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Amelioration of the hypertension of toxemia by postpartum curettage
Amelioration of the hypertension of toxemia by postpartum curettage CHARLES A. HUNTER, JR . , M .D. WILLIAM F. HOWARD, M.D. CHARLES O . McCORMICK, JR., M.D . Indianapolis, Indiana
Methods and material This study is based on the blood pressure response following postpartum uterine curettage of 70 patients. According to the American Committee on Maternal Welfare classification of toxemia of pregnancy, 60 patients had pre-eclampsia, 3 had eclampsia, 3 had chronic hypertensive vascular disease without superimposed toxemia, and 4 had superimposed toxemia. In 69 patients, the uterine curettage was performed immediately following the delivery of the placenta. One patient, with postpartum eclampsia, was not curetted until 33 hours post partum. This case is presented in more detail below. The uterine curettage was done with a specially made, large, sharp curette* as shown in Fig. 1. With as complete curettage as possible, approximately 8 to 20 grams of decidual tissue are obtained. In the majority of the patients, the blood loss has been minimal and no depression of the hemoglobin has been noted following this procedure. No uterine perforations have occurred. The only morbidity ascribed to the uterine curettage was one case of postpartum endometritis which was promptly controlled by antibiotic therapy. Following the curettage, all patients were placed on a regular diet without sodium re-
of the hypertension in toxemia of pregnancy has been attempted by diuretics, sedation, and antihypertensive drug therapy. The amelioration of the hypertensive state in the postpartum period is indicated to try to protect the mother from serious complications of this disease, namely, convulsions and cerehral vascular accidents. Specific therapy for control of the hypertension of toxemia during pregnancy should be directed toward the elimination of the pressor suhstance. A pressor substance (hystcrotonin) has been demonstrated in the decidua, amniotic fluid , and plasma in these pa tients. I. 2 Since the decidua has been found to have the highest concentration of hysterotonin, the removal of this tissue at the time of delivery seemed to be a plausihle approach. Patients with toxemia of pregnancy were curetted immediately following delivery of the placenta. The observation that the blood pressure returned to a normotensive level in a much shorter period of time than in the patients not treated in this manner is the basis of this report. CON T R 0 L
From the Department of Obstetrics and Gynecology, Indiana Uni versity Medical Center and Marion County General Hospital. Presented at the Twenty-eighth Annual Me eting of the Central Association of Obstetricians and G ynecologists, Kansas City, Missouri, Oct. 6-8, 1960.
*Availablc from Ht'mathcrmall'ol Corp ., Indlanal)ulis 4. Indiana.
884
VOlume 81 Number 5
striction and neither sedation nor antihypertensive medication was administered. The blood pressure was recorded before, during, and after delivery at least every hOur for the first 12 hours following the curettage and then every 6 hours for the remainder of the hospitalization. Results
The response of the blood pressure in a severely pre-eclamptic patient following delivery without curettage 'is illustrated in Fig. 2. This is representative of the gradual return of the blood pressure in these patients, according to reports by Stander, 8 Eastman/ Dieckmann,5 and Peckham. G Fig. 3 illustrates the blood pressure reCordings following uterine curettage in a patient with severe pre-eclampsia. It will be observed that the return to normotensive levels is much faster than the response noted in similar cases not curetted. The amelioration of the hypertension in a patient with postpartum eclampsia is shown in Fig. 4. This patient was a 17-yearold gravida i, para 0, who was admitted to the hospital with a blood pressure of 150/100 mm. Hg and a total weight gain of 42 POunds during pregnancy. Labor started Spontaneously shortly after admission to the hospital and she was delivered vaginally. Immediately post partum, the patient was given morphine sulfate, 15 mg., and reserpine, 0.25 mg., three times a day. Approximately 23 hours after delivery, the blood pressure was 170/90 mm. Hg and she had the first eclamptic convulsion. In spite of sedation and antihypertensive therapy, the blood pressure remained elevated and a second convulsion occurred 5 hours later. A third convulsive seizure ensued in 8 hours. One hour after the third convulsion, a postpartum curettage was done under general anesthesia. A large amount of decidua-like material was removed from the uterine cavity. All medications were discontinued following the curettage and the blood pressure dropped to 118/70 mm. Hg within 8 hours. For the remainder of her hospitalization, she remained normotensive.
