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Similar to Intracranial hemorrhage newborn
Intracranial hemorrhage newborn
- 3. Incidence varies from 2% to >30% in newborns depends on the gestational age (GA) at birth and the type of ICH Diagnosis typically depends on clinical suspicion The presence and severity of parenchymal injury is the best predictor of outcome
- 4. Rupture of the draining veins and sinuses of the brain molding, fronto-occipital elongation, and torsional forces acting on the head during delivery provoke laceration of dural leaflets of tentorium cerebelli or falx cerebri
- 5. Often results from trauma in the full-term infant SDH in the supratentorial space results from rupture of the bridging veins
- 6. large headsize, rigid pelvis (e.g., in a primiparous or older multiparous mother), nonvertex presentation (breech, face, etc.), very rapid or prolonged labor or delivery, difficult instrumental delivery, or rarely, a bleeding diathesis
- 7. Large collection especially in infratentorial SDH results in rapid deterioration. Systemic signs like hypovolemia and anemia Seizures may occur in up to half of neonates with SDH, particularly with SDH over the cerebral convexity
- 8. suspected on the basis of history and clinical signs and confirmed with a computed tomography (CT) scan. ultrasonic imaging subdural space is inadequate MRI- timing of the lesion and for detecting other lesions Lumbar puncture after CT
- 9. Most infantswith do not require surgical intervention prompt stabilization with volume replacement Open surgical evacuation of the clot in case of large SDH The outcome for infants with nonsurgical SDH is usually good
- 10. Primary SAH is probably frequent but clinically insignificant. normal “trauma” associated with the birth process. sourceof bleeding is usually ruptured bridging veins of the subarachnoid space or ruptured small leptomeningeal vessels
- 11. Usual scenar io i s a w l el appear i ng t er m i nf ant devel opi ng SAH on day 2 or 3 of l i f e
- 12. Clinical presentation is similar to other forms of ICH Thediagnosis is best established with a CT scan or MRI, or by LP to confirm or diagnose small SAH Ultrasonography is not sensitive for the detection of small SAH Management of SAH usually requires only symptomatic therapy, such as anticonvulsant therapy for seizures
- 13. Rare Intracerebral or intracerebellar variety More commonly a secondary event Hypoxic ischemic brain injury, venous infarction or thrombosis, ECMO therapy, large ICH in another compartment
- 14. Presentation and management similar to SDH MRI – extent and age of hemorrhage and other associated parenchymal lesions LP to rule out meningitis Symptomatic management Treatany coexisting pathology or predisposing factors Monitoring for hydrocephalus
- 15. 15-20% at <32 weeks gestation Venous (or sinus)thrombosis and thalamic infarction in term infants Relatedto birth trauma or perinatal asphyxia No identifiable risk factors in 25%
- 16. Intravascular factors • Ischemia/Reperfusion • Fluctuating or increase (Pressure passive circulation) CBF • Increase in cerebral venous pressure • Platelet dysfunction • Coagulation disturbances Vascular factors • Fragile, involuting capillaries with large diameter lumen Extravascular factors • Deficient vascular support • Excess fibrinolytic activity
- 17. Usually a clinically silent syndrome in preterms Term newborns – seizures, apnea, irritability, lethargy, vomiting, full fontanelle Catastrophic presentation less likely Complications
- 18. Routine CUS in all infants born at <32 weeks and in older infants at risk for IVH Days 3,7,30 and 60 days Monitoring for complications Gradingof GMH/IVH is important for determining management and prognosis
- 19. Grading Severity Description Papile (CT) I Isolated GMH (no IVH) II IVH without ventricular dilatation III IVH with ventricular dilatation IV IVH with parenchymal hemorrhage Volpe I GMH with no or minimal IVH (<10% (CUS) ventricular volume) II IVH occupying 10-50% of ventricular area on parasagittal view III IVH occupying >50% of ventricular area, usually distending lateral ventricle Separate Periventricular echodensity notation
- 20. Antenatal steroids Slow infusion of colloid or hyperosmolar solutions Avoidrapid fluctuations in CBF and hypotension Sedativeor paralytic medication in ventilated babies
- 21. Supportivecare andwatch for complications Maintaining Normal BP electrolytes and , blood gases Transfusions as necessary Correctthrombocytopenia and coagulation disturbances
- 22. Supportive care and treatment of seizures Serial LPs and eventual VP shunts Prognosis relates to factors other than IVH alone
- 23. Monitor OFC andfontanelle daily, Serial CUS q2-7 days to assess ventricle size, shape and RI No PVD Slowly Progressive Rapidly progressive Ventricular dilation ventricular dilatation (over weeks) (over days) No further Close surveillance for 2-4 wk treatment Dilatation stops Continued dilatation No therapy, close Serial LP Every 1-3 d, observation for 1 yr depending on rate of ventricular dilatation