Pre-eclampsia

Pre-eclampsia

Pre-eclampsia is a multisystem hypertensive disorder of pregnancy, defined as new-onset hypertension after 20 weeks’ gestation accompanied by proteinuria or evidence of maternal organ dysfunction (renal, hepatic, hematologic, or neurologic) or fetal growth restriction. It arises from abnormal placentation and uteroplacental malperfusion, and its imaging footprint spans three systems radiologists are called on to evaluate: the uteroplacental circulation on obstetric ultrasound, the brain on CT/MRI when eclampsia or severe neurologic symptoms develop (posterior reversible encephalopathy syndrome, PRES), and the liver on ultrasound/CT when HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) complicates the picture.

Quick Reference

  • Diagnostic criteria: hypertension (≥140/90 mmHg) after 20 weeks’ gestation + proteinuria OR maternal organ dysfunction (renal insufficiency, liver involvement, neurologic complications, hematologic complications) OR fetal growth restriction — proteinuria is no longer required for diagnosis
  • Severe features: BP ≥160/110 mmHg, thrombocytopenia, impaired liver function, renal insufficiency, pulmonary edema, new visual/cerebral symptoms
  • Uterine artery Doppler (screening): performed at 11–14 weeks, optionally repeated at 20–24 weeks; abnormal = PI above the gestational-age-specific 95th percentile, RI ≥ ~0.70, and/or a persistent bilateral early diastolic notch beyond 24–26 weeks
  • Doppler predictive performance: elevated PI + bilateral notching has the highest predictive value (positive likelihood ratio ~21 in high-risk women, ~7.5 in low-risk women); an RI cutoff of 0.695 has been reported with ~86% sensitivity and ~98% specificity for preeclampsia
  • Placental MRI: reduced T2* signal (BOLD effect of impaired oxygenation), abnormal lobulation, and increased placental granularity in preterm pre-eclampsia
  • Neurologic complication (PRES): seen on MRI in ~51% of eclampsia and ~20% of severe pre-eclampsia patients undergoing neuroimaging; classic pattern is symmetric vasogenic edema in the parieto-occipital subcortical white matter
  • Hepatic complication (HELLP): wedge-shaped/geographic areas of hypoattenuation on CT or altered echogenicity on US, subcapsular hematoma, or hepatic infarction/rupture in severe cases
  • Management impact: abnormal Doppler prompts aspirin prophylaxis and surveillance; PRES/eclampsia and hepatic hemorrhage on imaging are indications for expedited delivery and escalated maternal monitoring

Background and Definition

Pre-eclampsia complicates roughly 3–5% of pregnancies and remains a leading cause of maternal and perinatal morbidity and mortality worldwide. It is classically attributed to defective trophoblastic invasion of the maternal spiral arteries in early pregnancy, producing a high-resistance uteroplacental circulation, relative placental hypoxia, and release of antiangiogenic factors (soluble fms-like tyrosine kinase-1, soluble endoglin) into the maternal circulation. These factors drive systemic maternal endothelial dysfunction, which manifests clinically as hypertension and the multi-organ findings that define the syndrome (Rana et al., 2019). Current diagnostic frameworks no longer require proteinuria: hypertension after 20 weeks plus any one of proteinuria, maternal organ dysfunction, or fetal growth restriction is sufficient.

Imaging Anatomy

Three anatomic compartments are relevant to imaging in pre-eclampsia:

  • Uteroplacental circulation: the uterine arteries arise from the anterior division of the internal iliac arteries and normally undergo physiologic remodeling by invading extravillous trophoblast during the first and second trimesters, converting the spiral arterioles from high-resistance to low-resistance, high-capacitance vessels. In pre-eclampsia this remodeling is incomplete, leaving a persistently high-resistance uteroplacental bed that is directly interrogated by Doppler.
  • Brain, posterior circulation territory: the parieto-occipital watershed and subcortical white matter supplied by the posterior cerebral and superior cerebellar arteries are relatively sparse in sympathetic perivascular innervation, making them preferentially susceptible to breakthrough vasogenic edema when cerebral autoregulation fails at extremes of blood pressure — the anatomic basis for PRES.
  • Liver, peripheral/subcapsular parenchyma: hepatic involvement in HELLP centers on periportal and subcapsular sinusoidal fibrin deposition and hemorrhagic necrosis, typically in a peripheral, wedge-shaped or geographic distribution rather than a focal mass-like pattern.

