“…Although both eyes and visual pathways were damaged in HIE rats, the contribution of said damage to visual impairment was not defined [18]. Mangalesh [15]. In our study, the enrolled population did not present visual impairment, as we measured a best corrected visual acuity of 10/10 in all patients.…”
Section: Discussionmentioning
confidence: 78%
“…Experimental studies on murine models report damage to the inner retinal layers with HIE (ganglion cell layer, inner plexiform layer and inner nuclear layer) [11][12][13]. Mangalesh et al found ganglion cell and peripapillary nerve fibre layer impairment assessing HIE children with SD-OCT within the first two weeks of hypoxic-ischaemic insult [15]. Osborn et al showed greater susceptibility of inner retina to lack of oxygen compared to outer retinal layers.…”
Section: Discussionmentioning
confidence: 99%
“…Mangalesh et al found an association between retinal defects and MRI alterations evaluating 8 HIE children: newborns with low-grade MRI changes had no retinal findings, children with intermediate MRI damage had subretinal fluid or macular cystic spaces, while children with more severe MRI alterations had parafoveal cystoid spaces and loss of GCL/RNFL in the macula. Moreover, the author pointed out that children with intermediate MRI damage showed a different kind of retinal damage, suggesting a possible primitive eye injury independent from brain damage [ 15 ]. In our study, the enrolled population did not present visual impairment, as we measured a best corrected visual acuity of 10/10 in all patients.…”
Section: Discussionmentioning
confidence: 99%
“…Retinal and choroidal thinning, associated with subretinal fluid, was detected with spectral-domain optical coherence tomography (SD-OCT) in HIE newborns [ 14 ]. Other findings identified with SD-OCT in asphytic children are perimacular cystoid spaces, ganglionar cell and peripapillary nerve fibre layer thinning [ 15 ]. So far, no studies evaluated retinal and optic nerve long-term outcomes after neonatal HIE.…”
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.
“…Although both eyes and visual pathways were damaged in HIE rats, the contribution of said damage to visual impairment was not defined [18]. Mangalesh [15]. In our study, the enrolled population did not present visual impairment, as we measured a best corrected visual acuity of 10/10 in all patients.…”
Section: Discussionmentioning
confidence: 78%
“…Experimental studies on murine models report damage to the inner retinal layers with HIE (ganglion cell layer, inner plexiform layer and inner nuclear layer) [11][12][13]. Mangalesh et al found ganglion cell and peripapillary nerve fibre layer impairment assessing HIE children with SD-OCT within the first two weeks of hypoxic-ischaemic insult [15]. Osborn et al showed greater susceptibility of inner retina to lack of oxygen compared to outer retinal layers.…”
Section: Discussionmentioning
confidence: 99%
“…Mangalesh et al found an association between retinal defects and MRI alterations evaluating 8 HIE children: newborns with low-grade MRI changes had no retinal findings, children with intermediate MRI damage had subretinal fluid or macular cystic spaces, while children with more severe MRI alterations had parafoveal cystoid spaces and loss of GCL/RNFL in the macula. Moreover, the author pointed out that children with intermediate MRI damage showed a different kind of retinal damage, suggesting a possible primitive eye injury independent from brain damage [ 15 ]. In our study, the enrolled population did not present visual impairment, as we measured a best corrected visual acuity of 10/10 in all patients.…”
Section: Discussionmentioning
confidence: 99%
“…Retinal and choroidal thinning, associated with subretinal fluid, was detected with spectral-domain optical coherence tomography (SD-OCT) in HIE newborns [ 14 ]. Other findings identified with SD-OCT in asphytic children are perimacular cystoid spaces, ganglionar cell and peripapillary nerve fibre layer thinning [ 15 ]. So far, no studies evaluated retinal and optic nerve long-term outcomes after neonatal HIE.…”
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.
“…1 B; red). These differences in severity of injury are well documented responses of the central nervous system, including the retina and brain, in different individuals after HI exposure in both humans and preclinical Rice–Vannucci rodent model 58 , 59 , 63 , 64 . Figure 1 Abnormal dark-adapted electroretinogram (ERG) responses in juvenile mice after exposure to HI.…”
Ischemic stroke is a major cause of long-term disabilities, including vision loss. Neuronal and blood vessel maturation can affect the susceptibility of and outcome after ischemic stroke. Although we recently reported that exposure of neonatal mice to hypoxia–ischemia (HI) severely compromises the integrity of the retinal neurovasculature, it is not known whether juvenile mice are similarly impacted. Here we examined the effect of HI injury in juvenile mice on retinal structure and function, in particular the susceptibility of retinal neurons and blood vessels to HI damage. Our studies demonstrated that the retina suffered from functional and structural injuries, including reduced b-wave, thinning of the inner retinal layers, macroglial remodeling, and deterioration of the vasculature. The degeneration of the retinal vasculature associated with HI resulted in a significant decrease in the numbers of pericytes and endothelial cells as well as an increase in capillary loss. Taken together, these findings suggest a need for juveniles suffering from ischemic stroke to be monitored for changes in retinal functional and structural integrity. Thus, there is an emergent need for developing therapeutic approaches to prevent and reverse retinal neurovascular dysfunction with exposure to ischemic stroke.
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