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Hypoxic ischemic encephalopathy modified


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radiology seminar

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Hypoxic ischemic encephalopathy modified

  1. 1. Pediatric perinatal insult: HYPOXIC ISCHEMIC ENCEPHALOPATHY Dr. Mohit Goel, JRIII 19/5/14
  2. 2. INTRODUCTION  Hypoxic-ischemic injury (HII) to the brain is a devastating occurrence that frequently results in death or profound long-term neurologic disability in both children and adults.
  3. 3. Imaging findings in HII are highly variable and depend on a number of factors, including : • Brain maturity • Severity • Duration of insult • Type and timing of imaging studies
  4. 4. PATHOPHYSIOLOGY  Regardless of the specific cause of injury, the common underlying physiologic processes that result in HII are diminished cerebral blood flow (ischemia) and reduced blood oxygenation (hypoxemia).  In general, infants and children are more likely to suffer asphyxial events, which result in hypoxemia and brain hypoxia.  With prolonged hypoxemia, cardiac hypoxia occurs, leading to diminished cardiac output and, ultimately, to brain ischemia.
  5. 5. Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang, MD, MPH and Mauricio Castillo, MD. Doi: 10.1148/rg.282075066 March 2008 RadioGraphics, 28, 417-439.
  6. 6.  Areas of the brain with the highest concentrations of glutamate or other excitatory amino acid receptors (primarily located in gray matter) are more susceptible to excitotoxic injury that occurs as a result of hypoxia-ischemia.  Areas of the brain with the greatest energy demands become energy depleted most rapidly during hypoxia-ischemia, and are therefore injured early on.  Because of delayed cell death from apoptosis, some injuries may not be evident until days after the initial insult has occurred
  7. 7. Patterns of brain injury in mild to moderate hypoperfusion. how the vascular supply changes with maturation and affects the pattern of brain injury in HIE. The premature neonatal brain has a ventriculopetal vascular pattern, and hypoperfusion results in a periventricular border zone of white matter injury. Premature Term In the term infant, a ventriculofugal vascular pattern develops as the brain matures, and the border zone during hypoperfusion is more peripheral with subcortical white matter and parasagittal cortical injury. Neonatal Hypoxic-Ischemic Encephalopathy: Multimodality Imaging Findings. Christine P. Chao, MD, Christopher G. Zaleski, MD and Alice C. Patton, MD. Doi: 10.1148/rg.26si065504 October 2006 RadioGraphics, 26, S159-S172.
  8. 8. Causes of HIE. Chao C P et al. Radiographics 2006;26:S159-S172 ©2006 by Radiological Society of North America
  9. 9. IMAGING MODALITIES : Accurate identification and characterization of the severity, extent, and location of brain injury rely on the selection of appropriate neuroimaging modalities, including 1. Ultrasonography 2. Computed tomography 3. Magnetic resonance imaging.
  10. 10.  Radiation  Less sensitive Why Not CT ??
  11. 11. TERM NEONATE Antepartum risk factors  maternal hypotension  infertility treatment  multiple gestation  prenatal infection  thyroid disease Intrapartum factors  forceps delivery  breech extraction  umbilical cord prolapse  abruptio placentae  tight nuchal cord  maternal fever Antepartum factors in combination with intrapartum factors.
  12. 12. “1-2-3-4 sign” Imaging Findings in Neonatal Hypoxia: A Practical Review. E. Ralph Heinz1 and James M. Provenzale The four components of the 1-2-3-4 sign are : 1. Increased signal intensity in the basal ganglia on T1-weighted images 2. Increased signal intensity in the thalamus on T1-weighted images 3. Absent or decreased signal intensity in the posterior limb of the internal capsule on T1-weighted images “absent posterior limb sign” 4. Restricted water diffusion on diffusion-weighted images.
  13. 13. SEVERE ASPHYXIA IN TERM NEONATES Central pattern of injury involving the deep gray matter  putamina  ventrolateral thalami  hippocampi  dorsal brainstem  lateral geniculate nuclei  occasionally perirolandic cortex.  actively myelinating areas are the most susceptible to neonatal HII
  14. 14. USG  Early findings - global increase in cerebral echogenicity and obliteration of the CSF containing spaces, suggesting diffuse cerebral edema.  1st week but more readily apparent after 7 days. Increased echogenicity in the basal ganglia, thalami, and brainstem
  15. 15. USG  Late findings include prominence of the ventricles and extraaxial CSF- containing spaces, likely due to atrophy.  The presence of diminished resistive indexes (<60) in the anterior and middle cerebral arteries has been associated with a poor clinical outcome, even in the absence of other US abnormalities.
