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Uterine contractility in the fourth stage of labor and blood loss at delivery
Uterine contractility in the fourth stage of labor and blood loss at delivery JERZY Lddi,
CUPRYN,
M.D.
Poland
Uterine contractility in the fourth stage of labor was recorded in 100 women. No effect of parity, duration of labor, time of rupture of fetal membranes, or fetal weight on postpartum uterine contractility was demonstrated. The rate of contractions decreased with time. No differences were stated between the two groups of patients: i.e., those who lost up to 250 ml. of blood at delivery and those whose blood loss was 251 to 500 ml. The presumable cause of this lack of difference is that the role of contractility of the uterus as a whole organ, for postpartum hemostasis, is negligible. The essential factor is contractility of the myometrium within the region of the placental site.
THE FOURTH, or postplacental stage of labor, i.e., the period extending from expulsion of the placenta through 2 hours thereafter, was recognized as a definite phase of labor as early as 1946 by Greenberg.13 However, the problems of uterine contractility in this stage of labor have been little studied, in spite of their great importance to the clinical course of this stage. This study was carried out to determine the main features of uterine contractility in the fourth stage of labor and their effect upon blood loss at delivery.
Material
and
in the supine position. The records were continued for 30 to 120 minutes. Observations were recorded (of the mean rate of contractions per 30 minutes, contraction intensity and uterine tonus in millimeters; and duration of contractions in seconds) in nonmedicated patients. They were grouped according to parity, duration of labor, time of rupture of fetal membranes, fetal weight, and blood loss at delivery. Mean values for the nonmedicated patients were compared then to those for the 25 women who received oxytocic drugs. Significance of mean differences was tested using the Student t test (p < 0.01). In the nonmedicated group there were 46 patients whose blood loss did not exceed 250 ml. at delivery and 29 whose loss was greater, but not in excess of 500 ml. If the quantity of blood lost was still greater, the patient received oxytocic drugs, which then made it impossible to compare the postpartum tocographic values to those of the lower blood loss group,
methods
Material consisted of 100 healthy women, who underwent spontaneous term deliveries. Half of these patients were nulliparas. Seventy-five patients received no medication, and 25 received 5 I.U. of oxytocin and 0.2 mg. of methergine intramuscularly at the moment of fetal delivery. Within 5 to 60 minutes of expulsion of the placenta, a recording of uterine contractions was begun with a Lorand’s tocograph (adjusted to record contractions after delivery81 “). The patients were lying quietly From the 2nd Clinic Gynecology, Medical Lddk, Poland.
of Obstetrics Academy,
Results
Mean values of rate, intensity, and duration of contractions and uterine tonus in the nonmedicated group compared to those in the oxytocic group are shown in Table I.
and
490
Uterine
Table 1. Mean
values of the fourth stage tocographic records obtained from women receiving no medication, compared to those from women who received 5 I.U. oxytocin and 0.2 mg. methergine intramuscularly at delivery - - --..-.-.OxytocinNonmedication group
Rate of contractions per 30 minutes Intensity of contractions (mm. ) Uterine tonus (mm.1 Duration of contractions (ser. 1 *DifTrtenre I).I~l).
III
the
5.52
3.37
methergine group+
14.2 2 5.0
contractility
2.98
6.9 +_ 2.66 129 rmans
C 29.8 statistically
stage
of
labor
491
Table II. Mean values of the two halves recordings of uterine contractility in the fourth stage of labor First
Rate of contractions per 30 minutes Intensity of contractions (mm.) Uterine tonus (mm.1 Duration of contractions i sec.1 ‘Diffwence
7.7+
in fourth
of
1 Second
half
6.0+-
2.15
4.52
7.8 t
3.30
8.9 k. 1 o:!
7.6?
2.93
6.5 t
127
means
half
of
+ 30.7
statistically
1 i-i*
‘/.I%
134 23i.i
significant
(p
<
ii.01 /.
5.6% 2.25 9.1 f
2.85
Table III.
