Intracranial Hemorrhage in Newborns: Incidence, Types and Management

Intracranial Hemorrhage in Newborns: Incidence, Types and Management

This article discusses the incidence, types, pathogenesis, clinical presentation, diagnosis, management and prognosis of intracranial hemorrhage (ICH) in newborns, which can occur within different compartments of the skull. The article emphasizes how these factors relate to the gestational age of the infant.

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3. The incidence of intracranial hemorrhage (ICH) varies from 2% to >30% in new-borns, depending on gestational age (GA) at birth and the type of ICH. Bleeding within the skull can occur : (i) external to the brain into the epidural, subdural, or subarachnoid spaces; (ii) into the parenchyma of the cerebrum or cerebellum; or (iii) into the ventricles from the subependymal germinal matrix or choroid plexus.

4. The incidence, pathogenesis, clinical presentation, diagnosis, management, and prognosis of ICH varies according to the ICH location and size, and the infants GA . There is often a combination of two or more types of ICH, as an ICH in one location often extends into an adjacent compartment; for example, extension of a parenchymal hemorrhage into the subarachnoid space or ventricles.

5. Diagnosis usually depends on clinical suspicion when an infant presents with typical neurologic signs, such as seizures, irritability, depressed level of consciousness, and/or focal neurologic deficits referable either to the cerebrum or brain stem. Diagnosis is confirmed with an appropriate neuroimaging study.

6. The American Academy of Neurology (AAN) states that all infants with a birth GA of <30 weeks should undergo routine cranial ultrasound (CUS) between 7-14 days and optimally repeated between 36 to 40 weeks postmenstrual age,

7. Management varies according to the size and location of the ICH and the presenting neurologic signs. In general, only very large hemorrhages with clinical signs require surgical intervention More commonly, management is focused on treating complications such as seizures or the development of posthemorrhagic hydrocephalus.

9. GMH/IVH :- A. Aetiology and pathogenesis GMH/IVH is found principally in the preterm infant, where the incidence is currently 15% to 20% in infants born at <32 weeks' GA, but is uncommon in the term newborn. The etiology and pathogenesis are different for term and preterm infants. A. Aetiology and pathogenesis

10. GMH/IVH :- A. Aetiology and pathogenesis 1. In the term newborn a- IVH typically originates in the choroid plexus. b- In association with venous ( sinus) thrombosis and thalamic infarction, c- IVH may also occur in the small remnant of the subependymal germinal matrix.

11. GMH/IVH :- A. Aetiology and pathogenesis 2. In the preterm infant, GMH/IVH originates from the fragile involuting vessels of the subependymal germinal matrix There are numerous risk factors that have been identified in the etiology of IVH a- Maternal factors such as infection/inflammation and hemorrhage, lack of antenatal steroids.

12. GMH/IVH :- A. Aetiology and pathogenesis b- External factors such as mode of delivery or neonatal transport to another hospital, and increasingly recognized genetic factors that predispose some newborns to IVH. However these risk factors all contribute to the basic pathogenesis of GMH/IVH , which relates to alterations in blood flow and coagulation. Thus, the pathogenesis of GMH/IVH in preterm newborns has been shown to be largely related to intra-vascular, vascular, and extravascular factors

13. GMH/IVH :- A. Aetiology and pathogenesis Ischemia/reperfusion (e.g., volume infusion after hypotension) Fluctuating CBF (e.g., with mechanical ventilation) Increase in CBF (e.g., with hypertension, anemia, hypercarbia) Increase in cerebral venous pressure (e.g., with high intrathoracic pressure, usually from ventilator) Platelet dysfunction and coagulation disturbances Intravascular factors Weak, involuting capillaries with large luminal diameter Vascular factors Deficient vascular support Extra vascular factors

14. GMH/IVH :- A-Intravascular factors 1- Ischemia/reperfusion:- this scenario often occurs shortly after birth, when a premature infant may have hypovolemia or hypotension that is treated with infusion of colloid, normal saline, or hyperosmolar solutions such as sodium bicarbonate. Rapid infusions of such solutions are thought to be particularly likely to contribute to GMH/IVH. 2- Fluctuating CBF:- The large fluctuations typically occurred in infants breathing out of synchrony with the ventilator, but such fluctuations have also been observed in infants with large patent ductus arteriosus or hypotension A. Aetiology and pathogenesis