  16. 16. MRI Diffusion-weighted imaging  Sensitive for the detection of injury in the first 24 hours, during which time conventional T1- and T2-weighted images may appear normal.  Demonstrate increased signal intensity in the region of the ventrolateral thalami and basal ganglia particularly the posterior putamina in the perirolandic regions and along the corticospinal tracts
  17. 17. MRI - Pseudonormalization.  Although diffusion-weighted images seemingly improve and appear relatively normal by the end of the 1st week, this finding does not imply that there has been improvement or reversal of underlying disease.
  18. 18. MRI  Day 1 ---- Conventional T1- and T2-weighted MR images are frequently normal , therefore less useful than DWI  Day 2 ---- Injured areas may demonstrate hyperintensity on both T1- and T2-weighted images.  2 weeks --- T2 hypointensity subsequently develops in the thalami & posterior putamina.  Several months --- TI hyperintensity in thalami, basal ganglia & perirolandic cortex may persisit.  ‘T1WI & T2WI ARE MOST DIAGNOSTICALLY USEFUL AT THE END OF 1st WEEK, WHEN DWI PSEUDONORMALIZE’.  Chronic stage of injury - atrophy of the injured structures - T2 hyperintensity in the ventrolateral thalami, posterior putamina, and corticospinal tracts.
  19. 19. 13 days old, male baby Term baby with history of respiratory distress and hypotonia at birth, followed by 2 episodes of seizures.
  20. 20. 11 days old, male baby. History of one episode of seizure , known case of HIE
  21. 21. T1WI
  22. 22. Severe neonatal HII in a 7-day-old term infant. T1WI shows increased signal intensity in the lentiform nuclei and ventrolateral thalami. T2WIshows decreased signal intensity in the posterior aspects of the putamina and ventrolateral thalami. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  23. 23. DWI shows a relative lack of hyperintensity in the locations cited earlier, findings that represent pseudonormalization. Only the left globus pallidus shows high signal intensity. Corresponding ADC map shows hypointensity Huang B Y , and Castillo M Radiographics 2008;28:417-439
  24. 24. Severe neonatal HII in a 5-day-old term infant who suffered profound birth asphyxia. T1WI show hyperintensity in the ventrolateral thalami, basal ganglia and perirolandic cortex. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  25. 25. T2WI obtained approximately 7 months later show diffuse atrophy as well as hyperintensity (gliosis) in the ventrolateral thalami, posterior putamina, and perirolandic regions. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  26. 26. PARTIAL ASPHYXIA TERM NEONATES In mild to moderate hypoxic-ischemic ----  brainstem  cerebellum  deep gray matter structures are generally spared since autoregulatory mechanisms maintain perfusion. Moderate insults of short duration in neonates cause little or no injury to the brain Prolonged insults in neonates result in injury to the intervascular boundary (watershed) zones, which are relatively hypoperfused as a result of this shunting.
  27. 27. MRI TERM NEONATE  DWI (earliest to change) First 24 hrs ---demonstrate cortical and subcortical WM restriction most pronounced in the parasagittal watershed territories.  T2WI By day 2 --- cortical swelling with loss of gray and white matter differen. hyperintensity in the cortex and subcortical WM in the parasagittal watershed zones occasionally involving the hemispheres diffusely.
  28. 28. Partial neonatal HII in a 2-day-old term infant who experienced seizures shortly after birth . T1WI & T2WI are normal.
  29. 29. DWI and corresponding ADC map show restricted diffusion in the cortex and subcortical white matter in a parasagittal watershed distribution.
  30. 30. PRETERM NEONATE  HII is more common in preterm neonates than in term neonates.  HII in preterm infants, particularly those of very low birth weight is difficult to diagnose clinically early on because signs may be lacking or mistaken to result from developmental immaturity.
  31. 31. PRETERM NEONATES Manifest predominantly as damage to the deep gray matter structures and brainstem. Events of mild to moderate severity manifest as germinal matrix–intraventricular hemorrhages or periventricular leukomalacia.
  32. 32. SEVERE ASPHYXIA IN PRETERM  Injury to the thalami, basal ganglia, hippocampi, cerebellum, and corticospinal tracts can be seen.  The thalami, anterior vermis, dorsal brainstem are most frequently involved.  Involvement of basal ganglia is less severe compared with involvement of the thalami particularly among neonates born at less than 32 weeks gestation.  Germinal matrix hemorrhages and periventricular white matter injury also may be seen.
