Preeclampsia (PE) is an obstetrical complication characterized by new-onset hypertension or super-imposed hypertension with or without one systemic condition including proteinuria, hepatic dysfunction, neurologic symptoms, renal insufficiency, pulmonary edema, or thrombocytopenia during the second half of pregnancy.
The clinical manifestations of severe preeclampsia can be confusing for the clinician, as several subjective symptoms such as headache, epigastric pain, or right upper quadrant pain can be benign findings in pregnancy. Although hypertension in pregnancy is acknowledged to be a continuum of risk, and early delivery is indicated for many women, identifying an objective measure of lower risk could be useful in stratifying the need for early term delivery to avoid complications of premature delivery, and subsequent maternal management.
The clinical neurologic manifestations of preeclampsia and/or eclampsia have multiple theories about pathogenesis. One theory is that hyper perfusion of the brain due to decreased cerebrovascular resistance leads to vasogenic edema, similar to hypertensive encephalopathy(1, 2). Hypertensive encephalopathy is hypothesized to be an overperfusion injury causing disordered cerebral autoregulation and subsequent globally decreased cerebral blood flow with extravasation of fluid into the cerebral parenchyma(3, 4). Similarly, the results of noninvasive studies of cerebral blood flow and resistance suggest that vascular barotrauma and loss of cerebral vascular autoregulation contribute to the cerebral vascular pathology in preeclampsia(5–7). Radiologically, this can be visualized via computed tomography and magnetic resonance imaging demonstrating cerebral edema in some women with severe preeclampsia or eclampsia(1).
Cerebral edema is believed to cause this increase in intracranial pressure. The subarachnoid spaces surrounding the optic nerve communicate with the intracranial cavity, and changes in cerebrospinal fluid pressure are transmitted along the distensible optic nerve sheath to increase sheath diameter(8, 9). Two recent meta-analyses suggest that optic nerve sheath diameters can be used as surrogate markers for elevated intracranial pressure, but cite a range of cut-off from 4.8 to 6.3mm based on the multiple studies which were included (10, 11). The wide range in potentially significant ONSD measurements raises the question of what an expected ONSD in an obstetric population is. In a comparison of ocular ultrasonography with gold standard measures of intracranial pressure (ICP) via invasive devices such as intraventricular catheters, values of ONSD above 5.8 mm were shown to be associated with a 95% risk of raised ICP (i.e. more than 20 mmHg)(12), which is why we chose to use this threshold, but the optimal ONSD cuff off value for raised ICP is unknown.
To date, there have been four studies evaluating ONSD in preeclampsia and eclampsia. Dubost et al evaluated a total of 51 women: 26 preeclamptic patients, of which 13 had severe preeclampsia, and 13 had preeclampsia without severe features. A self-reported weakness of the Dubost study was the small percentage of severe preeclampsia patients with neurologic symptoms, limiting the ability to determine a relationship with ONSD enlargement(13). Only 8 women with preeclampsia had headaches, which included both severe (n=7) and non-severe preeclamptic (n=1) patients. The sample included preeclampsia patients predominantly diagnosed (54%) with severe features by renal dysfunction, which is reported only in approximately 1% of women with severe preeclampsia(14). They found that approximately 19% of severe preeclamptic patients had ONSD values indicating intracranial pressures above 20 mmHg(13).
Simenc et al assessed 30 severe preeclampsia patients and compared their ONSD and optic disc height (ODH) measurements to control patients(15). They did not assess preeclamptics without severe features or differentiate patients by subjective or objective features of severe preeclampsia. They found 43% of patients with severe preeclampsia had ONSD measurements >5.8mm and 77% with an ODH ≥ 1mm, compatible with intracranial hypertension(15). Ortner et al evaluated point of care ultrasound (POCUS) in 95 severe preeclampsia patients, which included the incidence of elevated ONSD in this population(16). However, their primary outcome was the relationship of albumin to POCUS for pulmonary edema or elevated ONSD above 5.8 mm(16). Singh and Bhatia evaluated 75 pregnant patients, in cohorts of 25 patients of severe preeclampsia, eclampsia, and control groups. They found significant differences between the ONSD measurements in the three cohorts with 44% of preeclampsia patients and 66% of eclampsia patients demonstrating elevations of ONSD values ≥ 5.7mm(17). Of note, they had included patients with IUGR for diagnosis of severe preeclampsia, and excluded those with blurred vision, moderate-to-severe renal or hepatic dysfunction or coagulopathy(17). Exclusion of patients with laboratory criteria for severe preeclampsia would remove 7.3% of patients with preeclampsia, especially as the frequency of abnormal laboratory values in women with pregnancy-associated hypertension increases with disease severity(18). Evaluating ONSDs in a North American population with severe preeclampsia by ACOG criteria is a necessary step to begin assessing utility of this point of care technique to our obstetric population.
This aim of this study was to estimate the incidence of elevated ONSD in severe preeclampsia patients with neurologic features compared to non preeclamptic patients. The secondary objective was to determine baseline optic nerve sheath diameters in patients with severe preeclampsia with and without neurologic criteria and preeclampsia without severe features. We anticipated correlation of clinical features of severe preeclampsia to elevated ONSD representing vasogenic edema.