Numerous physiologic effects occur within the body during pregnancy, and the eye is no exception. This article outlines both normal physiologic changes and pathological changes in the eye that can occur from pregnancy. In the physiological changes in pregnancy, changes in cornea, intraocular pressure, visual field changes, and external changes have been discussed. In pathologic ocular changes, pregnancy induced hypertension, central serous retinopathy, benign intracranial hypertension, occlusive vascular disorders, and other miscellaneous disorders have been discussed.
Physiologic Ocular Changes Occurring During Pregnancy
Cornea: Corneal sensitivity is reduced in the majority of pregnant women, with the majority of alterations occurring in the third trimester and then reversing in the postpartum period. One such explanation is the modest increase in corneal thickness that might occur as a result of corneal 0edema. There may also be an increase in corneal curvature and steepening. These alterations have been observed to occur even during breastfeeding in the postpartum period. Corneal curvature, on the other hand, is reversible after nursing is stopped. A change in corneal curvature, increased corneal thickness/edema, or an altered tear film can all cause contact lens discomfort during pregnancy. In any event, it is advised to wait several weeks after delivery before prescribing a new refraction. During pregnancy or the postpartum period, diminished or transitory loss of accommodation may also occur. Krukenberg spindles that have recently evolved have been discovered early in pregnancy. The mechanism is most likely linked to hormonal changes (e.g., low progesterone levels). Krukenberg spindles are generally reduced or absent by the third trimester due to an increase in progesterone and aqueous outflow [1].
Intraocular Pressure
During pregnancy, there is a drop in intraocular pressure that lasts for several months after the baby is born. An increase in aqueous outflow; a decrease in systemic vascular resistance, leading to lower episcleral venous pressure; generalized enhanced tissue elasticity, leading to decreased scleral rigidity; and generalized acidemia during pregnancy have all been proposed as possible explanations. The improvement of glaucoma during pregnancy has been recorded in a few cases, therefore this drop in intraocular pressure could have consequences for pregnant women with preexisting glaucoma [2].
Visual Field Changes
The extent and mechanism of visual field changes that may occur in pregnant women are the subject of much debate. Bitemporal loss, concentric constriction, and increased blind patches are all examples of field loss. Changes to the pituitary gland, which may influence the optic chiasm, are among the proposed mechanisms. These asymptomatic modifications in the visual field were shown to be entirely reversible after childbirth. Pregnant women with symptomatic visual field loss, on the other hand, should be investigated further.
External Changes
There has been a documented decrease in conjunctival capillaries and an increase in the granularity of conjunctival venules, both of which are reversible during the postpartum period. Changes in the skin, known as chloasma, are another common outward effect of pregnancy. Some pregnant women develop heightened pigmentation around the eyes and cheeks as a result of higher hormone levels (i.e. progesterone). Postpartum, the pigmentation alterations tend to diminish slowly.
Pathologic Ocular Changes during Pregnancy
Pre-eclampsia: The emergence of hypertension (>140/90 after 20 weeks) in a pregnant woman who is otherwise normotensive and has proteinemia (>300 mg/24 hours) is the bare minimum required to diagnose preeclampsia [3]. Furthermore, if these changes are accompanied by seizures
that cannot be explained by any other factor, the condition is categorized as eclampsia. Preeclampsia affects about 5% of pregnant women, and it is more common in primigravids, younger and older mothers, and those with maternal systemic disorders. This disease usually appears after the 20th week of pregnancy [4].
Preeclampsia has a variety of effects on both the mother and the fetus. Ocular sequelae have been recorded in up to a third of cases. Visual blurriness is the most prevalent ocular complaint, but additional symptoms such as photopsia’s, scotomas, and diplopia have also been reported. Retinopathy, optic neuropathy, serous detachments, and occipital cortical alterations are just few of the visual symptoms.
The changes that occur in preeclampsia-related retinopathy are comparable to those that occur in hypertensive retinopathy. Focused retinal arteriole narrowing, which can potentially be diffuse, is the most prevalent finding. Retinal hemorrhages, edema, exudates, nerve fiber layer infarcts, and vitreous hemorrhage related to neovascularization are all possible changes. Although there is a link between the severity of preeclampsia and the severity of retinopathy, most changes are reversible if the preeclampsia goes away. With underlying diabetes, persistent hypertension, or renal failure, preeclampsia retinopathy can be more severe. Papilledema, acute ischemic optic neuropathy, and optic atrophy are some of the optic nerve alterations that have been observed. In severe preeclampsia or eclampsia, exudative retinal detachments can occur. Bilateral, bullous, and preeclampsia retinopathy alterations are common. The underlying process is assumed to be linked to choroidal nonperfusion and subretinal leaking as a result. The majority of individuals with serous detachments get symptom relief within a few weeks of giving birth [5].
Although an uncommon consequence, cortical blindness has been documented as a cause of visual loss in preeclampsia patients. Vision loss is thought to be caused by cerebral edema. The cerebral edema could be explained by one of two explanations. According to one idea, vasospasm induces temporary ischemia and cytotoxic edema. Preeclampsia, according to the alternative idea, generates increased permeability due to circulatory dysregulation, resulting in vasogenic edema. Preeclampsia and the resulting cerebral edema are frequently treated or resolved at the same time as visual recovery. Preeclampsia can produce conjunctival vascular spasm or tortuosity, papillary mydriasis, ptosis, and nystagmus, all of which are not vision-threatening.
Central Serous Retinopathy
Central serous retinopathy (CSR) has been found to occur during pregnancy, which is unusual. It is more common in the third trimester, but it can also happen in the first or second. The problem normally goes away on its own during the first few months after delivery, although it has been known to reoccur in subsequent pregnancies, usually in the same eye. The mechanism behind it is yet unknown [6].
Benign Intracranial Hypertension
Increased intracranial pressure and its possible repercussions are classified as benign intracranial hypertension (BIH), also known as pseudotumor cerebri, with normal cerebrospinal fluid composition and normal neuroimaging. Obese females in their third decade of life are more likely to develop it. Surprisingly, pregnancy has little effect on the development of BIH. If BIH does develop, it usually does so during the first trimester, but it can also happen later.
BIH has no prenatal implications and has the same visual outcome in pregnant and non-pregnant patients. With a few exceptions, treatment for BIH in pregnancy is comparable to that for non-pregnant individuals. For starters, rapid weight reduction is not advised due to the risk of fetal viability. Second, carbonic anhydrase inhibitors are not recommended during pregnancy due to the risk of fetal harm. Finally, diuretics have the potential to cause electrolyte and placental blood flow abnormalities. There have been reports of spontaneous improvement in optic nerve function with no treatment and extremely close follow-up care. However, therapies such as bed rest, lumbar puncture, optic nerve sheath decompression, and lumboperitoneal shunting have been documented in cases of visual compromise.
Miscellaneous Disorders
Ptosis is a condition that can arise during and after a normal pregnancy and is usually unilateral. The mechanism is considered to be caused by abnormalities in the elevator aponeurosis caused by fluid, hormonal, and other changes during labor and delivery [7].
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