Blindness from retinal lesions is caused either by serous retinal detachment or rarely by retinal infarction, which is termed Purtscher retinopathy 40-13). Serous retinal detachment is usually unilateral and seldom causes total visual loss. In fact, asymptomatic serous retinal detachment is relatively common with preeclampsia (Saito, 1998). In most cases of eclampsiaassociated blindness, visual acuity subsequently improves. However, if blindness is caused by retinal artery occlusion, vision may be permanently impaired (Lara-Torre, 2002; Moseman, 2002; Roos, 2012).
Clinical manifestations suggesting widespread cerebral edema are worrisome. During 13 years at Parkland Hospital, 10 of 175 women (6 percent) with eclampsia were diagnosed with
FIGURE 40-1 3 Purtscher retinopathy caused by choroidal ischemia and infarction in preeclampsia syndrome. Ophthalmoscopy shows scattered yellowish, opaque lesions of the retina (arrows). (Reproduced with permission from Lam OS, Chan W: Images in clinical medicine. Choroidal ischemia in preeclampsia. N Engl J Med 344(1o0):739,o2001o.) symptomatic cerebral edema (Cunningham, 2000). Symptoms ranged from lethargy, confusion, and blurred vision to obtundation and coma. In most cases, symptoms waxed and waned. Mental status changes generally correlated with the degree of involvement seen with CT and MR imaging studies. These women are very susceptible to sudden and severe blood pressure elevations, which can acutey worsen the already widespread vasogenic edema. Thus, careful blood pressure control is essential. In the 10 women with generalized edema, three became comatose and had imaging indings of trans tentorial herniation, from which one died. Consideration is given for treatment with mannitol or dexamethasone.
Compromised utero placental perfusion is almost certainly a major culprit in the greater perinatal morbidity and mortality rates seen with preeclampsia (Harmon, 2015). Defects in endovascular trophoblastic invasion with the preeclampsia syndrome were discussed earlier (p. 714). hus, measurement of uterine, intervillous, and placental blood low would likely be informative. Attempts to assess these in humans have been hampered by several obstacles that include inaccessibility of the placenta, the complexity of its venous eiuent, and the need for radioisotopes or invasive techniques.
Measurement of uterine artery blood low velocity has been used to estimate resistance to uteroplacental blood low (Chap. 17, p. 339). Vascular resistance is estimated by comparing arterial systolic and diastolic velocity waveforms. By the completion of placentation, impedance of uterine artery blood low is markedly decreased, but with abnormal placentation, abnormally high resistance persists (Everett, 2012; Ghidini, 2008; Napolitano, 2012). Earlier studies were done to assess this by measuring peak systolic:diastolic velocity ratios from uterine and umbilical arteries in preeclamptic pregnancies. In some cases, but certainly not all, there was higher resistance (Fleischer, 1986; Trudinger, 1990).
Another Doppler waveform-uterine artery "notching"has been associated with elevated risks for preeclampsia or fetal-growth restriction (Groom, 2009). In the MFMU Network study reported by Myatt and colleagues (2012a), however, notching had a low predictive value except for early-onset severe disease.