- Email: [email protected]
The etiology of fetal acidosis as determined by umbilical cord acid-base studies
The etiology of fetal acidosis as determined by umbilical cord acid-base studies John W.C. Johnson, MD, and Douglas S. Riehards, MD Gainesville, Florida OBJECTIVE: Our purpose was to determine whether umbilical cord acid-base values might be used to differentiate abruptio placentae from cord prolapse. STUDY DESIGN" By use of a retrospective study design, umbilical cord blood acid-base values of 32 cases of severely acidotic acute abruptio placentae were statistically compared with those of 19 cases of severely acidotic acute cord prolapse with Fisher's exact test, Mann-Whitney U tests, and receiveroperator curve characteristic analyses. RESULTS: No significant differences in electronic fetal heart rate record interpretations were detected. Highly significant differences in umbilical arterial and umbilical venous blood gas values were noted between the two groups. Most notable were the differences between umbilical venous and arterial blood gas values in the cord prolapse group. Receiver-operator characteristic curve analysis demonstrated that an umbilical venous-arterial pH difference of 0.15 was an effective cutoff value in differentiating cord prolapse from abruptio placentae (accuracy 92%). CONCLUSION: Umbilical arterial blood gas values combined with umbilical venous blood gas values can assist in determining the pathogenesis of marked fetal acidosis. (Am J Obstet Gynecol 1997;177:274-82.)
Key words: Fetal acidosis, abruptio placentae, umbilical cord prolapse, umbilical artery and umbilical venous acid-base data
The interpretation of fetal heart rate (FHR) tracings is problematic) Tracings interpreted as normal have high specificity in predicting fetuses without significant acidosis. But the etiology of abnormal tracings is often obscure. 2 Even with ominous FHR tracings and fetal acidosis it is often difficult to determine the cause of the acidosis) It would be of great assistance to clinicians if they had an objective, accurate means of identifying the mechanism of fetal intrapartum compromise. Clearly, cord blood gases have become the gold standard in determining the presence or absence of acidosis in the fetus at delivery, as well as the severity of that acidosis. Might such measurements also define the pathogenesis of fetal acidosis? The purpose of this study was to test the hypothesis that patients with severe decreases in maternal blood flow to the placenta (acute abruptio placentae) have umbilical cord blood gas values that are distinctly different from those observed in patients who primarily have a From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Florida College of Medicine. Supported by the Department of Obstetricsand Gynecology, University of Florida College of Medicine. Presented at the Fifty-ninth Annual Meeting of The South Atlantic Association of Obstetricians and Gynecologists, Hot Springs, Virginia, January 25-28, 1997. Reprint requests:John W. C.Johnson, MD, Departmentof Obstetricsand Gynecology, University of Florida College of Medicine, P.O. Box 100294, Gainesville, FL 32610-0294. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/6/82719 274
reduction in the fetal perfusion of the placenta (acute umbilical cord compression). Over the years, a n u m b e r of investigators have observed that u n d e r circumstances of severe umbilical cord compression umbilical arterial blood gas values indicate fetal acidosis, whereas umbilical venous blood gas values tend to remain near normal. 4' ~ There have been animal studies demonstrating that umbilical cord occlusion is associated with significant umbilical arterial acidemia but relatively normal blood gas values in the umbilical venous blood. 6 By contrast, the general clinical observation has been that, when maternal blood flow to the placenta is reduced, both umbilical arterial and umbilical venous blood display acidosis. ~'7 These observations have not been documented in a rigorous way in h u m a n pregnancies. Methods
With use of a previously described computerized database that included all deliveries at our institution from Jan. 1, 1987, through Dec. 31, 1995, 8 we identified those patients with a discharge diagnosis of acute abruptio placentae or acute cord prolapse. Only those patients with severe acidosis, defined as an umbilical arterial pH <7.13, were included in the study. An umbilical arterial pH of <7.13 constitutes the mean value minus 2 SDs for term deliveries analyzed at this institution.9 Among these patients with severe acidosis at delivery, only those delivered by cesarean section with convincing diagnostic criteria for abruptio placentae or cord prolapse were
Johnson and Richards
Volume 177, Number 2 Am J Obstet Gynecol
included. In the case of abruptio placentae, only cases with retroplacental clots n o t e d at the time of cesarean section delivery were acceptable for inclusion in this study. In the case of prolapsed cord, only those cases in which m a n u a l elevation of the presenting part was req u i r e d before e m e r g e n c y delivery were included. Cases without umbilical arterial and umbilical venous blood gas values at delivery were excluded. Umbilical b l o o d gases were collected and analyzed as previously described, a° In an effort to exclude cases in which anesthesia complications m i g h t have altered the cord gas values, we reviewed the specific anesthesia records for evidence of cardiovascular or respiratory complications associated with the anesthesia. W h e n such complications were identified, those cases were e x c l u d e d f r o m the analysis. Electronic fetal m o n i t o r i n g interpretations were available through the obstetric data system and these were e x a m i n e d for differences between the two study groups. Statistical analysis was p e r f o r m e d with the Statgraphics Plus (Statistical Graphics, Princeton, N.J.) p r o g r a m for m i c r o c o m p u t e r . Differences between groups were tested with use of the Student t test for normally distributed data. T h e X2 test was used for categoric data analysis, unless the sample size was small, in which case Fisher's exact test was used. T h e blood gas data were not normally distributed, so they were c o m p a r e d with the MannWhitney U test. Values that m i g h t differentiate abruptio placentae f r o m cord prolapse were evaluated with receiver-operator characteristic curves. ~a This project was reviewed by our Institutional H u m a n E x p e r i m e n t a t i o n Review Board and approved u n d e r an e x e m p t e d status. T h e study was g r a n t e d an e x e m p t e d status because it involved the analysis of existing data and the subjects were n o t identifiable.
