Abstract
PurposeTo 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.MethodsForty-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.ResultsChildren 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).ConclusionsThickness 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.
Highlights
Neonatal hypoxic–ischaemic encephalopathy (HIE) is a clinical syndrome characterised by abnormal neurologic behaviour in the neonatal period due to inadequate blood flow and oxygen provision to the brain as a result of hypoxic–ischaemic events [1, 2]
& SII-III/therapeutic hypothermia (TH)+ subgroup: 18 children with Sarnat score II-III treated with TH
Age difference between subgroups can be explained due to TH being performed based on the severity of HIE and TH being available in the Neonatal Intensive Care Unit from 2010: children of SII-III/TH- subgroup were born between 2003 and 2009 when TH was not available, children of SII-III/TH+ subgroup were born between 2010 and 2014 and where treated with TH, while the children of SI/TH, that did not need TH, were born between 2003 and 2014
Summary
Neonatal hypoxic–ischaemic encephalopathy (HIE) is a clinical syndrome characterised by abnormal neurologic behaviour in the neonatal period due to inadequate blood flow and oxygen provision to the brain as a result of hypoxic–ischaemic events [1, 2]. Sarnat score divides HIE into three clinical stages (mild—grade I, moderate—grade II and severe— grade III-), based on different parameters: level of consciousness, neuromuscular control, complex reflexes, autonomic nervous system activity, seizures and electroencephalogram findings [3]. The standard of care for moderate and severe HIE includes therapeutic hypothermia (TH), which reduces core temperature to 33 °C–34 °C, with neuroprotective effects. TH improves neurological outcomes in children with HIE, it does not provide complete protection: about 30% of treated children present different degrees of disability at 18 months of life [2, 5]
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