Amelioration of hypertension of toxemia
885
The results of the blood pressure response in the immediate postpartum period following uterine curettage are shown in Table I. In the majority of patients with mild preeclampsia, the blood pressure returns to normotensive levels within 4 to 12 hours after curettage. The majority of patients with severe pre-eclampsia become normotensive within a period of 24 hours. Occasionally, a "rebound phenomenon" with slight elevation of the blood pressure is observed on the second or third postpartum day. This secondary elevation is not marked and is transitory in nature, usually less than 6 hours, followed by a return to normal levels for the remainder of the hospital stay. Comment
The role of true toxemia as the initiating factor in residual hypertension following
Fig. 1. Comparison of a normal-sized uterine curette with the special large curette used for postpartum curettage.
May, 1961
886 Hunter, Howard, and McCormick
.
'"
200 180 180
'0:" "'"
140
'"
100
0 0
..,
80
'"
00
'"'0:"
Am .
120
Q
40 20 39
40 DAY S
WEEKS (Alter Slander)
Fig. 2. Blood pressure response of a p atient with pre-eclampsia not curetted.
1'\"'' 1
200
.
180 180
'e" 140 a
'"0: "'" '"'"0: '"
120 100 80
,,/
"""=
-
~
Q
0 0
.,..,
~
80
--.....
40 20 39 40 WEEKS
,1
12
2.
38
.8
80
72
84
96 .
HOURS IN HOS PI T A L
Fig. 3. Blood pressure response of a patient with severe pre-eclampsia following curettage.
) 00
180 ~
'"
I'" 1<0
~
. ~
" ~
12O
100
Q
0
:::
=
80
60 40
on H OU R S I N HOS PIT A L
Fig. 4. Blood pressure response of a patient with postpartum eclampsia treated with uterine curettage.
J. Obst. & Gyne c .
pregnancy is still controversial. However, all observers agree that prolongation of the puerperal hypertension is not beneficial. The objective of this study was directed toward the amelioration of the hypertension resulting from acute toxemia of pregnancy. No specific therapy was directed toward correction of the albuminuria and edema. Whether or not these two manifestations of toxemia are influenced directly by lowering of the blood pressure is questionable. In the majority of cases, the onset of postpartum eclampsia is within 48 hours after delivery; therefore, it appears that the time of occurrence of postpartum eclampsia is related directly to the viability of the decidua. From the results of this study, approximately 87 per cent of the pre-eclamptic patients curetted demonstrated a return of the blood pressure to normotensive levels within 12 to 44 hours. A long-term followup study of these patients will be necessary to determine the presence of residual hypertension. The mqst dramatic response obtained to date has been the case reported of postpartum eclampsia. This patient failed to respond to antihypertensive and sedative medications. After the removal of the decidual tissue, the patient returned to normotensive levels within 8 hours. Associated with the amelioration of the hypertension, there was also a marked improvement in the patient's sensorium. This marked improvement of the patient, following the curettage, strongly suggests that removal of the decidua was the factor responsible for the patient's improvement. The 2 antepartum eclamptic patients also demonstrated immediate and persistent returns to normotensive levels. The duration of the prepartum eclamptic process was short in both cases. We can only hypothesize that the response would not be as dramatic in cases of eclampsia of long duration. In these patients, we believe that the persistent hypertension is the result of renal pressor substances which are secondary to pressor substances of decidual origin. Patients with essential hypertension have
Volume 81 Number 5
Amelioration of hypertension of toxemia
887
uterine curettage, (2) unsuspected essential hypertension, and (3) secondary renal ischemia with activation of the renin pressor mechanism. The blood pressure response, following uterine curettage of patients with toxemia of pregnancy, substantiates our concepts on the etiology of the hypertension in this disease. Summary
failed to respond to curettage. This is quite reasonable when one considers that this condition is extrauterine in origin. However, in cases in which the essential hypertension is complicated by superimposed toxemia, the blood pressure will revert to the prep regnancy levels by this procedure. Failures with this type of therapy are Probably the result of: (1) inadequate
-
REFERENCES
1. Hunter, C. A., Jr., and Howard, W. F.: AM.
J. OIlST. & GYNEC. 79: 838, 1960. 2. Hunter, C. A., Jr., and Howard, W. F.: AM. 1. OnsT. & GYNEC. (In press.) 3. Stander, H. J.: Textbook of Obstetrics, rev. 3, New York, 1945, D. Appleton-Century Company, p. 600.
