INTRAVENTRICULAR HEMORRHAGE Mohammed PGY 2  I IVH is an intracranial hemorrhage that originates in the periventricular subependymal germinal matrix with entrance of blood into by mikeholy

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									INTRAVENTRICULAR
  HEMORRHAGE
     Mohammed PGY-2
   I. IVH is an intracranial hemorrhage that originates in the
    periventricular subependymal germinal matrix with entrance of
    blood into the ventricular system. It is predominantly a disorder
    of preterm infants.
   Early IVH:IVH diagnosed at <72 h after birth
   Late IVH:IVH diagnosed > 72 h of life.

   II. Incidence. The overall incidence of IVH has decreased in
    recent years from 40-60% to ~20% or less in infants weighing
    <1500 g at birth. The incidence and severity of IVH are inversely
    proportional to gestational age. Although cases of prenatal IVH
    have been reported, the "risk period" is during the first 3-4
    postnatal days: ~50% of IVH occurs in the first 6-12 h of life,
    75% by the second day, and 90% by the third day. 10 to 65% of
    infants with early IVH have progression of the hemorrhage, with
    maximal extent occurring within 3-5 days of the initial diagnosis.
                                   Pathogenesis
      A. The germinal matrix (GM) is a weakly supported and highly vascularized area that is
    located between the caudate nucleus and the thalamus at the level of, or slightly posterior to, the
    foramen of Monro. The blood vessels in these areas represent the "watershed" zone of the
    ventriculofugal and ventriculopedal vessels of the immature cerebrum and are prone to hypoxic-
    ischemic injury. These vessels are irregular, with large luminal areas, and are prone to rupture.
    The GM begins to involute after 34 weeks' postconceptional age (PCA).

      B. Fluctuations in cerebral blood flow (CBF) play an extremely important role because sick
    premature infants have pressure-passive cerebral circulation. A sudden rise in systemic blood
    pressure can result in an increase in CBF with subsequent rupture of the GM vessels. Decreases
    in CBF can result in ischemic injury to the GM vessels, which rupture on reperfusion.

      C. The deep venous circulation takes a U-turn in the subependymal region at the level
    of the foramen of Monro. This unique venous anatomy and the open communication between
    the GM vessels and the venous circulation contribute to the importance of increased cerebral
    venous pressure.

     D. Rupture through the GM ependymal layer results in entrance of blood into the lateral
    ventricles. Eighty percent of IVH cases are accompanied by the spread of blood throughout the
    ventricular system.
                      Consequences of IVH
    A. GM is the site of production of neurons and glial cells of the cerebral cortex and basal ganglia.
    GM destruction may result in impairment of myelinization, brain growth, and subsequent cortical development.


      B. Periventricular hemorrhagic infarction is a venous infarction that is associated with severe and
    usually asymmetric IVH in ~85% of cases and invariably occurs on the side with the larger amount of
    intraventricular blood.


      C. PHH is more common in those infants with the highest grade of hemorrhage. It is most frequently
    attributable to obliterative arachnoiditis either over the convexities of the cerebral hemispheres with occlusion
    of the arachnoid villi or in the posterior fossa with obstruction of outflow of the fourth ventricle. Rarely,
    aqueductal stenosis is caused by an acute clot or reactive gliosis.


      D. Periventricular leukomalacia (PVL) is a frequent accompaniment of IVH but is not caused by IVH
    itself. PVL is the ischemic, usually nonhemorrhagic, and symmetric lesion of periventricular white matter
    resulting from hypotension, apnea, and other ischemic events known to decrease CBF. Preterm infants born to
    mothers with prolonged rupture of membranes or chorioamnionitis are at an increased risk for PVL.
                                       Risk factors
     A. Strong risk factors

       1. Extreme prematurity.
        2. Presence of labor (early IVH).
       3. Birth asphyxia (early IVH).
        4. The need for vigorous resuscitation at birth (early IVH).
       5. Pneumothorax.
       6. Ventilated preterm infants, especially those who breathe out of synchrony with the ventilator.
       7. Seizures.
        8. Sudden elevation in arterial blood pressure as in rapid volume expansion and administration of
    hypertonic sodium bicarbonate.

