Pregnancy and retinal and retinal vascular complications
Review Article

Pregnancy and retinal and retinal vascular complications

Anushua Bhattacharya1, Sruthi R. Arepalli2

1Emory University School of Medicine, Atlanta, GA, USA; 2Emory Eye Center, Emory University, Atlanta, GA, USA

Contributions: (I) Conception and design: SR Arepalli; (II) Administrative support: SR Arepalli; (III) Provision of study materials or patients: SR Arepalli; (IV) Collection and assembly of data: Both authors; (V) Data analysis and interpretation: Both authors; (VI) Manuscript writing: Both authors; (VII) Final approval of manuscript: Both authors.

Correspondence to: Sruthi R. Arepalli, MD. Emory Eye Center, Emory University, 1365B Clifton Road, Building B, Suite 2400, Atlanta, GA 30322, USA. Email: sruthiarepalli@gmail.com.

Abstract: Pregnancy requires several changes in the body of the mother to successfully carry and deliver a child. Multiple alterations occur, including changes in cardiovascular system to meet the increased demands of the mother and placenta, the tilting of the hypercoagulable status to a more pro-coagulable state to prevent excessive blood loss post-delivery, and immunologic manipulations to protect the mother and fetus and decreasing the risk of a fatal immunologic response to the allogeneic fetus. These alterations are physiologically normal and expected, but can become pathologic when thresholds are crossed. Pregnancy may cause or exacerbate underlying retinal vascular diseases, a class of disorders compromised predominantly of retinal vein occlusion (RVO), retinal artery occlusion (RAO), central serous retinopathy (CSR), diabetic retinopathy, and hypertensive-related retinopathy, which includes pre-eclampsia, eclampsia, and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. The majority of the literature on retinal changes associated with pregnancy has focused on diabetic retinopathy, while the knowledge regarding the pathogenesis and treatment options of other pregnancy-related vascular diseases remains scarce. Understanding the implications pregnancy has on these rare, but severe, retinal vascular complications can help guide clinical management and potential treatment modalities. This paper aims to serve as a review of the retinal manifestations of diseases outside of diabetic retinopathy.

Keywords: Pregnancy; retinal vascular complications; central serous chorioretinopathy (CSCR)

Received: 25 April 2023; Accepted: 25 September 2023; Published online: 26 October 2023.

doi: 10.21037/aes-23-31

Introduction

Background

Pregnancy, a state in which the human body goes through physiologic changes in order to support the adapting mother and growing fetus, can come with systemic and ocular complications. These ocular manifestations can range from mild to visually destructive.

Rationale and knowledge gap

Out of protection for the fetus, more invasive studies are prohibited, which limits our knowledge of deeper pathophysiology, cost-benefits ratio of treatments, and certain treatment outcomes in pregnant patients.

Objective

This review article aims to highlight certain retinal vascular conditions more common in pregnancy, such as central or branch retinal artery occlusion (CRAO and BRAO, respectively), central or branch retinal vein occlusion (CRVO and BRVO, respectively), central serous retinopathy (CSR), pre-eclampsia related retinopathy and retinopathy secondary to hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. Overall, the current regimens and outcomes are anecdotal and require the cooperation of hematologists, cardiologists, obstetricians, and ophthalmologists.

Normal physiologic changes during pregnancy

Pregnancy induces several physiological changes in the mother to both nurture the developing fetus and help prepare the mother for labor and delivery. These include, but are not limited to: cardiovascular manipulations to meet the placental metabolic demands, the induction of a hypercoagulable state to prevent excessive blood loss post-delivery, and immunologic adaptations to protect the mother and fetus while avoiding a fatal immunologic response to the allogeneic fetus (1). These alterations are physiologically normal, but can become pathologic when protective thresholds are crossed.

