Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Intracranial hemorrhage newborn


Published on

  • Can you provide me with any citations or other information on the prevalence and clinical insignificance of Subarachnoid hemorrhage in newborns?
    Are you sure you want to  Yes  No
    Your message goes here

Intracranial hemorrhage newborn

  1. 1.  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
  2. 2.  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
  3. 3.  Often results from trauma in the full-term infant SDH in the supratentorial space results from rupture of the bridging veins
  4. 4.  large head size, 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
  5. 5.  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
  6. 6.  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
  7. 7.  Most infants with 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
  8. 8.  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
  9. 9. Usual scenar i o i s a w l el appear i ng t er m i nf antdevel opi ng SAH on day 2 or 3 of l i f e
  10. 10.  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
  11. 11.  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
  12. 12.  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
  13. 13.  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%
  14. 14. Intravascular factors • Ischemia/Reperfusion • Fluctuating or increase(Pressure passive circulation) CBF • Increase in cerebral venous pressure • Platelet dysfunction • Coagulation disturbancesVascular factors • Fragile, involuting capillaries with large diameter lumenExtravascular factors • Deficient vascular support • Excess fibrinolytic activity
  15. 15.  Usually a clinically silent syndrome in preterms Term newborns – seizures, apnea, irritability, lethargy, vomiting, full fontanelle Catastrophic presentation less likely Complications
  16. 16.  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
  17. 17. Grading Severity DescriptionPapile (CT) I Isolated GMH (no IVH) II IVH without ventricular dilatation III IVH with ventricular dilatation IV IVH with parenchymal hemorrhageVolpe 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
  18. 18.  Antenatal steroids Slow infusion of colloid or hyperosmolar solutions Avoidrapid fluctuations in CBF and hypotension Sedativeor paralytic medication in ventilated babies
  19. 19.  Supportivecare and watch for complications Maintaining Normal BP electrolytes and , blood gases Transfusions as necessary Correctthrombocytopenia and coagulation disturbances
  20. 20.  Supportive care and treatment of seizures Serial LPs and eventual VP shunts Prognosis relates to factors other than IVH alone
  21. 21. Monitor OFC and fontanelle daily, Serial CUS q2-7 days to assess ventricle size, shape and RINo PVD Slowly Progressive Rapidly progressive Ventricular dilation ventricular dilatation (over weeks) (over days)No further Close surveillance for 2-4 wktreatment Dilatation stops Continued dilatation No therapy, close Serial LP Every 1-3 d, observation for 1 yr depending on rate of ventricular dilatation