Imaging Findings

Obstetric ultrasound: uterine artery Doppler

Uterine artery Doppler performed at 11–14 weeks (and optionally repeated at 20–24 weeks) is the primary screening tool. It is obtained transabdominally, insonating each uterine artery where it crosses the external iliac vessels near the internal cervical os, angle of insonation under 30°, averaging at least three similar consecutive waveforms per side. An elevated pulsatility index (PI), particularly when combined with a persistent bilateral diastolic notch, is the most predictive Doppler finding for subsequent pre-eclampsia. In a systematic review and meta-analysis of over 79,000 patients, an increased PI with notching carried a positive likelihood ratio of 21.0 in high-risk women and 7.5 in low-risk women for predicting pre-eclampsia, with second-trimester PI outperforming first-trimester measurement alone (Cnossen et al., 2008). Longitudinal data show that the normal physiologic decline in PI between 11–13+6 and 21–24+6 weeks is blunted in pregnancies that go on to develop pre-eclampsia, so the trajectory of PI — not just a single measurement — adds predictive value beyond a single-timepoint cutoff (Plasencia et al., 2008).

The diastolic “notch” is a transient early-diastolic dip in flow velocity reflecting persistently high downstream resistance in non-remodeled spiral arterioles. A unilateral notch is common and usually benign in the first trimester, but a bilateral notch — especially one persisting past 24–26 weeks — is the clinically significant abnormal pattern and should be explicitly stated in the report. Resistive index (RI) is sometimes reported alongside PI: a mean RI cutoff of approximately 0.695 has been associated with roughly 86% sensitivity and 98% specificity for preeclampsia in high-risk populations, with diagnostic accuracy above 95%. In practice, Doppler indices are most predictive when combined with maternal risk factors and serum angiogenic markers (e.g., PlGF) in a first-trimester combined screening algorithm rather than interpreted as an isolated cutoff, and findings should always be reported alongside gestational age, since normal PI decreases progressively through pregnancy.

Placental MRI

Placental MRI is not yet routine but is increasingly used in research and complex cases to characterize the placental phenotype directly. T2* mapping exploits the blood oxygen level–dependent (BOLD) effect: hypoxic placental tissue has a higher relative concentration of deoxyhemoglobin and therefore a shorter T2*. In preterm pre-eclampsia, whole-placenta mean T2* is significantly reduced compared with gestation-matched controls, and affected placentas show abnormal lobulation, increased granularity, and substantial areas of low signal intensity on T2-weighted sequences (Ho et al., 2020). These findings correlate with the degree of villous hypoxia seen histologically and may eventually help stratify pregnancies at highest risk for early, severe disease.