Early on, the mother’s cardiovascular system changes drastically: cardiac output increases around 40% due to an increase in stroke volume and heart rate, while peripheral vasodilation leads to a 25–30% decrease in systemic vascular resistance due to estradiol and nitric oxide upregulation (2). Despite the increase in plasma volume and cardiac output, pregnant women are physiologically hypotensive due to progesterone release, which relaxes the blood vessel walls and increases blood flow to mother and fetus. The coagulation system is altered during pregnancy to produce a hypercoagulable state to ensure hemostasis after delivery. Clotting factors such as factors VIII, IX, and X increase while endogenous anticoagulants such as antithrombin and protein S decrease (3). While the maternal immune system has not been fully understood, it’s known that a balance between pro-inflammatory and anti-inflammatory changes leads pregnant women to being susceptible to infections (4).

Retinal vascular occlusion

Retinal vascular occlusions, which can occur in either arteries (RAOs), or veins (RVOs), typically occur in the fifth decade or later and are attributed to various systemic risk factors, such as hypertension, hyperlipidemia, and diabetes. Other risk factors include inherited disease states that predispose to clot formation, including, but not limited to: patent foramen ovale, antiphospholipid syndrome, factor V Leiden mutation, low protein S, and increased factor VIII (5). Although pregnancy occurs in ages younger than the fifth decade, the physiological changes associated with gestation can lead to spontaneous occurrences of RAOs and RVOs. The prevalence of retinal vascular occlusions is not well documented. Maurya et al., report a 2-year prospective study at an outpatient setting for ophthalmology and for obstetrics and gynecology and found 16.36% of pregnant-related vascular disorders to be that of RVO (6). In another study by Park et al. over a 4-year period found out of the 1.8 million births, 33 pregnancies were complicated by RVO (7).

CRVO

The risk of RVO instances during pregnancy is reported to be between 0.05% and 1.8% and occurs most often in the third trimester (8). Patients typically present with acute, painless visual decline as the blocked, damaged vasculature leads to macular edema. Additionally, the lack of oxygenation induces a release of vascular endothelial growth factor (VEGF), with subsequent abnormal neovascularization, and in certain cases, vitreous hemorrhage or tractional retinal detachments (9).

A few reports exist in the literature detailing RVOs in pregnancy. Li et al. report a case of a 30-year-old woman who developed a bilateral CRVO at month 7 in her pregnancy (10). The patient was monitored but not treated. Post-partum, her sight returned to normal in both eyes at the 1-year mark. Several other reports have opted for observation as well (10-14). When treatment was initiated, therapies ranged from intravitreal corticosteroid injections, panretinal photocoagulation, and systemic administration of anti-coagulation (5,15-19).

RAO

Pregnancies with RAO are usually complicated with pre-eclampsia or hypercoagulability due to acquired or congenital deficiency in hemostatic factors. The incidence of RAO is also not well documented; in one retrospective case series of 147 patients who developed acute visual loss during the pregnancy, 4.1% (n=2) were due to RAO (20). Treatment of pregnancy-induced RAOs in the literature has mainly been anticoagulants and observation (5,11,12,18).

Interestingly, the development of a RAO in pregnancy has led to the diagnosis of a systemic condition. Kurtz et al. identified a unilateral BRAO during pregnancy which led to a previously undetected diagnosis of familial thrombophilia (11). The authors describe a 32-year-old, who presented with a BRAO at 13 weeks of gestation. She had no prior thrombotic events, though family history was significant for deep venous thrombosis and lethal pulmonary embolism in maternal grandmother. At the time of presentation, she was evaluated for thrombophilia-hypofibrinolysis and revealed a protein S deficiency and a high factor VIII count. Likewise, Askim et al. describe the first case of a BRAO due to hereditary hemorrhagic telangiectasia (HHT) during pregnancy (21). In this case, a pregnant woman presented with sudden scotoma in her left eye. A work-up revealed HHT that ran through her family. A thoracic computed tomography (CT) and pulmonary angiography revealed a pulmonary arteriovenous malformation (PAVM). The authors propose that HHT should be screened for PAVMs prior to pregnancy; if already pregnant, the patient should undergo an echocardiography to confirm PAVM.

Central serous chorioretinopathy (CSCR)

CSCR is reported to be ten times more common in men, but pregnancy is a risk factor for CSCR development (8). CSCR is characterized by elevated endogenous cortisol and catecholamines leading to a permeable blood-retinal barrier (22). An accumulation of subretinal fluid leads to neurosensory retinal detachment in the macula at the level of the retinal pigment epithelium (RPE) (23).

