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Stroke and Severe Preeclampsia and Eclampsia: A Paradigm Shift Focusing on Systolic Blood Pressure

Martin, James N. Jr MD*; Thigpen, Brad D. DO*; Moore, Robert C. MD*; Rose, Carl H. MD*; Cushman, Julie RN*; May, Warren PhD

doi: 10.1097/01.AOG.0000151116.84113.56
Original Research

OBJECTIVE: To identify important clinical correlates of stroke in patients with preeclampsia and eclampsia.

METHODS: The case histories of 28 patients who sustained a stroke in association with severe preeclampsia and eclampsia were scrutinized with particular attention to blood pressures.

RESULTS: Stroke occurred antepartum in 12 patients, postpartum in 16. Stroke was classified as hemorrhagic-arterial in 25 of 27 patients (92.6%) and thrombotic-arterial in 2 others. Multiple sites were involved in 37% without distinct pattern. In the 24 patients being treated immediately before stroke, systolic pressure was 160 mm Hg or greater in 23 (95.8%) and more than 155 mm Hg in 100%. In contrast, only 3 of 24 patients (12.5%) exhibited prestroke diastolic pressures of 110 mm Hg or greater, only 5 of 28 reached 105 mm Hg, and only 6 (25%) exceeded a mean arterial pressure of 130 mm Hg before stroke. Only 3 patients received prestroke antihypertensives. Twelve patients sustained a stroke while receiving magnesium sulfate infusion; 8 had eclampsia. Although all blood pressure means after stroke were significantly higher than prestroke, only 5 patients exhibited more than 110 mm Hg diastolic pressures. In 18 of 28 patients, hemolysis, elevated liver enzymes, low platelets syndrome did not significantly alter blood pressures compared with non–hemolysis, elevated liver enzymes, low platelets. Mean systolic and diastolic changes from pregnancy baseline to prestroke values were 64.4 and 30.6 mm Hg, respectively. Maternal mortality was 53.6%; only 3 patients escaped permanent significant morbidity.

CONCLUSION: In contrast to severe systolic hypertension, severe diastolic hypertension does not develop before stroke in most patients with severe preeclampsia and eclampsia. A paradigm shift is needed toward considering antihypertensive therapy for severely preeclamptic and eclamptic patients when systolic blood pressure reaches or exceeds 155–160 mm Hg.


Although all patients exhibit severe systolic hypertension before stroke with preeclampsia and eclampsia, few develop prestroke severe diastolic hypertension or mean arterial pressure greater than 130 mm Hg.

From the Departments of *Obstetrics and Gynecology and †Preventive Medicine, University of Mississippi Medical Center, Jackson, Mississippi.

Reprints are not available. Address correspondence to: James N. Martin Jr, MD, Department of Obstetrics and Gynecology, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216–4505; e-mail:

Received May 4, 2004. Received in revised form September 27, 2004. Accepted October 7, 2004.

Stroke is a feared but fortunately infrequent complication of severe preeclampsia or eclampsia. Cerebral hemorrhage has been reported to be the most common cause of death in patients with eclampsia,1,2 and stroke is known to be the most common cause of death (45%) in women with hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome who receive traditional nonsteroid obstetric and medical management.3 A decade ago Sharshar et al4 demonstrated that eclampsia is the main cause of both nonhemorrhagic stroke and intraparenchymal hemorrhage in the pregnant patient, with the latter associated with a particularly poor prognosis. Pathan and Kittner5 also demonstrated that eclampsia is strongly related to stroke in pregnancy. Although severe diastolic hypertension greater than 110 mm Hg was observed to be infrequently present in pregnant or puerperal patients with stroke due to hemorrhage or infarction,6 sometimes in association with preeclampsia and eclampsia, the role of severe systolic hypertension as an important factor for stroke in the pregnant female with severe preeclampsia and eclampsia has not been explored or emphasized.