15. GMH/IVH :- A-Intravascular factors 3- Increase in CBF:- Sustained increases in CBF may contribute to GMH/IVH and can be caused by seizures, hypercarbia, anemia, and hypoglycemia, which result in a compensatory increase in CBF. 4-Increase in cerebral venous pressure|:- intrathoracic pressure is high (e.g., high continuous positive airway pressure), pneumothorax, tracheal suctioning, and both labor and delivery, where fetal head compression likely results in significantly increased venous pressure. Indeed, a higher incidence of GMH/IVH is found in preterm infants with a longer duration of labor and in those delivered vaginally compared with those delivered via caesarean section. A. Aetiology and pathogenesis

16. GMH/IVH :- A-Intravascular factors Several studies have shown that preterm infants, particularly asphyxiated newborns, have an impaired ability to regulate CBF in response to blood pressure changes (hence, "pressure-passive") . Such impaired autoregulation puts the infant at increased risk for rupture of the fragile germinal matrix vessels in the face of significant increases in cerebral arterial or venous pressure, and particularly when ischemia precedes such increased pressure. 5- Platelet dysfunction and coagulation disturbances:- Finally, impaired coagulation and platelet dysfunction are also intravascular factors that can contribute to the pathogenesis of GMH/IVH. A. Aetiology and pathogenesis

17. GMH/IVH :- B-Vascular factors Vascular factors that contribute to GMH/IVH include the fragile nature of the involuting vessels of the germinal matrix. There is no muscularis mucosa and little adventitia in this area of relatively large diameter, thin-walled vessels; all of these factors make the vessels particularly susceptible to rupture . A. Aetiology and pathogenesis

18. GMH/IVH :- C-Extra vascular factors Extravascular risk factors for GMH/IVH include deficient extravascular support and likely excessive fibrinolytic activity in preterm infants. A. Aetiology and pathogenesis

19. GMH/IVH :- B-Complications of GMH/IVH. The two major complications of GMH/IVH are:- 1-Periventricular hemorrhagic infarction (PVHI) 2-Posthemorrhagic ventricular dilation (PVD). *********** 1-Periventricular hemorrhagic infarction (PVHI) PVHI has previously been considered an extension of a large IVH Recently,it is not accepted as an extension of the original IVH, but is a separate lesion consisting of a venous hemorrhagic infarction. a- Neuropathologic studies demonstrate the fan-shaped appearance of a typical hemorrhagic venous infarction in the distribution of the medullary veins that drain into the terminal vein, resulting from obstruction of flow in the terminal vein by the large ipsilateral IVH. B-Complications of GMH/IVH.

20. GMH/IVH :- b- PVHI occurs on the side of the larger IVH, and Doppler US studies show markedly decreased or absent flow in the terminal vein on the side of the large IVH . c- The ependymal lining of the lateral ventricle separating IVH and PVHI has been observed to remain intact in some cases, demonstrating that the IVH did not ""extend" into the adjacent cerebral parenchyma. Risk factors for the development of PVHI include low birth GA, low Apgar scores, early life acidosis, patent ductus arteriosus, pneumothorax, pulmonary hemorrhage, and need for significant respiratory or blood pressure support B-Complications of GMH/IVH.

21. GMH/IVH :- 2-Posthemorrhagic ventricular dilation (PVD). or posthemorrhagic hydrocephalus (PHH-terminology varies), may occur days to weeks following the onset of GMH/IVH. Not all ventricular dilation progresses to established hydrocephalus The pathogenesis of progressive posthemorrhagic ventricular dilation: a- I mpaired CSF resorption and/or obstruction of the aqueduct or the foramina of Luschka or Magendie by particulate clot b- High levels of transforming growth factor -1(TGF -1) are found in the CSF following IVH, particularly in infants with PVD; TGF-pl upregulates genes for extracellular matrix proteins that elaborate a "scar," which may obstruct CSF flow and/ or CSF reabsorption B-Complications of GMH/IVH.

22. GMH/IVH :- B-Complications of GMH/IVH. The pathogenesis of the brain injury resulting from PVD is probably related in large part to : a- Regional hypoxia-ischemia and mechanical distension of the periventricular white matter. b- The presence of non-protein-bound iron in the CSF of infants with PVD may lead to the generation of reactive oxygen species that in turn contribute to the injury of immature oligodendrocytes in the white matter .The brain injury associated with PVD is principally a bilateral cerebral white matter injury.

