2016 Volume 4 Issue 1 Pages 33-37
Preeclampsia is often complicated by visual disorder, but retinal detachment is comparably rare. We experienced two cases of serous retinal detachment in life-threatening placental abruption and preeclampsia. Both patients complained of visual disorder after the onset of placental abruption. Magnetic resonance imaging, scanning laser ophthalmoscopy, and optical coherence tomography were useful in the diagnosis of serous retinal detachment, which spontaneously resolved after several months in both cases. In a severe case of placental abruption, serous retinal detachment should be considered if the patient has disordered vision, although the prognosis is typically good.
Visual disorders occur in 25 to 50% of patients with severe preeclampsia (PE).1) Representative ophthalmic disorders associated with PE include cortical blindness and posterior reversible encephalopathy syndrome (PRES), with retinal detachment occurring less frequently.2) Retinal detachment accompanying placental abruption is rare and, to date, only a few case reports have been published. Here, we report two cases of serous retinal detachment that occurred in life-threatening placental abruption with PE. Multiple diagnostic modalities, including magnetic resonance imaging (MRI), scanning laser ophthalmoscopy, and optical coherence tomography, were useful in these cases.
A 28-year-old primigravida was transferred to our hospital at 38 weeks and 1 day of gestation with severe lower abdominal pain. She had no history of hypertension or ophthalmic disease. At a previous clinic visit at 36 weeks and 0 days of gestation, her blood pressure was elevated at 144/77 mmHg and there was positive urinary protein by dipstick and poor fetal growth on ultrasonography. At 38 weeks and 1 day of gestation, she visited the clinic due to sustained severe abdominal pain and uterine tenderness. Her blood pressure was 190/110 mmHg and ultrasonography revealed no fetal heartbeat. During the transfer to our hospital, she experienced diplopia. On arrival, she was alert though her face was pale, and uterine tenderness and edema of both legs were prominent. Her blood pressure was 159/107 mmHg and dipstick urine protein was 3+. On ultrasonography, extensive retroplacental hematoma was observed. Under the diagnosis of placental abruption with intrauterine fetal death and PE, labor induction by oxytocin was initiated, and a 2,290 g stillborn infant was vaginally delivered. Blood transfusion was required because the total amount of bleeding was 3,480 g. Blood pressure was maintained between 120–130 and 60–70 mmHg by nicardipine infusion during labor.
Diplopia and bilateral blindness continued after delivery. Since PRES was suspected, brain MRI was performed on postpartum day 1. MRI showed bilateral retinal detachment (Figure 1A). In the posterior lobe of the brain, however, there were no signs of PRES, such as a high signal in the occipital lobe in T2-weighted images (Figure 1B). Ophthalmologic examination determined the patient’s bilateral visual acuity to be 20/200. Scanning laser ophthalmoscopy showed bilateral serous retinal detachment (Figure 1C). Serial observations revealed the gradual improvement of retinal detachment. Five months after onset, the patient’s bilateral visual acuity completely recovered to 20/13, and scanning laser ophthalmoscopy showed a complete recovery of retinal detachment (Figure 1D).
Case 1.
(A and B) T2-weighted image of brain MRI on postpartum day 1. Transverse view at the eye (A) and posterior lobe (B) levels. Arrows in (A) show retinal detachment in both eyes. (C and D) Scanning laser ophthalmoscopy of the left eye (left panel) and right eye (right panel), examined on postpartum day 1 (C) and 5 months after onset (D). Note that retinal detachment marked by arrows in (C) completely improved by 5 months after delivery (D).
The patient was a 26-year-old primigravida with no medical or family history. She was admitted at a previous clinic visit due to mild abdominal pain and genital bleeding at 33 weeks and 2 days of gestation. Under the diagnosis of preterm labor, tocolysis with ritodrine was started. At 34 weeks and 2 days of gestation, her blood pressure was elevated at 140/90 mmHg, and oral hydralazine was started. Intrauterine fetal death and retroplacental hematoma were found on transabdominal ultrasonography at 35 weeks and 1 day of gestation. The patient was transferred to our hospital, and on arrival, she was alert though her face was pale, and had uterine tenderness and edema in both legs. Blood pressure was 147/102 mmHg and dipstick urine protein was 3+. Under the diagnosis of placental abruption and PE, induction of labor with oxytocin was started, and a 2,414 g stillborn infant was vaginally delivered. Blood transfusion was required given the total amount of bleeding of 2,653 g.
The patient experienced right eye blindness on postpartum day 1. A dark spot also appeared in the right eye. On the 3rd day postpartum, the blindness worsened. As PRES was suspected, brain MRI was performed, though both eyes looked normal (Figure 2A) and there were no abnormal signals in the posterior lobe of the brain in T2-weighted images (Figure 2B). Ophthalmologic investigation revealed that her left eye visual acuity was 20/13 and that of her right was 20/30. Optical coherence tomography revealed prominent serous retinal detachment in the right eye, while the left eye was normal (Figure 2C). With careful observation, her vision gradually improved. Three month after onset, visual acuity of the right eye completely recovered to 20/13.