Recently there were several patients treated for preeclampsia-related strokes at our tertiary care center in Jackson, Mississippi, and a number of others have come to our attention through the forensic review process. Because appropriate care consistent with current recommended practice for the use of antihypertensive agents in patients with preeclampsia and eclampsia seemed to be rendered in many instances and yet stroke still occurred, we decided to scrutinize further the peripartum courses of women with this disorder who also had a stroke. We hoped to identify any clinical correlates of stroke previously missed and to determine whether current recommendations for the treatment of hypertension in patients with severe preeclampsia and eclampsia merited reassessment.

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After receiving approval from the Institutional Review Board, we identified and reviewed the medical records of all patients with pregnancy-related stroke managed at the University of Mississippi Medical Center, Wiser Hospital for Women and Infants, between 1980 and 2003. All patients fulfilled contemporary American College of Obstetricians and Gynecologists criteria for the diagnosis of preeclampsia and eclampsia.7 The forensic review process contributed an additional 21 patients with similar clinical circumstances whose data were combined with the University of Mississippi Medical Center patients to preserve confidentiality and prevent individual patient identification from either primary source. Patients were included in the analysis only if they were free of other potential causes for development of stroke such as a preexisting central nervous system lesion or a medical disorder like sickle hemoglobinopathy. Available data from each patient's prenatal, hospital, and postpartum course were extracted from medical records and entered into a Microsoft Access (Microsoft Corp., Redmond, WA) database. Particular attention was given to signs and symptoms recorded by medical and nursing staff in the 6–12 hour period immediately before and after stroke. These variables included dipstick urinalysis for protein, weight, amount of edema (1–4+), and location, nausea and vomiting, epigastric pain (right upper quadrant, mid epigastrium), headache, change in sensorium, and eclamptic seizure. Timing of stroke was estimated to coincide with the sudden onset of symptomatology and physical findings indicative of a central nervous system event, confirmed by computed tomography or magnetic resonance imaging. When available, laboratory findings obtained immediately before and immediately after stroke were accessed. Site(s) of cerebral hemorrhage or thrombosis or infarction were determined by review of the imaging reports. Both immediate and remote clinical sequelae were assessed. Administration of antihypertensive agents, magnesium sulfate, and corticosteroids around the time of stroke was recorded. Pertinent obstetric and neonatal data were obtained as well as information about anesthesia use for delivery.

Systolic blood pressure (BP), diastolic BP, pulse pressure, and mean arterial pressure (MAP) were recorded when available for pregnancy baseline as the value recorded either just before pregnancy or the earliest prenatal measurement. Last prenatal values were those derived from the last prenatal visit before hospital admission and delivery. Preevent and postevent values are those derived from available records and represent either the highest single recorded value or mean of up to 6 readings taken during the 6- to 12-hour period before and after the stroke for each patient. When available, values that were poststroke and pretreatment for hypertension were assessed. Change from pregnancy baseline to preevent and postevent was calculated for each pressure measure and derivative. Intracranial Doppler studies were neither available nor evaluable for most patients.

The presence of developing HELLP syndrome before or after stroke was determined. For the purposes of this report, patients were assigned to HELLP classifications as previously described8,9 based not on entire clinical course, but rather on patient status before stroke: Class 1 HELLP syndrome is defined by a platelet count of 50,000/μL or less, total l-lactate dehydrogenase (LDH) 600 IU/L or greater, and aspartate transaminase (AST) 70 IU/L or greater; Class 2 HELLP is defined as a platelet count greater than 50,000 but 100,000/μL or less with similar LDH and AST values as Class 1; and Class 3 HELLP syndrome is identified by platelets between 100,000 and 150,000/μL or less in association with total LDH 600 IU/L or greater and AST 40 IU/L or greater. In some cases, the HELLP syndrome disease process was clearly in rapid transition between classification groups during evolution of the stroke itself, but for the purposes of this investigation the classification immediately before stroke is used. Patients for whom there was no evidence whatsoever of HELLP syndrome by the Mississippi classification were termed NoHELLP.