Neuroimaging: eclampsia and PRES

When a pre-eclamptic or eclamptic patient develops headache, visual disturbance, altered mental status, or seizure, MRI (or CT when MRI is unavailable or the patient is unstable) is obtained to evaluate for PRES. The classic appearance is symmetric, confluent T2/FLAIR hyperintensity in the subcortical and cortical parieto-occipital white matter, reflecting vasogenic edema; frontal, temporal, cerebellar, and brainstem involvement occurs less commonly but is well described. Diffusion-weighted imaging typically shows facilitated diffusion (elevated ADC) in these regions, distinguishing vasogenic edema from the restricted diffusion of infarction — restricted diffusion or hemorrhage should raise concern for a superimposed ischemic or hemorrhagic complication rather than uncomplicated PRES. On CT, findings are often subtler and may show only symmetric hypoattenuation in the same posterior distribution, or may be normal despite clinically significant PRES, which is why MRI is preferred whenever the patient can be safely imaged. PRES is common in this population: a systematic review of 29 studies (1,519 women) found PRES on neuroimaging in 51.4% of eclamptic women and 19.8% of women with severe pre-eclampsia who underwent imaging, with a pooled maternal death rate of 5.3% among affected women (Tawati and Chan, 2023). Among women with preeclampsia or eclampsia who specifically had neurologic symptoms prompting MRI, PRES was identified in 92.3% of eclamptic patients versus 19.2% of preeclamptic patients (Mayama et al., 2016), and a high incidence of PRES-typical cortical/subcortical hyperintensity has also been reported in severely pre-eclamptic women presenting with headache alone, even without seizure (Fisher et al., 2016).

Hepatic imaging: HELLP syndrome

Imaging of the liver is not required for the diagnosis of HELLP syndrome, which is made biochemically, but ultrasound or CT is obtained when a patient has right upper quadrant or epigastric pain, or when hemorrhage or rupture is suspected. On ultrasound, hepatic involvement appears as irregular, peripheral, wedge-shaped areas of altered (typically increased) echogenicity corresponding to infarction or hemorrhage, and subcapsular hematoma appears as a crescentic, complex echogenic fluid collection along the hepatic capsule, most often over the right lobe. On CT, the most characteristic finding is an inhomogeneous, low-attenuation, wedge-shaped or geographic area, often peripheral, with normal enhancing vessels traversing the abnormal parenchyma — a pattern that helps distinguish infarction/hemorrhage from a discrete mass. Subcapsular and perihepatic hematoma, hemoperitoneum from capsular rupture, and, rarely, active contrast extravasation are the findings that most urgently change management (Nunes et al., 2005). Imaging abnormalities are present in only a minority of HELLP cases overall, so a normal liver ultrasound or CT does not exclude the diagnosis.

Differential Diagnosis and Imaging Pitfalls

  • PRES vs. acute ischemic stroke: PRES shows vasogenic edema with facilitated diffusion in a posterior, often symmetric distribution; stroke shows restricted diffusion in a vascular territory. Distinguishing the two changes anticoagulation and blood-pressure management decisions.
  • PRES vs. cerebral venous sinus thrombosis: both can occur in the peripartum period and both can cause edema/hemorrhage; venous imaging (CT or MR venography) should be considered, especially with atypical or hemorrhagic edema patterns.
  • Elevated uterine artery PI: can also be seen with fetal growth restriction in the absence of maternal hypertension, so an abnormal Doppler alone is not specific for pre-eclampsia and must be interpreted with clinical/laboratory context.
  • Hepatic infarction/hematoma of HELLP vs. acute fatty liver of pregnancy: both present with abnormal liver tests in the third trimester; AFLP tends to show diffuse fatty infiltration (low hepatic attenuation on CT, diffuse signal drop on opposed-phase MRI) rather than the focal wedge-shaped/subcapsular pattern typical of HELLP.

Clinical Impact

Imaging findings directly shape management. A high-risk uterine artery Doppler pattern in the first trimester supports initiation of low-dose aspirin and closer surveillance for growth restriction and pre-eclampsia. PRES identified on MRI in a pre-eclamptic or eclamptic patient confirms a hypertensive neurologic emergency and typically prompts aggressive blood pressure control, magnesium sulfate continuation, and expedited delivery planning; most PRES-related imaging abnormalities resolve on follow-up imaging once blood pressure is controlled, consistent with the syndrome’s “reversible” designation, though delayed or absent imaging in symptomatic patients is associated with worse outcomes. Hepatic imaging showing subcapsular hematoma or active hemorrhage in a patient with HELLP syndrome is a surgical/interventional radiology emergency requiring immediate multidisciplinary escalation.

