Intraventricular hemorrhage

1. INTRAVENTRICULAR HEMMORHAGE Dr zulfiqar butt

2. DEFINITION Intracranial hemorrhage that originates in periventricular sub ependymal germinal matrix with subsequent entrance of blood into the ventricular system. EARLY IVH: IVH develop within 72hrs after birth. LATE IVH: IVH develop after 72hrs of life.

3. EPIDEMIOLOGY The overall incidence has decreased over the past decades as a result of improved perinatal care. Incidence and severity is inversely proportional to gestation age and birth weight 30 percent premature infants less than 1500 grams may develop IVH. 7 % of 1 kg to 1.5 kg 14 % of 750 to 1000 grams 24% of less than 750 grams infants develop severe IVH(grade 3 or 4).

4. PATHOGENESIS IVH in preterm occurs in sub ependymal germinal matrix This is located between caudate nucleus and the ependymal lining of the lateral ventricle This area is site of origin of embryonal neurons and fetal glial cells This area is highly vascularized and weakly supported The blood vessels in this area are immature and are prone to hypoxic ischemic injury

5. CONTINUED: Fluctuation in cerebral blood flow play an important role in developing IVH. A sudden rise in systemic blood pressure may result in an increase in cerebral circulation with subsequent rupture of the germinal matrix vessels. Decreases in cerebral blood flow can result in ischemic injury to germinal matrix vessels, which rupture on re-perfusion.

6. RISK FACTORS Prematurity is the most important risk factor for IVH. Rapid volume expansion Hypertension Coagulopathies Hypoxic-ischemic insults Respiratory disturbances Acidosis Infusions of hypertonic solutions Anemia Vacuum-assisted delivery Frequent handling Tracheal suctioning

7. Clinical Features IVH may be totally asymptomatic (especially in some cases of grade I & II IVH hemorrhage) or there may be subtle symptoms. e.g. Apnea Bradycardia Acidosis Cutaneous mottling A bulging fontanel High pitched cry Absent Moro reflex

8. 8) Seizures 9) A sudden drop in hematocrit 10) Failure to suck well 11) Change in muscle tone or level of consciousness In large IVH, there may be: Rapid onset of coma Seizures Decerebrate posturing Pupils fixed to light Respiratory irregularities.

9. DIAGNOSIS Intraventricular hemorrhage is diagnosed on the basis of : History Clinical manifestations cranial ultrasonography or CT scan

10. continued: The clinical signs of IVH are non specific , so therefore , it is recommended that cranial ultrasound should be done in premature infants <32 week of gestation . Infants <1000g are at highest risk and should undergo cranial ultrasonography within, first 3-7 days of age after birth.

11. GRADING OF IVH Severity of hemorrhage may be defined on CT Scan. Grade I:Isolated germinal matrix hemorrhage Grade II: IVH without ventricular dilatation Grade III: IVH with ventricular dilatation Grade IV : There is IVH and parenchymal hemorrhage.

12. Another grading system describes 3 levels of IVH detected on ultrasound. Grade-I: bleeding is confined to the germinal matrix – sub ependymal region or to <10% of the ventricle Grade-II: Defined as IVH bleeding with 10-50% filling of the ventricle. Grade-III: >50% of the ventricle is involved with dilated ventricles.

13. PREVENTION ANTENATAL PREVENTION Avoid preterm delivery VIT k should be given before delivery to all women receiving phenobarbitone or phenytoin during pregnancy C section of high risk deliveries A single course of antenatal corticosteroids is recommended in pregnancies 24-34 weeks of gestation that are at risk for preterm delivery

14. POSTNATAL PREVENTION Avoid birth asphyxia Avoid large fluctuation in blood pressure Avoid excessive handling Avoid rapid infusion of volume expander or hypertonic solutions Correct acid base balance Correct coagulation abnormalities Prophylactic administration of low dose indomethacin (0.1mglkglday) for 3 days, reduces the incidence of severe IVH.

15. COMPLICATION OF IVH Posthemorrhagic Hydrocephalus Seizures Irreversible brain damage Shock Death

16. MANAGEMENT OF IVH N o specific treatment is available for IVH, it may be associated with other complications that require therapy. Maintain ABC. Seizures are aggressively treated with anticonvulsant drugs Anemia and coagulopathies requires transfusion with packed red blood cells or fresh frozen plasma. Shock and acidosis are treated with slow administration of sodium bicarbonate and fluid resuscitation.

17. CONTINUED: Follow up serial imaging (Cranial USG or CT Scanning) to detect progressive hydrocephalus. Insertion of a ventriculoperitoneal shunt is the preferred method to treat progressive and symptomatic post-hemorrhagic hydrocephalus. Serial lumbar punctures, diuretics, and acetazolamide have no role in the management of posthemorrhagic hydrocephalus.

18. PROGNOSIS There are no death as a result of grade I and II hemorrhage, whereas grade III and IV hemorrhage carry a mortality rate of 10-20 %. Post hemorrhagic hydrocephalus is rarely seen in grade I hemorrhage but is seen in 54-87 % of grade II-IV hemorrhage

19. CONTINUED: The degree of IVH and the presence of PVL are strongly linked to neuro developmental impairment . For infants less than 1000 gms the incidences of severe neurologic impairment are about: 40% infants with grade 1 IVH 50% infants with grade 2 IVH 55% infants with grade 3 IVH 70% infants with grade 4 IVH

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