Inasmuch as this was mainly a descriptive study, summary statistics were reported either as a proportion, mean plus standard deviation, or median with interquartile range. Although missing data are present, we report results for available data, and paired data analyses use only those observations for which both measures are present. Changes over time in continuous blood pressure measures are reported as mean plus standard deviation and analyzed using separate paired t tests for each pair without adjustment for multiple testing. Blood pressure measures were also categorized according to important clinical cut points and reported as proportions. Changes over time for categorical variables were analyzed using McNemar's test without adjustment for multiple testing. Subgroup analyses comparing blood pressure measures for those with and without HELLP syndrome were undertaken using a mixed model approach with a Satterthwaite approximation for the degrees of freedom due to suspected variance heterogeneity. The model included main effects for HELLP compared with NoHELLP, time (before to after), and an interaction term. Some comparisons were made using contrasts based on a repeated-measures cell means model, again without adjustment for multiple testing. A P < .05 was considered significant for all comparisons.

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A total of 31 patients was identified between 1980 and 2003 who received obstetric care at The University of Mississippi Hospitals and Clinics with a diagnosis either of stroke during the index pregnancy or in a prior gestation before the index pregnancy. Within this group of patients there were 7 whose stroke occurred antepartum or postpartum in association with severe preeclampsia and eclampsia uncomplicated by any other attributable cause. A further 21 patients with severe preeclampsia and eclampsia-related stroke were identified from forensic sources. The combined study group of 28 women provided the data upon which this report was based.

Maternal demographic characteristics are shown in Table 1. Study subjects were derived from a varied geographic base of 13 states, with an age range of 14 to 42 years; the majority were parous (n = 17, 61%) and 65.4% were 30 years or older. All events occurred either antepartum (n = 12, 43%) or in the first 5 days postpartum (n = 16, 53%), usually in association with a late third-trimester pregnancy (mean gestational age at admission = 37.5 weeks, range 21–41 weeks). Only 1 patient reported current tobacco use, and 2 others had a history of chronic hypertension, but were normotensive without medication during the first 2 trimesters.

Table 1

Table 1

Blood pressure data for initial prenatal visit, immediately before stroke (“prestroke”) and immediately after stroke (“poststroke”) is shown for systolic BP, diastolic BP, pulse pressure, and MAP in Figure 1. Blood pressures were available immediately prestroke in 24 of 28 patients; exceptions were the 4 patients presenting to the hospital postpartum with stroke already in process. As shown in Table 2, systolic blood pressure was more than 160 mm Hg immediately before stroke in 23 of 24 (96%); the exception was a patient with systolic values in the 155–159 mm Hg range. In contrast, only 5 patients equaled or exceeded a diastolic pressure of 105 mm Hg (20.8%), and only 3 a diastolic pressure of more than 110 mm Hg (12.5%). Mean increases in blood pressures after stroke compared with prestroke values were significant (P < .05) for systolic (13.4 + 27.4), diastolic (11.8 + 17.0), and mean arterial blood pressures (11.8 + 18.3 mm Hg), despite the immediate interventions used in most cases to reduce blood pressure quickly.



Table 2

Table 2

The change from initial pregnancy baseline blood pressure to prestroke values were, on average, approximately double the now obsolete criteria (> 30 mm Hg systolic increase or > 15 mm Hg diastolic increase or both) proposed to diagnose “pregnancy-induced hypertension” before 1996. The changes in pressure from the last recorded prenatal visit to prestroke values revealed mean increases of systolic (44.9 + 18.4 mm Hg), diastolic (20.2 + 16.3 mm Hg), and mean arterial pressures (28.6 + 16.5 mm Hg; all P < .001). Only 3 patients in the entire patient series received antihypertensive medication during the 6 hours before stroke.