23. GMH/IVH :- C. Clinical Presentation 1-GMH/IVH in the preterm newborn is usually a clinically Silent syndrome and thus is recognized only when a routine CUS is performed. The vast majority of these hemorrhages occur within 72 hours after birth Infants with large IVH may present with decreased levels of consciousness and spontaneous movements, hypotonia, abnormal eye movements. Rarely, coma, severe hypotonia and lack of spontaneous movements, OR generalized tonic posturing that is often thought to be seizure, but does not have an electrographic correlate by electroencephalogram. C. Clinical Presentation

24. GMH/IVH :- 2-The term newborn with IVH typically presents with signs such as seizures, apnea, irritability or lethargy, vomiting with dehydration, or a full fontanel. 3-Posthemorrhagic ventricular dilation (PVD) may develop over days to weeks following IVH, particularly in premature infants, and may present with increasing head growth (crossing percentiles on the growth chart), bulging fontanelle, splitting of sutures, decreased level of consciousness, sunsetting sign, apnea, worsening respiratory status, or feeding difficulties. However, PVD may be relatively asymptomatic in preterm newborns C. Clinical Presentation

25. GMH/IVH :- Grading of GMH/IVH Grading system Severity of GMH/1VH Description of findings Papile I Isolated GMH (no IVH) II IVH without ventricular dilatation III IVH with ventricular dilatation IV IVH with parenchymal hemorrhage Grading of GMH/IVH

26. GMH/IVH :- E. Management and Prognosis Management and Prognosis Prevention of GMH/IVH should be the primary goal 1- Antenatal administration of glucocorticoids has clearly been shown to decrease the incidence of GMH/IVH. 2- Aantenatal phenobarbital, vitamin K, and magnesium sulfate have not been conclusively demonstrated to prevent GMH/IVH. 3- Minimizing risk factors as infusions of colloid or hyperosmolar solutions should be given slowly. 4- Efforts should be directed to avoiding hypotension and large fluctuations or sustained increases in arterial blood pressure or cerebral venous pressure. 5- Elimination of CBF fluctuation related to mechanical ventilation

27. GMH/IVH :- Management of GMH/IVH in the premature newborn largely consists of : A- Supportive care and monitoring for and treatment of complications of GMH/IVH. 1- Supportive care should be directed toward maintaining stable cerebral perfusion by maintaining normal blood pressure, circulating volume, electrolytes, and blood gases. 2- Transfusions of packed red blood cells may be required in cases of large IVH to restore normal blood volume and hematocrit. 3- Thrormbocytopenia or coagulation disturbances should be corrected. Management and Prognosis

28. GMH/IVH :- B- Treatment of seizures during the acute phase. C- Careful monitoring of ventricle size by serial CUS and appropriate intervention when needed to reduce CSF accumulation, such as serial LPs to remove CSF, surgical interventions to divert CSF flow, and rarely, medications to reduce CSF production Management and Prognosis

29. GMH/IVH :- The long-term prognosis for infants with GMH/IVH varies considerably depending on the severity of IVH, complications of IVH or other brain lesions, the birth weight/GA, and other significant illnesses that affect neurologic outcome. Several recent studies suggest that preterm infants with grades I and II IVH have an increased risk of CP and/or cognitive impairment Management and Prognosis

30. GMH/IVH :- Infants with the two major complications of IVH, namely PVHI and PVD, are at much higher risk of neurologic impairments than those with IVH alone. Infants with PVD/PHH requiring significant intervention often manifest spastic diparesis and cognitive impairments due to bilateral peri-ventricular WMI. Quadriparesis and significant cognitive deficits (including mental retardation) are more likely if the PVHI is extensive or bilateral, or if there is also coexisting PVL Management and Prognosis

31. GMH/IVH :- Outcome in term newborns with IVH relates to factors other than IVH alone, as uncomplicated small IVH in this population has a favorable prognosis. Infants with a history of trauma or prenatal asphyxia, or with neuroimaging evidence of thalamic hemorrhagic infarction, hypoxic- ischemic brain injury, or other parenchymal lesions, are at high risk for significant cognitive imparments. Management and Prognosis


36. INTRAPARENCHYMAL HEMORRHAGE Etiology and pathogenesis A. Etiology and pathogenesis 1. Primary cerebral hemorrhage is uncommon in all newborns, An intracerebral hemorrhage may occur rarely as a primary event related to rupture of an arteriovenous malformation or aneurysm, from a coagulation disturbance (e.g., hemophilia, thrombocytopenia), or from an unknown cause. More commonly, cerebral intraparenchymal hemorrhage (IPH) occurs as a secondary event, such as hemorrhage into a region of hypoxic-ischemic brain injury 2. Intracerebellar hemorrhage occurs more commonly in preterm than term newborns and may be missed by routine CUS.

37. INTRAPARENCHYMAL HEMORRHAGE Clinical presentation B. Clinical presentation. The presentation differs depending on the size and location of the IPH . In the preterm infant, IPH is often clinically silent unless the hemorrhage is quite large . In the term infant , intracerebral hemorrhage typically presents with focal neurologic signs such as seizures, asymmetry of tone/movements along with irritability or depressed level of consciousness. Diagnosis. MRI is the best imaging modality for IPH, but CUS may be used in the preterm infant or when a rapid bedside imaging study is necessary.