     B. Other antenatal risk factors include heavy cigarette smoking and alcohol consumption,
    chorioamnionitis, use of indomethacin for tocolysis, and ominous fetal heart rate tracing.

      C. Other neonatal risk factors include hypothermia, hypotension, hypercarbia, acidosis, exchange
    transfusion, elevated central venous pressure, "restlessness," PDA, PDA ligation, decreased hematocrit
    resulting in decreased arterial oxygen content, hypoglycemia, heparin use, and disturbances of hemostasis. Even
    those procedures that we perceive as routine in the care of premature infants may also be contributory: tracheal
    suctioning, abdominal examination, handling, and instillation of mydriatics.
                 Classification
   Developed by Papile (developed for CT but, it
    has been applied to ultrasonography)

Grade I: GM hemorrhage
Grade II: IVH without ventricular dilatation
Grade III: IVH with ventricular dilatation
Grade IV: GM hemorrhage or IVH with
 parenchymal involvement.
Images
                Clinical presentation
   The clinical presentation is extremely diverse, and diagnosis
    requires neuroimaging confirmation.
   IVH may be totally asymptomatic, or there may be subtle
    symptoms (eg, a bulging fontanelle, a sudden drop in hematocrit,
    apnea, bradycardia, acidosis, seizures, and changes in muscle
    tone or level of consciousness).
   Catastrophic syndrome is characterized by rapid onset of
    stupor or coma, respiratory abnormalities, seizures, decerebrate
    posturing, pupils fixed to light, eyes fixed to vestibular
    stimulation, and flaccid quadriparesis.
                                                 Diagnosis

      A. Ultrasonography is the procedure of choice for screening and diagnosis.
        Sonograms are done via the anterior fontanelle. If normal sized ventricles, scanning through the posterior fontanelle may
    increase the rate of detection of IVH. Although CT scanning and MRI are acceptable alternatives, they are more expensive and
    require transport from the intensive care unit to the imaging device.

        Indications
           a. All infants with birth weight <1500 g.
           b. Larger infants, if risk factors are present or if there is evidence of increased ICP or hydrocephalus.

        Obtained on the first day of life in selected infants with risk factors for early IVH because 50% of cases of IVH occur during
    the first 6-12 h of life. And some also obtain a sonogram, CT, or MRI before discharge or at 36 weeks' PCA
         A scan obtained at 4-7 days of life will detect 90-100% of all hemorrhages.

       Periventricular white matter injury (detected as intraparenchymal echodensities [IPEs]) and PHH may be detected on
    scans obtained at 2 weeks of life.

      B. Laboratory studies
         LP. Examination of CSF is normal in up to 20% of infants with IVH. Initially elevated red and white blood cells, with
    elevated protein concentration. The degree of elevation of CSF protein correlates with the severity of the hemorrhage. Sometimes
    difficult to distinguish IVH from a "traumatic tap." A few days after hemorrhage, the CSF becomes xanthochromic, with
    decreased glucose. Often, the CSF shows a persistent increase in white blood cells and protein and a decreased glucose level,
    making it difficult to rule out meningitis except by negative cultures.

        Elevated counts of absolute nucleated erythrocytes beyond day 1 of life may be a marker for impending or existing
    severe IVH.
                                            Management
     A. Prenatal prevention

        1. Avoidance of premature delivery.

        2. Transportation in utero.

        3. Active labor may be a risk factor for early IVH and that there may be a protective role for cesarean (C-) section. Studies
    have shownC-section before the active phase of labor resulted in a lower frequency of severe IVH and of progression to severe
    IVH, although it did not affect the overall incidence of IVH.

         4. Tocolysis using indomethacin probably should be avoided because it has been associated with an increased rate of
    necrotizing enterocolitis, IVH, PDA, respiratory distress syndrome (RDS), and bronchopulmonary dysplasia.

