Characteristic changes in systemic blood pressure in eclampsia

Abstract

Aim: It has been reported that eclampsia might be caused by vasogenic edema from impaired autoregulation of cerebral blood flow, potentially due to elevated systemic blood pressure (BP). This study retrospectively investigated changes in systemic BP around eclampsia onset.

Methods: Eight women with eclampsia were enrolled. Three received antihypertensive drugs. Four had labor pains. Systolic and diastolic BP and heart rate were evaluated. Mean arterial pressure (MAP) and changes in BP (ΔBP) just before and after eclampsia onset were calculated.

Results: Systemic BP markedly increased just before eclampsia onset, then decreased to lower than before onset. The ΔBP1 (each BP just before eclampsia onset−mean BP) was 21±9 mmHg (21±11%), and the ΔBP2 (each BP just after eclampsia onset−BP just before eclampsia onset) was −40±18 mmHg (−31±12%) in MAP. The heart rate rapidly increased just after onset (75±8 vs. 128±6 bpm). Fetal cardiac monitoring showed prolonged deceleration in all pregnant patients.

Conclusions: It was suggested that both marked increase and decrease in BP around the onset of eclampsia might cause strong damage in not only maternal but also fetal blood circulation.

Introduction

Eclampsia is a rare but serious obstetric complication. It is a major cause of maternal and perinatal morbidity and death in Japan and in certain other populations.^1,2) Although once widely believed to reflect the effects of vasospasm and thrombosis,^3,4) neurologic deficits in patients with hypertensive encephalopathy are now believed to be most commonly caused by vasogenic edema attributable to fluid that escapes from the intravascular compartment into the interstitium due to impaired autoregulation.^1,2,5,6) The clinical and radiographic signs in patients with eclampsia might be related to acutely elevated systemic blood pressure (BP), which impairs the autoregulation of cerebral blood flow due to hypertensive encephalopathy. Our previous study demonstrated that the increase in BP, as well as the oscillation of BP just before eclampsia onset, might greatly influence the onset of eclampsia.⁷⁾

Just after eclampsia onset, a marked decrease in systemic BP is sometimes seen. Furthermore, fetal cardiac monitoring showed the effects of impairment of uterine blood circulation. Thus, systemic BP might dramatically change around eclampsia onset; however, this has remained unclear.

The purpose of the present study was to observe systemic BP just before and after eclampsia onset to investigate characteristic changes of blood circulation in both mother and fetus.

Methods

Eclamptic women were investigated retrospectively in the present study subjects. In 8 of the patients, 1-day serial BP measurements before and after the development of eclampsia were available. Of the eclamptic patients, 7 were administered in Nagoya City West Medical Center and 1 was administered in a private hospital.

Preeclampsia and eclampsia were defined according to the criteria of the Japan Society for the Study of Hypertension in Pregnancy (JSSHP).⁸⁾

All patients were diagnosed with eclampsia by observation of vasogenic edema (posterior reversible encephalopathy syndrome, PRES) on cerebellar MRI within a week (0–6 days) after the onset of seizures.

Systolic and diastolic BP and heart rate were measured, and the mean arterial pressure (MAP) was calculated using the following equation before and after onset of eclampsia: ([systolic BP+diastolic BP×2]/3).

The changes in BP (ΔBP1 and ΔBP2) were calculated as follows: ΔBP1=each BP just before eclampsia onset−mean BP, ΔBP2=each BP just after eclampsia onset−BP just before eclampsia onset (Figure 1).

Figure 1.

Analysis of serial blood pressure (BP) measurements obtained 1 day before eclampsia onset.

The changes in BP (ΔBP1 and ΔBP2) was calculated as: ΔBP1=each BP just before onset−mean BP, ΔBP2=each BP just after eclampsia onset−BP just before eclampsia onset.

Statistical analysis

All results are expressed as mean±SD. Student’s paired t-test was used for the statistical analysis. The level of significance was set at P<0.05.

Results

Clinical data of the 8 eclamptic women are shown in Table 1. The onset of eclampsia occurred antepartum (in 2 patients), intrapartum (3 patients), and postpartum (3 patients).

