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Obstetrics & Gynecology 1999;94:361-363
© 1999 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

Ophthalmic Artery Velocimetry in Normotensive and Preeclamptic Women With or Without Photophobia

YASUMASA OHNO, MD, MICHIYASU KAWAI, MD, YASUNORI WAKAHARA, MD, TAKESHI KITAGAWA, MD, MASAKI KAKIHARA, MD and YOSHITARO ARII, MD

From the Department of Obstetrics and Gynecology and Ophthalmology, Toyohashi Municipal Hospital, Toyohashi, Japan.

Address reprint requests to: Yasumasa Ohno, MD 165 Tomyoan Shimohonmachi Iwakura 482, Aichi Japan


    Abstract
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 Abstract
 Materials and Methods
 Results
 Discussion
 References
 
Objective: To compare ophthalmic arterial velocimetry in normotensive and preeclamptic gravidas with and without photophobia.

Methods: Ophthalmic arteries were studied by color-flow Doppler ultrasonography in 118 normotensive pregnant women, 20 gravidas with preeclampsia and no visual symptoms, and 11 with preeclampsia, photophobia, and retinal edema.

Results: The ophthalmic arterial pulsatility index (PI) correlated negatively with gestational age (y = -0.01x + 1.84, r = -0.41, P < .01). Pulsatility index in preeclamptics with photophobia (0.71 ± 0.17) was lowest among the three groups (P < .01) and was highest in normotensive pregnant women (1.41 ± 0.21, P < .01). Mean velocity in normotensive pregnant women (0.19 ± 0.05 m/second) was highest among the groups (P < .01) and was not significantly different in preeclamptic women with no visual symptoms (0.27 ± 0.03 m/second) and with photophobia (0.30 ± 0.02 m/second).

Conclusion: Preeclamptic women, especially those with photophobia, have orbital vascular vasodilation or hyper-perfusion, or both.

Cerebral circulatory effects of preeclampsia are still unclear but are thought to involve breakthrough of cerebral circulatory autoregulation, endothelial damage, and ischemia caused by vasospasm. Retinal changes have long been associated with preeclampsia. Visual disturbances such as photophobia, visual field defect, and poor vision are found in some preeclamptic women; however, orbital and cerebral circulatory effects of preeclampsia, with or without visual disturbance, have not yet been clarified.

Color-flow Doppler ultrasonography now makes it possible to identify reliably blood flow characteristics of specific vessels in the eye. We examined ophthalmic arterial velocimetry using color-flow Doppler ultrasonography in normotensive gravidas and preeclamptic women with or without photophobia.


    Materials and Methods
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 Abstract
 Materials and Methods
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Maternal, ophthalmic, arterial blood-flow velocimetry was assessed by Doppler velocimetry in 118 normotensive pregnant women (from 20–41 weeks’ gestation) during routine prenatal visits, and in 31 preeclamptic women admitted to Toyohashi Municipal Hospital between 1995 and 1997. Preeclampsia was defined as development of hypertension (systolic blood pressure exceeding 140 mmHg and diastolic exceeding 90 mmHg) and proteinuria more than 30 mg/dL, with no history of hypertension or renal disease. Preeclamptic women were subdivided into those with no visual symptoms (n = 20), and those with photophobia (n = 11). Photophobia was defined as the presence of visual disturbance due to dazzling. Subjects with multiple pregnancies, fetal anomalies, diabetes, and chronic hypertension, defined as elevation of blood pressure (BP) before pregnancy or before 20 weeks’ gestation, were excluded from the study.

Color-flow Doppler imaging and pulsed Doppler ultrasonography (LOGIQ 500, GE Yokogawa Medical System, Tokyo, Japan) with a 5-MHz transducer were used for all studies. Each subject was placed recumbent with a 15° left-lateral tilt in a quiet room. Gel was applied to the closed eyelid and the transducer placed on the eyelid with care not to apply pressure to the eye and create artifacts. The blood flow waveform of the ophthalmic artery was easily obtained nasally, superior to the optic nerve.1,2 An angle-correction indicator was used to ensure an angle of insonation of the ophthalmic artery of less than 20° during spectral analysis. The frequency shift was corrected for angle. The spatial peak temporal average intensity was less than 80 mW/cm2. Systolic velocity, end-diastolic velocity, mean velocity, and pulsatility index (PI) on both sides were averaged, and the average was taken as the final value for the subject. Subjects had less than 15% differences in PI and mean velocity between both eyes, assessed before the administration of antihypertensive agents, magnesium sulfate, and epidural anesthesia. Gestational age was estimated from the first day of the last menstrual period (LMP) and confirmed by first-trimester ultrasonographic examinations (crown-rump length and biparietal diameter measurement). Fundal examination was done for all preeclamptic women by an experienced ophthalmologist using dilating drops (tropicamide and phenylephrine hydrochloride) and indirect examination.

