Hypoxic ischaemic encephalopathy refers to collection of abnormal neurological signs like decreased activity, poor suck, respiratory difficulty due to antenatal or perinatal hypoxia and associated postnatal morbidity like cerebral palsy, mental retardation, epilepsy etc. This condition is associated with considerable long term morbidity and therefore an early diagnosis can obviate serious neurological damage.
Etiology
The causation of HIE is multifactorial, however the common causes for this are
1. Maternal diabetes.
2. Pregnancy induced hypertension.
3. Intrauterine growth retardation.
4. Severe bleeding.
5. Placental insufficiency.
6. Prolonged labour.
7. Dystocia.
Anatomical and physiological factors as related to imaging-
Fetal brain is different from adults with regards to cerebral blood supply. In adults the watershed region is the superomedial aspect of cerebral hemispheres, the region between the vascular territories of anterior, middle and posterior cerebral arteries. However in preterm infants this region is in the periventricular white matter. On one side is the germinal matrix with its rich blood supply and on the other side are branches from leptomeningial vessels. The intervening area is most susceptible to the hypoxic changes. With the maturation of the fetal brain this watershed region shifts to the sub cortical white matter.
Physiologically too, the fetal brain responds differently than the adults to hypoxia. The cerebral circulation lacks auto regulation and is in the ‘Pressure-passive’ state i.e. the cerebral perfusion changes as the intravascular pressure changes. This auto regulation is further impaired by hypoxemia and hypercarbia.
So, on one hand hypotension can lead to an ischaemic insult to the brain, increase in vascular pressure can cause hemorrhage.Since the fetal life arterial partial pressure of oxygen is quite low, hypoxic ischaemic disturbances are primarily a consequence of hypoperfusion.Certain evidences also indicate that certain excitatory neurotransmitters (i.e. amino acids esp. glutamate) are released excessively at the synaptic clefts during conditions of hypoxic- ischaemia. These may play a role in neuronal damage.
Imaging in HIE
Close coordination between a pediatrician and neuroradiologist is essential for correct interpretation of imaging features of HIE.
Sonography is the most frequent and widely used modality. As the anterior fontanels is open in the neonatal period it allows quick, bedside examination of the neonatal brain without the hazards of ionizing radiation and at a fraction of a cost of the NCCT or MRI. However the major drawback is the intra. and interobserver variation in the interpretation of the findings as this modality is highly operator dependent. NCCT is more objective modality for the imaging especially in the presence of acute hemorrhages.
MRI has now emerged as more sensitive and specific modality for the evaluation of HIE. Not only it can detect early ischaemic and hemorrhages changes, it can also better characterize the findings picked on initial sonography. It in turn helps in predicting the prognosis of the infants with HIE. Now, the reports of detection of ischaemic changes in first few hours of life with MR diffusion and MR spectroscopy has shifted the focus from merely detecting the abnormalities to the early detection when medical interventions might still be helpful.
Major patterns of HIE on imaging
1. Periventricular hemorrhage
2. Periventricular leukomalacia
3. Cerebral edema.
4. Subcortical/ parasaggital leukomalacia.
5. Focal cerebral ischaemias.
6. Cerebral atrophy.
Periventricular Hemmorhage
Occurs mainly in the preterm infants and refers to germinal matrix hemorrhage with or without associated intraventricular or parenchymal hemorrhages. Caudo-thalamic groove is the most common site. On sonography and NCCT acute hemorrhage appear as bright hyperechoic areas in the periventricular region. In few weeks time they either resolve completely or change into subependymal or porencephalic cysts. These cystic changes are better picked on NCCT.
Grading of IVH (Papile et al)
Grade-1 Hemorrhage confined to the germinal matrix.
Grade-2 IVH without ventricular dilatation
Grade-3 IVH with ventricular dilatation.
Grade-4 Associated parenchymal hemorrhage.
Periventricular Leukomalacia-
It is the term given to the ischaemic changes occurring in the periventricular region in the preterm infants. Classically the lesions of PVL are bilateral, symmetrical and located in peritrigonal white matter or in the areas around the frontal horns.
On ultrasound in the acute stage it appear as periventricular hyperechoic areas or PV flare with echogenecity similar or more than that of the adjacent choroids plexus. They have to be differentiated from the periventricular blush seen in normal infants.
On NCCT they are seen as hypodense areas in the above mentioned location. Here it is difficult to differentiate them from normal unmyelinated white matter seen in immature brain.
Conventional MRI depicts these lesions as the areas of abnormal signal intensity both on T1WI andT2WI. MRI is more sensitive in detecting the areas of hemorrhage occurring in PVL, which on sonography may be completely missed or seen merely as areas of inhomogenecity in periventricular flares.
Chronic PVL
There is change in the periventricular region with in 3-4 weeks and may completely resolve(within months). The periventricular changes are not appreciated on USG or NCCT or result in ventriculomegaly. However, MRI is a sensitive modality to detect the chronic changes, which are seen as-
1. B/L symmetrical, hyperintense foci in periventricular white matter on PD and T2WI.
2. Reduction in periventricular white matter leading to abutting of deep cortical sulci to the ventricular wall.
3. Irregular ventriculomegaly.
Grading of PVL
Grading of PVL has been proposed by many authors however one given by De Vries et al is most followed.
Grade-1 periventricular echodense areas persisting for seven days or more
Grade-2 periventricular echodense areas evolving into small fronto-parietal cysts.
Grade-3 periventricular echodense areas evolving into multiple cysts in the parieto-occipital white matter.
Grade-4 echodense areas in the deep white matter evolving into multiple subcortical cysts.
Subcortical Leukomalacia And Cerebral Edema
The subcortical region is the watershed area in the term infants, thus the ischaemic changes are noted in this area. When the hypoperfusion in profound and for a long period, whole brain is affected and features of diffuse cerebral edema are seen. On sonography the edematous brain appears as diffuse increase in the echotexture of cerebral hemispheres. NCCT the findings of diffuse low attenuation involving both hemispheres are noted.
Prognosis
The prognosis is predicted mainly by the clinical scoring systems which use clinical signs as well as EEG findings to stage the disease. However certain imaging features are associated with poor prognosis. In general the prognosis is in direct relation to the grade of injury. Higher the grade poorer the prognosis. In a study by V. Pierrat et al. 29 out of 30 patients with grade2/3 PVL developed cerebral palsy. Diffuse decrease density on CT in term infants is also associated with poor prognosis. Resistive index of less than 60 in cerebral arteries on Doppler scanning is associated with poor outcome. On MRS decrease in ATP is associated with death in the neonatal period.
Conclusion
Hypoxic ischaemic encephalopathy is a frequent problem in preterm and at term infants and the early diagnosis of this entity can help in management and can alter the long-term prognosis. Various radiological modalities are available like USG, CT and MRI. No single modality is sufficient for complete diagnosis and follow-up. Close coordination between the pediatrician and radiologist is required to adequately manage this entity.
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