In pregnant women specifically, CSCR can present with white subretinal exudation. One study reported white fibrous subretinal exudates are found in 90% of pregnancy-associated CSCR (pCSCR) compared to 20% of general cases (24). Risk factors during pregnancy include glucocorticoid use, Cushing syndrome, obstructive sleep apnea, hypertension, and emotional stress. In pregnancy in particular, elevated cortisol levels, preeclampsia, and hypertension are risk factors (25).

There are cases which document the spontaneous resolution of CSR after delivery (23,26).

However, there are also reports detailing permanent visual loss in patients. CSCR can also recurrently present in subsequent pregnancies and, over time, lead to subretinal fibrin-fibrosis and scarring of the macula (27,28).

Pre-eclampsia-complicated retinopathy

Pre-eclampsia is a leading cause of both maternal and fetal morbidity and mortality worldwide and is characterized by hypertension, proteinuria, and maternal organ dysfunction between mid-gestation to 6 weeks post-partum. Mild pre-eclampsia is reported to impact 0.5% of women and severe pre-eclampsia impacts 2–3% of women (29). Ophthalmologic complications associated with pre-eclampsia include cortical blindness, serous retinal detachment, Purtscher-like retinopathy, CRVOs, and retinal or vitreous hemorrhages (30). Most reports document the improvement of vision after delivery but in some cases, Purtscher-like retinopathy resulted in permanent vision loss (31,32).

While vision changes can be transient in the settings of pre-eclampsia, some courses of pregnancy can lead to permanent vision loss as was the case in Kotlyar et al. (33). A 27-year-old primigravida patient presented at 31 weeks with pre-eclampsia. She was treated with hydralazine and labetalol to maintain blood pressure control. Unfortunately, after delivery, she developed decreased visual acuity that was limited to counting fingers. Fundus exam showed diffuse retinal whitening, optic nerve pallor, and retinal hemorrhages. At 3-month follow-up, the patient had visual acuity limited to 20/150 and 20/250.

HELLP-complicated retinopathy

HELLP syndrome is a pregnancy complication that usually presents in women with underlying pre-eclampsia or eclampsia. Risk factors are shared with pre-eclampsia and include pre-existing hypertension or diabetes, advanced maternal age. The pathophysiology of Purtscher-like retinopathy is not well understood in the pregnant state. In the setting of HELLP syndrome, it is thought chronic inflammation of the placenta may cause complement activation leading to neutrophil and leukocyte embolization. Interestingly, in 15% of HELLP patients, no signs of pre-eclampsia are present (34).

Much like the rare case of Purtscher-like retinopathy in the setting of pre-eclampsia, Stewart et al., report on a 25-year-old primigravida patient who developed Purtscher-like retinopathy in the setting of HELLP syndrome (35). Unfortunately, her vision remained impaired on follow up, with fundus exam showing severe optic atrophy and retinal thinning. In another instance, a 23-year-old primigravida patient developed HELLP syndrome and 2 days after delivery, noticed diminution of her vision. A fundus exam revealed bilateral serous detachment involving the macula. Her vision recovered completely 3 weeks post-partum (36).

HELLP syndrome has also been documented in the setting of posterior reversible encephalopathy syndrome (PRES). In this case, a 26-year-old pregnant female developed acute, bilateral vision loss due to serous retinal detachments and cortical vision loss during her post-partum period (37). She also developed systolic blood pressure in the 200s and laboratory tests showed thrombocytopenia, diffuse intravascular coagulopathy, and elevated liver function tests. She continued to deteriorate with worsening headaches and acute encephalopathy. HELLP syndrome was diagnosed and subsequent magnetic resonance imaging (MRI) confined vasogenic cerebral edema and PRES. Unfortunately, her visual acuity never improved.