77 + 26.9 significant
(p
<
Mean values of the records of uterine contractility in the fourth stage of labor in patients with blood loss at delivery” __---..-~_.._____ ___-. -. / Blood 10s~
j o-250 ml. In the nonmedicated group no effect of parity, duration of the first stage of labor (up to 24 hours), time of rupture of fetal membranes, or fetal weight was demonstrated upon the fourth stage uterine contractility. These recordings, which were continued for 45 minutes or more, were divided into halves. Comparison of mean values for each half showed that a decrease in frequency of contractions was the only change appearing with elapse of time (Table II) . No correlation was noted between uterine contractility in the fourth stage and blood loss at delivery (up to 500 ml.). This is shown in Table III. Comment In our material uterine contractions continued throughout the 2 hours following expulsion of placenta. A typical fourth stage tocogram is shown in Fig. 1, A. Contraction rates were observed as low as 2.5 per 30 minutes( Fig. 1, B) , or as high as 15.0 per 30 minutes. These observations were similar to those of Guggisberg.‘” However, contraction rates as high as 10 per 10 minutes which \vert: reported by Alvarez and CaldeyroHarcia’ were not seen. Furthermore, in our material it would not be possible, because the short& duration of contractions was
Rate of contractions per 30 minutes Intensity of contractions (mm.) Uterine tonus (mm. ) Duration of contractions (ser. ) ---__ *Differences
of
nwans
/ 252-500 ml.
5.42
2.29
5.82
7.3 t
2.61
Ii.-4 -e 3.32
7.3 k 2.70
6.4 t 2.56
129 a~ e
+ 28.7 not
121
significant
2.46
210.9 ~tatl4rally
ip < 0.01).
63 seconds. Ijifferences in applied methods must be remembered. However, Moir.‘” using the same method as used by Alvarez and Caldeyro-Barcia,’ obtained results rather similar to ours. Intensity of contractions and uterine tonus \vere similar to the results of Lorantl and Szecsi’” but are not comparable to those of other authors’, I9 who used different methods. Fig. 1, B shows a recording with very low uterine tonus and high intensity of contractions. Mean duration of the fourth stagts contractions in our material (126 seconds’) is much longer than reported by others.“” “’ We have observed contractions lasting 200 seconds and longer (Fig. 1, C) Some feel that the fourth stage contractions arc qular,“’ while others observed uncoordinated contractions but never as early as lvithin 2 hours post partum. I8 We ohserved i rc-
492
Cupryn
Fig. 1. Recordings of uterine contractility in the fourth stage of labor. A, typical record; B, a record showing low rate and high intensity of contractions as well as low uterine tonus; C, contractions of long duration; D, irregular uterine contractions in the fourth stage of labor (the recording was started 25 minutes after delivery of fetus and 20 minutes after expulsion of placenta); E, this patient received 5 I.U. oxytocin and 0.2 mg. mrthergine intramuscularly at the moment of delivery of the fetus (the recording was started in 60 minutes after administration of the drugs).
cordings of irregular contractions. In one of these (Fig. 1, D) the change into a regular pattern is visible. Unlike others,l”J I33 w *CJwe did not demonstrate a difference in the fourth stage tocographic values with regard to parity. Similar results were reported by Lorand and Szecsi.23 The effect of the clinical course of the earlier phases of labor upon the fourth stage uterine contractility could be studied only partially. It was useless to compare records obtained after operative deliveries to those after normal deliveries because of use of anesthesia, oxytocics, etc., in the former group. No effect of the duration of the first stage (up to 24 hours), time of rupture of fetal membranes, or fetal weight could be demonstrated. It is possible that such effects
would be demonstrable if cases of prolonged labor, hydramnios, or multiple births were included. The effect of oxytocin and methergine on fourth stage uterine contractility resembled the results of many authors. Compare a typical recording after oxytocin-methergine medication (Fig. 1, E) to Fig. 1, A. As seen from Table II, the rate of contractions lowered with time, while other values showed no change. This was also observed by others.ll IQ, 26 Some feel that intensity of contractions decreases as well.“9 ” In a normal labor the effect of an increasing rate of oxytocin infusion upon the uterus consists of three phases: first increased intensity of contractions, then rate of contractions, and finally augmentation of uterine tonus. Slowing down the infusion rate causes first a decrease in tonus, then frequency of
Uterine