Regression analysis was used to correlate gestational week and the subject Doppler indices. Statistical analysis for comparison of those indices among groups was done with analysis of variance and Tukey multiple-comparison test. P < .05 was considered statistically significant.


    Results
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 Abstract
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Clinical data for subjects are given in Table 1Go. There were no significant differences in maternal age, parity, and gestational week among the groups.


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Table 1. Clinical Characteristics of Normotensive and Preeclamptic Women With and Without Photophobia
 
Ophthalmic arterial PI showed a significant negative correlation with gestational age (y = -0.01x + 1.84, r = -0.41, P < .01). Mean velocity did not change significantly throughout gestational age (y = 0.002x + 0.13, r = 0.22).

The mean ophthalmic arterial PI was lowest in preeclamptic women with photophobia (P < .01) and highest in normotensive pregnant women (P < .01; see Table 2Go). Pulsatility index was significantly lower in preeclamptic women with photophobia than in women with no visual symptoms (P < .05). The mean velocity in normotensive pregnant women was highest among the groups (P < .01). There was no significant difference in mean velocity between preeclamptic women with no visual symptoms and those with photophobia. Mean arterial BP did not correlate significantly with PI and mean velocity. Fundal examinations did not identify any abnormalities in any of the normal subjects or in preeclamptic women with no visual symptoms, but diffuse retinal edema without detachment, arterial spastic change, and hemorrhage were seen in all preeclamptic women with photophobia.


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Table 2. Ophthalmic Arterial Pulsatility Index and Mean Velocity in Each Group
 

    Discussion
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 Abstract
 Materials and Methods
 Results
 Discussion
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In our study, the ophthalmic arterial PI showed a significant negative correlation with gestational age, which might be caused by decreasing vascular resistance during pregnancy. Mackenzie reported that central retinal arterial PI showed significant negative correlation with gestational age.1

In preeclamptic women, we found significant lower ophthalmic arterial PI and higher mean velocity, compared with those in normotensive gravidas. Pulsatility index in preeclamptic women with photophobia was significantly lower than in women with no visual symptoms. Hata showed the decrease of ophthalmic artery PI in severe preeclampsia,3 but there is no report showing change of ophthalmic artery velocity and PL Pulsatility index and velocity are necessary to evaluate blood circulatory change and we examined those values in a larger group.

Pulsatility index is believed to represent impedance to blood flow downstream from the point of sampling.4 Decreased PI values suggest a lowering of resistance in the vascular bed, distal to the region of insonation, whereas an increase in mean velocity of cerebral vessels, such as the middle cerebral artery and internal carotid artery, had been believed to indicate a narrowing of the region of insonation. However, Clyde reported that high mean velocity of middle cerebral artery was associated not with vasoconstriction but high local cerebral blood flow measured by xenon computed tomography (CT).5 Decreasing PI value and increasing mean velocity in the ophthalmic artery in preeclamptic women suggests decreased vascular resistance or hyper-perfusion in at least orbital vessels. Decrease of orbital vascular resistance and increase of orbital perfusion are much stronger in photophobia and retinal edema.

There are two hypotheses on the pathogenesis of eclampsia. Some investigators reported that eclampsia might be caused by brain ischemia after cerebrovascular spasms,6,7 which were found in some eclamptic women.8,9,10 Whether or not eclamptic attacks are caused by cerebrovascular spasms has not been determined. Others reported that eclampsia might be caused by a breakthrough in the autoregulation of cerebral hemodynamics.11,12 Our findings support the latter hypothesis.

Retinal edema is found in some preeclamptic women. Severe retinal edema can result in retinal detachment. Photophobia in preeclamptic women is caused by retinal edema. Increased permeability of retinal vessels is believed to be the main mechanism of retinal edema; however, the correlation between initiation of retinal edema and orbital circulatory change has not been clarified. Our findings suggest the hyperdynamic change of orbital circulation is stronger in preeclamptic women with photophobia and retinal edema.

