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Spectral-domain OCT changes in retina and optic nerve in children with hypoxic-ischaemic encephalopathy
L Grego1,2, S Pignatto1,2, E Busolini3
1Department of Medicine, Ophthalmology, University of Udine, Udine, Italy.
Insights
Neonatal hypoxic-ischaemic injury can cause retinal and optic nerve damage, particularly in severe encephalopathy. Ocular issues correlate with inflammation and cerebral edema, but higher bilirubin levels may be protective.
Area of Science:
- Ophthalmology
- Neonatology
- Neurology
Background:
- Neonatal hypoxic-ischaemic encephalopathy (HIE) poses significant risks to infant health.
- The long-term effects of HIE on ocular structures, including the retina and optic nerve, require further investigation.
Purpose of the Study:
- To assess the impact of neonatal hypoxic-ischaemic injury on the retina and optic nerve.
- To correlate ocular damage with systemic factors, laboratory results, neurological imaging, and therapeutic hypothermia.
Main Methods:
- A cohort study included 41 children with HIE and 38 healthy controls.
- Spectral-domain optical coherence tomography measured retinal and optic nerve layers.
- Clinical data included perinatal parameters, blood tests, and neurological imaging.
Main Results:
- Inner retinal layers and peripapillary nerve fiber layer thickness were reduced in HIE patients with severe encephalopathy.
- Ocular damage correlated with C-reactive protein, lactate dehydrogenase, and cerebral edema.
- Higher total bilirubin levels showed a protective effect against retinal damage.
Conclusions:
- Reduced inner retinal thickness and optic nerve fiber layer impairment are linked to HIE severity.
- Ocular damage in HIE is associated with inflammation and cerebral edema.
Purpose:
To evaluate the effect of neonatal hypoxic-ischaemic injury on the retina and the optic nerve and to correlate ocular damage with systemic parameters, laboratory tests, neurological imaging and therapeutic hypothermia at birth.
Methods:
Forty-one children with hypoxic-ischaemic encephalopathy (HIE) at birth (9.09 ± 3.78 years) and a control group of 38 healthy subjects (9.57 ± 3.47 years) were enrolled in a cohort study. The HIE population was divided into three subgroups, based on the degree of encephalopathy according to Sarnat score and the treatment with therapeutic hypothermia (TH): Sarnat score I not treated with hypothermia, Sarnat score II-III treated with TH and Sarnat score II-III not subjected to TH. Total macular thickness, individual retinal layers and peripapillary nerve fibre layer thickness were measured with spectral-domain optical coherence tomography. Clinical data of perinatal period of HIE children were collected: APGAR score, pH and base excess of funiculus blood at birth, apnoea duration, brain ultrasound, cerebral MRI ischaemic lesions and blood chemistry tests.
Results:
Children with Sarnat score I did not show a reduction of peripapillary nerve fibres and ganglion cell layer compared to the control group (p = 0.387, p = 0.316). Peripapillary nerve fibre layer was 109.06 ± 7.79 μm in children with Sarnat score II-III treated with TH, 108.31 ± 7.83 μm in subjects with Sarnat score II-III not subjected to TH and 114.27 ± 6.81 μm in the control group (p = 0.028, p = 0.007). Ganglion cell layer was thinner in children with Sarnat score II-III treated with TH (50.31 ± 5.13 μm) compared to the control group (54.04 ± 2.81 μm) (p = 0.01). Inner retinal layers damage correlated with C-reactive protein and lactate dehydrogenase increase, while higher levels of total bilirubin were protective against retinal impairment (p < 0.05). Cerebral oedema was related to peripapillary nerve fibre layer damage (p = 0.046).
Conclusions:
Thickness reduction of inner retinal layer and peripapillary nerve fibre impairment was related to encephalopathy severity. Ocular damage was associated with inflammation and cerebral oedema following hypoxic-ischaemic damage.
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