Intracranial hemorrhage in newborns

Intracranial hemorrhage in newborns

    * Introduction
    * Subdural hemorrhage
    * Primary subarachnoid hemorrhage
    * Hemorrhage primary intracerebeloasa
Intracranial hemorrhage include hemorrhagic lesions of the nervous system all conditioned by the act of birth (obstetrical trauma), cerebral hypoxia or hemorrhagic syndrome of the newborn. Common cause permanent neurological sequelae.
Intracranial hemorrhage may have different locations and classifying them causing hemorrhage: the germinative matrix and the ventricles, the posterior fossa (subdural hemorrhage), subarachnoid hemorrhage, bleeding in the brain parenchyma. Bleeding in the brain ventricles and germinative matrix is the most common form of intracranial hemorrhage and occurs almost exclusively in premature infant.
Intraventricular hemorrhage
This type of bleeding occurs in approximately 25-30% of children weighing less than 1500 grams and gestational age below 32 weeks. In 50% of cases bleeding occurs in the first days of life and 90% of cases within 4 days postnatally.
Pathophysiology:
The starting point is the matrix of germline subependimara bleeding - place of glial proliferation and neuronal cells in the first two trimesters of pregnancy. At 25 weeks of gestation the majority of neurons in the cortex are formed, axono-dendritic tree is up and begin to form synapses. Germ is rich matrix containing large vessels and blood supply, irregular, with a poor organization of membrane protein or glial support. Bleeding may remain localized in the matrix germination, or it may extend to the lateral ventricles. The size and exact location of bleeding is determined by the age of gestation. In the first trimester of pregnancy bleeding body extends from the head of caudate nucleus, the foramen Monro. With increasing age of gestation bleeding is reabsorbed, that time is completely lost in most cases. In the newborn period may present a residual germ matrix that occasionally can be the origin of ventricular bleeding, among other sources of intraventricular hemorrhage in the newborn period, as the choroid plexus and venous thrombosis. Efficient self-regulation, cerebral blood flow increases with gestation age. Thus, the developing brain is susceptible to ischemia during disturbances both hypotensive and hypertensive bleeding during disturbances. It seems that the choroid plexus hemorrhage is due to the limited capacity of cerebral blood flow autoregulation. Despite matrix primitive germline cells remain active until 32-34 weeks of gestation and is an area with increased vascularization, the risk of haemorrhage is 4-5 days of life.
Etiology:
Intraventricular hemorrhage is caused by a number of factors associated with acute onset of bleeding: too vigorous resuscitation, respiratory distress syndrome, hypoxemia, acidosis, bicarbonate administration, pneumothorax, seizures.
Of intravascular factors include: fluctuations in cerebral blood flow, increased cerebral blood flow, decreased cerebral blood flow, platelet and coagulation disorders, this ductus arteriosus. Other etiologic agents include: apnea, seizures, handling of the newborn, hiperosmotice infusion solutions, and ECMO hypertension, congestive heart failure, pneumothorax, birth.
Vascular factors include: the integrity of the vascular coats, normal involution of germinal matrix vessels, relatively high blood flow to deep brain structures (in the second and third trimester of pregnancy), hypoxic-ischemic insult in germ matrix and vessels.
Extravascular factors include: weak perivascular support vessels germ matrix, this fibrinolytic enzymes, this bleeding diatheses.
Classification: After intraventricular hemorrhage affected area is classified in three grades: Grade I-matrix hemorrhage in germination and / or minimal intraventricular hemorrhage (less than 10% of ventricular area in section parasagitala), grade II intraventricular hemorrhage less than 50% of the surface ventricular, intraventricular hemorrhage grade III more than 50% of the ventricular surface.
Another popular classification: grade I-subependimara hemorrhage, grade II intraventricular haemorrhage without dilatation, grade III intraventricular hemorrhage with dilation, grade IV intraventricular hemorrhage with dilation and parenchyma.
Clinical signs:
Clinical manifestations may occur in the first zilede life from the 4 and even up to the 21th. In 50-75% of cases are silent, although children may be hemorrhage of grade III or IV. Another manifestation is the catrastrofala with impaired general condition, severe respiratory distress, hypotonia, lethargy, shock, convulsions, coma. Usually these children die. Other specific signs of pathology: a bulging fontanelle, hypotonia, excessive sleepiness, thermal instability, apnea, jaundice or excessive pallor.
Diagnosis:
Dagnosticul put on clinical and paraclinical examination. Of Trans ultrasound examinations should be done in the laboratory on the 3rd or 4th life, followed by a 2nd ultrasound to 7 days to establish the extent of bleeding. Moreover, if severe clinical phenomena ultrasound should be performed weekly to monitor ventricular size. Ultrasonography can identify the full spectrum of severity of haemorrhage, major bleeding Destruction isolated parenchymal bleeding lay. Ultrasound can also view the two major complications of intraventricular hemorrhage: periventricular hemorrhagic infarction and posthemoragica ventriculomegalia (periventricular leukomalacia).
Blood picture reveals decreased hematocrit (Ht) and hemoglobin (Hb) to about 75% of children without clinical symptoms, and thrombocytopenia, with prolonged PT and TPT. Acid-base balance is altered in favor of metabolic acidosis. Monitoring of blood gas shows: hypoxemia, and respiratory acidosis hipercarbie. Hyperbilirubinemia is present and the lumbar puncture is distinguished performance liquid proteinorahie bleeding with 1, 5 g% o

Complications May be complicated by intraventricular hemorrhage: germinal matrix destruction with secondary cystic organization, periventricular leukomalacia, hydrocephalus posthemoragica, hemorrhage and periventricular infarction.
Treatment:
Prophylactic treatment is ideal. Primordial is to avoid premature labor and birth, if it can not be avoided is preferred infant in utero transport to a specialized center of Perinatology, because transport of newborn after birth can influence later neuologic status. Administration of betamethasone 48 hours before birth is thought to be direct consequences to decrease the incidence of intraventricular hemorrhage. The resort and magnesium sulfate tocolysis.
Depending on the aggressiveness of therapy also provides intravascular factors: the prevention or correction of major hemodynamic disorders including cerebral flow fluctuations and increased cerebral venous pressure with a special value in reducing the incidence of bleeding. Pharmacological agents used are phenobarbital, indomethacin, vitamin K, fresh frozen plasma Depending on use etamsilatul vascular factors and vitamin E. Depending on the factors utilized extravascular prolactin.