Normal blood flow through the retina is autoregulated within normal mean arterial pressure limits, with little help from the sympathetic nervous system.4 Cerebral blood flow autoregulation normally operates at mean arterial pressures between 60 and 150 mrnHg.13,14,15,16 Beyond the upper limit, hypertensive encephalopathy can occur. Severe cerebral hyperperfusion caused by a breakthrough in autoregulation might break the blood-brain barrier17 and injure the endothelial cells, resulting in cerebral vascular spasm or dilation. In our study, mean arterial pressures of all subjects were below 150 mmHg, and had no significant negative correlation with PI or positive correlation with mean velocity. Effect of pregnancy and preeclampsia on normal mean arterial pressures at which cerebral blood flow autoregulation operates is not clear.


    Footnotes
 
PII S0029-7844(99)00294-X

Received November 12, 1998. Received in revised form February 2, 1999. Accepted February 18, 1999.


    References
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 Abstract
 Materials and Methods
 Results
 Discussion
 References
 
1. MacKenzie F, De Vermette R, Nimrod C, Boisvert D, Jackson B. Doppler sonographic studies on the ophthalmic and central retinal arteries in the gravid woman. J Ultrasound Med 1995;14:643–7.[Abstract]

2. Belfort MA. The effect of magnesium sulphate on blood flow velocity in the maternal retina in mild preeclampsia: A preliminary colour Doppler study. Br J Obstet Gynaecol 1992;99:641–5.[Medline]

3. Hata T, Hata K, Moritake K. Maternal ophthalmic artery Doppler velocimetry in normotensive pregnancies and pregnancies complicated by hypertensive disorders. Am J Obstet Gynecol 1997;177: 174–8.[Medline]

4. Thompson RS, Trudinger BJ, Cook CM. Doppler ultrasound waveform indices: A/B ratio, pulsatility index, Pourcelot ratio. Br J Obstet Gynaecol 1988;95:581–8.[Medline]

5. Clyde BL, Resnick DK, Yonas H, Smith HA, Kaufmann AM. The relationship of blood velocity as measured by transcramal Doppler ultrasonography to cerebral blood flow as determined by stable xenon computed tomographic studies after aneurysmal subarachnoid hemorrhage. Neurosurgery 1996;38:896–905.[Medline]

6. Byrom FB, Lond MD. The pathogenesis of hypertensive encephalopathy and its relation to the malignant phase of hypertension. Lancet 1954;31:201–11.

7. Dinsdale HB, Robertson DM, Haas RA. Cerebral blood flow in acute hypertension. Arch Neurol 1974;31:80–7.[Medline]

8. Kanayama N, Nakajima A, Maehara K, Halim A, Kajiwara Y, Isoda Y, et al. Magnetic resonance imaging angiography in a case of eclampsia. Gynecol Obstet Invest 1993;36:56–8.[Medline]

9. Trommer BL, Homer D, Milhael MA. Cerebral vasospasm and eclampsia. Stroke 1988;19:326–9.[Abstract/Free Full Text]

10. Ito T, Sakai T, Inagawa S, Utsu M, Bun T. MR angiography of cerebral vasospasm in preeclampsia. Am J Neuroradiol 1995;16: 1344–6.[Abstract]

11. Skinhoj E, Strandgaard S. Pathogenesis of hypertensive encephalopathy. Lancet 1973;801:461–2.

12. MacKenzie ET, Strandgraard S, Graham DI, Jones JV, Harper AM, Farrar JK. Effect of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral flow, and the blood-brain barrier. Circ Res 1976;39:33–41.[Abstract/Free Full Text]

13. Strandgaard S. Autoregulation of cerebral blood flow in hypertensive patients. The modifying influence of prolonged antihypertensive treatment on the tolerance to acute, drug-induced hypotension. Circulation 1976;53:720–7.[Abstract/Free Full Text]

14. Strandgaard S, Olesen J, Skinhoj E, Lassen NA. Autoregulation of brain circulation in severe arterial hypertension. BMJ 1973;2:507–10.

15. McHenry LC Jr, West JW, Cooper ES, Goldberg HI, Jaffe ME. Cerebral autoregulation in man. Stroke 1974;5:695–706.[Abstract/Free Full Text]

16. Paulson OB, Strandgaard S, Edvinsson L. Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990;2:161–92.[Medline]

17. Bill A. Blood circulation and fluid dynamics in the eye. Physiol Rev 1975;55:383–417.[Abstract/Free Full Text]




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This Article
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