38. INTRAPARENCHYMAL HEMORRHAGE Management Management 1. Small hemorrhages require only symptomatic treatment and support. 2. Large IPH with severe neurologic compromise should prompt neurosurgical intervention . It is important to diagnose and treat any coexisting pathology, such as infection or sinus venous thrombosis

39. INTRAPARENCHYMAL HEMORRHAGE Prognosis Prognosis The long term prognosis largely relates to location and size of the IPH and GA of the infant. A small IPH may have relatively few or no long-term neurologic consequences. A large cerebral IPH may result in a life- long seizure disorder, hemiparesis or other type of cerebral palsy (CP), feeding difficulties, and cognitive impairments ranging from learning disabilities to significant intellectual disability, depending on the location. Cerebellar hemorrhage in the term newborn often has a relatively good prognosis, although it may result in cerebellar signs of ataxia, hypotonia, tremor, nystagmus, and mild cognitive deficits.


42. SUBDURAL HEMORRHAGE Etiology and pathogenesis A. Etiology and pathogenesis. The pathogenesis of SDH relates to rupture of the draining veins and sinuses of the brain that occupy the subdural space. Vertical molding, fronto-occipital elongation, and torsional forces acting on the head during delivery may provoke laceration of dural leaflets of either the tentorium cerebelli or the falx cerebri. These lacerations can result in rupture of the vein of Galen, inferior sagittal sinus, straight sinus and/or transverse sinus

43. SUBDURAL HEMORRHAGE Clinical presentation B. Clinical presentation. 1- When the accumulation of blood is rapid and large, as occurs with rupture of large veins or sinuses, the presentation follows shortly after birth as infratentorial SDH, where compression of the brain stem may result in nuchal rigidity or opisthotonus, obtundation or coma, apnea, other abnormal respiratory patterns, and unreactive pupils .With increased intracranial pressure (ICP), there may be a bulging fontanelle arid/or widely split sutures.

44. SUBDURAL HEMORRHAGE Clinical presentation 2- Seizures may occur in up to half of neonates with SDH, 3- Finally, a chronic subdural effusion may gradually develop over months, presenting as abnormally rapid head growth, Diagnosis. The diagnosis should be suspected on the basis of history and clinical signs and confirmed with a neuroimaging study. CT scan is the study of choice for diagnosing SDH or EH for acute emergencies, if MRI cannot be obtained quickly. US is often inadequate.

45. SUBDURAL HEMORRHAGE Management Management. Most infants with SDH do not require surgical intervention and can be managed with supportive care and treatment of any accompanying seizures.

46. Epidural hemorrhage (EH) Epidural hemorrhage (EH). There are approximately 20 case reports of neonatal EH in the literature. EH appears to be correlated with trauma and a large cephalohematoma or skull fracture was found in about half the reported cases of EH. Removal or aspiration of the hemorrhage was performed in the majority of cases, and the prognosis was quite good except when other ICH or parenchymal pathology was present.


50. SUBARACHNOID HEMORRHAGE Etiology and pathogenesis A.Etiology and pathogenesis. Subarachnoid hemorrhage (SAH) is a common form of ICH among newborns, Primary SAH (i.e., SAH not due to extension from ICH in an adjacent compartment) is probably frequent but clinically insignificant. In these cases, SAH may go unrecognized because of a lack of clinical signs. For example, hemorrhagic or xanthochromic CSF may be the only indication of such a hemorrhage in infants who undergo a CSF exam to rule out sepsis.

51. SUBARACHNOID HEMORRHAGE Etiology and pathogenesis SAH may also result from extension of SDH (e.g., particularly in the posterior fossa) or a cerebral contusion (parenchymal hemorrhage). Finally, subpial hemorrhage may occur, mostly in the otherwise healthy term newborn, and is usually a focal hemorrhage likely caused by local trauma resulting in venous compression or occlusion in the setting of a vaginal delivery.

52. SUBARACHNOID HEMORRHAGE Clinical presentation. Clinical presentation. As with other forms of ICH, clinical suspicion of SAH may result because of blood loss or neurologic dysfunction. More often, neurologic signs manifest as seizures, irritability, or other mild alteration of mental status, particularly with SAH The diagnosis is best established with a MRI (or CT) scan,

53. SUBARACHNOID HEMORRHAGE Management and prognosis. Management and prognosis. Management of SAH usually requires only symptomatic therapy, such as anticonvulsant therapy for seizures and nasogastric feeds or intravenous fluids if the infant is too lethargic to feed orally. The majority of infants with small SAH do well with no recognized sequale