M. Nabil El-Tabbakh, MD

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.

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M. Nabil El-Tabbakh, MD

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