contraction, and finally a lower intensity of contractions.“” Sica-Blanc0 and SalaZs after stopping oxytocin infusion observed a decrrase in frequency and later in intensity of contractions. The highest dose used was probably too low to initiate the third phase of oxytocin effect. The quantity of endogenous oxytocin released from the neurohypophysis at the end of normal labor may be recognized as optirnal, i.e., sufficient to induce the second phase (high intensity and rate of contractions) After delivery, the level of oxytocin diminishes,” probably because Ferguson’s reflrx is no longer completed. During the fourth stage of labor uterine activity decreases gradually and a diminishing contraction rate seems to be the first sign of this. Scvrral hours later a decrease in intensity probably would appear. Opinions on the role of the main factors in postpartum hemostasis differ greatly. 1. It is well known that placental separation is very important for postpartum hemostasis (Duncan versus Schultze mechanism) . If penetration of uterine wall by placental villi does not exceed normal, separation of the placenta depends upon two factors: (a) uterine contractility in the third stage of labor’” (it appears, however, that the third stage tocograrns in labors complicated by hernorrhage do not differ from those in labors with normal blood loss”) and (b) plart9tal position in utero (a placenta located in the lower uterine segment or in the cornual area often separates abnormally). ‘fhis is probably due to poor contractility of the myometrium in these parts of the uterus. The dependence between uterine contractility and placental separation is reciprocal? as sholvn by hemorrhages accompanying residua placenta?. 2. Uterine contractility in the fourth stage of labor is one of the main factors in postpartum hemostasis.‘, 1p-14, lG, 21 The mechanism of its action is compression of placental site vessels. Blood loss is greater after labors complicated by uterine hypertonia or uncoordinated contractions.“2 Many authors feel that the quantity of blood lost at deliv-
contractility
in
fourth
stage
ot
labor
493
ery parallels the height of uterine tonus post partunl. Some feel that, in cases of hemorrhage, uterine tonus is low.‘> “‘. ” The opillion of others is that in “atonic” bleeding uterine tonus may be normal, while uterinr hypotonia is not necessarily accompanietl 1)) increased blood ~oy.2. 15. 23. 3, Insufficient uterine contractility after. drlivery may be caused by rupture or distention of muscular fibers (hydramnios, multiple pregnancy I, replacrment of contractile e/emvnts by connective tissue (grand ~nulmilieu in tiparity j , change in the chemical dehydration, and llytissues (exhaustion poxia in prolonged ‘labors ! , or rapid wept ying of uterus (operative deliveries j 3. Vasoconstriction within the placcmtal site is also important for postpartum titlmostasis.” Some investigators feel that IIIVOmetrial contractions and those of the ~ur~st*lrs of the placental site vessels are synchronous, but poorly musculated vessels in the deep layers of the decidua undergo compression.’ Others maintain that placental sit{, at terks constrict, while vpins arc compressed.‘” 4. Blood coagulation in stumps of pia~ntal site \.essc:ls completes definite henlostasis.:!. ‘* Some authors lriaintain that the tllost important is coagulation it I veins and constriction in artrries.” It secbms then that in lack of traull~a to pelvic organs the blood loss at deli,.e,,y depends upon four main factors, one: of \vtiich is uterine contractility in the fourth stage. The group of patients studied consisted of women whose blood loss at delivery did not exceed 500 n11. Nevertheless, it might be expected that the effect of postpartum Ilterinc contractility on blood loss would hr dernonstrated. However, no significant difcrenre was noted brtwren patients with nnnimal and greater, yet normal, blood loss. It is possible that this difference ~vould l)e evident if women with abnormal I morp than 500 ml.) blood loss were included, It also may be that even then such an &feet would not be demonstrable. It seems that, for postpartum hemostasis, contractility of 1.h~ myometrium within the placental site, not of the whole uterus. is essential. In this region,
494
Cupryn
uterine muscle contracts more weakly than in other parts of the organ because of the so-called “local progesterone block.““9 J5 Probably the chief reason that uterine contractility is “similar” in cases of varying blood loss is that in those with greater blood loss the uterus contracts normally beyond the placental site. If the recording device collects impulses from the myometrium above the placental site, it records contractions of just this part of uterine muscle (placental location on the anterior wall in 33 per cent, postpartum placental site diameter 7 cm.). Otherwise it records contractility of other parts of myometrium, which play no role in postpartum hemostasis. Thus, it seems that in cases of atonic bleeding the record may show normal contractility pattern, unless atonia of placental
site muscle is accompanied by that of the whole myometrium. As early as in 1941, Weibel”” admitted that atonia may be liruited to a part of uterus. Lorand and Szecsi’)” tried to explain cases of “atonic” bleeding with high uterine tonus in the fourth stage in this way. Probably, local atonia is responsible only for some cases of atonic bleeding. In many cases of atonic bleeding, an obstetrician palpates the uterus as a big, soft organ. However, sometimes in a healthy woman, showing no coagulation disorders, after normal labor without trauma to the birth canal, severe postpartum hemorrhage appears, though the uterus “contracted well.” These cases may be explained by local atonia, limited to placental site myometrium. Results of this study, as well as data published earlier-,$ support this view.