Disseminated intravascular coagulation (DIC)-complicated retinopathy

DIC itself is associated with pregnancy complications such as pre-eclampsia, HELLP syndrome, placental abruption, retained stillbirth, and amniotic fluid embolism. Pregnancy-associated DIC secondary is estimated to be around 1–5% of all pregnancies in countries in Western hospitals (38). Two reports in the literature detail vision loss in the context of DIC in pregnancy. In one case, vision improved, while in the other, it did not. Both cases presented with serous retinal detachments, which were thought to be secondary to intravascular coagulation occluding the choriocapillaris in the poster pole, subsequently damaging the RPE-cells and their ability to supply the retina and subretinal space (39).

Amniotic fluid embolism-complicated retinopathy

Amniotic fluid embolism is a dangerous and life-threatening complication of pregnancy where the amniotic fluid enters the maternal pulmonary circulation shortly after giving birth and causes cardiorespiratory collapse. Risk factors include advanced maternal age, multiparity, trauma, and induction of labor (40). Amniotic fluid embolism occurs in 2 to 8 per 100,000 deliveries and is the second leading cause of peripartum maternal death in the United States (41). These amniotic fluid emboli can also occlude retinal arteries in pregnant patients, causing occlusion and serious vision consequences. Kim and Choi present a dramatic case of amniotic fluid embolism in a 28-year-old female who was admitted for an elective abortion at 16 weeks (42). Three hours later, the patient reported reduced vision in her left eye with initial best-corrected visual acuity (BCVA) was count fingers. Fluorescein angiography showed an occlusion in the infratemporal branch retinal artery. Three days later, two more arteries were occluded. The final BCVA never improved.

Current treatments

Out of ethical constraints for the well-being of the fetus, exploration of effective treatment during pregnancy are mostly anecdotal, leading to limitations on consensus for treatment. Anti-VEGF has growing literature supporting its use and is further discussed in the diabetic retinopathy section review paper (15,16,43).

Conclusions

One proposed intervention is laser photocoagulation, especially in the setting of neovascular complications which can arise from ischemia (8). Intravitreal corticosteroids are also well tolerated and can be used to target macular edema (16,17). Systemic anti-coagulants such as low-molecular-weight heparin (LMWH) have been used as well in an effort to lessen the burden of ischemic vascular injury, but the evidence for this is sparse. The literature also documents several cases of observation, as spontaneous resolution has been documented with time and/or after delivery. These treatments and outcomes are listed in Table 1.