Case 2.
(A and B) T2-weighted image of brain MRI on postpartum day 4. Transverse view at the eye (A) and posterior lobe (B) levels. Retinal detachment is unclear by MRI. (C and D) Optical coherence tomography of the left eye (C) and right eye (D) on postpartum day 4. A cross-section of the vertical (right panel) and horizontal (lower panel) view is shown in each figure. Retinal detachment is apparent in the right eye (arrows) while the left eye was normal; retinal detachment completely improved after 3 months.
Only 4 case reports have been published on retinal detachment associated with placental abruption.3,4,5,6) Hoines et al. reported a woman of 40 weeks of gestation with vaginal bleeding, dizziness, and blurred vision.4) Although her systolic blood pressure was normal (110–120 mmHg), laboratory data showed disseminated intravascular coagulopathy (DIC) with positive proteinuria. A dead fetus and large retroplacental blood clot were delivered by cesarean section. Blurred vision continued after the operation, and fluorescein angiogram revealed serous retinal detachment, which reattached 4 weeks later. Bjerknes et al. reported a woman with acute lower abdominal pain, headache, nausea, and mild blurred vision at 29 weeks of gestation.3) Her blood pressure was 180/100 mmHg with proteinuria (3+). Ultrasonography revealed a dead fetus and retroplacental hematoma. During labor, sudden blurring of vision occurred, and serous retinal detachment required 5 weeks for complete recovery. Watanabe et al. reported a woman with chronic hypertension.5) At 28 weeks of gestation, her blood pressure was elevated at 170/107 mmHg with proteinuria (4+). Placental abruption occurred at 31 weeks of gestation, and emergent cesarean section saved the infant. She complained of visual disturbance and double vision soon after cesarean section, and left third nerve palsy and serous retinal detachment were diagnosed. Nerve palsy improved 3 days postpartum but retinal detachment required 2 months for recovery. Finally, Younis et al. reported a woman of 31 weeks of gestation feeling unwell.6) Her blood pressure was 174/112 mmHg with proteinuria (4+). Intrauterine fetal death was confirmed, and she delivered a dead infant with a large retroplacental clot. Shortly after labor, she experienced blurred vision, flashing lights, and visual loss. Fundoscopy revealed bilateral serous exudative retinal detachment, which normalized 3 months later.
Serous retinal detachment occurs in 1 to 2% of patients with severe PE.2) The pathophysiology of serous retinal detachment caused by PE is not completely understood. Choroidal ischemia caused by vasospasm of the choroidal and retinal arteries results in increased vascular permeability and leakage of serous fluid into the subretinal space, which can lead to retinal detachment.7) A combination of severe hypertension, microangiopathic hemolysis, and hypoalbuminemia in the choroidal vessels also reportedly leads to retinal detachment.8)
Placental abruption increases the pressure within the intervillous space due to retroplacental clots, forcing a large release of thromboplastin into maternal circulation and causing severe consumptive coagulopathy or DIC.9) Moreover, placental abruption causes massive bleeding during labor, which leads to a sudden loss of circulatory fluid volume and, in some cases, temporal hypotension. Blood transfusion may be required to correct volume loss and DIC, which can lead to volume overload. We hypothesize that such instability of circulation and coagulation would further damage the choroidal and retinal vessels in cases of placental abruption. Although most cases of retinal detachment are seen in severe PE and eclampsia,7) the severity of retinal detachment does not necessarily correlate with the degree of hypertension, as seen in our second case (blood pressure 147/102 mmHg) and Hoines’s case (systolic blood pressure 110–120 mmHg). We speculate that vasospasm and microangiopathy of choroidal arterial would rather impair retina.
All 6 cases (the 4 previous cases mentioned above and our 2 cases) resulted in spontaneous resolution of retinal detachment, even in the severe case (Case 1). In general, retinal detachment associated with PE gradually improves and patients completely recover their vision.2) However, there are a few reports of permanent blindness due to retinal artery occlusion.10) As such, if a patient complains of visual symptoms during the treatment of PE, ophthalmologic examination is necessary.
In our 2 cases, we first suspected PRES as the cause of visual disturbance, so MRI was performed. In the first case, retinal detachment was apparent on MRI, so the patient was seen by an ophthalmologist. In the second case, although there were no findings by MRI, blindness worsened, and ophthalmologic examination led to a diagnosis of retinal detachment. The reason why MRI was able to detect retinal detachment in the first case is presumably because the degree of detachment was severer (visual acuity 20/200) than that in the second case (visual acuity 20/30). In other words, subtle changes in retinal structure cannot be detected by MRI. Although fundoscopy is the first diagnostic tool, our case demonstrates that scanning laser ophthalmoscopy and optical coherence tomography are also useful for the diagnosis of retinal detachment.
We thank Dr. Saeko Imai and Dr. Rin Mizuno (Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan) for the clinical treatment of the patient. This work was supported by JSPS KAKENHI Grant Number 25861488 and MEXT KAKENHI “Constructive Developmental Science” 24119004.
The authors report no conflicts of interest.
