Late onset vitamin K deficiency intracranial hemorrhage

Intracranial hemorrhage due to late-onset vitamin K deficiency Intracranial hemorrhage has a high mortality and disability rate, and survivors often have varying degrees of neurological sequelae. The common causes of intracranial hemorrhage include late-onset VitK deficiency (VKD), cerebrovascular malformation and craniocerebral trauma, etc. VKD, also known as Vit K-dependent hemorrhage, develops after 8 days of life and is called late-onset VKD, which is more common and is briefly described as follows: 1. Epidemiology The peak age of onset of the disease is 4-8 weeks after birth, 89% of exclusively breastfed children, 92% of children with intracranial hemorrhage; more in rural than urban areas. More than urban. Often with infection. Late onset VKD is the main cause of intracranial hemorrhage in infants aged 1 to 6 months. Subdural hemorrhage, subarachnoid hemorrhage and cerebral parenchymal hemorrhage are the common sites of intracranial hemorrhage, and the mortality rate of the disease is 19%-33%, and 21%-67% of patients are left with neurological sequelae. 2. Etiology VitK deficiency is the direct cause of this disease. Infants <3 months of age, exclusive breastfeeding, cytomegalovirus (CMV) infection, diarrhea, and abnormal liver function have been reported as high-risk factors for intracranial hemorrhage from VKD. 3. Symptoms Most children with late onset VKD causing intracranial hemorrhage are healthy before the disease and are mostly breastfed with sudden onset. The child has progressive pallor, fever or temperature does not rise, and the extremities are cold. Sudden onset of acute or subacute intracranial pressure increase and disorders of consciousness, manifested as vomiting, restlessness or screaming, disorders of consciousness or even coma; irregular breathing, convulsions, full fontanelle or cranial suture splitting; severe cases of unequal pupils, weakening or loss of light reflex; children may show brain herniation. Other parts of the bleeding are: skin and mucous membrane bleeding, nasal bleeding, gastrointestinal bleeding, injection or puncture site bleeding more than. 4, laboratory tests: peripheral blood cell count may have anemia, and infected patients can have elevated white blood cells, platelets are generally in the normal range. Coagulation function tests: bleeding time and prothrombin time are normal, coagulation time is mostly prolonged, activated partial thromboplastin time and prothrombin time are prolonged, and fibrinogen is normal. Lumbar puncture or lateral ventricular puncture may have bloody cerebrospinal fluid. 5. Prognosis The prognosis of brain parenchymal hemorrhage and multi-location hemorrhage is the worst. The neurological damage caused by intracranial hemorrhage from late-onset VKD is mainly due to secondary cerebral hypoxia-ischemia and cerebral infarction. The neurological localization of the hemorrhage site, the amount of hemorrhage, the speed of hemorrhage and the duration of compression of brain tissue determine the corresponding clinical manifestations. Long-term follow-up of the disease reveals that children with severe hemorrhage mostly have sequelae such as limb paralysis, cerebral palsy and epilepsy and intellectual abnormalities; the incidence of microcephaly and intellectual abnormalities is 45% and 50%, respectively. Prevention The prognosis of this disease is poor, but prevention is simple. Therefore, all newborns should be routinely given vitamin K after birth, and infants under 3 months of age who are breastfed should be routinely given vitamin K to prevent this disease when they are seen for any illness.