The majority of patients before stroke did not have an elevated mean arterial pressure more than 130 mm Hg. Mean pulse pressure for the patient group almost doubled from a pregnancy baseline of 43.6 + 6.7 mm Hg to the prestroke level of 77.4 + 13.8 mm Hg, with further increases generally after stroke. All patients in this series had a pulse pressure before stroke of at least 60 mm Hg, an approximate 50% increase above baseline.

The effect of concurrent HELLP syndrome upon blood pressures was investigated in the 18 affected patients (64.3%) and compared with the group of 10 NoHELLP patients. Before stroke 6 patients had developed Class 1 HELLP syndrome, 6 patients had Class 2, and 6 patients had Class 3 HELLP syndrome. No patient in the series was a recipient of any type of glucocorticoid therapy for fetal or maternal reasons during the 48-hour period before stroke. At least 8 of the 18 patients with HELLP syndrome were rapidly worsening during stroke development and would have been ultimately reclassified as a more advanced group if poststroke status had been assigned instead of prestroke status. A repeated-measures analysis to assess changes in blood pressure measures over time for those with or without HELLP syndrome present did not reveal evidence of a significant interaction for any measure or HELLP classification group. Poststroke blood pressure measurement differences were significantly greater than prestroke values in both HELLP and NoHELLP patients (P < .001).

The spectrum of recorded symptomatology for patients before stroke is shown in Table 3. Headache, nausea and vomiting, epigastric or abdominal pain, edema, and occasional subtle changes in neurologic status and sensorium were most commonly exhibited. Significant dipstick proteinuria (3–4+) was observed in slightly more than half of the patients (58.3%). Oliguria and hematuria were very infrequent. Significant change in laboratory measures before and after stroke was observed only for laboratory measures of HELLP syndrome (platelet count, AST, and total LDH, all P < .05) and not for hematocrit, white cell count, uric acid, alanine transaminase, dipstick proteinuria, serum albumin, or total protein. Magnesium sulfate by continuous infusion was ongoing at the time of stroke in 12 patients (42.9%), only 3 of whom were receiving the drug for treatment of eclampsia. The other 5 of 8 total patients with eclampsia received magnesium sulfate only after the seizure or stroke event occurred. Five patients had received betamethasone for fetal lung maturation purposes earlier, 2 within the 7 days before stroke but none less than 48 hours before. No patient in the study was receiving high-dose dexamethasone per the Mississippi protocol for HELLP syndrome.

Table 3

Table 3

Radiologic evaluations were undertaken by computed tomography (n = 22, 78.6%), magnetic resonance imaging (n = 5, 17.9%), or both (n = 3, 10.7%) to determine the location(s) of stroke in 27 of the 28 patients. Almost all strokes were described as arterial hemorrhagic (n = 25, 89.3%), 2 were determined to be arterial thrombotic (n = 2, 7.1%), and 1 remained unknown (scan results unavailable). Sites of involvement as shown in Table 4 were varied and without a dominant pattern; in 10 of 27 patients there were multiple areas (37%) of the brain affected, although the majority had an isolated single site of hemorrhage.

Table 4

Table 4

Subsequent to stroke there were multiple maternal morbidities as listed in Table 5. Fifteen patients died after stroke, a mortality rate of 53.6%. Only 3 patients escaped any significant long-term morbidity without residual deficit. Details of poststroke management are beyond the scope of this study and were not investigated.

Table 5

Table 5

Delivery was evenly divided between vaginal and abdominal routes. Nine of 14 cesareans were undertaken for the maternal indication of worsening preeclampsia and eclampsia, 3 were undertaken primarily for fetal indications, and 2 were planned repeat cesarean deliveries. General anesthesia was used for 8 cesareans, 9 patients received regional blocks, and 11 had local or no analgesia at delivery. Mean birth weight was 2,259 ± 1,067 g for the 18 patients with evaluable data; there were no small for gestational age fetuses. The only 2 pregnancy losses in the study were stillbirths weighing less than 1,000 g.

