A.A. Raouf

Objective: To evaluate the effect of immediate postpartum curettage upon  maternal recovery from severe Preeclampsia.

Methods: Sixty parturient women with severe Preeclampsia were randomly  assigned to either undergo ultrasound directed curettage following delivery  (n=30)or to have no curettage (controls=30).

Results: Subjects who underwent immediate postpartum curettage had a  significant decrease in mean arterial pressure at 16 hours post delivery  (p<0.0002). The mean urine output after uterine curettage was significantly  greater after the first 12 hours post delivery compared to controls (p<0.0002).  Platelet count increased in the curettage group from 12 to 24 hours following  curettage, while controls exhibited a decrease in the platelet count from 12 to  24 hours (p<0.02).

Conclusion: Immediate puerperal uterine curettage of the parturient with  severe Preeclampsia appears to accelerate disease recovery with no adverse  sequelae.

Preeclampsia is considered as an endothelial cell disorder observed only in  the pregnant human female(1). Defined classically as the development of  hypertension, proteinuria and/or edema in the second half of pregnancy in a  woman who has previously been normotensive and otherwise clinically well (2). It  occurs in 7% of all pregnancies and is associated with increased maternal and  perinatal morbidity and mortality (3).

There are many maternal complications of Preeclampsia such as abruptio  placenta, thrombocytopenia, hepatic hemorrhage and rupture, eclampsia,  disseminated intravascular coagulation, stroke, intracerebral hemorrhage, acute  renal failure, and the syndrome of hemolysis, elevated liver enzymes and low  platelet count. (HELLP).(4)

Accelerated recovery from this disease process following delivery could avert  these complications and shorten the time required for intensive care and  hospitalization.

The subjects of this study were 60 pregnant women who presented to labor and  delivery department, Al-Hussein University Hospital, with physical findings  consistent with severe Preeclampsia.

  Severe Preeclampsia was defined as combinations of the following:1-Blood pressure at least 160/110mmHg on two occasions at least 6 hours  	apart.
 	2-At least 3+ proteinuria on a semi qualitative assay
 	3-Less than 400 ml of urine output over 24 hours.  	

Because hypertension, proteinuria and oliguria are not always present  	consistently and concurrently in patients with severe Preeclampsia,  	additional criteria involved verifying the diagnosis of severe disease.  	These include:1-Cerebral or visual disturbances such as altered consciousness,  	headaches, scotoma, or blurred vision.
 	2-Pulmonary edema or cyanosis.
 	3-Epigastric or right upper quadrant pain
 	4-Impaired liver function of unclear etiology
 	5-Thrombocytopenia, or
 	6-Fetal growth retardation. 

Subjects signed informed consent and a computer-generated random card was  drawn and the patients were assigned to receive immediate postpartum curettage  or no curettage.

At admission, evaluation included mean arterial pressure (MAP), hemoglobin  and hematocrit, urine dipstick for presence of proteinuria, quantitative  platelet count, uric acid and serum creatinine, liver function tests,  neurological examination and Ophthalmological examination of the fundus.

Thirty patients underwent uterine curettage after vaginal or caesarian  delivery. At Caesarian , the presumed area of the decidua basalis was curetted  with large banjo curette (fig.1). Patients who delivered vaginally were sedated  with intravenous butorphanol tartrate (Stadol, Bristol Laboratories, Evansville,  IN, USA) and promethazine hydrochloride (Phenergan,Wyeth, Ayerst,  Philadelphia,PA) and underwent ultrasound guided curettage using large Banjo  curette (fig.1).

All curettage specimens were sent for pathological examination.

During the immediate puerperium, all subjects were observed in the obstetric  recovery room until disease remission was apparent. Intensive postpartum  surveillance maintained for 24 hours,and included hourly measurement of MAP,  hourly urine output, hemoglobin and hematocrit with platelet count every 6  hours, and uric acid and creatinine assessment at 12 and 24 hours.