Results During the 9 years of obstetric e x p e r i e n c e abstracted in the c o m p u t e r database, this hospital r e c o r d e d 30,888 deliveries. During these years a total of 167 patients were diagnosed with abruptio placentae, for a frequency of 0.54% or 1 in every 185 deliveries. T h e diagnosis of prolapsed Umbilical cord was m a d e 97 times, for a frequency of 0.314% or 1 every 322 deliveries. O n e h u n d r e d thirty-five (81%) of the cases diagnosed as abruptio placentae did n o t m e e t o u r inclusion criteria, leaving 32 study cases. Seventy-eight (80%) of those cases diagnosed as umbilical cord prolapse did not m e e t o u r inclusion criteria, leaving 19 cases for analysis. T h e majority of the exclusions in b o t h groups were cases in which the umbilical arterial p H was >7.12. We excluded two cases because of significant cardiorespiratory complications in the mothers, which were related to anesthesia difficulties. O n e set o f twins was included in the abruptio placentae group. After a spontaneous vaginal delivery of twin A,
275
Table I. Maternal characteristics
Maternal age (yr) Maternal race White Black Singleton pregnancy Nulliparous Prior abortion General anesthesia
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance
25 -+ 6*
25 -+ 7
NS
53.1%]46.9% 96.9% 31.3% 43.7% 84.4%
57.9% 42.1% 84.2% 36.8% 31.6% 89.5%
NS NS NS NS NS
NS, Not significant. *Mean -+ 1 SD. tPercent of total within each group.
abruptio placentae o c c u r r e d in twin B, necessitating e m e r g e n c y cesarean delivery. T h e r e were three sets of twins in the cord prolapse group. In o n e set twin A was delivered by spontaneous vaginal delivery and then the cord prolapsed in twin B, requiring cesarean section. In two o t h e r sets of twins, twin A was d e t e r m i n e d to have cord prolapse, necessitating e m e r g e n c y cesarean delivery. In all four cases of twins the cord b l o o d gas values of the unaffected twins were within n o r m a l limits and these cases were n o t included in the analyses. In a statistical comparison of d e m o g r a p h i c characteristics of the mothers, no significant differences were d e t e c t e d between the 32 cases of abruptio placentae and the 19 cases of cord prolapse (Table I). In b o t h groups of patients general anesthesia was most c o m m o n l y used for cesarean section and the mothers received supplemental oxygen frequently. T h e inspired oxygen concentrations varied from 21% to 100%. T h e a m o u n t of assisted respiration was n o t ascertainable. Maternal arterial Po 2 values were n o t d e t e r m i n e d at delivery. No statistically significant differences were n o t e d in the infants with regard to their gestational ages, birth weights, sexes, or Apgar scores (Table II). Most of the patients had electronic fetal m o n i t o r i n g p e r f o r m e d before delivery, although 6% of the cases of abruptio placentae did n o t and 21% of the cases of cord prolapse did not (Table III). T h e r e were m o r e decelerations in the abruptio placentae group (p < 0.03). Otherwise, no significant differences were n o t e d between the two groups with regard to the electronic fetal monitor tracing interpretations. Deceleration and bradycardia w e r e the most c o m m o n abnormalities noted. Variable decelerations were m o r e c o m m o n l y seen in the cord prolapse group, and late decelerations were m o r e commonly seen in the abruptio placentae group, but their fi'equencies within each g r o u p were not significantly different. R e d u c e d variability was very u n c o m m o n and tachycardia was n o t observed. T h e umbilical arterial b l o o d gas values of the abruptio
276 Johnson and Richards
August 1997 Am J Obstet Gynecol
Table II. N e o n a t a l characteristics
Gestational age (wk) Birth weight (gin) Neonatal sex male Apgar score --<3 at 1 rain Apgar score <7 at 1 rain Apgar score -<3 at 5 min Apgar score <7 at 5 min
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance
