Intracranial hemorrhage is well known and frequent in the neonatal period, and four types are generally reported: subarachnoid hemorrhage, intracerebral hematoma, intraventricular hemorrhage, and subdural hematoma. In 1894 Charles Townsend originally described the syndrome of neonatal cerebral hemorrhagic disease, which generally occurs on days 1-5 after birth in newborns with hemophilia. Vitamin K is an important fat-soluble vitamin that was discovered by Danish biologists in 1929, and is the first letter of the word “blood clotting”. There are two types of vitamin K: K1 and K2, K1 comes from plant or vegetable oils and is absorbed in the small intestine, depending on the presence of bile salts; K2 is synthesized by the intestinal flora. Vitamin K1 does not readily cross the placenta, and its concentration in maternal blood does not exceed 10%, so that the newborn receives very small amounts from the mother’s blood at the time of birth. Blood levels of the coagulation system will gradually decrease during the first 1-2 weeks of life and will not return to normal levels until 6 weeks – 6 months. Coagulation factors II, VII, IX and X in the body are dependent on vitamin K. Neonatal vitamin K deficiency hemorrhage can be divided into three types according to the time when the bleeding occurs after birth: early vitamin K deficiency hemorrhage (bleeding that occurs within 24 hours after birth), typical vitamin K deficiency hemorrhage (bleeding that occurs 2-7 days after birth), and late vitamin K deficiency hemorrhage (bleeding that occurs one week after birth). bleeding). It has been reported that more than 50% of delayed vitamin K deficiency hemorrhages are intracranial hemorrhages. Therefore, we studied 43 cases of children admitted to our hospital from 2009 to 2011, and we report them as follows: I. General information and methods. All the cases in this group were full-term births, gestational age at birth ≥ 37 weeks, and age at birth within 1 month. 29 of the 43 cases were male and 14 were female; the age interval ranged from 1 day-4 weeks (mean 20, 4 ± 4, 9 days); so the children were born spontaneously, with no history of forceps and fetal suction, no history of trauma, no record of drug use, and no family history of hemorrhage. The child presented with acute neurological symptoms, especially seizures, and a specific state of lethargy. Emergency cranial CT examination revealed intracranial hemorrhage. Laboratory tests showed prolonged PT and APTT (excluding anemia and platelet abnormalities), and the APTT improved significantly 6-12 hours after receiving vitamin K therapy. The diagnosis of vitamin K deficiency relied mainly on the severely abnormal PT and APTT, and normal PT and APTT could be obtained after vitamin K treatment. The diagnosis and staging of intracranial hemorrhage relied on CT examination, and surgical treatment was based on the clinical manifestations and imaging of the children, and all children were treated with antiepileptic treatment with phenobarbital. dehydration therapy, 9 children were given acetazolamide to reduce cerebrospinal fluid secretion, 31 patients required ventilator ventilation therapy, and 25 children required dobutamine to maintain blood pressure. II. Results. The age at presentation of symptoms was 20,4±4,9 days, with a male ratio of 2,07:1 (29:14). Neurological symptoms included seizures, irritability and impaired consciousness, anterior fontanelle tension, progressive cranial enlargement, bilateral “sunset signs”, irritability, diminished or absent neurological reflexes, and muscle spasms or hypotonia. The general clinical picture also includes pallor, respiratory distress, lethargy or irritability, and bleeding at other sites. The mean PT of the child before the administration of vitamin K was 72,1±45,0 seconds and the APTT was 112,4±57,6. The PT was 14,6±1,6 seconds and the APTT was 34,4±1,0 seconds when retested 6-12 hours after vitamin K treatment. The hemoglobin level was 7,8±2,5 g/dl (fluctuating range 3,5-12,3 g/dl). 3 cases had early vitamin K deficiency hemorrhage, 11 cases had typical vitamin K deficiency hemorrhage, and 29 cases had late hemorrhage. All children underwent cranial CT examination, which revealed acute subdural hematoma in 24 cases, intracerebral hematoma in 11 cases, and acute subdural hematoma with intracerebral hematoma, intraventricular hemorrhage and/or subarachnoid hemorrhage in a total of 8 cases. All infants were treated with vitamin K at 1 mg per kg body weight intramuscularly, 12 (27,9%) were given fresh frozen plasma infusion, and 24 (55,8%) were given red blood cell therapy to correct anemia. All children underwent surgical removal of the intracranial hematoma after correction of PT and APTT with free bone flap or with bone flap. Postoperatively, 8 children died, and 35 children developed different degrees of neurological deficits during the subsequent follow-up, including 7 cases of hydrocephalus, 16 children with residual seizures, 7 cases of limb movement disorders, and 5 cases of vegetative survival. III. Discussion. Intracranial hemorrhage in neonates, especially subdural hemorrhage, has a high mortality and disability rate. The coagulation activity of neonatal blood is only 20-25% of that of adults, and lack of vitamin K supplementation after birth, exclusive breastfeeding, chronic diarrhea, and the application of antibiotics can lead to vitamin K deficiency hemorrhage in infants. There are three types of vitamin K deficiency hemorrhage, namely 1 early type 2 typical type 3 and late type. The early type occurs within the first 24 hours of life and is commonly associated with prolonged and regular use of certain drugs during maternal pregnancy, such as antiepileptic drugs (barbiturates, phenytoin sodium), anti-tuberculosis drugs (rifampin), and antagonistic drugs of vitamin K. All three children underwent