All medications given in the obstetric recovery room were recorded. All women  received magnesium sulfate by continuous IV infusion at a rate of 1.3g/hour  during the study interval. None of the patients received fluid challenge in the  obstetric recovery area. Discharge criteria from this area included:1)adequate  diuresis (output>100ml/hour sustained for at least 2 consecutive hours), 2)  blood pressure control, with diastolic values below 100mmHg and systolic below  160mmHg, and 3), rising platelet count above 50,000/ml.

The time each patient spent in the obstetric recovery room were recorded.

Longitudinal data between groups were analyzed by repeated measure analysis  of variance over time. Grouped demographic data were analyzed by X2 or Fisher  exact test as appropriate. Group means were analyzed by unpaired t test. Data  are expressed as mean ± Standard deviation (SD). P<0.05 was considered  statistically significant.

The age, number of pregnancies, and duration of gestation were similar in  both groups (table 1). The initial MAP in all patients was more than 110 mmHg.

As shown in table 1, laboratory indices of renal function, uric acid and  platelet count was similar in both groups.

On pathological examination, the curettage specimens revealed many decidua  with minimal placental tissue.(fig.2,3)

The MAP of the curettage group was significantly reduced compared with  controls at each 12 hours intervals after delivery (fig.4) with the largest  difference at 14 hours postpartum (p<0.0002).

Mean urine output for the curettage group was significantly greater than for  the non-curettage group at 4-hour interval postpartum (fig.5). The smallest  difference between both groups was observed at 4 hours and the largest  difference at 20 hours postpartum (p<0.0002).

Platelet counts also demonstrated a significant change over time after  delivery (fig.6) with the concentration increasing from 159,000/ml at 12 hours  to 162,000/ml at 24 hours postpartum in the curettage group. On contrast, the  non-curettage group had a mean platelet count of 148.500/ml at 12 hours  postpartum, decreasing to 135,000/ml at 24 hours (p<0.05).

Mean serum levels of uric acid, urea and creatinine were not significantly  different between both groups at 12 and 24 hours postpartum (table 2).

Also, there was no significant difference in the frequency of medications  administered to either group. In the group with curettage 8 patients had  eclamptic fits before delivery, none of them had further fits after delivery and  curettage, while 2 out of 6 patients with antepartum fits had further fits after  delivery in the non-curettage group.

There were no complications from curettage. Twenty-two patients who underwent  curettage were eligible for discharge from the obstetric recovery room at 24  hours, compared with nineteen controls, a non significant difference.

Follow-up for all curettage patients revealed that 11 had onset of  menstruation within 6 weeks and 19 had had lactation amenorrhea, non had  infection or hemorrhagic complications after the curettage.

For control group 14 had onset of menstruation within 6 weeks of delivery and  16 had lactation amenorrhea.

Demographic Characteristics and admission criteria

Articles

Subjects who underwent immediate postpartum curettage had a significant decrease in mean arterial pressure at 16 hours post delivery (p

Effect of Immediate Postpartum Curettage on the Recovery of Severe Preeclampsia

Human Placental Lactogen (HPL) and         Estriol (E3) levels in serum were measured by radioimmunoassay in 50         normal (group I), 50 diabetic (group II) and 50 pre-eclamptic women         (group III) at 32 and 36 weeks. Ultrasonography was also done at 16, 18,         32, 36 weeks of pregnancy and immediately before delivery. The mean         serum HPL and E2 showed progressive increase with the advance of         pregnancy in all groups. However, the pre-eclamptic group showed lower         mean serum HPL and E3 concentrations. While diabetic group showed higher         serum HPL and E3 concentrations than the control group. There was a         positive correlation between birth weight, placental weight and HPL         levels at 32 and 36 weeks in all groups and between E3 level and birth         weight in pre-eclamptic group only. A significant correlation was found         between ultrasonic fetal weight and birth weight in all groups.