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Since the publication of Schauta in 1881 (cited by Dieck-mann10) and more recently the patient series by Govan,11 it has been known that cerebral hemorrhage is an important cause of death in patients with eclampsia. What has been less emphasized in recent obstetric literature is that cerebral hemorrhage is also an important cause of maternal morbidity and mortality in patients with severe preeclampsia. The patients presented in this study make a strong statement for the consideration of patients with severe preeclampsia and eclampsia, particularly when significant severe systolic hypertension more than 160 mm Hg develops either with or without associated symptomatology or diastolic hypertension, to have developed a hypertensive emergency. These patients seem to have merited this status even though most of them (80%) did not exhibit a sustained diastolic pressure or more than 105 mm Hg before stroke.

In his 1978 classic text, Chesley12 wrote that “one of the chief aims in the use of antihypertensive drugs in the management of severe preeclampsia and eclampsia is to reduce the risk of such (fatal cerebral) hemorrhages.” In addition, he included among his primary objectives of management for patients with preeclampsia not only to prevent convulsions, but also to prevent cerebrovascular hemorrhage.13 For adult male and female patients in general the risk of hemorrhagic stroke correlates directly with the degree of elevation of systolic blood pressure and is less related to, but not independent of, the diastolic blood pressure.14 Exactly how to use this epidemiologic data for the pregnant woman and apply it to Chesley's admonition for the obstetric patient with preeclampsia and eclampsia has so far eluded precise determination.

Precise, evidence-based recommendations for the use of antihypertensive agents to treat severe hypertension in patients with preeclampsia–eclampsia do not exist. Consensus is lacking among obstetric providers, and a variety of clinical guidelines based largely on anecdotal experience influence practice. Dr. Jack Pritchard's Parkland Hospital policy in Dallas, elaborated in 1975 with a dominant influence upon American obstetricians that persists to this day, is to “institute treatment when the diastolic pressure is maintained at 110 mm Hg or higher…the objective is to reduce it to about 90 to 100 mm Hg.”15 In the 2000 National Institutes of Health Working Group Report on High Blood Pressure in Pregnancy,16 after noting that “some experts would treat persistent diastolic levels of 105 mm Hg or higher” and “others would withhold treatment until diastolic blood pressure levels reach 110 mm Hg,”17,18 the final recommendation is made to treat acute severe hypertension in preeclampsia when systolic BP is more than 160 mm Hg or diastolic BP is sustained more than 105 mm Hg or both. The definition of “sustained” remains unspecified.

The most recent American College of Obstetricians and Gynecologists Practice Bulletin on the subject (Number 33, January 2002)7 also emphasizes diastolic blood pressure as a primary determinant for intervention, commenting that “antihypertensive therapy is generally recommended for diastolic blood pressure levels of 105–110 mm Hg or higher” using either hydralazine or labetalol. Based on the above publications and the practice and court testimony of many obstetrician–gynecologists, it is the senior author's contention that most practicing obstetricians in the United States currently use the diastolic threshold of 110 mm Hg, whether single or sustained, to initiate antihypertensive therapy in preeclamptic and eclamptic patients, paying little heed to the associated systolic pressures to direct therapy.

Should obstetric practice guidelines focus on antihypertensive therapy initiation for patients with preeclampsia at a certain systolic or diastolic threshold or both, or should a range of blood pressure be the goal comparable to the current approach to diabetes mellitus management with maintenance of blood sugar in tightly controlled ranges? Based on our review of these 28 patient case histories, it seems reasonable to urge that a threshold for the initiation of antihypertensive therapy in the patient with preeclampsia and eclampsia should be recommended once a threshold range of 155–160 mm Hg is reached until further research can be undertaken to confirm our findings. Such a change from diastolic focus almost exclusively would require a major paradigm shift in the thought process of most American obstetrician–gynecologists. The great majority of the patients in the present case series never exhibited a single or a sustained diastolic blood pressure at the 110 or even 105 mm Hg level before the stroke itself, usually manifested as a hemorrhage in 1 or more sites rather than a thrombosis.