         5. Antenatal pharmacologic interventions
           a. Antenatal steroids. Several large, trials have shown a clear efficacy of antenatal steroids in reducing IVH.

           b. Phenobarbital. Clinical trials from the early 1990s strongly suggested an overall reduction in the total incidence of IVH
    in preterm infants. However due to newer studies, currently, antenatal phenobarbital is not recommended for prevention of IVH.
   B. Postnatal prevention

        1. Avoid birth asphyxia.
         2. Avoid large fluctuations in blood pressure.
        3. Avoid overly rapid infusion of volume expanders or hypertonic solutions.
        4. Use prompt but cautious cardiovascular support to prevent hypotension.
        5. Correct acid-base abnormalities.
         6. Correct abnormalities of coagulation.
        7. Avoid poorly synchronized mechanical ventilation.
         8. Blood sampling from umbilical arterial catheters (UACs) produces fluctuations
    in CBF velocity and may contribute to IVH.
         9. Surfactant therapy may cause a transient increase in CBF velocity and
    cerebral blood volume as well as electroencephalographic depression, but the effects
    are generally not marked.      10. Postnatal pharmacologic interventions may be
    considered. None of the following regimens have been definitively proven to be safe
    and effective.
           a. Indomethacin. Indomethacin prophylaxis for IVH highly controversial.
           b. Pancuronium Is not currently recommended for the prevention of IVH
           c. Vitamin E. The timing, dosage, and route remain controversial.
        Management of acute hemorrhage

        1. General supportive care to maintain a normal blood volume and a stable acid-base status.

        2. Avoid fluctuations of arterial and venous blood pressures.


        3. Follow-up serial imaging (ultrasonography or CT scanning) to detect progressive hydrocephalus.


   D. Prevention of PHH


        1. LPs. Several randomized controlled trials of infants with IVH failed to show a difference between
    infants undergoing LPs with supportive care and those receiving supportive care only.


        2. Intraventricular fibrinolytic therapy (tissue-type plasminogen activator, urokinase, and
    streptokinase). Data from preliminary studies are encouraging, but further studies are needed. The CSF
    plasminogen level is lower in neonates with IVH than in those without hemorrhage, and the potential for
    intraventricular fibrinolytic treatment may be limited by low concentrations of plasminogen.
                       Prognosis and outcome
      A. Short-term outcome is related to the severity of IVH, with a mortality rate and PHH rate of 5-10% and 5-20%,
    respectively, for infants with mild to moderate IVH; 20% and 55%, respectively, for infants with severe IVH (blood filling the
    ventricles); and ~50% and ~80%, respectively, for those with severe IVH and parenchymal involvement.

      B. Long-term major neurologic sequelae depend primarily on the extent of associated parenchymal injury, ranging
    from 5-15% in infants with minor degrees of hemorrhage to 30-40% in infants with severe hemorrhage, and as high as 100% in
    those infants with parenchymal involvement.

       1. Markers for poor prognosis include severe IVH, persistent or transient cerebral ventriculomegaly, persistent or transient
    IPEs, cystic PVL, and cranial midline shift.

        2. The incidence of major motor and cognitive deficits is markedly increased in infants with extensive IPEs compared
    with that in infants with localized IPEs.

         3. Resulting motor deficits correlate with the topography of the IPEs and usually manifest as either spastic hemiparesis or
    asymmetric spastic quadriparesis. Longitudinal studies have shown that there can be significant motor recovery in the first 2 years
    of life, especially in infants with grades III-IV IVH.

        4. Visual impairment can result from ventriculomegaly or from extensive periventricular white matter loss with
    involvement of the striate and parastriate cortex.

        5. Hearing impairment can result from injury to the auditory radiations.

        6. Children who were at high risk for IVH should be assessed periodically until school age because some studies have shown
    an increased risk of disability at 5-8 years of age in children who had no hemorrhage or minor hemorrhage.
             Markers Better Prognosis

          a. A less severe grade of IVH.

           b. A normal sonogram at discharge from the neonatal
    intensive care unit (NICU).
           c. Absence of ventricular dilation.

          d. Absence of periventricular white matter injury.

          e. Shorter neonatal hospitalization.

          f. Higher social and environmental status.

								
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