34.4 -+ 5* (range 25-40) 232l -+ 946 62.5% 72% 91% 16% 59%
34.2 -+ 6 (range 26-42) 2521 -+ 1234 57.9% 53% 84% 5% 47%
NS NS NS NS NS NS NS
NS, Not significant. *Mean -+ 1 SD. ~-Percent of total within each group. Table IlL Electronic F H R r e c o r d i n t e r p r e t a t i o n
Abruptio placentae (n = 32) No electronic fetal monitoring Electronic fetal monitoring No decelerations Variability Bradycardia (>10/min) Tachycardia (>10/min) Variable decelerations Late decelerations Other
2 30 0 1 22 0 2 5 3
(6%) (93.7%) (0%) (3%) (73%) (0%) (6%) (16%) (10%)
Cord pwlapse (n = 19) 4 15 3 0 10 0 2 1 0
Significance (Fisher's exact test)
(21%) (79%) (20%) (0%) (66%) (0%) (13%) (6%) (0%)
p p p p p
= 0.15 = 0.15 = 0.03 = 1.0 = 0.9 NS p = 0.5 p = 0.8 p = 0.5
Values are number and percentage. Percentages within each group exceed 100% because a few cases had several abnormalities. NS, Not significant. Table IV. Umbilical arterial a n d umbilical v e n o u s values
Umbilical arterial pH Po2(mm Hg) Pco2(mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (%) Oxygen content (vol/100 ml) Umbilical venous pH Po 2 (mm Hg) PCO2 (mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (%) Oxygen content (vol/100 ml) Hemoglobin (gm/dl)
Ab~ptio placentae (n = 32)
Cord prolapse (n = 19)
Significance (Mann-Whitney U test)
6.87 (6.78-7.05) 11 (7.5-12) 90.5 (76-105.5) 17.2 (13.9-20.6) - 13.9 ( - 17.9 to - 7.7) 5 (2.5-7.5) 0.9 (0.6-1.5)
7.05 (6.98-7.07) 16 (10-20) 83 (76-95) 20.7 (19-22.6) -7.5 (-11.6 to -6.1) 11 (5-17) 2.2 (1.1-2.9)
p = 0.01 p = 0.009 NS p = 0.005 p = 0.005 p = 0.002 p = 0.003
6.97 (6.84-7.13) 17 (14-23) 75 (66.5-92) 18.4 (14.1-20.2) -12.4 (-15.5 to -6.9) 11.4 (7.3-18.2) 2.2 (1.3-4.2) 14.6 + 1.7"
7.28 (7.24-7.33) 40 (27-46) 48 (45-51) 22.2 (20.9-23.6) -2.5 (-5.8 to -1.4) 67.6 (58.4-78.9) 12.3 (9.6-14.8) 14.3 -+ 1.9"
p p p p p p p
= = = = = = =
2.9 × 1.8 × 2.8 × 3.1 × 2.8 x 4.2 x 6.4 × NS
10 -8 10 -6 10 -v 10 -5 10 -v 10 - s 10 - s
Values are medians with lower and upper quartiles in parentheses. NS, Not significant. *Mean -+ 1 SD (hemoglobin only).
p l a c e n t a e g r o u p were significantly less t h a n those o f the c o r d p r o l a p s e group, e x c e p t for the Pco 2 m e a n values,
e n c e s in the umbilical v e n o u s b l o o d gas values were m u c h m o r e striking t h a n t h o s e in the umbilical arterial
w h i c h were n o t significantly different (Table IV). T h e umbilical v e n o u s b l o o d gas values o f the a b r u p t i o pla-
samples. T h e differences b e t w e e n the umbilical v e n o u s a n d
c e n t a e g r o u p were significantly different f r o m those o f the c o r d p r o l a p s e g r o u p , e x c e p t for the plasma h e m o globin c o n c e n t r a t i o n (Table IV). In general, the differ-
arterial b l o o d gas values were c o m p u t e d in each case a n d the m e d i a n s o f the two p a t i e n t g r o u p s were c o m p a r e d (Table V). T h e differences b e t w e e n the umbilical v e n o u s
Volume 177, Number 2 Am J Obstet Gynecol
J o h n s o n and R i c h a r d s
277
o
.~
4--
o.. L.
D'I 0 r-
.Q
QJ
0"
QJ
C. LL
D. o
L 0. "0 L o
5
o -5
14
34
54
74
UVaUA 02 Sa~ D i ~ Fig. 1. This frequency histogram demonstrates umbilical venous (UI0 minus umbilical arterial (UA) oxygen saturation values for abruptio placentae group and cord prolapse group. Table V, Differences in umbilical v e n o u s - u m b i l i c a l arterial values
UV-UA pH UV-UA PO 2 UV-UA PCO 2 UV-UA bicarbonate UV-UA base excess UV-UA oxygen saturation UV-UA oxygen content
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance (Mann-Whitney U test)
0.6 (0.05-0.09) 7 (4-12) -12.5 ( - 1 5 to -6) 0.05 (-0.55 to 0.7) 1.1 (0.7-2.0) 6.2 (3.0-11.8) 1.4 (0.5-2.5)
0.25 (0.19-0.3) 25 (16-30) - 4 0 ( - 4 4 to 23) 0.2 (-1.1 to 4.4) 4.5 (2.8-7.5) 54.7 (42.2-64.8) 10.4 (7.9-12.3)
p ~ 1.5 M 10 - 7 p = 2.9 X 10 -5 p = 5.8 × 10 -6 NS p = 3.3 X 10 -5 p = 3.3 x 10 -s p = 7.5 x 10 -9
Values are medians with lower and upper quartiles in parentheses. UV, Umbilical venous; UA, umbilical arterial; NS, not significant.