REFERENCES
1.
2. 3.
4.
5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
Alvarez,
H., and Caldeyro-Barcia, R.: Proc. Seq. Congr. Latino-am. obst. e ginec., S. Pablo, 1954. Bieniarz, J.: Zentralbl. GynHk. 78: 1369, 1956. Caldeyro-Barcia, R., Alvarez, H., Poseiro, J. J., Pose, S. V., and Mendez-Batter, C.: Proc. Nov. Congr. Argent. obst. e ginec., Buenos Aires, 1955. Coch, J. A., Brovetto, J., Cabot, H., Fielitz, C. A., and Caldeyro-Barcia, R.: AM. J. OBST. & GYNEC. 91: 10, 1965. Csapo, A. I., Lipman, J,, and Wood, C.: AM. J. OBST. & GYNEC. 85: 819, 1963. Csapo, A. I., and Lloyd-Jacob, M. A.: AM. J. OBST. & GYNEC. 85: 806, 1963. Csapo, A. I., Takeda, H., and Wood, C.: AM. J. OBST. & GYNEC. 85: 813, 1963. Cupryn, J.: Ginek. polska 36: 473, 1965. Cupryn, J.: Gynaecologia 160: 183, 1965. Embrey, M. P.: Triangel 6: 199, 1964. Embrey, M. P.: J. Obst. & Gynaec. Brit. Emp. 62: 1, 1955. Gorodovsky, J., Florek, E. N., and Wulff, G.: AM. J. OBST. & GYNEC. 88: 612, 1964. Greenberg, E.: AM. J. OBST. & GYNEC. 52: 746, 1946. Greenhill, J. P.: Obstetrics, Philadelphia and London, 1961, W. B. Saunders Company. Guggisberg, H.: Helvet. med. acta 4: 13, 1937. Guggisberg, H.: Cah. mens. Med. 4: 477, 1948. von Gyory, G., and Domahidy, F.: Ztschr. Geburtsh. u. GynPk. 118: 192, 1944. Hendricks, C. H., Eskes, T. H., and Saameli, K.: AM. J. OBST. & GYNEC. 83: 890, 1962.
19. 20.
21.
22. 23. 24.
25. 26.
27. 28.
29. 30. 31.
Huber, R.: Zentralbl. GynPk. 78: 748, 1956. Huffman, J. W.: Gynecology and Obstetrics, Philadelphia and London, 1962, W. B. Saunders Company. von Jaschke, R.: Die normale Geburt, in SeitzAmreich: Biolorrie und Patholoeie des Weibes. Berlin-Wien, 162, Urban-Schwarzenberg. ’ JaSkiewicz, J., and Wicifiski, R.: Ginek. polska 31: 441, 1960. Lorand, S., and Szecsi, K.: Acta med. Acad. SC. Hungary 4: 111, 1953. von Mikulicz-Radecki: F.: Geburtshilfe des praktischen Antes, Leipzig, 1954, Barth Verlag. Moir, C.: J. Obst. Gynaec. Brit. Emp. 51: 181, 1944. Miiller, H. A.: Qualitative and Quantitative Studies of the Effect of Oxytocin on Uterine Contractility, in Caldeyro-Barcia, R., and Heller, H.: Oxytocin, Oxford-London-New York-Paris, 1961, Pergamon Press, Inc. Miiller, H. A., and Stroker, W.: Arch. GynPk. 191: 369, 1959. Sica-Blanco, Y., and Sala, N. L.: Uterine Contractility at the Beginning and End of an Oxytocin Infusion, in Caldeyro-Barcia, R., and Heller, H. : Oxytocin, Oxford-LondonNew York-Paris, 1961, Pergamon Press, Inc. Weibel. W.: Lehrbuch der Frauenheilkunde. Berlin-Wien, 1941, Urban-Schwarzenberg. ’ Wicifiski, R.: III Weltkongr. Gynlk. u. Geburtsh., Wien, 1961. Winzeller, H.: Zentralbl. Gynak. 66: 1477, 1942. ul. Crerwona Lddi, Poland
3 a
CUPRYN,
M.D.
