INTRAVENTRICULAR HEMORRHAGE

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INTRAVENTRICULAR HEMORRHAGE

• Mohammed PGY-2

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• 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 IVHIVH diagnosed at lt72 h after birth
• Late IVHIVH diagnosed gt 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 lt1500 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.

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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.

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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.

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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.

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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.

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Images
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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.

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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 lt1500 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.

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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.

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• 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. 

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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.
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• 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.   

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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.

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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.