Pulse pressure, a surrogate measure of arterial compliance, has been shown to be higher in women with a pregnancy-related hypertensive disorder compared with women with uncomplicated pregnancies. Thadhani and colleagues19 reported that late first and early second trimester pulse pressures were 45 ± 6 mm Hg, significantly higher than normotensive women (41.8 ± 8 mm Hg). These values obtained prospectively are consistent with the ones observed retrospectively in the present investigation. Higher pulse pressures were recorded around the time of stroke, without differences between patients with or without HELLP syndrome as previously suspected.9 The development of a pulse pressure of more than 60 mm Hg in association with a systolic blood pressure increase over baseline also of more than 60 mm Hg could be a significant combination risk factor for stroke in patients with severe preeclampsia and eclampsia.

Cerebral autoregulation of cerebral blood flow in the nonpregnant individual normally is maintained over a mean arterial pressure range of 60–150 mm Hg.20,21 During normal pregnancy it may be altered by chronic hyperventilation.22 A precise understanding of cerebral autoregulation changes secondary to the development of severe preeclampsia and eclampsia remains elusive, although Oehm and colleagues23 in Germany report a substantial disturbance of dynamic cerebral autoregulation in patients they studied with eclampsia. The upper limit of autoregulation may be reduced in such patients, breached by rapid and severe systolic pressure rises with consequent forced overdistention of the cerebral vasculature.24 Zeeman and coworkers recently reported that magnetic resonance imaging–calculated cerebral blood flow is significantly increased in patients with severe preeclampsia.25 Belfort's group26 and Williams’ group27 have shown that patients with severe preeclampsia have high cerebral perfusion pressure compared with controls, placing the cerebral vasculature at risk for barotraumas and vessel damage. Both of these groups also have shown that increased cerebral flow velocities in patients with preeclampsia persist postpartum for at least the first week and likely in some cases for months thereafter.28,29 When cerebral autoregulation is disrupted, interstitial extravasation of proteins and fluid would be expected to lead to vasogenic edema in some vascular beds, whereas rupture and hemorrhage might occur in others. The affected patient would be expected to express rapidly progressive signs and symptoms of the neurologic syndrome known as hypertensive encephalopathy that is characterized by headache, nausea, visual problems, altered sensorium, focal neurologic signs and seizures. Labetalol in our hands is the preferred antihypertensive because it has been shown to effectively reduce cerebral perfusion pressure without compromising cerebral perfusion, primarily by decreasing systemic blood pressure.30

It is likely that blood pressure alone, whether systolic or diastolic or a derivative, is not the only or even the dominant factor related to stroke occurrence in the patient with severe preeclampsia or eclampsia. At least 2 lines of reasoning lend support to this opinion. One is that in our experience and that of others31 cerebral hemorrhage is relatively infrequent in women with eclampsia, even with sustained severe hypertension. Stroke also occurs infrequently in the total population of pregnant women whose systolic pressures exceed 160 mm Hg at any time during the course of antepartum, intrapartum, or postpartum management. The second is the interesting finding of rapidly worsening characteristics of HELLP syndrome in many of the patients studied in this series points to disordered vascular endothelial pathophysiology that may injure the normal protective blood-brain barrier systems in the brain while also causing or contributing to higher blood pressures. A number of case reports consistent with this possibility have been published recently describing central nervous system abnormalities in patients with HELLP syndrome.32–37

Simply lowering blood pressure below a certain systolic or diastolic threshold may not be enough in certain patients. Specific subpopulations of patients may be particularly susceptible, such as adolescents, older gravidas or patients acutely developing HELLP syndrome. Our extensive clinical and research experience leads us to hold the firm opinion and recommendation that a practice guideline of early, aggressive intravenous dexamethasone use in patients developing HELLP syndrome averts much maternal morbidity.38,39 Given the absence of this intervention before stroke in all 18 patients with HELLP syndrome reviewed for this study, we consider it probable and worthy of future investigation that the use of this modality in combination with magnesium sulfate and appropriate antihypertensive therapy to reduce systolic hypertension might considerably reduce stroke in this clinical setting.