and arterial b l o o d gas values were uniformly greater in the cord prolapse g r o u p than in the abruptio placentae group, with the e x c e p t i o n of the bicarbonate values, which were n o t different. T h e differences between umbilical venous and arterial b l o o d gas values were most m a r k e d in the c o r d prolapse g r o u p ' s oxygen saturation (Fig. 1), p H (Fig. 2), and oxygen c o n t e n t values. In an effort to d e t e r m i n e w h e t h e r differences in the umbilical arterial and venous values m i g h t be used to differentiate abruptio placentae from cord compression as the cause of severe fetal acidosis, receiver-operator characteristic curves were constructed for the umbilical venous minus the umbilical arterial oxygen saturation values (Fig. 3), and for umbilical venous minus umbilical arterial p H values (Fig. 4). In the receiver-operator characteristic curve analysis for the umbilical venous m i n u s umbilical arterial oxygen saturation difference, the b r e a k p o i n t o c c u r r e d at an oxygen saturation difference o f >-24%. Any value >-24% d e m o n s t r a t e d a sensitivity of 95% (95% confidence interval 74% to 100%) and a specificity of 91% (95% c o n f i d e n c e interval 75% to 98%) in the diagnosis of cord
prolapse. T h e area u n d e r the curve was 97% and the accuracy of this b r e a k p o i n t was 92% (Fig. 3). T h e receiver-operator characteristic curve analysis for umbilical vein minus umbilical artery p H differences (Fig. 4) indicated a b r e a k p o i n t at a p H difference of 0.15. Designating any case with a p H difference of -----0.15 as cord prolapse had a sensitivity of 89% (95% confidence interval 67% to 99%) and specificity of 94% (95% confidence interval 79% to 99%). The area u n d e r the curve was 92% and the accuracy of this breakpoint was 92% (Fig. 4). We also c o m p a r e d the m e a n b l o o d gas values of the two study groups to the m e a n reference values for a p r e t e r m obstetric p o p u l a t i o n ) As expected, we f o u n d the umbilical arterial blood gas values in b o t h patient groups to be significantly less than the r e f e r e n c e values for p r e m a t u r e infants, with the exception of the Pco 2 values, which were significantly higher. T h e umbilical venous b l o o d gas values of the abruptio placentae g r o u p were significantly m o r e h y p o x e m i c and acidemic than were the r e f e r e n c e values. Within the c o r d prolapse group, the umbilical venous p H and base excess were significantly less, but the umbilical venous Po 2, P c o 2 ,
August 1997 AmJ Obstet Gynecol
278 Johnson and Richards
c
0
i :
Break
O.
I7oi nt
t o
4 o c (11 D 0" O t kL
o oJ 111 IL co
4
o
t o. "o L
o t_) 0
0,1
0.2
0.3
0.4
0.5
OU-UA pH D i ~ Fig. 2. This frequency histogram demonstrates umbilical venous (UD minus umbilical arterial (UA) pH values for abruptio placentae group and cord prolapse group. 1"
A
,
¢J
•
~ ) ~ ~ O 2 Sat Diff 19 0"8 7 + - ~ ~O2 S a t D i f f 24
i;
0,6-~/
0,4" 0.2
Area Under Curve = 97% 0'~
0
01,1
01.2
01.3
01.4
I
0.5
I
0.6
017
018
019
1 - Specificity
Fig. 3. Receiver-operator characteristic curve analysis for umbilical venous-umbilical arterial oxygen saturation difference. Breakpoint is oxygen saturation difference of ->24% with sensitivity of 95%, specificity of 91%, and accuracy of 92%.
oxygen saturation, and oxygen content were all significantly greater than the reference values (Table VI). Comment
The frequencies of acute abruptio placentae and prolapsed cord for this hospital are compatible with those reported in other obstetric departments. 12 After our specific exclusions, the numbers remaining for study were small, representing only 20% of the total diagnostic group. We felt it was important to include cases that would have a high probability of adequately testing our hypothesis (i.e., cases with significant fetal acidosis and a definite clinical diagnosis). Clearly, other unsuspected pathologic events could have contributed to the blood
gas changes seen in our study cases, but we attempted to limit those by excluding cases without specified diagnostic criteria and those noted to have anesthetic complications. The two patient populations were very similar in terms of their general demographic characteristics. The umbilical arterial blood values tended to be more acidotic in the patients with abruptio placentae patients, which is probably an indication of the severity of the pathologic process. It has been suggested by others that umbilical cord compression tends to be characterized by fetal respiratory acidosis with elevated umbilical arterial Pco 2 values and near-normal bicarbonate or base deficit values. I3 Our results do not support these findings. The umbilical
Volume177,Number2
Johnson and Richards
279
Am J Obstet Gynecol
~ f f 0.125 0.8- [~-pl-IDiff0.15 pH Diff0.175 "r. e-
0.6" I 0,4-
°i!