1. Seventy patients with toxemia of pregnancy were subjected to postpartum uterine curettage in an attempt to ameliorate the hypertension. 2. In the 67 patients classified as having acute toxemia, 64 exhibited prompt returns of the blood pressure to normotensive levels. 3. Three patients with essential hypertension without superimposed toxemia of pregnancy showed no blood pressure response by this procedure. 4. The removal of the decidua post partum in patients with acute toxemia substantiates our concepts on the etiological mechanisms involved in hypertension of this disease.
4. Eastman, N. J., editor: Williams Obstetrics, ed. 11, New York, 1956, Appleton-CenturyCrofts, Inc., p. 697. 5. Dieckmann, W. J.: The Toxemias of Pregnancy, St. Louis, 1952, The C. V. Mosby Company, p. 490. 6. Peckham, C. H.: AM. J. OUST. & GVNEC. 42: 638, 1941.
Discussion DR. WILLIAM E. COPELAND, Columbus, Ohio. Dr. Hunter and his associates are to be complimented not only on their excellent work in the identification of hysterotonin, but also for their approach to solving this problem and to proving clinically the rationale of their original concept. The rather prompt amelioration of hypertension in 64 of 67 patients by postpartum curettage is an excellent response to therapy and does substantiate their earlier work. Certain features of this investigation may not be uniformly accepted and deserve further comment.
1. Assuming that in the maJonty of women with toxemia, ultimate delivery is of prime consideration in treatment of the disease, antepartum or intrapartum therapy may have some beneficial effect that extends over into the postpartum period. 2. It is generally felt that prolongation of antepartum toxemia will result in a longer period of residual hypertension post partum, and under these circumstances we would expect the same results or response as noted here. 3. The ability of specific drug antagonists to block the action of serotonin has been demon-
888
May, 1961 Am . J. Obst. & Gynec.
Hunter, Howard, and McCormick
strated previously and it has been stated that proteolytic enzymes from the kidney can inactivate polypeptides such as hysterotonin. In toxemia is the kidney incapable of neutralizing hysterotonin, or is it possible that production is so increased that the proteolytic enzymes are incapable of keeping pace? 4. Finally, the minimal complications and morbidity in these 70 patients suggest postpartum curettage as a relatively safe procedure. However, postpartum curettage is still potentially hazardous. Uterine perforation, hemorrhage, and infection will be potential sources of concern and may at times be more hazardous to the patient than the risk of postpartum hypertension treated medically. It would be of interest to know about the long-range follow-up of these patients regarding resumption of normal menses, the possible deveIopmC'nt of Asherman's disease, and the subsequent development of permanent vascular or rc~ na I change's.
