancillary examinations All children were examined by CT plain scan before surgery to determine the lesion site, scope, degree of hematoma ossification and skull shape (Figures 2-4). In some cases, the corresponding cranial deformity was seen by X-ray plain film examination (Figure 5). Treatment All children underwent surgical treatment. 7 cases underwent resection of the ossified shell of the hematoma and 1 case underwent cranioplasty and repositioning due to significant pressure of the skull into the skull. Results Cranioplasty was performed in all 8 children. According to the operator’s custom, a longitudinal shuttle, S-shaped, horseshoe-shaped or straight incision of the hematoma could be made to remove part of the expanded excess scalp, open the periosteum, separate along the surface of the ossified mass to its base, and expose the whole ossified hematoma, and in some cases, ossification of the top of the hematoma was not completed (Figure 6), and the parietal part of the ossified hematoma was removed by electric knife, bone chisel or biting forceps to open and enter the interior of the hematoma, and a layer of membranous tissue lining the inner wall of the hematoma was visible The thickness of the hematoma is related to the duration of the disease, and is thicker in those with longer disease duration, and the hematoma is mostly filled with iron-containing heme deposits and partially fibrotic tissue. The base of the hematoma was normal cranial cap bone, and all eight children had obvious cranial compression and deformation, losing the normal rounded structure. In one 4-year-old child, the cranial appearance was only mildly abnormal, and the shell of the ossified hematoma was mildly elevated, but the normal cranial bone was obviously compressed. The hematoma shell was used as a bone flap to repair the bone window defect, and glue was fixed to the edge of the normal skull (Figure 7). Afterwards, the periosteum, subcutaneous and scalp were sutured layer by layer, and according to the intraoperative bleeding 5 children received red blood cell transfusion and 3 did not, and most of them required postoperative drainage tube placement and were discharged from the hospital in 5 days. Pathology confirmed the ossification of the cranial hematoma and the presence of collagenization of the fibrous capsule wall with focal calcification. At postoperative follow-up from 2 months to 6 years, the children grew and developed well without neurological complications and without recurrence of cranial deformities. Discussion Cranial hematoma is caused by the accumulation of blood under the periosteum, not exceeding the bone suture. It occurs mostly in the neonatal period, is very rare in other ages, and has a very different clinical course in infancy and childhood than in adolescence and adulthood. The incidence of cranial hematoma in live births has been reported in the literature as 0.4% to 2.49%, and there is a history of difficult births, but less often combined with skull fractures. The local periosteum is elevated after hematoma formation and a mass appears in the head, which, if left untreated, tends to resolve spontaneously within 3 weeks. In rarer cases, subperiosteal osteogenesis occurs within the hematoma, and the perimeter of the hematoma begins to mechanize and gradually ossify, resulting in significant local cranial deformity. The incidence of ossification of cranial hematomas has not been reported. The pathogenesis of hematoma formation is not clear and may be related to trauma. The hematoma formation is caused by direct force or shear between the periosteum and the skull due to the compression and pull of the head by the birth canal during prolonged labor and delivery, or the application of delivery aids. The newly formed hematoma is mostly located at the top, with high tension, difficult to push, and a localized mass with obvious fluctuation, confined to the periosteum and skull bone suture attachment. The head position at birth is associated with the occurrence of cranial hematoma. Hartley et al. found that neonates born in the anterior and transverse occipital positions were significantly more likely to develop a cranial hematoma than those born in the posterior occipital position. In contrast, Churchill et al. reported that cranial hematoma did not occur if cesarean delivery was performed before labor was initiated, but hematoma occurred if cesarean delivery was performed after labor was initiated, suggesting that the compression of the fetal head by the birth canal after labor was initiated is closely related to the formation of cranial hematoma. However, it has also been reported that not all cases of cranial hematoma have a history of trauma, and Winter and Petrikovsky et al. have reported cranial hematoma in fetuses without an obvious history of trauma. In our group, four children had a clear history of obstructed labor, prolonged labor, and use of delivery aids, including one case with a history of transient hypoxic asphyxia, one case born after a difficult birth was turned into a cesarean section, and one child born without cranial hematoma who developed after trauma, while the remaining three cases had no clear history of trauma. Therefore, it can be assumed that trauma is the main cause of cranial hematoma, but its pathogenesis cannot be fully explained yet. Fortunately, most of the children do not meet with intracranial injury, but only with cranial lesions. After the formation