Intracranial hemorrhage in newborns

Cranial hemorrhage includes all bleeding lesions of the nervous system act conditioned by birth (obstretical trauma), cerebral hypoxia or hemorrhagic syndrome of the newborn. Frequently cause permanent neurological sequelae.
Intracranial hemorrhage may have different locations and classifications of them causing hemorrhage: the germ matrix and ventricles, the posterior fossa (subdural hemorrhage), subarachnoid hemorrhage, bleeding in the brain parenchyma.Bleeding in the brain ventricles and germ matrix is ​​the most common form of intracranial hemorrhage and occurs almost exclusively in premature babies.
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 on the first day of life and 90% in first 4 days postnatally.
Pathophysiology:
The starting point of germinal matrix hemorrhage is subependimara - instead of glial cells and neuronal proliferation in the first two trimesters of pregnancy. At 25 weeks gestation most neurons in the cortex are formed, axono-dendritic tree is up and begin to form synapses. Matrix germ is rich blood supply, and contains large vessels, irregular, with poor organization of the membrane protein or glial support. Bleeding may remain localized in the matrix germ, or may extend to the lateral ventricles.The size and exact location of bleeding is determined by gestational age. In the first trimester of pregnancy bleeding body extends from head to tail nuclei, the foramen Monro. With increasing age of gestation bleeding is reabsorbed, that time is completely missing in most cases. The term infant may present a residual germ matrix that occasionally can be the origin of ventricular bleeding, among other sources of intraventricular hemorrhage in term newborn, such as venous thrombosis and choroid plexuses.Effective self-regulation increases cerebral blood flow with gestational age. Thus, the developing brain is susceptible to ischemia during disturbances both hypotensive and haemorrhage during disturbances in hypertensive patients. It seems that the choroid plexus haemorrhage is due to the limited capacity of cerebral blood flow autoregulation. Despite the primitive cells in the germinal matrix remain active up to 32-34 weeks of gestation and is an area with increased vascularization, the risk of bleeding is 4-5 days of life.
Etiology:
Intraventricular hemorrhage is caused by several factors associated with acute onset of bleeding: too vigorous resuscitation, respiratory distress syndrome, hypoxemia, acidosis, administration of bicarbonate, pneumothorax, seizures.
Of intravascular factors include: fluctuations in cerebral blood flow, increased cerebral blood flow, decreased cerebral blood flow, platelet and clotting disorders, this ductus arteriosus. Other etiologic agents include: apnea, seizures, handling of the newborn, infusion solutions hiperosmotice, hypertension, and ECMO, congestive heart failure, pneumothorax, birth.
Vascular factors include: the integrity of the vascular tunics, involution of germinal matrix vessels normal, relatively high blood flow to deep brain structures (in the second quarter and third of pregnancy), hypoxic-ischemic insult in germ matrix and vessels.
Extravascular factors are: support weak vessels perivascular matrix germ, this fibrinolytic enzymes, this bleeding diatheses.
Classification:After intraventricular hemorrhage affected area is classified in three grades: Grade I-matrix hemorrhage in germ and / or minimal intraventricular hemorrhage (less than 10% of the ventricular section parasagitala) grade II intraventricular hemorrhage less than 50% of the ventricular; grade III intraventricular hemorrhage more than 50% of the ventricular surface.
Another popular classification: grade I-subependimara hemorrhage, grade II intraventricular hemorrhage 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 4 and even up to the 21st.In 50-75% of cases are silent, although children may hemorrhage 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: bulging fontanelle, hypotonia, excessive sleepiness, temperature instability, apnea, jaundice or excessive pallor.
Diagnosis:
Dagnosticul put on clinical examination and laboratory.Of laboratory examinations should be done transfontanelara ultrasound on day 3 or 4 of life, followed by a 2nd ultrasound to 7 days to establish the extent of bleeding. Moreover, if severe clinical phenomena echography should be performed weekly to monitor ventricular size. Ultrasonography can identify the full spectrum of severity of bleeding, the bleeding isolated in major bleeding with large parenchymal destruction. Ultrasound can also view the two major complications of intraventricular hemorrhage: periventricular hemorrhagic infarction and posthaemorrhagic ventriculomegalia (periventricular leukomalacia).
Blood picture reveals decreased hematocrit (Ht) and hemoglobin (Hb) to about 75% of children without clinical symptoms and thrombocytopenia with prolongation of 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 to perform lumbar puncture is emphasized with hemorrhagic fluid proteinorahie 1, 5 g% o

Complications:May be complicated by intraventricular hemorrhage: germinal matrix destruction with secondary cystic organization, periventricular leukomalacia, hydrocephalus posthaemorrhagic, periventricular haemorrhage and 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 transporting the newborn after birth may influence later neuologic status.Administration of betamethasone 48 hours before birth would seem to have direct consequences on diminishing the incidence of intraventricular haemorrhage.The use and tocolysis with magnesium sulfate.
Depending on the aggressiveness of therapy also provides intravascular factors: prevention or correction of major hemodynamic disorders including cerebral flow fluctuations and increased cerebral venous pressure with a great value in reducing the incidence of bleeding.Pharmacological agents used are: phenobarbital, indomethacin, vitamin K, fresh frozen plasmaDepending on use etamsilatul vascular factors and vitamin E.Depending on extravascular factors used prolactin.