the procedure can be done more quickly. So far I have been fortunate not to perforate a uterus. I want to emphasize again that these patients are otherwise treated post partum as normotensive patients are treated. They are put on a regular diet, with no restriction as to salt intake, and they get up as soon as any postpartum patient. I think postpartum curettage of toxemic patients will de.c rease the incidence of, if not entirely eradicate, postpartum eclampsia. Just before this study of routinely curetting all toxemic patients, I had 2 patients with postpartum eclampsia. Since performing this operation, I have had no instance of postpartum eclampsia. As to how long the toxemia has been present before delivery, and what effect that will have on residual hypertension, I will submit the data in Table I. I do not intend to draw final conclusions from this, because the series is too small. In this total series of toxemic patients, w~ have had the opportunity of examining 34 of them after they left the hospital. One of these 34 patients was examined for the first time 6 months post partum. This patient had a blood pressure of 160/90. The remainder of these patients were. examined at least 6 weeks post partum. In the group with severe pre-eclampsia, th~ other case of residual hypertension may not he considered as such. This patient had a blood pressure of 140/84 6 weeks after delivery. The 2 patients with {'c1ampsia had no residual
DR. C. O. MCCORWCK, JR., Indianapolis, Indiana. I would like to elaborate a bit on our technique for curettage. It is a relatively simple operative procedure. We usually use ring forcrps and put them on the anterior lip of the cervix, hold them ourselws, or have our assistant hold them. If the assistant does not hold them, we have him hold the uterus. This procedure can be done in about 5 minult's. I have llsed both of the curettes presented in Fig. 1, but I prefer the larger one be'cause
Table I. Hypertension following postpartum curettement of toxemic patients Duration of toxemia (weeks)
Cases
6-8 weeks posl parium
Cases
6 months post parium
5
0
Mild pre-eclampsia
1-2
3-4 5-6 7-8
Total
13
6 I
0 20
0 0 0
0 0
2 0 0 -7
0
1 0
0 0
I
0
Sel'ere pre-eclampsia
1-2 3-4
5
3
0
3
0
7-8
0
1
0 0
I
2
0
0
0
0
5-6
Total
I
12
1
0
--
Hclamp .. i"
1-2
2
Volume 81 Number 5
hypertension at the time of their 6 weeks' examination. DR. WILLIAM B. STROMME, Minneapolis, Minnesota. I would like to ask simply whether Dr. Hunter and his associates have had any experience with postpartum amenorrhea following such thorough curettage. DR. HUNTER (Closing). I am one of the first to agree that the duration of the process prior to delivery influences the rapidity with which the blood pressure returns to normal after delivery. It is well documented by many good observations that the duration, rather than the severity, of the hypertension is the significant factor, in that the longer the process persists, the longer it will take before the blood pressure returns to normal. Admittedly, in this series, as
Amelioration of hypertension of toxemia
889
you may recall from Table I, many of these patients' hypertension was of relatively short duration. Concerning the question about the proteolytic enzymes in the kidney and their effects on the circulating polyppptide, be it hysterotonin, angiotensin, or what, it appears that these proteolytic enzymes, which are in the substance of the kidney, arc not capable of gaining access to thl' maternal circulation and inactivating it. This holds true not only in toxemia but also in the unilateral renal disease process in which angiotensin is an incriminating factor. This disease is relatively infrequent. As far as thl' question is concerned about postpartum ampnorrhea, we have not had any patient who has been classified in this category. To our knowledge, the patients we have followed have all started to menstmatp.
Methods and material This study is based on the blood pressure response following postpartum uterine curettage of 70 patients. According to the American Committee on Maternal Welfare classification of toxemia of pregnancy, 60 patients had pre-eclampsia, 3 had eclampsia, 3 had chronic hypertensive vascular disease without superimposed toxemia, and 4 had superimposed toxemia. In 69 patients, the uterine curettage was performed immediately following the delivery of the placenta. One patient, with postpartum eclampsia, was not curetted until 33 hours post partum. This case is presented in more detail below. The uterine curettage was done with a specially made, large, sharp curette* as shown in Fig. 1. With as complete curettage as possible, approximately 8 to 20 grams of decidual tissue are obtained. In the majority of the patients, the blood loss has been minimal and no depression of the hemoglobin has been noted following this procedure. No uterine perforations have occurred. The only morbidity ascribed to the uterine curettage was one case of postpartum endometritis which was promptly controlled by antibiotic therapy. Following the curettage, all patients were placed on a regular diet without sodium re-
of the hypertension in toxemia of pregnancy has been attempted by diuretics, sedation, and antihypertensive drug therapy. The amelioration of the hypertensive state in the postpartum period is indicated to try to protect the mother from serious complications of this disease, namely, convulsions and cerehral vascular accidents. Specific therapy for control of the hypertension of toxemia during pregnancy should be directed toward the elimination of the pressor suhstance. A pressor substance (hystcrotonin) has been demonstrated in the decidua, amniotic fluid , and plasma in these pa tients. I. 2 Since the decidua has been found to have the highest concentration of hysterotonin, the removal of this tissue at the time of delivery seemed to be a plausihle approach. Patients with toxemia of pregnancy were curetted immediately following delivery of the placenta. The observation that the blood pressure returned to a normotensive level in a much shorter period of time than in the patients not treated in this manner is the basis of this report. CON T R 0 L
From the Department of Obstetrics and Gynecology, Indiana Uni versity Medical Center and Marion County General Hospital. Presented at the Twenty-eighth Annual Me eting of the Central Association of Obstetricians and G ynecologists, Kansas City, Missouri, Oct. 6-8, 1960.