surgery to remove the intracranial hematoma, and two died, presumably due to high intracranial hemorrhage and low preoperative GCS scores. Typical vitamin K deficiency hemorrhage occurs 2-7 days after birth and is mainly due to the lack of vitamin K intake after birth, with a low mortality rate. Hemorrhage often occurs in the gastrointestinal tract, skin and intracranially. Nine (20,9%) of our cases belonged to this type, and all nine children were given vitamin K supplementation after birth, and two of them died due to severe gastrointestinal bleeding. Delayed vitamin K deficiency hemorrhage occurs after the first week of life, with a higher incidence of intracranial hematoma in this type of child, and another common feature is widespread profound petechiae or nodular petechiae. This type of hemorrhage has also been reported to be associated with severe hepatic impairment, particularly cholestatic liver disease. Thirty-one of our cases (72,1%) belonged to this type, and two of the children presented with biliary atresia and died of rapid liver failure soon after surgery. The clinical manifestations of intracranial hemorrhage in neonates are not specific and several manifestations are the most dominant (e.g., strong grip, fever, reduced state of consciousness, generalized hypotonia, increased intracranial pressure). hanigan [] et al. reported that the most common clinical manifestations of intracranial hemorrhage in neonates within the first 2 days of life were seizures, respiratory distress, and asphyxia in 24 of 33 infants (72%). Another study [] [showed that the most common clinical manifestations were pallor (77,4%), seizures (58%), altered state of consciousness (58%), vomiting (44%), and nausea (35%). The anterior fontanelle fluctuated in 61% of cases while the fontanelle was elevated in 26%, and seven children (22.5%) had been on antibiotics. In a more recent study, the initial clinical manifestations of intracranial hemorrhage were seizures in 11 cases (46%), pallor in 7 cases (29%), shortness of breath in 5 cases (21%), fever in 1 case (4%), failure to increase body temperature in 1 case (4%), and dyspnea in 1 case (4%). These findings are consistent with the present findings. Symptoms of anemia were also present in more than half of the children with intracranial hemorrhage at term in this group of cases. Anemia or hematologic abnormalities often suggest internal bleeding, including intracranial hemorrhage, the most frequent of which is a subdural hematoma. In some cases subdural hematomas within the skull are considered when no clear etiology for the anemia can be found. Therefore, anemia in full-term newborns can often alert the physician to the possibility of intracranial hemorrhage in the child. A recent study showed that the most common form of intracranial hemorrhage was acute subdural hematoma (56,3%), followed by intracerebral hematoma (31,3%) and multisite hemorrhage (12,5%). In our study, all children were supplemented with vitamin K preoperatively and anemia was corrected if present. Fresh frozen plasma contains all the clotting factors and is recommended for transfusion in children with vitamin K deficiency bleeding. The usual dose of transfusion is 10-20 ml per kilogram of body weight every 12-24 hours depending on the clinical condition, of course in combination with dehydrating drugs for intracranial hypertension. Early craniotomy or minimally invasive surgery is performed to remove intracerebral or subdural hematomas. For complex cases of intracranial multisite hemorrhage Zhang Jian et al. used multipoint puncture and drainage method can rapidly reduce intracranial hypertension, that is, to relieve the high-risk state, which is of some significance to save the child and improve the prognosis. For intracranial hematoma Liang et al. believe that the amount of bleeding >30ml and confined, with obvious occupying effect, the hematoma should be removed by craniotomy. The prognosis of children with vitamin K deficiency hemorrhage depends on early diagnosis, rapid and adequate correction of coagulation defects, the general condition of the patient, and anemia realization and surgical and early intervention. It has been shown that symptomatic neonates with intracranial hemorrhage exhibit a low mortality rate (11%) at the subsequent 3-year follow-up, but neurological deficits remain in the survivors. Our study revealed a higher incidence of sequelae in survivors. Jhawar et al. followed a group of children with intracranial hemorrhage and found that 80% of children with acute subdural hemorrhage had no sequelae in mental and limb movement, whereas children with subarachnoid hemorrhage or multiple forms of intracranial hemorrhage had a poorer prognosis. The prognosis of our five children with multiple forms of intracranial hemorrhage was not favorable. Vitamin K deficiency hemorrhage is quite threatening in newborns, but the disease is completely preventable, as safe and inexpensive as immunization, so all injections of vitamin K should be recommended for newborns to prevent the disease. There is evidence that intramuscular injection of vitamin K is more effective than oral administration, and if one dose of intramuscular injection is sufficient, more than three doses may be required for oral administration. IV. Conclusion. Vitamin K deficiency hemorrhage, especially late hemorrhage, is the most important cause of intracranial hemorrhage in newborns. The most common type of intracranial hemorrhage is subdural hematoma, and focal seizures, impaired consciousness, anterior fontanelle tension, unexplained anemia, and respiratory distress are the predominant clinical manifestations, although early surgical treatment of children has a high mortality rate and most survivors are left with neurological deficits. Application of vitamin K at birth may reduce the incidence of this disorder.