Spectral-domain OCT changes in retina and optic nerve in children with hypoxic–ischaemic encephalopathy

Abstract

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.

Optical coherence tomography as retinal imaging biomarker of neuroinflammation/neurodegeneration in systemic disorders in adults and children

“…Optical coherence tomography (OCT) has emerged as a fast, non-invasive and affordable imaging modality to assess the retina and optic nerve and, therefore, lends itself to evaluate ocular changes in neuroinflammatory/neurodegenerative disorders [ 7 – 14 ]. Research on systemic diseases, such as diabetes mellitus, multiple sclerosis and CNS diseases, especially Alzheimer and Parkinson diseases, has identified inflammatory and neurodegenerative changes in the retina that can be evaluated through specific biomarkers, that recently has gained more importance.…”

“…Several studies of infants with hypoxic ischaemic encephalopathy (HIE) sought to find noninvasive methods to assess neurologic damage from ischaemia and to predict the association with future neurologic dysfunction or abnormalities in structural CNS features. Although few studies have been done, non-invasive OCT does not require sedation and can be done at the bedside [ 13 , 14 ], most recently demonstrated in a hypothermia treatment trial [ 14 ].…”

Hypothermic Shock Applied After Perinatal Asphyxia Prevents Retinal Damage in Rats

“…Based on the results obtained in previous animal experimentation, the use of hypothermia is currently the standard of care to treat episodes of severe PA-ischemia in humans (World Health Organization, 1991;Thoresen, 2015;Rivero-Arias et al, 2019). Nevertheless, most clinical studies still focus on the positive effects of hypothermia in the brain while studies on the beneficial effects on the visual system are still scarce (Akin et al, 2019;Grego et al, 2020).…”

Continuous Hypoxia Reduces Retinal Ganglion Cell Degeneration in a Mouse Model of Mitochondrial Optic Neuropathy

“…It is clear that profound hypoxia (as may occur in the setting of vascular occlusions or global hypoperfusion of the central nervous system) may result in RGC degeneration and optic atrophy. 31 , 32 However, overt RGC injury was not observed in mice subjected to a more moderate level of hypoxia similar to that used in the studies by the Mootha laboratory. 33 Therefore, we were interested in exploring the potential therapeutic value of hypoxia in our model of RGC-specific ndufs4 deletion.…”