Area
Under
Curve
= 94%
0'., 0'.2 0'.3 o'.4 .'.5 o'.6 °'.7 o'.s o; 1 - Specificity
Fig. 4. Receiver-operator characteristic curve analysis for umbilical venous-umbilical arterial pH
difference. Breakpoint is difference of ->0.15 pH units with sensitivity of 89%, specificity of 94%, and accuracy of 92%.
Table VI. C o r d prolapse versus r e f e r e n c e umbilical venous values
Cord prolapse pH (mm Hg) Pco 2 (mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (vol/100 ml) Oxygen content PO 2
7.28 37.8 49.2 22 -3.3 63.6 12.4
+ 0.07 + 11 +- 8 + 2.2 -+ 3 +- 20.3 -+ 4.4
Reference values 7.35 27.9 41.7 21.8 -2.1 47.9 9.2
-+ 0.08 +_ 8.5 -+ 10 -+ 2.6 -+ 2.2 +_ 18.5 -+ 3.6
Significance (t test) p < 0.005 p < 0.005 p < 0.01 NS p = 0.02 p < 0.005 p < 0.005
Values are mean + 1 SD, NS, Not significant. arterial P c o 2 values were significantly elevated in both the abruptio placentae group and the cord prolapse group but were not significantly different from each other. Metabolic acidosis was present in both groups, as reflected by umbilical arterial base excess and bicarbonate levels significantly less than noted in the reference population. The most striking differences between the two groups were in umbilical venous values. These were acidotic in the abruptio placentae group but near normal in the cord prolapse group. The individual differences between umbilical venous and umbilical arterial blood gas values were strikingly greater in the cord prolapse population. The receiver-operator characteristic curve indicated that a large difference in umbilical venous-umbilical arterial p H effectively distinguishes cord prolapse from abruptio placentae. A large umbilical venous-arterial oxygen saturation difference was a more sensitive marker for umbilical cord prolapse. However, because oxygen values may be affected by the technique of administration of oxygen to the mother and because many institutions do not measure the oxygen characteristics of umbilical blood gases, 14 we feel that the p H difference might prove to have greater clinical utility.
For obstetricians to further reduce the frequency and severity of intrapartum fetal acidosis, m o r e knowledge is n e e d e d regarding the etiologic associations. In general, there are two major mechanisms that may p r o d u c e fetal acidosis: (1) r e d u c e d m a t e r n a l placental oxygen delivery and (2) r e d u c e d fetal placental b l o o d flow. T h e determinants of umbilical v e n o u s - u m b i l i c a l arterial b l o o d gas gradients can be derived in simple terms f r o m the Fick blood flow and m e m b r a n e diffusion equations, a° Factors affecting these gradients include placental b l o o d flow, oxygen diffusion, oxygen capacity, oxygen tissue demands, etc. A l t h o u g h these o t h e r physiologic factors may influence the umbilical v e n o u s - u m b i l i c a l arterial b l o o d gas gradients, changes in either maternal or fetal placental b l o o d flow appear to be the most likely factors o p e r a t i n g intrapartum. O n the basis of these assumptions, a small umbilical v e n o u s - u m b i l i c a l arterial p H difference or oxygen saturation difference would be e x p e c t e d to characterize n o t only abruptio placentae but also o t h e r causes of r e d u c e d maternal oxygen delivery to the placenta, such as r e d u c e d maternal cardiac o u t p u t (maternal hypotension), increased uterine arterial resis-
280
Johnson and Richards
tance (maternal hypertension, uterine hypersystole), and maternal hypoxemia, a m o n g others. O n the o t h e r hand, a large umbilical v e i n - u m b i l i c a l artery p H difference or oxygen saturation difference would be e x p e c t e d to characterize r e d u c e d fetal perfusion of the placenta as in r e d u c e d umbilical arterial flow (cord prolapse), r e d u c e d fetal cardiac output (acute hypovolemia, fetal sepsis, or fetal myocarditis, etc.), and possibly increased intravillous vessel resistance. In c o m p a r i n g the umbilical venous values of the cord prolapse with our reference values, we f o u n d that the umbilical venous Po2, oxygen saturations, and oxygen contents were all significantly greater a m o n g the umbilical prolapse cases. T h e fact that the fetal tissues are markedly acidotic (low umbilical artery pH) in the face of elevated umbilical venous oxygen c o n t e n t seems paradoxical. However, the rate of umbilical venous oxygen delivery is a function n o t only of umbilical venous oxygen c o n t e n t but also of the rate of blood flow. In cord prolapse umbilical blood flow is significantly reduced. T h e r e f o r e the rate of oxygen delivery to fetal tissues is also r e d u c e d in spite of a near-normal umbilical vein oxygen content. The increased umbilical venous oxygen values in the babies with cord prolapse could be explained by increased oxygen diffusion across the placenta caused by high maternal arterial oxygen values and p r o l o n g e d transit time of fetal placental blood. T h e r e have b e e n animal studies m indicate that, especially in the case of umbilical cord obstruction, administration of oxygen to the m o t h e r has an i m p o r t a n t beneficial effect on fetal oxygenation. 6 T h e current data suggest that careful analysis of umbilical arterial and venous b l o o d gas values may enable clinicians to differentiate m a r k e d fetal acidosis resulting from maternal factors (abruptio placentae, etc.) from that resulting from fetal factors (cord prolapse, etc.). It is unlikely that umbilical cord b l o o d gas analysis will be helpful in differentiating these causes when they lead to less severe acidosis or if they occur in combination. In investigational studies of m a r k e d fetal acidosis, the analysis of umbilical arterial and venous b l o o d gas values could serve as an accurate m e t h o d of assessing cause. An i m p r o v e d u n d e r s t a n d i n g of the mechanisms of fetal c o m p r o m i s e m i g h t lead to m o r e effective diagnostic and therapeutic measures in future intrapartum care. Additional studies in o t h e r patient populations are n e e d e d to verify the cutoff values derived from this study.