Table 1. Clinical data of study subjects at onset of eclampsia

Case	Onset time	Type	Symptom	Chemical data	Just before eclampsia	Anti-HT drugs	Delivery (week)	Birth weight	abdominal findings of CTG
1	39 w	antepartum	headache	no change	mild PE	−	C/S (39 w)	2,750 g	prolonged deceleration
2	40 w	antepartum	headache	no change	severe PE	+	C/S (40 w)	3,594 g	prolonged deceleration
3	39 w	intrapartum	headache	not done	mild GH	−	Vaginal (39 w)	3,430 g	prolonged deceleration
			visual disturbance
4	41 w	intrapartum	headache	no change	LOH	+	C/S (41 w)	2,974 g	prolonged deceleration
			visual disturbance
			nausea
5	39 w	intrapartum	headache	no change	LOH	−	C/S (39 w)	2,814 g	prolonged deceleration
			visual disturbance						late deceleration
6	2 DP	postpartum	headache	no change	mild PE	+	C/S (37 w)	2,694 g	−
7	2 DP	postpartum	headache	HELLP syndrome	severe PE	+	C/S (36 w)	1,930 g	−
8	0 DP	postpartum	headache	no change	severe GH	−	C/S (36 w)	2,342 g	−
								2,004 g

All the eclamptic women showed posterior reversible encephalopathy syndrome. DP, day of postpartum; PE, preeclampsia; GH, gestational hypertension; LOH, labor onset hypertension; HT, hypertension; C/S, cesarean section; CTG, cardiotocogram.

All women were primiparous and presented with clinical symptoms that included headache, nausea, and visual disturbance. Four patients had preeclampsia, and one had mild gestational hypertension 2 days before the onset of eclampsia. Two patients had hypertension after labor onset. When the BPs were more than 160 mmHg systolic and/or 110 mmHg diastolic, respectively, antihypertensive drugs were administered. Accordingly, four patients were given antihypertensive drugs. Nobody received magnesium sulfate before eclampsia. Four patients received intravenously diazepam just after onset of eclampsia. Furthermore, 2 patients received intravenously both diazepam and magnesium sulfate just after the onset.

Systemic BP markedly increased just before eclampsia onset (150±12 vs. 178±5 mmHg in systolic [P<0.0001], 87±15 vs. 107±16 mmHg diastolic [P=0.001], and 108±14 vs. 129±10 mmHg MAP [P<0.001]), then decreased to lower than before onset (114±17 mmHg in systolic, 71±14 mmHg in diastolic and 89±15 mmHg in MAP) (Figure 2A).

Figure 2.

Representative changes in eclampsia.

(A) Blood pressure (BP) just before and after eclampsia onset.

(B) Fetal heart rates just after eclampsia onset. Prolonged deceleration was shown just after eclampsia onset.

C/S, cesarean section.

The ΔBP1 was 28±9 mmHg (19±8%) systolic, 22±12 mmHg (26±17%) diastolic and 21±9 mmHg (21±11%) MAP. The ΔBP2 was −64±17 mmHg (−36±10%) systolic, −36±17 mmHg (−32±13%) diastolic and −40±18 mmHg (−31±12%) MAP. The heart rate rapidly increased just after onset (75±8 vs. 128±6 bpm) (Table 2).

Table 2. Characteristic changes in blood pressure (BP) immediately before and after eclampsia onset

A

Case	Systolic BP (mmHg)
	Mean	Before			After
		BP	ΔBP1 (%)		BP	ΔBP2 (%)
1	134±28	180	46 (34)		150	−30 (−17)
2	163±15	197	34 (21)		136	−61 (−37)
3	140±15	168	28 (20)		110	−58 (−35)
4	157±15	183	26 (17)		136	−47 (−26)
5	149±29	178	29 (19)		120	−58 (−32)
6	129±29	174	45 (35)		88	−86 (−49)
7	163±15	182	19 (12)		93	−89 (−49)
8	163±16	181	18 (11)		135	−46 (−25)
	150±12	178±5*	28±9		114±17*†	−64±17
			(19±8)			(−36±10)

B

Case	Diastolic BP (mmHg)
	Mean	Before			After
		BP	ΔBP1 (%)		BP	ΔBP2 (%)
1	61±21	85	39 (57)		64	−21 (−25)
2	105±10	133	28 (27)		91	−42 (−32)
3	82±7	89	7 (9)		60	−29 (−29)
4	98±9	110	12 (12)		90	−20 (−18)
5	91±16	121	30 (32)		64	−57 (−47)
6	70±15	103	33 (48)		58	−45 (−44)
7	105±9	120	15 (14)		69	−61 (−51)
8	87±4	95	8 (9)		85	−10 (−11)
	87±15	107±16*	22±12		71±14*†	−36±17
			(26±17)			(−32±13)

