Pathologic Ocular Changes During Pregnancy
Can pregnancy affect eyes badly in any case?
@keaon Pregnancy-induced hypertension (preeclampsia)
The onset of hypertension (>140/90 after 20 wk) in an otherwise normotensive pregnant woman with proteinemia (>300 mg/24 h) is the minimal criteria needed to diagnose a patient with preeclampsia.  Furthermore, if these changes are associated with seizures, which are not attributed to any other cause, then the disorder is classified as eclampsia. The incidence of preeclampsia is approximately 5%, and it is more common in primigravids, in younger and older women, and in those patients with maternal systemic diseases. The onset of this disorder is usually after the 20th week of gestation.
Preeclampsia has various maternal and fetal consequences. In up to one third of cases, ocular sequelae have been reported. The most common ocular complaint is visual blurriness; however, other symptoms have also been noted, including photopsias, scotomas, and diplopia. The protean ocular manifestations include retinopathy, optic neuropathy, serous detachments, and occipital cortical changes.
The changes that occur in retinopathy due to preeclampsia are similar to changes from hypertensive retinopathy.  The most common finding is focal retinal arteriole narrowing, which also may be diffuse. Other changes may include retinal hemorrhages, edema, exudates, nerve fiber layer infarcts, and vitreous hemorrhage secondary to neovascularization. A positive correlation exists between the severity of preeclampsia and the degree of retinopathy; however, most changes are reversible once preeclampsia resolves. Preeclampsia retinopathy may be more severe with underlying diabetes, chronic hypertension, and renal disease.
Optic nerve changes that have been reported include papilledema, acute ischemic optic neuropathy, and optic atrophy.
Serous exudative retinal detachments may occur in severe preeclampsia or eclampsia. They tend to be bilateral, bullous, and with preeclampsia retinopathy changes. The underlying mechanism is thought to be related to choroidal nonperfusion and resultant subretinal leakage. Most patients with serous detachments have resolution of symptoms a few weeks within postpartum.
Cortical blindness, although a rare complication, has been a reported cause of vision loss in patients with preeclampsia. Cerebral edema is believed to be the mechanism of vision loss. Two proposed theories may account for the cerebral edema. One theory suggests that vasospasm causes transient ischemia and produces cytotoxic edema. The other theory explains that preeclampsia causes increased permeability from circulatory dysregulation, thus providing vasogenic edema. Treatment or resolution of preeclampsia and the resultant cerebral edema usually parallels visual recovery.
Preeclampsia may cause certain non–vision-threatening changes in the eye, including conjunctival vascular spasm or tortuosity, papillary mydriasis, ptosis, and nystagmus.
Central serous retinopathy
Although not typical, central serous retinopathy (CSR) has been reported to occur during pregnancy. Although more common in the third trimester, it may also occur during the first or second trimesters. The condition resolves spontaneously in the first few months postpartum and has been known to recur in future pregnancies, usually in the same eye. The underlying mechanism remains unclear.
Benign intracranial hypertension
Benign intracranial hypertension (BIH), also known as pseudotumor cerebri, is defined as increased intracranial hypertension and its possible sequelae, with normal cerebrospinal fluid composition and normal neuro-imaging. It typically occurs in obese females in their third decade of life. Interestingly, pregnancy does not increase the risk of developing BIH. If BIH does occur, it usually presents in the first trimester but may occur later.
BIH does not carry any fetal consequences and carries the same visual outcome in nonpregnant patients. Treatment for BIH in pregnancy is similar to that in nonpregnant patients with a few considerations. First, intense weight loss is not recommended because of risk to fetal viability. Second, carbonic anhydrase inhibitors are contraindicated during pregnancy due to the potential fetal teratogenic effects. Thirdly, the use of diuretics poses the risk of electrolyte and placental blood flow changes. Reports exist of spontaneous improvement with no treatment and very close follow-up care of optic nerve function. However, with visual compromise, interventions, such as bed rest, lumbar puncture, optic nerve sheath decompression, and lumboperitoneal shunting, have been reported.
Occlusive vascular disorders
It is well appreciated that pregnancy represents a hypercoagulable state, through various changes that occur with platelets, clotting factors, and arteriovenous flow dynamics. Such changes may be related to the development of retinal artery and vein occlusions, disseminated intravascular coagulopathy (DIC), thrombotic thrombocytopenic purpura (TTP), amniotic fluid embolism, and cerebral venous thrombosis.
Both branch and central retinal artery occlusions have been reported to occur in pregnancy. Although a hypercoagulable workup may detect an abnormality, routine hematological workup may be unremarkable. A case report exists of bilateral central retinal artery occlusion from amniotic fluid embolism, which in and of itself is a potentially fatal condition. Retinal vein occlusions are less common than arterial occlusions.
DIC is characterized by widespread small vessel thrombosis often associated with hemorrhage and tissue necrosis. It may occur with complications in pregnancy, such as abruptio placentae, severe preeclampsia, complicated abortion, and intrauterine death. The choroid is the most common location in the eye for DIC to manifest. Patients often complain of visual loss from choroidal infarction or hemorrhage, retinal pigment epithelial, or serous detachments usually located in the posterior pole. Visual recovery usually occurs once the DIC resolves; however, mild pigmentary changes may persist.
TTP is a rare disorder characterized by small vessel thrombosis, thrombocytopenia, microangiopathic hemolytic anemia, neurologic and renal dysfunction, and fever. Visual symptoms may occur due to serous retinal detachment, retinal artery narrowing, retinal hemorrhage, and optic nerve head edema. The central nervous system may be involved, and the most common visual complaint is a homonymous hemianopia.
Antiphospholipid antibody syndrome is another condition that warrants consideration. In this syndrome, patients are in a thrombophilic state and are prone to recurrent arterial and/or venous thrombosis. Diagnostic criteria include clinical evidence of recurrent pregnancy loss or thrombosis in any organ or tissue as well as laboratory evidence of circulating antiphospholipid antibodies or lupus anticoagulant. Ophthalmic manifestations may present in the form of vascular thrombosis of the retina, the choroid, the optic nerve and visual pathway, and ocular motor nerves.
Ptosis has been reported to occur during and after normal pregnancy and usually is unilateral. The mechanism is thought to be due to defects that develop in the levator aponeurosis from fluid, hormonal, and other changes due to the stress of labor and delivery.
Endogenous candidal endophthalmitis, although rare, has been associated with pregnant or postpartum women with indwelling intravenous catheters, systemic antibiotic use, and surgery. However, postpartum candidal endophthalmitis has also been reported in an otherwise uncomplicated labor and delivery.