Cerebral injury usually occurred by hemorrhage rather than thrombosis, in every instance thought to involve arterial rather than venous vessels. Stroke had no predilection for a certain site of the brain in this study, affecting both cortical and basal areas. In addition, often there were multiple sites involved. Although the posterior basal cerebral circulation or “centrencephalon” has been reported to be the most commonly affected by hypertension-induced breaches in cerebral autoregulation of nonobstetric patients, our patient series did not closely reflect such a pattern.

A careful analysis of the clinical courses of these 28 patients leads the authors to emphasize that preeclampsia represents a spectrum of signs and symptoms reflective of a long-standing and insidious developing disease process that is not inherently a hypertensive condition.40 Its terminal clinical expression is eventually elevated blood pressure in most cases, but the sum total of the disease expression includes many “soft” characteristics that frustrate quantification by the clinician. It is critically important for the provider to consider the composite clinical picture presented by the patient in reaching decisions about treatment or nontreatment. Clearly, a patient with preeclampsia who has nausea, headache, epigastric pain, and considerable edema is more ill than another patient without these findings and a comparable blood pressure reading. In addition, the patient's preeclampsia state is also more than the sum of her laboratory values. In individual circumstances the change in laboratory values of HELLP syndrome, for instance, can change very quickly and become concerning only after a cerebral hemorrhage has already happened. Thus a cautious approach to patients with preeclampsia who seem ill and are approaching blood pressure thresholds that merit intervention require bedside intensive care by providers, including transfer to hospital settings where close attention can be optimally rendered.

The authors are aware of the limitations of the present investigation, selection bias being a major one. We believe that most patients with preeclampsia and eclampsia who reach the systolic threshold of 155–160 mm Hg do not have strokes, even when a diastolic threshold of 105–110 is met or exceeded. Why then did these particular women suffer a stroke? Obviously there are contributing factors other than systemic blood pressure alone, and further investigation is needed to better define prospectively the patient at risk of stroke. Until those studies are undertaken and a more complete understanding is of this complex process is achieved, we believe it is prudent for obstetrician-gynecologists to be aware of the potential risk to their patient with preeclampsia or eclampsia and to take steps to prevent, to the extent possible, progression to stroke. Withholding antihypertensive therapy in the presence of sustained severe systolic hypertension, because the diastolic pressures have not yet reached 105–110 mm Hg, seems to be ill-advised in this clinical setting. Similarly, withholding potent glucocorticoids in the clinical setting of rapidly developing HELLP syndrome with severe systolic hypertension may also be proven to be hazardous to the mother's potential for hemorrhagic stroke. Prospective, large-scale, multicenter investigations in heterogeneous patient populations are required to explore these issues. Investigation may be most fruitful if it seeks to elucidate whether a practice policy of blood pressure maintenance within certain ranges is preferable to a policy of withholding antihypertensive therapy until certain systolic thresholds such as 155–160 mm Hg are reached or exceeded.

In conclusion, we were surprised to find that a systolic blood pressure threshold of approximately 155–160 mm Hg, usually in association with diastolic pressures at levels less than 105 mm Hg, preceded stroke in the majority of this select group of 28 patients with severe preeclampsia and eclampsia. We believe that women who have severe preeclampsia or eclampsia and severe systolic hypertension (> 160 mm Hg) are at special risk for hemorrhagic stroke. These patients deserve immediate and special attention, intensive care, and antihypertensive therapy to reduce their risk of such strokes.

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