REFERENCES
1. American College of Obstetricians and Gynecologists. Fetal heart rate patterns: monitoring, interpretation, and management. Washington: The College; 1995. Technical Bulletin No.: 207. 2. Low JA, Cox MJ, Karchmar EJ, McGrath MJ, Pancham SR, Piercy WN. The prediction of intrapartum fetal metabolic
August 1997 A_mJ Obstet Gynecol
3. 4. 5.
6.
7. 8. 9. 10. 11. 12. 13. 14.
acidosis by fetal heart rate monitoring. AmJ Obstet Gynecol 1981;139:299-305. Silver RK, Dooley SL, MacGregor SN, Depp R. Fetal acidosis in prolonged pregnancy cannot be attributed to cord compression alone. A m J Obstet Gynecol 1988;159:666-9. Quilligan EJ, Katigbak E, Hofschild J. Correlation of fetal heart rate patterns and blood gas values. Am J Obstet Gynecol 1965;91:1123-32. Tejani NA, Mann LI, Sanghavi M, Bhakthavathsalan A, Weiss RR. The association of umbilical cord complications and variable decelerations with acid-base findings. Obstet Gynecol 1977;49:159-62. Edelstone DI, Peticca BB, Goldblum LJ. Effects of maternal oxygen administration on fetal oxygenation during reductions of umbilical blood flow in fetal lambs. Am ] O b s t e t Gynecol 1985;152:351-8. Gordon A, JohnsonJWC. Value of umbilical blood acid-base studies in fetal assessment. J Reprod Med 1985;30:329-36. JohnsonJWC, LongmateJA, Frentzen B. Excessive maternal weight and pregnancy outcome. Am J Obstet Gynecol 1992;167:353-72. RileyWJ,JohnsonJWC. Collecting and analyzing cord blood gases. Clin Obstet Gynecol 1993;36:13-24. Boesel RR, Olson AE, Johnson JWC. Umbilical cord blood studies help assess fetal respiratory status. Contemp O b / Gyn 1986;28:63-74. Gur D, KingJL, Rockette HE, Britton CA, Thaete FL, Hoy RJ. Practical issues of experimental ROC analysis: selection of controls. Invest Radiol 1990;25:583-6. Cunningham FG, MacDonald PC, Leveno KJ, Gant NF, Gilstrap LC, editors. Williams' obstetrics. 19th ed. Norwalk (CT): Appleton & Lange; 1993. Wible JL, Petri RH, Koons A, Perez A. The clinical use of umbilical cord acid-base determinations in perinatal surveillance and management. Clin Perinatol 1982;9:387-97. JohnsonJWC, Riley W. Cord blood gas studies: a survey. Clin Obstet Gynecol 199;336:99-101.