Table 1

Pregnancy and retinal and retinal vascular complications

Authors Number of patients Demographics Retinal findings (CRVO, BRVO, CRAO, BRAO, CSR, etc.) Vision in impacted
eye		 Ocular complications
(CME, NVE, etc.) or remarkable systemic findings		 Treatment Resolution with delivery Final vision
Jürgens et al., 2022 3 Patient 1: 32 YO, 19 weeks CLRAO w/non-ischemic CRVO 5/200 No Acetylsalicylic acid (100 mg PO) Vision improved, while the inner retina layers and superior half of optic disc showed atrophy 20/20
Patient 2: 30 YO, 10 weeks; PFO identified during work-up CLRAO 20/20 No Acetylsalicylic acid (100 mg PO) Vision unimpacted, while the inner retina layers on OCT revealed progressive atrophy 20/20
Patient 3: 32 YO, 16 weeks PAMM Not available Not available Not available Not available Not available
Wester and Murray, 2010 1 26 YO, 26 weeks Retinal AVM with multiple BRVOs 20/50-2 CME Bevacizumab No, poor visual and anatomical outcomes 6/200E
Li et al., 2019 1 30 YO, 7 months CRVO bilaterally 20/63, 20/40 CME bilaterally Not available No, poor visual outcome 20/125, 20/200
Kurtz et al., 2016 3 Patient 1: 35 YO, 8 weeks BRAO—left eye Not reported Not available Enoxaparin 40 mg BID, switched to once a day Not available Not available
Patient 2: 32 YO, 13 weeks BRAO—right eye Not reported Not available Enoxaparin 1.5 mg/kg per day Not available Not available
Patient 3: 55 YO, 15 years post delivery CRVO left eye Not reported Not available – Not available Not available
Pokroy et al., 2022 1 39 YO, 7 weeks CRVO right eye 20/200 CME Deferred treatment until 2nd trimester: intravitreal dexamethasone implant at 16 weeks Yes, visual recovery VA of 20/30
Ozdamar et al., 2010 1 25 YO, 1 week post delivery Combined CLRAO and incomplete CRVO of right eye 20/20, 20/20 Elevated D-dimer (1.64, NL is 0–0.5 mg/mL) Not available Not available Not available
Mee et al., 2017 1 30 YO, 28 weeks Bilateral CRVO 20/40, 20/40 NVE Right eye treated with PRP No, VA worsened 20/63
Gonzalvo et al., 2000 1 30 YO, 28 weeks CRVO in right eye CF, 20/200 Severe pre-eclampsia and HELLP Not available Symptoms worsened after 10 days after delivery 20/125
Bahar et al., 2022 1 36 YO, 36 weeks CRVO with CLRAO CF Not available LMWH 40 mg subcutaneously daily for 7 days No, VA worsened 10/125
Zhang and Reddy, 2017 1 ~30s YO (exact age unspecified), 20 weeks Bilateral CRVO 20/50, 20/40 Protein S level decreased (61%), heterozygous for factor V Leiden deficiency Not available Patient lost to follow-up Patient lost to follow-up
Al-Mujaini et al., 2008 3 Patient 1: 27 YO, 7 months CSCR 20/200 Not available No, spontaneous resolution of CSCR Yes 20/20
Patient 2: 28 YO, 7 months CSCR 20/200 Not available No, spontaneous resolution of CSCR Yes 20/20
Patient 3: 25 YO, 6 months CSCR 20/180 Not available No, spontaneous resolution of CSCR Yes 20/20
Al-Mujaini and Wali, 2014 2 31 YO, 6 months CSCR 20/25 RPE detachment No, spontaneous resolution of CSCR No 20/200
Maggio et al., 2015 1 35 YO CSCR 20/20, 20/200 No Not available Yes Worsened BCVA due to atrophy
Chakraborti et al., 2014 1 30 YO, third trimester Bilateral CSCR 20/25, CF Serous macular detachment Not available No 20/200
Hirji et al., 2010 1 37 YO, 5 days post delivery CSCR 20/80 Not available Not available No 20/200
Normalina and Alias, 1998 1 39 YO, 30 weeks CSCR 20/320, 20/200 Not available Not available Yes Exact vision not disclosed
Lopez-Yang and Garcia, 2015 1 40 YO, 6 months pregnant CSCR 20/30, 20/20 Not available Single dose of 0.05 cc intravitreal bevacizumab in right eye on presentation No 20/30, 20/20
Motulsky et al., 2018 1 32 YO, 31 weeks CRVO 20/25, 20/200 Not available Single dose of 4 mg triamcinolone acetonide intravitreal injection in left eye No 20/20-2
Pole et al., 2020 1 34 YO, 32 weeks CSCR 20/30, 20/20 Serous neurosensory detachment Not available No 20/20
Komoto et al., 2019 1 31 YO, post C-section delivery at 37 weeks PIH HM, HM Bilateral retinal detachment associated with SRFM Not available No, presented after delivery 20/25, 20/20
Van Rysselberge et al., 2022 1 25 YO, 5 months HELLP 20/200, 20/20 Serous retinal detachments Beta blockers and MgSO4 protocol for HTN management, emergent C-section No 20/20, 20/20
Tsui and Kolomeyer, 2022 1 36 YO, 4 days post emergent C-section HELLP Listed as bilateral blindness Bilateral Purtscher-like retinopathy Not available Not available Not available
Haque et al., 2021 1 23 YO, 2 days post emergent C-section HELLP Not available Bilateral serous retinal detachment Not available Not available Complete recovery
Lin et al., 2012 1 20 YO, 2 days post emergent C-section HELLP 20/100, 20/200 Bilateral serous retinal detachment Not available Presented after delivery 20/25, 20/25
Velazquez-Villoria et al., 2019 1 36 YO, does not list start of symptoms HELLP HM, HM Pigment epithelial detachments Not available Not available 20/25, 20/25
Jayaraj et al., 2020 1 29 YO, 4 hours after C-section at 37 weeks Pre-eclampsia CF, CF Bilateral serous retinal detachment Treatment for high blood pressure Presented after delivery 20/30, 20/30
Raposo et al., 2020 1 37 YO, POD 1 at 36 weeks Pre-eclampsia Listed as decreased vision in both eyes Bilateral serous retinal detachment Enoxaparin and nifedipine Presented after delivery Recovery to baseline
Santoro et al., 2021 1 39 YO, 34 weeks 1 hour post delivery Pre-eclampsia without HTN 20/400, 20/400 Bilateral serous retinal detachment Treatment was deferred Presented after delivery 20/20, 20/20
Gupta and Sheidow, 2019 1 33 YO, post-partum period Pre-eclampsia 20/400, 20/200 Bilateral serous retinal detachment Not available Presented after delivery Not available
Raval and Das, 2019 1 20 YO, 2 days post C-section Severe pre-eclampsia CF, CF Diagnosis of bilateral Purtscher-like retinopathy with gross macular ischemia in preeclampsia secondary to antiphospholipid syndrome Tapering dose of oral corticosteroid for 4 weeks Presented after delivery 20/200, CF
Zamora et al., 2022 1 37 YO, 34 weeks, post delivery HELLP 20/50, 20/50 Bilateral serous retinal detachment Diuretics for HTN Presented after delivery 20/200, 20/200
Leff et al., 1990 1 33 YO, 7 months HELLP VA was 20/30 RE, 20/100 LE Vitreous hemorrhage, presumed NVE Not available Yes 20/30
Lanzetta, 1999 1 Age unspecified, post placental abruption and IUD at 34 weeks Eclampsia and DIC Not available RPE rip Not available Presented after IUD 20/20, 20/20
Kim and Choi, 2000 1 28 YO, 16 weeks, post dilatation and curettage for elective abortion BRAO secondary to amniotic fluid embolism Listed as diminished, HM Not available Not available No HM
Hoines and Buettner, 1989 1 30 YO, 40 weeks post C-section DIC secondary to placental abruption Not available Bilateral serous retinal detachment Not available Not available Not available
Stewart et al., 2007 1 25 YO, 38.5 weeks HELLP syndrome CF, CF Bilateral Purtscher-like retinopathy Not available No Permanent vision loss
Kini et al., 2021 1 26 YO, post-partum HELLP syndrome 20/50, 20/50 Not available Not available Not available Not available
Patel et al., 2005 1 40 YO, post-partum PIH CF, CF DIC Not available Not available 20/200, 20/120