C

Case	MAP (mmHg)
	Mean	Before			After
		BP	ΔBP1 (%)		BP	ΔBP2 (%)
1	85±23	116	31 (36)		97	−19 (−16)
2	124±12	137	13 (10)		106	−31 (−23)
3	101±10	115	14 (14)		77	−38 (−33)
4	119±10	134	15 (15)		105	−29 (−22)
5	111±15	140	29 (26)		83	−57 (−41)
6	91±19	127	36 (40)		68	−59 (−46)
7	123±11	141	18 (15)		70	−71 (−50)
8	111±7	123	12 (11)		101	−22 (−18)
	108±14	129±10*	21±9		89±15*†	−40±18
			(21±11)			(−31±12)

ΔBP1 is calculated as BP just before–mean BP, ratio is ΔBP1/mean BP×100, ΔBP2 is calculated as just before BP–just after BP, ratio is ΔBP2/just before BP×100. Data are shown as mean±SD. * P<0.05 vs. mean BPs, † P<0.05 vs. before BPs. BP, blood pressure; MAP, mean arterial pressure.

In 4 patients received intravenously diazepam, the ΔBP2 was −60±21 mmHg (−34±11%) in MAP. However, the decrease in blood pressure just after onset of eclampsia was similarly in 4 patients without the medication. (59±16 mmHg, −34±10%, P=0.98). Furthermore, two patients received intravenously both diazepam and magnesium sulfate. The ΔBP2 in MAP just after onset of eclampsia was not different in both groups (75±14 mmHg, 43±6% vs. 54±17 mmHg, −31±10%, P=0.23).

Fetal cardiac monitoring showed prolonged deceleration in all pregnant patients (Figure 2B and Table 1).

Discussion

Eclampsia is potentially life-threatening to the mother and fetus owing to the associated increase in systemic BP. Drastic changes of blood circulation in both mother and fetus might be present around eclampsia onset.

Maternal changes in blood circulation

In patients with eclampsia, edema develops in the subcortical white matter and cortex and predominantly involves the occipital lobes, and is usually evident upon examination by cerebral imaging. These findings are identical to those of hypertensive encephalopathy.⁹⁾ Through focusing on the changes in BP just before eclampsia onset, a previous study demonstrated that large oscillation in BP might influence the onset of eclampsia.⁷⁾

In the present study, a large increase in BP was seen just before eclampsia onset. Furthermore, a large decrease in BP was seen just after eclampsia onset, together with an increase in the maternal heart rate. Drastic changes in BP occurred around eclampsia onset. Although eclampsia onset is characterized by an acute increase in BP, due to impairment of the autoregulation system in the cerebellar blood circulation, some patients with eclampsia did not show this phenomenon. There might be two reasons: 1) the threshold might be lower in patients with endothelial cell damage, such as in patients with preeclampsia; and 2) an acute increase in BP might be masked by the decrease in BP just after eclampsia onset. The results of the present study suggested that this masking of the acute increase in BP at eclampsia onset might often occur in patients with obstetrical emergency.

Furthermore, the increase in maternal heart rate might indicate a pivotal change in maternal blood circulation around eclampsia onset.

Fetal changes in blood circulation

Fetal cardiac monitoring showed prolonged deceleration in all pregnant patients. It was suggested that eclampsia onset might damage the fetal blood circulation, together with failure of the maternal systemic blood circulation. We speculated that strong disorder of the cerebral blood circulation might cause the drastic various changes in systematic blood circulation, including deep decrease in BP seen just after onset of eclampsia. The disorder of fetal heart rates just after the onset might support the drastic changes in systematic blood circulation, including uterine blood circulation.

In conclusion, a large increase in BP was seen before the development of eclampsia, and a large decrease in BP was seen just after the onset of eclampsia, together with disordered fetal heart rate.

The observations of the present study suggested that the changes in BP seen in eclampsia might cause strong damage to both the maternal and fetal blood circulation.

Acknowledgments

This work was supported by a Grant-in-Aid for Japan Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology (23592408 and 23791848).

Conflict of interest

None.

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