Frequently Asked Questions

What is the difference between pre-eclampsia and eclampsia?

Pre-eclampsia is new-onset hypertension after 20 weeks’ gestation with proteinuria or other maternal organ dysfunction; eclampsia is the occurrence of new-onset generalized tonic-clonic seizures in a patient with pre-eclampsia that cannot be attributed to another cause. Eclampsia is considered a severe, life-threatening progression of pre-eclampsia.

Does every patient with pre-eclampsia need a brain MRI?

No. Neuroimaging is reserved for patients with new neurologic symptoms — headache unresponsive to treatment, visual disturbance, altered mental status, or seizure — rather than being performed routinely on all pre-eclamptic patients.

What does PRES look like on MRI in a pre-eclamptic patient?

The typical pattern is symmetric, bilateral T2/FLAIR hyperintensity involving the subcortical white matter of the parietal and occipital lobes, with facilitated diffusion (elevated ADC) reflecting vasogenic rather than cytotoxic edema. Frontal, temporal, cerebellar, and brainstem involvement can also occur.

Can uterine artery Doppler rule out pre-eclampsia?

Uterine artery Doppler has better performance as a predictor than as a rule-out test; a normal Doppler reduces but does not eliminate risk, and screening is typically combined with maternal risk factors and biomarkers (such as PlGF) for more accurate risk stratification.

Is liver imaging required to diagnose HELLP syndrome?

No, HELLP syndrome is a laboratory diagnosis (hemolysis, elevated liver enzymes, low platelets). Ultrasound or CT is obtained selectively when there is right upper quadrant pain or concern for hepatic hemorrhage, infarction, or rupture.

Does PRES resolve after delivery?

In most cases, yes — PRES-associated imaging abnormalities typically resolve on follow-up imaging within days to weeks once hypertension is controlled and the pregnancy is delivered, which is why the syndrome is termed “reversible.” Delayed treatment or hemorrhagic transformation can result in permanent injury.

References

  1. Rana S, Lemoine E, Granger JP, Karumanchi SA. Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circ Res. 2019;124(7):1094-1112. PMID: 30920918
  2. Cnossen JS, Morris RK, ter Riet G, et al. Use of uterine artery Doppler ultrasonography to predict pre-eclampsia and intrauterine growth restriction: a systematic review and bivariable meta-analysis. CMAJ. 2008;178(6):701-711. PMID: 18332385
  3. Plasencia W, Maiz N, Poon L, Yu C, Nicolaides KH. Uterine artery Doppler at 11+0 to 13+6 weeks and 21+0 to 24+6 weeks in the prediction of pre-eclampsia. Ultrasound Obstet Gynecol. 2008;32(2):138-146. PMID: 18634131
  4. Ho AEP, Hutter J, Jackson LH, et al. T2* Placental Magnetic Resonance Imaging in Preterm Preeclampsia: An Observational Cohort Study. Hypertension. 2020;75(6):1523-1531. PMID: 32336233
  5. Fisher N, Saraf S, Egbert N, Homel P, Stein EG, Minkoff H. Clinical Correlates of Posterior Reversible Encephalopathy Syndrome in Pregnancy. J Clin Hypertens (Greenwich). 2016;18(6):522-527. PMID: 26293622
  6. Mayama M, Uno K, Tano S, et al. Incidence of posterior reversible encephalopathy syndrome in eclamptic and patients with preeclampsia with neurologic symptoms. Am J Obstet Gynecol. 2016;215(2):239.e1-5. PMID: 26902987
  7. Tawati DA, Chan WS. A systematic review of posterior reversible encephalopathy syndrome in pregnant women with severe preeclampsia and eclampsia. Obstet Med. 2023;16(4):236-241. PMID: 38074208
  8. Nunes JO, Turner MA, Fulcher AS. Abdominal imaging features of HELLP syndrome: a 10-year retrospective review. AJR Am J Roentgenol. 2005;185(5):1205-1210. PMID: 16247135

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