*Availablc from Ht'mathcrmall'ol Corp ., Indlanal)ulis 4. Indiana.
884
VOlume 81 Number 5
striction and neither sedation nor antihypertensive medication was administered. The blood pressure was recorded before, during, and after delivery at least every hOur for the first 12 hours following the curettage and then every 6 hours for the remainder of the hospitalization. Results
The response of the blood pressure in a severely pre-eclamptic patient following delivery without curettage 'is illustrated in Fig. 2. This is representative of the gradual return of the blood pressure in these patients, according to reports by Stander, 8 Eastman/ Dieckmann,5 and Peckham. G Fig. 3 illustrates the blood pressure reCordings following uterine curettage in a patient with severe pre-eclampsia. It will be observed that the return to normotensive levels is much faster than the response noted in similar cases not curetted. The amelioration of the hypertension in a patient with postpartum eclampsia is shown in Fig. 4. This patient was a 17-yearold gravida i, para 0, who was admitted to the hospital with a blood pressure of 150/100 mm. Hg and a total weight gain of 42 POunds during pregnancy. Labor started Spontaneously shortly after admission to the hospital and she was delivered vaginally. Immediately post partum, the patient was given morphine sulfate, 15 mg., and reserpine, 0.25 mg., three times a day. Approximately 23 hours after delivery, the blood pressure was 170/90 mm. Hg and she had the first eclamptic convulsion. In spite of sedation and antihypertensive therapy, the blood pressure remained elevated and a second convulsion occurred 5 hours later. A third convulsive seizure ensued in 8 hours. One hour after the third convulsion, a postpartum curettage was done under general anesthesia. A large amount of decidua-like material was removed from the uterine cavity. All medications were discontinued following the curettage and the blood pressure dropped to 118/70 mm. Hg within 8 hours. For the remainder of her hospitalization, she remained normotensive.
Amelioration of hypertension of toxemia
885
The results of the blood pressure response in the immediate postpartum period following uterine curettage are shown in Table I. In the majority of patients with mild preeclampsia, the blood pressure returns to normotensive levels within 4 to 12 hours after curettage. The majority of patients with severe pre-eclampsia become normotensive within a period of 24 hours. Occasionally, a "rebound phenomenon" with slight elevation of the blood pressure is observed on the second or third postpartum day. This secondary elevation is not marked and is transitory in nature, usually less than 6 hours, followed by a return to normal levels for the remainder of the hospital stay. Comment
The role of true toxemia as the initiating factor in residual hypertension following
Fig. 1. Comparison of a normal-sized uterine curette with the special large curette used for postpartum curettage.
May, 1961
886 Hunter, Howard, and McCormick
.
'"
200 180 180
'0:" "'"
140
'"
100
0 0
..,
80
'"
00
'"'0:"
Am .
120
Q
40 20 39
40 DAY S
WEEKS (Alter Slander)
Fig. 2. Blood pressure response of a p atient with pre-eclampsia not curetted.
1'\"'' 1
200
.
180 180
'e" 140 a
'"0: "'" '"'"0: '"
120 100 80
,,/
"""=
-
~
Q
0 0
.,..,
~
80
--.....
40 20 39 40 WEEKS
,1
12
2.
38
.8
80
72
84
96 .
HOURS IN HOS PI T A L
Fig. 3. Blood pressure response of a patient with severe pre-eclampsia following curettage.
) 00
180 ~
'"
I'" 1<0
~
. ~
" ~
12O
100
Q
0
:::
=
80
60 40
on H OU R S I N HOS PIT A L
Fig. 4. Blood pressure response of a patient with postpartum eclampsia treated with uterine curettage.