  33. 33. USG IN PRETERM NEONATES  May be normal particularly in the first 2 days. OR  Demonstrate increased echogenicity in the thalami by 48–72 hours
  34. 34. MRI  1st day Conventional MR may be normal or show only subtle abnormalities.  Diffusion abnormalities are usually evident in the thalami within 24 hours .  After 2 days, T2 prolongation can be seen in the thalami and basal ganglia.
  35. 35. MRI  3rd day - T1 hyperintensity will be seen in the injured areas.  3–5 days - DW abnormalities most apparent subsequently begin to pseudonormalize .  7 days - T2 hypointensity develops in the injured areas T1 hyperintensity persists into the chronic stage.
  36. 36. T1WI 19 days old, male baby Preterm, AGA. History of cardiac arrest at 30 hours of life. Baby was ventilated.
  37. 37. T2WI
  38. 38. MILD TO MODERATE ASPHYXIA PRETERM  Weighing less than 2000 gms  Prevalence of intraventricular hemorrhage approximately 25%  Bleeding occurs within the first 24 hours of life.  Prevalence is inversely related to gestational age and weight at birth.  Majority of intraventricular hemorrhages are associated with germinal matrix hemorrhages.
  39. 39. Sonographic grading system proposed by Burstein and Papile Grade I restricted to subependymal region / germinal matrix which is seen in the caudothalamic groove Grade II extension into normal sized ventricles and typically filling less than 50% of the volume of the ventricle Grade III extension into dilated ventricles Grade IV grade III with parenchymal haemorrhage 90% mortality. It should be noted that it is now thought that grade IV bleeds are not simply extensions of germinal matrix haemorrhage into adjacent brain, but rather represent sequelae of venous infarction Grading of neonatal intracranial haemorrhage
  40. 40. Grade I
  41. 41. Grade II
  42. 42. Grade III
  43. 43. Grade IV hemorrhage.
  44. 44. PVL Classification  Grade I – Transient Periventricular echo densities persisting for > 7 days  Grade II - Transient Periventricular echo density evolving into small, localized fronto-parietal cyst  Grade III - Periventricular echo densities evolving into extensive periventricular cystic lesions  Grade IV – Densities extending into the deep white matter evolving into extensive cystic lesions
  45. 45. Grade I PVL
  46. 46. Grade III PVL PARA SAG COR
  47. 47. Grade III PVL
  48. 48. MRI - PVL  Early WM injury will manifest as periventricular foci of T1 hyperintensity (without corresponding T2 hypointensity) within larger areas of T2 hyperintensity.  These foci are usually evident by 3–4 days, subsequently giving way to mild T2 hypointensity at 6–7 days .  In contrast, hemorrhage (reported to be present in 64% of cases of PVL) initially manifests with much lower signal intensity on T2- weighted images.
  49. 49. 1 yr male with history of right side focal seizurs with global developemental delay. USG AF done during neonatal period revealed bilateral germinal matrix hemorrhage.
  50. 50. T1WI FLAIR 1 yr male with history of hypoxic cerebral palsy with mental retardation and global developmental delay.
  51. 51. POSTNATAL INFANTS & YOUNG CHILDREN  Hypoxic-ischemic injuries in infants and young children are usually the result of drowning, choking, or non accidental trauma.  As myelination nears completion by about 2 years of age, injuries similar to the pattern seen in adults begin to appear.
  52. 52. SEVERE ASPHYXIA IN POSTNATAL INFANTS & YOUNG CHILDREN 1 and 2 years of age ---- Result in injury to the  Corpora striata  Lateral geniculate nuclei  Hippocampi  Cerebral cortex (particularly the anterior frontal and parieto-occipital cortex), with relative sparing of the thalami and perirolandic cortex.  Immediate perinatal period but before 1 year of age --- can demonstrate features of both birth asphyxia and later infantile asphyxia, with involvement of the basal ganglia (predominantly posteriorly), lateral thalami, and dorsal midbrain, as well as cortical injury.
  53. 53. CT < 24 hours of an insult --- may be negative or may demonstrate only subtle hypoattenuation of the deep gray matter structures . Subsequent CT --- will demonstrate  diffuse basal ganglia abnormalities along with diffuse cerebral edema, manifesting as cortical hypoattenuation  loss of normal “gray-white” differentiation  cisternal and sulcal effacement. 4–6 days --- may show hemorrhagic infarctions of the basal ganglia. Chronic phase ---- diffuse atrophy with sulcal and ventricular enlargement .