In cases where both eyes were impacted, the right eye VA is listed before the left eye. CRVO, central retinal vein occlusion; BRVO, branch retinal vein occlusion; CRAO, central retinal artery occlusion; BRAO, branch retinal artery occlusion; CSR, central serous retinopathy; CME, cystoid macular edema; NVE, neovascularization elsewhere; YO, years old; CLRAO, cilioretinal artery occlusion; PO, per os (taken by mouth); PFO, patent foramen ovale; OCT, optical coherence tomography; PAMM, paracentral acute middle maculopathy; AVM, arteriovenous malformation; BID, 2 times a day; VA, visual acuity; NL, normal; PRP, panretinal photocoagulation; CF, counting fingers; HELLP, hemolysis, elevated liver enzymes, and low platelets; LMWH, low-molecular-weight heparin; CSCR, central serous chorioretinopathy; RPE, retinal pigment epithelium; BCVA, best-corrected visual acuity; PIH, pregnancy-induced hypertension; HM, hand motion; SRFM, subretinal fibrin-like material; HTN, hypertension; RE, right eye; LE, left eye; IUD, intrauterine demise; DIC, disseminated intravascular coagulation.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editor (Kareem Moussa) for the series “The Retina and Systemic Disease” published in Annals of Eye Science. The article has undergone external peer review.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://aes.amegroups.com/article/view/10.21037/aes-23-31/coif). The series “The Retina and Systemic Disease” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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doi: 10.21037/aes-23-31
Cite this article as: Bhattacharya A, Arepalli SR. Pregnancy and retinal and retinal vascular complications. Ann Eye Sci 2023;8:19.

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