of a cranial hematoma, the local mass mostly resolves itself within 1 week without leaving any sequelae. In extremely rare cases, the resorption of the hematoma is impaired, and the periosteum, which has been lifted by the hematoma, initiates subperiosteal osteogenesis to form new bone tissue on the surface of the hematoma. Mechanization or ossification of the hematoma first occurs at the edge of the hematoma and gradually extends to the top of the hematoma, with early eggshell-like changes that harden in a few weeks and form bone tissue that protrudes from the normal skull surface, and its thickness seems to be related to the duration of the disease. The shortest duration of the disease in our children was 2 months, with only partial ossification at the top, like an eggshell, and thin walls, and significant ossification at the base. The longest disease duration was 4 years, with local hardness and thickness of about 0.6 cm, and the appearance of deformity was not obvious. The deformed skull was pressed into the skull and the brain tissue was deformed by pressure, and the ossified part was shaped as normal skull in surgery. Histopathological examination of the cyst wall of the inner wall of the ossified hematoma revealed multiple ossification centers and new bone tissue composed of dense fibrous connective tissue. Chung et al. concluded that the development of cranial hematoma occurred without calcification and was mainly an ossification process. However, in this group of cases, focal calcification occurred in addition to fibrous tissue hyperplasia and collagenization of the cyst wall. It is possible that the process of ossification is accompanied by calcification, so some scholars also call this condition “cranial hematoma calcification”. If care is taken to avoid trauma at birth, nearly half of all cranial hematomas can be prevented. If the hematoma does not resorb in 2 weeks, Morgan et al. suggest that aspiration should be performed to remove the hematoma to avoid the possibility of local mass calcification, but local aspiration also has the potential to cause infection. Surgical treatment is indicated after ossification of the hematoma. After ossification has formed, aspiration of its contents in the early stages of ossification does not seem to be effective, and the ossified tissue surrounding the hematoma will still gradually harden and thicken. If the disease is of long duration, ossified hematoma can cause significant deformity of the skull and may even compress the skull and affect the development of brain tissue. We believe that there are two main mechanisms by which the ossified hematoma affects the normal skull beneath it: first, the formation of the ossified hematoma acts as a fixation and restriction of the skull beneath it, preventing it from continuing to extend and augment with the normal growth of the rest of the child’s skull, and second, the direct compression of the cranial plate by the greater tension of the hematoma during the formation of the ossified hematoma. Both forces finally result in a compressive deformation of the skull. The ossified hematoma often protrudes significantly from the surface of the skull, causing cranial asymmetry, and may cause a heavy psychological burden during the growth and development of the child, so surgery should be performed at an early stage in order to relieve the child’s psychological stress, the restriction of brain tissue development by the deformed skull, and for cosmetic reasons. However, if the cranium is significantly compressed, it is necessary to reshape the cranial cover by cutting and reshaping the cranial bone. Resorbable materials are more widely used in cranioplasty because they are more biocompatible and do not remain permanently in the body. Most scholars believe that cranioplasty should be performed when the skull is compressed, but its indications are not clear. In this group of 8 children with obvious cranial compression, 7 cases were given hematoma removal and edge shaping, and a small grinding drill was applied to flatten the protruding hematoma ossification edge to form a continuous curve with the normal skull on both sides, without craniotomy shaping. In one child with obvious cranial compression, the cranial bone was removed and the ossified hematoma parietal part was slightly shaped and placed on the dural surface as a bone covered graft, which avoided surgical operations such as breaking the normal cranial bone, reshaping and titanium alloy fixation, and the shaping result was more satisfactory and cost-effective. All children showed partial improvement of skull depression and satisfactory appearance after long-term follow-up. We believe that, compared with depressed fractures, skull hematoma ossification is a relatively chronic process, and its compression of normal brain tissue is relatively more moderate. Therefore, for most of the infants and children with cranial compression, it is generally not necessary to reshape and reposition the compressed cranial bone after incision, but only to excise the ossified hematoma. In our group, only one case of 8 children was resected and repositioned, and the skull appearance of all children was close to normal. Conclusion Cranial hematoma in children should be prevented, and if it is not absorbed in 3-4 weeks after formation, it should be punctured and aspirated with local pressure bandage. If hematoma ossification is formed, early cranioplasty should be performed.