J. Obst. & Gyne c .
pregnancy is still controversial. However, all observers agree that prolongation of the puerperal hypertension is not beneficial. The objective of this study was directed toward the amelioration of the hypertension resulting from acute toxemia of pregnancy. No specific therapy was directed toward correction of the albuminuria and edema. Whether or not these two manifestations of toxemia are influenced directly by lowering of the blood pressure is questionable. In the majority of cases, the onset of postpartum eclampsia is within 48 hours after delivery; therefore, it appears that the time of occurrence of postpartum eclampsia is related directly to the viability of the decidua. From the results of this study, approximately 87 per cent of the pre-eclamptic patients curetted demonstrated a return of the blood pressure to normotensive levels within 12 to 44 hours. A long-term followup study of these patients will be necessary to determine the presence of residual hypertension. The mqst dramatic response obtained to date has been the case reported of postpartum eclampsia. This patient failed to respond to antihypertensive and sedative medications. After the removal of the decidual tissue, the patient returned to normotensive levels within 8 hours. Associated with the amelioration of the hypertension, there was also a marked improvement in the patient's sensorium. This marked improvement of the patient, following the curettage, strongly suggests that removal of the decidua was the factor responsible for the patient's improvement. The 2 antepartum eclamptic patients also demonstrated immediate and persistent returns to normotensive levels. The duration of the prepartum eclamptic process was short in both cases. We can only hypothesize that the response would not be as dramatic in cases of eclampsia of long duration. In these patients, we believe that the persistent hypertension is the result of renal pressor substances which are secondary to pressor substances of decidual origin. Patients with essential hypertension have
Volume 81 Number 5
Amelioration of hypertension of toxemia
887
uterine curettage, (2) unsuspected essential hypertension, and (3) secondary renal ischemia with activation of the renin pressor mechanism. The blood pressure response, following uterine curettage of patients with toxemia of pregnancy, substantiates our concepts on the etiology of the hypertension in this disease. Summary
failed to respond to curettage. This is quite reasonable when one considers that this condition is extrauterine in origin. However, in cases in which the essential hypertension is complicated by superimposed toxemia, the blood pressure will revert to the prep regnancy levels by this procedure. Failures with this type of therapy are Probably the result of: (1) inadequate
-
REFERENCES
1. Hunter, C. A., Jr., and Howard, W. F.: AM.
J. OIlST. & GYNEC. 79: 838, 1960. 2. Hunter, C. A., Jr., and Howard, W. F.: AM. 1. OnsT. & GYNEC. (In press.) 3. Stander, H. J.: Textbook of Obstetrics, rev. 3, New York, 1945, D. Appleton-Century Company, p. 600.
1. Seventy patients with toxemia of pregnancy were subjected to postpartum uterine curettage in an attempt to ameliorate the hypertension. 2. In the 67 patients classified as having acute toxemia, 64 exhibited prompt returns of the blood pressure to normotensive levels. 3. Three patients with essential hypertension without superimposed toxemia of pregnancy showed no blood pressure response by this procedure. 4. The removal of the decidua post partum in patients with acute toxemia substantiates our concepts on the etiological mechanisms involved in hypertension of this disease.
4. Eastman, N. J., editor: Williams Obstetrics, ed. 11, New York, 1956, Appleton-CenturyCrofts, Inc., p. 697. 5. Dieckmann, W. J.: The Toxemias of Pregnancy, St. Louis, 1952, The C. V. Mosby Company, p. 490. 6. Peckham, C. H.: AM. J. OUST. & GVNEC. 42: 638, 1941.
Discussion DR. WILLIAM E. COPELAND, Columbus, Ohio. Dr. Hunter and his associates are to be complimented not only on their excellent work in the identification of hysterotonin, but also for their approach to solving this problem and to proving clinically the rationale of their original concept. The rather prompt amelioration of hypertension in 64 of 67 patients by postpartum curettage is an excellent response to therapy and does substantiate their earlier work. Certain features of this investigation may not be uniformly accepted and deserve further comment.
1. Assuming that in the maJonty of women with toxemia, ultimate delivery is of prime consideration in treatment of the disease, antepartum or intrapartum therapy may have some beneficial effect that extends over into the postpartum period. 2. It is generally felt that prolongation of antepartum toxemia will result in a longer period of residual hypertension post partum, and under these circumstances we would expect the same results or response as noted here. 3. The ability of specific drug antagonists to block the action of serotonin has been demon-
888
May, 1961 Am . J. Obst. & Gynec.