Poland
Uterine contractility in the fourth stage of labor was recorded in 100 women. No effect of parity, duration of labor, time of rupture of fetal membranes, or fetal weight on postpartum uterine contractility was demonstrated. The rate of contractions decreased with time. No differences were stated between the two groups of patients: i.e., those who lost up to 250 ml. of blood at delivery and those whose blood loss was 251 to 500 ml. The presumable cause of this lack of difference is that the role of contractility of the uterus as a whole organ, for postpartum hemostasis, is negligible. The essential factor is contractility of the myometrium within the region of the placental site.
THE FOURTH, or postplacental stage of labor, i.e., the period extending from expulsion of the placenta through 2 hours thereafter, was recognized as a definite phase of labor as early as 1946 by Greenberg.13 However, the problems of uterine contractility in this stage of labor have been little studied, in spite of their great importance to the clinical course of this stage. This study was carried out to determine the main features of uterine contractility in the fourth stage of labor and their effect upon blood loss at delivery.
Material
and
in the supine position. The records were continued for 30 to 120 minutes. Observations were recorded (of the mean rate of contractions per 30 minutes, contraction intensity and uterine tonus in millimeters; and duration of contractions in seconds) in nonmedicated patients. They were grouped according to parity, duration of labor, time of rupture of fetal membranes, fetal weight, and blood loss at delivery. Mean values for the nonmedicated patients were compared then to those for the 25 women who received oxytocic drugs. Significance of mean differences was tested using the Student t test (p < 0.01). In the nonmedicated group there were 46 patients whose blood loss did not exceed 250 ml. at delivery and 29 whose loss was greater, but not in excess of 500 ml. If the quantity of blood lost was still greater, the patient received oxytocic drugs, which then made it impossible to compare the postpartum tocographic values to those of the lower blood loss group,
methods
Material consisted of 100 healthy women, who underwent spontaneous term deliveries. Half of these patients were nulliparas. Seventy-five patients received no medication, and 25 received 5 I.U. of oxytocin and 0.2 mg. of methergine intramuscularly at the moment of fetal delivery. Within 5 to 60 minutes of expulsion of the placenta, a recording of uterine contractions was begun with a Lorand’s tocograph (adjusted to record contractions after delivery81 “). The patients were lying quietly From the 2nd Clinic Gynecology, Medical Lddk, Poland.
of Obstetrics Academy,
Results
Mean values of rate, intensity, and duration of contractions and uterine tonus in the nonmedicated group compared to those in the oxytocic group are shown in Table I.
and
490
Uterine
Table 1. Mean
values of the fourth stage tocographic records obtained from women receiving no medication, compared to those from women who received 5 I.U. oxytocin and 0.2 mg. methergine intramuscularly at delivery - - --..-.-.OxytocinNonmedication group
Rate of contractions per 30 minutes Intensity of contractions (mm. ) Uterine tonus (mm.1 Duration of contractions (ser. 1 *DifTrtenre I).I~l).
III
the
5.52
3.37
methergine group+
14.2 2 5.0
contractility
2.98
6.9 +_ 2.66 129 rmans
C 29.8 statistically
stage
of
labor
491
Table II. Mean values of the two halves recordings of uterine contractility in the fourth stage of labor First
Rate of contractions per 30 minutes Intensity of contractions (mm.) Uterine tonus (mm.1 Duration of contractions i sec.1 ‘Diffwence
7.7+
in fourth
of
1 Second
half
6.0+-
2.15
4.52
7.8 t
3.30
8.9 k. 1 o:!
7.6?
2.93
6.5 t
127
means
half
of
+ 30.7
statistically
1 i-i*
‘/.I%
134 23i.i
significant
(p
<
ii.01 /.
5.6% 2.25 9.1 f
2.85
Table III.