  54. 54. CT  Within the first 24 hours, a small number of these patients may demonstrate the “Reversal sign,” in which there is reversal in the normal CT attenuation of gray matter and white matter.  “White cerebellum sign” --- diffuse edema and hypoattenuation of the cerebral hemispheres with sparing of the cerebellum and brainstem, resulting in apparent high attenuation of the cerebellum and brainstem relative to the cerebral hemispheres.
  55. 55. Unenhanced CT shows diffuse cortical swelling and hyperattenuation in the white matter relative to areas of preserved cortex, i.e ‘Reversal sign’ --poor prognosis. A small amount of extraaxial hemorrhage adjacent to the left frontal lobe is also seen. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  56. 56. Unenhanced CT demonstrates the ‘White cerebellum sign’. The cerebellar hemispheres are hyperattenuating relative to the supratentorial structures, which are hypoattenuating due to edema. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  57. 57. Unenhanced CT scan obtained at the level of the basal ganglia after cardiopulmonary arrest that lasted 30 minutes is essentially unremarkable. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  58. 58. DWI and T2WI obtained 4 days later show high signal intensity with corresponding T2 abnormalities in the caudate nuclei, lentiform nuclei, and occipital lobes. Huang B Y , and Castillo M Radiographics 2008;28:417-439
  59. 59. MRI  MR imaging is frequently performed in children with HII. Diffusion-weighted images will usually be abnormal within the first 12–24 hours, initially demonstrating bright signal intensity in the posterolateral lentiform nuclei ; thalamic involvement (when present) will usually involve the ventrolateral nuclei.  Over the next 48 hours, there is typically significant progression of involvement to include the remainder of the basal ganglia and the cortex
  60. 60. MRI  Conventional T1- and T2WI obtained in the first 24 hours are often normal and may appear so for up to 2 days.  By 48 hours, T2-weighted images will usually demonstrate diffuse basal ganglia and cortical signal intensity abnormality
  61. 61. MILD TO MODERATE ASPHYXIA IN POSTNATAL INFANTS & YOUNG CHILDREN  As in term neonates, milder anoxic events in older infants will generally result in watershed zone injuries involving the cortex and subcortical white matter.  White matter lesions are more common in children under 1 year of age. Relative sparing of the periventricular white matter will be seen.
  62. 62. Unenhanced head CT scan shows bilateral cortical and subcortical hypoattenuation in the parasagittal watershed regions
  63. 63. DWI obtained at the same level shows corresponding high-signal-intensity areas compatible with watershed infarcts.
  64. 64. OLDER CHILDREN & ADULTS  HII in adults is more often a result of cardiac arrest or cerebrovascular disease, with secondary hypoxemia.  Drowning and asphyxiation remain common causes of HII in older children.  Mild to moderate global ischemic insults to the brain usually result in watershed zone infarcts.  Severe HII in this population primarily affects the gray matter structures: the basal ganglia, thalami, cerebral cortex (in particular the sensorimotor and visual cortices, although involvement is often diffuse), cerebellum, and hippocampi
  65. 65. MRI  As in younger patients, conventional T1- and T2-weighted images are often normal or demonstrate only very subtle abnormalities.  Early subacute period (24 hours–2 weeks) --- conventional T2WI typically become positive and demonstrate increased signal intensity and swelling of the injured gray matter structures. DWI abnormalities usually pseudonormalize by the end of the 1st week .  2nd week --- Gray matter signal intensity abnormalities at conventional MR imaging may persist into the end of the.  Chronic stage --- T2WI may demonstrate some residual hyperintensity in the basal ganglia, and T1WI may show cortical necrosis , which is seen as areas of high signal intensity in the cortex
  66. 66. Axial T2W and DWI show diffuse WM hyperintensity. On the corresponding ADC map, the white matter is hypointense
  67. 67. MR SPECTROSCOPY  MR spectroscopy is perhaps more sensitive to injury and more indicative of the severity of injury in the first 24 hours after a hypoxic-ischemic episode, when conventional and diffusion- weighted MR imaging may yield false-negative findings or lead to significant underestimation of the extent of injury.
  68. 68.  MR spectroscopy will demonstrate substantial lactate elevation (appearing as a doublet centered in the deep gray nuclei, parieto- occipital region, or white matter of the parasagittal watershed zones by as early as 2–8 hours .  A glutamine-glutamate peak may also be detected , probably reflecting the release of glutamate that occurs in HII.
  69. 69. THANK YOU