A high risk pregnancy is defined as pregnancy in which there is a         risk of a serious adverse outcome in the mother and/or the baby that is         greater than the incidence of that outcome in the general population(1).

It has been recognized for many years that hypertension accompanying         pregnancy can directly affect both the placenta and the fetus and may         cause substantial maternal and fetal morbidity and mortality (2),(3).         The incidence of morbidity and unfavourable perinatal outcome are         significantly increased in diabetics when compared to non-diabetic         pregnancies(3).

Antenatal tests of fetal well-being depend indirectly on changes in         fetal and placental physiology(4). Two hormonal tests of fetal         well-being are popular; Estriol and Human Placental Lactogen(5).         Diagnostic ultrasound has emerged as an important tool for antepartum         fetal surveillance(6). The technical and methodological development of         diagnostic ultrasound has made possible a direct communication with the         fetus(7).

The aim of this work is to study the role of human placental lactogen         and free estriol levels in maternal serum and ultrasonography in normal,         diabetic and pre-eclamptic pregnancy and their relation to the outcome         of pregnancy.

This study involved 150 pregnant women divided into three groups:

  (50 cases) were normal         pregnant women served as a control group.

  (50 cases) were         diabetic pregnant women. All patients of this group were         insulin-dependant.

          (50 cases) were         pre-eclamptic pregnant patients. All the patients had been followed up         starting from the first trimester and attended at a regular antenatal         visits.

A special sheet for each patient was filled.

Ultrasonography was done for all the patients at 16, 18, 32, 36         weeks, and immediately before delivery. Fetal weight was estimated by         ultrasound according to modified Shepard equation (25).

10 ml of maternal venous blood were collected at 32

 weeks where radioimmunoassay of HPL and E3 was carried         out using the iodinated kits prepared by "Diagnostic Products         Corporation, California, USA".

Immediately after delivery, the babies were rescitated and examined,         weight and head circumference were recorded and Apgar scores were         estimated at one and five minutes. Also the placenta was examined and         its weights were recorded.

(links to tables and figures will         open in new windows)

Tables 1, 2, 3 and 4 represent the         antenatal ultrasonic, biochemical and pregnancy outcome data of the         studied groups. 

A significant correlation was found         between ultrasonic fetal weight and birth weight in group I and group         III (p<0.05). In group II the correlation was highly significant         (p<0.02).

In groups I and III the estimated         ultrasonic weight was more then the actual birth weight, while in group         II it was always less than the birth weight 

In the three groups the growth curve of         ultrasonic fetal weight was within normal range 

 Serum HPL         concentration was found between serum HPL levels and the biparietal         diameter (BPD) at 32

 weeks (p<0.05).         Also in this group there was significant correlation between HPL,         neonatal head circumference (p<0.05), placental weight (p<0.05)         and birth weight (p<0.05), 

. However, no         significant correlation was found between Apgar scores and HPL levels.

         weeks was positively correlated with birth weight (p<0.05) 

 and inversely correlated         with Apgar scores at one and five minutes (p<0.05), 

. No significant correlation was found between HPL levels and BPD         at 32

 weeks and head circumference in         the newborn.

In group III, a highly significant         correlation was found between HPL levels at 36

. A significant correlation was         found between HPL, placental weight (p<0.05), 

 weeks (p<0.002) and Apgar scores         at one and five minutes (p<0.05). Also a significant correlation was         found between HPL level at 32

 weeks and neonatal head         circumference (p<0.05).

 The mean E3 levels showed         progressive increase with advance of pregnancy 

In group I, a non significant correlation         was found between E3 levels and birth weight, placental weight, Apgar         scores at five minutes, neonatal head circumference and BPD. A         significant correlation between E3 levels and the other studied         parameters vs.. Birth weight, BPD, placental weight, neonatal head         circumference and Apgar scores (p<0.05).