77 + 26.9 significant
(p
<
Mean values of the records of uterine contractility in the fourth stage of labor in patients with blood loss at delivery” __---..-~_.._____ ___-. -. / Blood 10s~
j o-250 ml. In the nonmedicated group no effect of parity, duration of the first stage of labor (up to 24 hours), time of rupture of fetal membranes, or fetal weight was demonstrated upon the fourth stage uterine contractility. These recordings, which were continued for 45 minutes or more, were divided into halves. Comparison of mean values for each half showed that a decrease in frequency of contractions was the only change appearing with elapse of time (Table II) . No correlation was noted between uterine contractility in the fourth stage and blood loss at delivery (up to 500 ml.). This is shown in Table III. Comment In our material uterine contractions continued throughout the 2 hours following expulsion of placenta. A typical fourth stage tocogram is shown in Fig. 1, A. Contraction rates were observed as low as 2.5 per 30 minutes( Fig. 1, B) , or as high as 15.0 per 30 minutes. These observations were similar to those of Guggisberg.‘” However, contraction rates as high as 10 per 10 minutes which \vert: reported by Alvarez and CaldeyroHarcia’ were not seen. Furthermore, in our material it would not be possible, because the short& duration of contractions was
Rate of contractions per 30 minutes Intensity of contractions (mm.) Uterine tonus (mm. ) Duration of contractions (ser. ) ---__ *Differences
of
nwans
/ 252-500 ml.
5.42
2.29
5.82
7.3 t
2.61
Ii.-4 -e 3.32
7.3 k 2.70
6.4 t 2.56
129 a~ e
+ 28.7 not
121
significant
2.46
210.9 ~tatl4rally
ip < 0.01).
63 seconds. Ijifferences in applied methods must be remembered. However, Moir.‘” using the same method as used by Alvarez and Caldeyro-Barcia,’ obtained results rather similar to ours. Intensity of contractions and uterine tonus \vere similar to the results of Lorantl and Szecsi’” but are not comparable to those of other authors’, I9 who used different methods. Fig. 1, B shows a recording with very low uterine tonus and high intensity of contractions. Mean duration of the fourth stagts contractions in our material (126 seconds’) is much longer than reported by others.“” “’ We have observed contractions lasting 200 seconds and longer (Fig. 1, C) Some feel that the fourth stage contractions arc qular,“’ while others observed uncoordinated contractions but never as early as lvithin 2 hours post partum. I8 We ohserved i rc-
492
Cupryn
Fig. 1. Recordings of uterine contractility in the fourth stage of labor. A, typical record; B, a record showing low rate and high intensity of contractions as well as low uterine tonus; C, contractions of long duration; D, irregular uterine contractions in the fourth stage of labor (the recording was started 25 minutes after delivery of fetus and 20 minutes after expulsion of placenta); E, this patient received 5 I.U. oxytocin and 0.2 mg. mrthergine intramuscularly at the moment of delivery of the fetus (the recording was started in 60 minutes after administration of the drugs).
cordings of irregular contractions. In one of these (Fig. 1, D) the change into a regular pattern is visible. Unlike others,l”J I33 w *CJwe did not demonstrate a difference in the fourth stage tocographic values with regard to parity. Similar results were reported by Lorand and Szecsi.23 The effect of the clinical course of the earlier phases of labor upon the fourth stage uterine contractility could be studied only partially. It was useless to compare records obtained after operative deliveries to those after normal deliveries because of use of anesthesia, oxytocics, etc., in the former group. No effect of the duration of the first stage (up to 24 hours), time of rupture of fetal membranes, or fetal weight could be demonstrated. It is possible that such effects
would be demonstrable if cases of prolonged labor, hydramnios, or multiple births were included. The effect of oxytocin and methergine on fourth stage uterine contractility resembled the results of many authors. Compare a typical recording after oxytocin-methergine medication (Fig. 1, E) to Fig. 1, A. As seen from Table II, the rate of contractions lowered with time, while other values showed no change. This was also observed by others.ll IQ, 26 Some feel that intensity of contractions decreases as well.“9 ” In a normal labor the effect of an increasing rate of oxytocin infusion upon the uterus consists of three phases: first increased intensity of contractions, then rate of contractions, and finally augmentation of uterine tonus. Slowing down the infusion rate causes first a decrease in tonus, then frequency of
Uterine