Discussion
DR. WILLIAMA. COOK III, Lynchburg, Virginia (Official Guest). Measurements of umbilical cord blood gases are b e c o m i n g m o r e and m o r e a standard practice. Many advocate the use of umbilical cord gases at all deliveries. Others strongly suggest umbilical cord b l o o d analysis in all high-risk or c o m p l i c a t e d deliveries. The question that many clinicians have is what is the purpose of the test and does the cost justify the information gained by the test. In this study by J o h n s o n and Richards a value of obtaining cord b l o o d gases is illustrated. In this retrospective study by Drs. J o h n s o n and Richards an effort is m a d e to show a difference in the umbilical cord blood values in cases of abruptio placentae and umbilical cord prolapse. It has previously b e e n shown that in cases of umbilical cord compression that the umbilical arterial p H was m u c h lower than the umbilical venous pH. This has led to the r e c o m m e n d a tion that the umbilical arterial gas values may be the main and most i m p o r t a n t vessel sampled and that the umbilical arterial gases reflect the true fetal acid-base status. Some have r e c o m m e n d e d that this is the only value that is necessary. This study shows that by obtaining both the arterial and venous pHs o t h e r valuable information may be gained. T h e data also show that the oxygen saturation difference may be an even m o r e sensitive d e t e r m i n a n t between umbilical cord compression and disruption of placental b l o o d flow. Could the
Johnson and Richards
Volume 177, Number 2 AmJ Obstet Gynecol
oxygen saturation difference be more predictive in less overt cases of cord compression and diminished placental exchange? Umbilical cord pH discordance has been previously studied in various ways as it is related to cord compression. Riley and Johnson 1 showed a large difference in the umbilical arterial pH (7.03) to venous pH (7.35) in a case of cord prolapse to illustrate the importance of using the arterial pH in the determination of fetal acidemia. Gordon and Johnson 2 compared groups of patients in an effort to show a difference in the acid-base values in patients with nuchal cords, representing cord compression, and patients with Apgar scores < 7 and patients having cesarean section for fetal distress, hopefully representing uteroplacental insufficiency. They did show a greater arterial to venous pH difference (0.12) in the patients with nuchal cords. The other groups had a slightly lower difference in the arterial to venous pH, but some of this may represent some crossover in these latter groups. Tejani et al. 3 showed a large arterial to venous pH difference in pregnancies with umbilical cord complications and variable decelerations. Hankins et al. 4 also compared nuchal cord pregnancies with matched controls and showed an arterial to venous pH difference. Egan et al. 5 compared discordant arterial to venous pH groups with nondiscordant groups. The discordant group had a pH difference of >0.12. Vaginal delivery was associated with a higher incidence of discordance compared with cesarean section. This was also noted in the Gordon and Johnson 2 study. Vaginal delivery would be associated with a higher degree of cord compression, thus leading to the greater incidence of discordance. In the Egan et al. 5 study comparisons were made of various intrapartum factors. Of note were abruptio placentae with 9% of the nondiscordant group compared with 5.7% of the discordant group. Mso, nuchal cords were noted in 15.8% of the nondiscordant group versus 24.5% of the discordant group. The results, however, were not statistically significant because of relatively low numbers. There are other studies 6-1° that also show an arterial to venous pH difference, but none attempt to quantify the amount of the difference as to use the results as a diagnostic tool. Drs. Johnson and Richards mention that further studies need to be performed in different patient populations to help verify this study. Thanks to larger databases that are being kept this should not be hard to do. As an example, I was able to obtain information on cord prolapse and abruptio placentae from our deliveries in Lynchburg, Virginia, thanks in large part to Dr. Harry Jarrett, who helped to establish the database in the labor and delivery department at Virginia Baptist Hospital. From 1989 through 1996 there were 19,307 deliveries. There were only 14 cases of cord prolapse for an incidence of 0.072%. There were 43 case of abruptio placentae, for an incidence of 0.22%. These numbers are relatively low, but this may reflect a lower risk area and smaller high-risk referral base population. Following the same criteria as Drs. Johnson and Richards, only two of the
281
prolapse group and five in the abruptio placentae group were acceptable. Most of the exclusions were because no cord gas values were obtained. Both of the cord prolapse values had a pH difference of ->0.15. In the abruptio placentae group the pH difference was -<0.11. I realize these numbers are extremely small but I present this data mainly to show the ease with which the results of this study might be confirmed, again with the available databases. Of note in the article by Drs. Johnson and Richards is the greater degree of acidemia in the abruptio placentae numbers (median pH 6.87) versus the cord prolapse values (median pH 7.05,). Did the pregnancies with abruptio placentae have a greater degree of chronic diseases, such maternal hypertension, which led to a lower antepartum acidemia and possibly to the abruptio placentae itself?. It has been shown that in infants with arterial cord pHs <7.00 there is a greater incidence of seizures and other signs of asphyxia. Does one group versus the other have any more long-term problems? In conclusion, this study provides us with a diagnostic tool with high sensitivity and high specificity. It further supports the role of obtaining umbilical cord gases in high-risk pregnancies. I agree with the authors that the study needs to be verified in other populations. Also, studies might be done in less obvious signs of cord compression and of diminished placental perfusion. REFERENCES
1. RileyWJ,JohnsonJWC. Collecting and analyzing cordblood gases. Clin Obstet Gynecol 1993;36:13-24. 2. Gordon A, Johnson JWC. Value of umbilical acid-base studies in fetal assessment. J Reprod Med 1985;30:329. 3. Tejani NA, Mann LI, Sanghavi M, Bhakthavathsalan A, Weiss RR. The association of umbilical cord complications and variable decelerations with acid-base finding. Obstet Gynecol 1977;49:159-62. 4. Hankins GDV, Synder RR, Hauth JC, Gilstrap LC, Hammond T. Nuchal cords and neonatal outcome. Obstet Gynecol 1987;70:687. 5. Egan JFX, VintzileosAM, Campbell WA, et al. Arteriovenous cord blood pH discordancy in a high-risk population and its clinical significance. J Matern Fetal Med 1992;1:39. 6. Gilstrap LC, Cunningham GF. Umbilical cord blood acidbase analysis. In: Cunningham FG, MacDonald PC, Leveno KJ, Gant NF, Gilstrap LC, editors. Williams' obstetrics. 19th ed. Norwalk (CT): Appleton & Lange; 1993. 7. Thorp JA, Sampson DE, Parisi VM, Creasy RK. Routine umbilical cord blood determinations? Am J Obstet Gynecol 1989;161:600. 8. Johnson JWC, Richards DS, Wagaman RA. The case for routine umbilical blood acid-base studies at delivery. Am J Obstet Gynecol 1990;162:621. 9. Wible JL, Petrie RH, Koons A, Perez A. The clinical use of umbilical cord acid-base determinations in perinatal surveillance and management. Clin Perinatol 1982;9:387. 10. Boesel RR, Olson AE, Johnson JWC. Umbilical cord blood studies help assess fetal respiratory status. Contemp Ob/ Gyn 1986;28:63. DR. HERBERT G. HovwooD, Arlington, Virginia. Was the diagnosis of abruptio placentae a clinical diagnosis or a pathologic diagnosis? How many placentas actually had depressed cotyledons? How many of the cases of cord prolapse were genuine prolapse or what might be called "occult prolapse"?