In Group II, There was no significant         correlation between E3 levels and the other studied parameters vs.. Birth         weight, BPD, placental weight, neonatal head circumference and Apgar         scores.

In Group III, a significant correlation         was found between E3 levels at 32

 weeks         and birth weight (p<0.05) 

, Apgar scores at one and         five minutes (p<0.05) 

There was no significant correlation         between E3 levels and placental weight or BPD at 32

There are two main problems in the high risk pregnancy, the first is         the fetal weight either large or small for date, the second is the         prematurity. Both are accompanied by high perinatal morbidity and         mortality (8).

In the present study 150 pregnant women were selected. Fifty cases         were normal non complicated pregnancies served as control, 50 cases were         diabetic and fifty cases were pre-eclamptic pregnant women.

In this study there were significant correlation between serum level         of HPL at 36

 weeks and birth weight in normal,         pre-eclamptic and diabetic pregnant women. This is in accordance with         the finding of Spellacy (9) and kandil et al (10). This correlation         could be explained by somatotrophic activity as demonstrated by growth         promoting activity, baby weight gain, nitrogen retention and tibial         epiphysial growth (11).

The lower mean serum HPL in patients with pre-eclampsia may also be         due to impaired placental function.

No significant correlation was found between serum level of free         estriol at 36

 weeks and birth weight in normal pregnancy.         This is in agreement with Kandil et al (12) and against Hay and         Lorscheider et al(13). This confliction may be due to fluctation of         estriol level from day to day and variation in relation to meal and to         uterine contraction(11). There was a positive significant correlation         between E3 levels at 36

 week and birth weight in         pre-eclamptic pregnancy. This finding goes with Kloppers et al(14) but         against Kandil et al(12), however, no significant correlation was found         in diabetic pregnancy. Similar results were reported by Kandil et al(12)

In all groups, the mean ultrasonic fetal weight and birth weight were         within normal range.

Human Placental Lactogen can influence both fat and carbohydrate         metabolism and may be responsible for the diabetogenic state observed in         pregnancy(17), this action involves its direct action on adipose         tissues(18). The maternal concentration of HPL is directly related to         the amount of viable placental tissue (18,19).

In this study there was a progressive increase in the serum level of         HPL from 32

 weeks in all groups. This         was in agreement with previous studies(10,20).

There was lower levels of serum HPL in pre-eclamptic patients         compared with normal, while in diabetic patients the serum level of HPL         was higher than in normal. Similar results were reported by         others(10,11,21).

There was a significant correlation between HPL levels at 36

         weeks in pre-eclamptic and diabetic patients and both placental weight         and Apgar scores at 1 & 5 minutes... this is against the results         reported by Kandil et al(10).

In this study the serum level of E3 showed progressive rising from 32

 weeks of pregnancy in the studied groups. This         finding was in accordance with other studies (12,13,22).

In this study no significant correlation was found between E3 level         and birth weight and placental weight in the control group and the         diabetic group. This goes with the results reported by Kandil et al(12)         and against Allen and Lachelim (22), where they found a correlation         between serum E3 level and the mass of trophoblast.

In this study there was a significant correlation between E3 level in         normal pregnancy and Apgar score at one minute and insignificant         correlation in the first trimester but no correlation in the third         trimester.

In diabetic group no significant correlation was found between E3         level and BPD, neonatal head circumference and Apgar scores. This goes         with the finding of Kandil et al(12). The incidence of false abnormal         values of E3 was high(6,24).

From the presented work we concluded that serum HPL and ultrasonographic         assessment of fetal weight appeared to be more accurate tools in         assessment of feto-placental well-being in pre-eclamptic and diabetic         pregnancies than serum free estriol.

TABLE 1: Antenatal Data of Studied Groups 

Role of Maternal Human Placental Lactogen (HPL), Estriol (E3) and Ultrasonography in Monitoring High Risk Pregnancy and Its Outcome