contraction, and finally a lower intensity of contractions.“” Sica-Blanc0 and SalaZs after stopping oxytocin infusion observed a decrrase in frequency and later in intensity of contractions. The highest dose used was probably too low to initiate the third phase of oxytocin effect. The quantity of endogenous oxytocin released from the neurohypophysis at the end of normal labor may be recognized as optirnal, i.e., sufficient to induce the second phase (high intensity and rate of contractions) After delivery, the level of oxytocin diminishes,” probably because Ferguson’s reflrx is no longer completed. During the fourth stage of labor uterine activity decreases gradually and a diminishing contraction rate seems to be the first sign of this. Scvrral hours later a decrease in intensity probably would appear. Opinions on the role of the main factors in postpartum hemostasis differ greatly. 1. It is well known that placental separation is very important for postpartum hemostasis (Duncan versus Schultze mechanism) . If penetration of uterine wall by placental villi does not exceed normal, separation of the placenta depends upon two factors: (a) uterine contractility in the third stage of labor’” (it appears, however, that the third stage tocograrns in labors complicated by hernorrhage do not differ from those in labors with normal blood loss”) and (b) plart9tal position in utero (a placenta located in the lower uterine segment or in the cornual area often separates abnormally). ‘fhis is probably due to poor contractility of the myometrium in these parts of the uterus. The dependence between uterine contractility and placental separation is reciprocal? as sholvn by hemorrhages accompanying residua placenta?. 2. Uterine contractility in the fourth stage of labor is one of the main factors in postpartum hemostasis.‘, 1p-14, lG, 21 The mechanism of its action is compression of placental site vessels. Blood loss is greater after labors complicated by uterine hypertonia or uncoordinated contractions.“2 Many authors feel that the quantity of blood lost at deliv-
contractility
in
fourth
stage
ot
labor
493
ery parallels the height of uterine tonus post partunl. Some feel that, in cases of hemorrhage, uterine tonus is low.‘> “‘. ” The opillion of others is that in “atonic” bleeding uterine tonus may be normal, while uterinr hypotonia is not necessarily accompanietl 1)) increased blood ~oy.2. 15. 23. 3, Insufficient uterine contractility after. drlivery may be caused by rupture or distention of muscular fibers (hydramnios, multiple pregnancy I, replacrment of contractile e/emvnts by connective tissue (grand ~nulmilieu in tiparity j , change in the chemical dehydration, and llytissues (exhaustion poxia in prolonged ‘labors ! , or rapid wept ying of uterus (operative deliveries j 3. Vasoconstriction within the placcmtal site is also important for postpartum titlmostasis.” Some investigators feel that IIIVOmetrial contractions and those of the ~ur~st*lrs of the placental site vessels are synchronous, but poorly musculated vessels in the deep layers of the decidua undergo compression.’ Others maintain that placental sit{, at terks constrict, while vpins arc compressed.‘” 4. Blood coagulation in stumps of pia~ntal site \.essc:ls completes definite henlostasis.:!. ‘* Some authors lriaintain that the tllost important is coagulation it I veins and constriction in artrries.” It secbms then that in lack of traull~a to pelvic organs the blood loss at deli,.e,,y depends upon four main factors, one: of \vtiich is uterine contractility in the fourth stage. The group of patients studied consisted of women whose blood loss at delivery did not exceed 500 n11. Nevertheless, it might be expected that the effect of postpartum Ilterinc contractility on blood loss would hr dernonstrated. However, no significant difcrenre was noted brtwren patients with nnnimal and greater, yet normal, blood loss. It is possible that this difference ~vould l)e evident if women with abnormal I morp than 500 ml.) blood loss were included, It also may be that even then such an &feet would not be demonstrable. It seems that, for postpartum hemostasis, contractility of 1.h~ myometrium within the placental site, not of the whole uterus. is essential. In this region,
494
Cupryn
uterine muscle contracts more weakly than in other parts of the organ because of the so-called “local progesterone block.““9 J5 Probably the chief reason that uterine contractility is “similar” in cases of varying blood loss is that in those with greater blood loss the uterus contracts normally beyond the placental site. If the recording device collects impulses from the myometrium above the placental site, it records contractions of just this part of uterine muscle (placental location on the anterior wall in 33 per cent, postpartum placental site diameter 7 cm.). Otherwise it records contractility of other parts of myometrium, which play no role in postpartum hemostasis. Thus, it seems that in cases of atonic bleeding the record may show normal contractility pattern, unless atonia of placental
site muscle is accompanied by that of the whole myometrium. As early as in 1941, Weibel”” admitted that atonia may be liruited to a part of uterus. Lorand and Szecsi’)” tried to explain cases of “atonic” bleeding with high uterine tonus in the fourth stage in this way. Probably, local atonia is responsible only for some cases of atonic bleeding. In many cases of atonic bleeding, an obstetrician palpates the uterus as a big, soft organ. However, sometimes in a healthy woman, showing no coagulation disorders, after normal labor without trauma to the birth canal, severe postpartum hemorrhage appears, though the uterus “contracted well.” These cases may be explained by local atonia, limited to placental site myometrium. Results of this study, as well as data published earlier-,$ support this view.
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