Hunter, Howard, and McCormick
strated previously and it has been stated that proteolytic enzymes from the kidney can inactivate polypeptides such as hysterotonin. In toxemia is the kidney incapable of neutralizing hysterotonin, or is it possible that production is so increased that the proteolytic enzymes are incapable of keeping pace? 4. Finally, the minimal complications and morbidity in these 70 patients suggest postpartum curettage as a relatively safe procedure. However, postpartum curettage is still potentially hazardous. Uterine perforation, hemorrhage, and infection will be potential sources of concern and may at times be more hazardous to the patient than the risk of postpartum hypertension treated medically. It would be of interest to know about the long-range follow-up of these patients regarding resumption of normal menses, the possible deveIopmC'nt of Asherman's disease, and the subsequent development of permanent vascular or rc~ na I change's.
the procedure can be done more quickly. So far I have been fortunate not to perforate a uterus. I want to emphasize again that these patients are otherwise treated post partum as normotensive patients are treated. They are put on a regular diet, with no restriction as to salt intake, and they get up as soon as any postpartum patient. I think postpartum curettage of toxemic patients will de.c rease the incidence of, if not entirely eradicate, postpartum eclampsia. Just before this study of routinely curetting all toxemic patients, I had 2 patients with postpartum eclampsia. Since performing this operation, I have had no instance of postpartum eclampsia. As to how long the toxemia has been present before delivery, and what effect that will have on residual hypertension, I will submit the data in Table I. I do not intend to draw final conclusions from this, because the series is too small. In this total series of toxemic patients, w~ have had the opportunity of examining 34 of them after they left the hospital. One of these 34 patients was examined for the first time 6 months post partum. This patient had a blood pressure of 160/90. The remainder of these patients were. examined at least 6 weeks post partum. In the group with severe pre-eclampsia, th~ other case of residual hypertension may not he considered as such. This patient had a blood pressure of 140/84 6 weeks after delivery. The 2 patients with {'c1ampsia had no residual
DR. C. O. MCCORWCK, JR., Indianapolis, Indiana. I would like to elaborate a bit on our technique for curettage. It is a relatively simple operative procedure. We usually use ring forcrps and put them on the anterior lip of the cervix, hold them ourselws, or have our assistant hold them. If the assistant does not hold them, we have him hold the uterus. This procedure can be done in about 5 minult's. I have llsed both of the curettes presented in Fig. 1, but I prefer the larger one be'cause
Table I. Hypertension following postpartum curettement of toxemic patients Duration of toxemia (weeks)
Cases
6-8 weeks posl parium
Cases
6 months post parium
5
0
Mild pre-eclampsia
1-2
3-4 5-6 7-8
Total
13
6 I
0 20
0 0 0
0 0
2 0 0 -7
0
1 0
0 0
I
0
Sel'ere pre-eclampsia
1-2 3-4
5
3
0
3
0
7-8
0
1
0 0
I
2
0
0
0
0
5-6
Total
I
12
1
0
--
Hclamp .. i"
1-2
2
Volume 81 Number 5
hypertension at the time of their 6 weeks' examination. DR. WILLIAM B. STROMME, Minneapolis, Minnesota. I would like to ask simply whether Dr. Hunter and his associates have had any experience with postpartum amenorrhea following such thorough curettage. DR. HUNTER (Closing). I am one of the first to agree that the duration of the process prior to delivery influences the rapidity with which the blood pressure returns to normal after delivery. It is well documented by many good observations that the duration, rather than the severity, of the hypertension is the significant factor, in that the longer the process persists, the longer it will take before the blood pressure returns to normal. Admittedly, in this series, as
Amelioration of hypertension of toxemia
889
you may recall from Table I, many of these patients' hypertension was of relatively short duration. Concerning the question about the proteolytic enzymes in the kidney and their effects on the circulating polyppptide, be it hysterotonin, angiotensin, or what, it appears that these proteolytic enzymes, which are in the substance of the kidney, arc not capable of gaining access to thl' maternal circulation and inactivating it. This holds true not only in toxemia but also in the unilateral renal disease process in which angiotensin is an incriminating factor. This disease is relatively infrequent. As far as thl' question is concerned about postpartum ampnorrhea, we have not had any patient who has been classified in this category. To our knowledge, the patients we have followed have all started to menstmatp.