282
Johnson and Richards
DR. LAWRENCED. DEvon., Augusta, Georgia. You've attacked two etiologies that at least clinically should be very obvious and easy to diagnosis at the time of their occurrence. I am puzzled by the inability to distinguish between these two entities on the basis of the electronic tracings because there are characteristic patterns associated with both. I think that there is an opportunity to look at other causes for fetal compromise that might not be as obvious as cord prolapse and abruptio placentae (i.e., the issues of fetal anemia and substance abuse). I wonder if you identified subsets of infants in your population that might give us data in this area? DR. JOHNSON (Closing). I want to thank Dr. Cook for verifying in his own hospital that their cord acid-base values seem to be in agreement with ours. The fact that our abruptio placentae cases were more acidotic than the cord prolapse cases is probably related to the more catastrophic nature of acute abruptio placentae. In the case of cord prolapse, while awaiting delivery, the physician may be able to temporarily ameliorate the condition by elevating the presenting part. But there is no ameliorative treatment for the fetus in acute abruptio placentae that I know of except delivery. Whether the umbilical venous arterial oxygen saturation difference could discriminate occult cases of cord compression from cases of diminished maternal perfusion is something we hope to study in the future. We have not investigated the long-term neurologic sequelae of our babies born
August 1997 AmJ Obstet Gynecol
with marked umbilical arterial acidemia. In reply to Dr. Hopwood's questions, we only studied cases in whom the clinical diagnoses were definite. All were delivered by cesarean section. The diagnosis of abruptio placentae required the detection of retroplacental clots. The placentas were not assessed for depressed cotyledons. The cases of cord prolapse were genuine cases of cord prolapse into the vagina, requiring manual elevation of the presenting part. I agree with Dr. Devoe that it is puzzling the electronic FHR tracings did not differentiate these two major pathologic entities, but I know of no clinical studies that assess the diagnostic accuracy of FHR tracings. It may have been that the acuity and severity of our cases resulted in deep and prolonged decelerations not interpretable as late or variable decelerations. Whatever the explanation, in this study we didn't find that FHR tracings were very helpful in establishing the diagnosis. We suspect that this may not be unusual in circumstances of severe fetal acidosis. So far, we have not studied other etiologic categories of fetal acidosis, such as fetal anemia or maternal substance abuse. The hypothesis we are presenting is that cord blood gases might provide in retrospect a more accurate analysis of the pathophysiologic mechanisms in cases of severe fetal acidosis. Refinements in our general knowledge about such mechanisms might provide improvements in prevention and treatment in the future.
Availability of Journal back issues As a service to our subscribers, copies of back issues of the American Journal of Obstetrics and Gynecology for the preceding 5 years are maintained and are available for purchase from Mosby until inventory is depleted at a cost of $15.00 per issue. The following quantity discounts are available: 25% off on quantities of 12 to 23 and one third off on quantities of 24 or more. Please write to Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318, or call (800)453-4351 or (314)453-4351 for information on availability of particular issues. If back issues are unavailable from the publisher, photocopies of complete issues may be purchased from UMI, 300 N. Zeeb Road, Ann Arbor, MI 48106-1346. Tel.: (313)761-4700.
Key words: Fetal acidosis, abruptio placentae, umbilical cord prolapse, umbilical artery and umbilical venous acid-base data
The interpretation of fetal heart rate (FHR) tracings is problematic) Tracings interpreted as normal have high specificity in predicting fetuses without significant acidosis. But the etiology of abnormal tracings is often obscure. 2 Even with ominous FHR tracings and fetal acidosis it is often difficult to determine the cause of the acidosis) It would be of great assistance to clinicians if they had an objective, accurate means of identifying the mechanism of fetal intrapartum compromise. Clearly, cord blood gases have become the gold standard in determining the presence or absence of acidosis in the fetus at delivery, as well as the severity of that acidosis. Might such measurements also define the pathogenesis of fetal acidosis? The purpose of this study was to test the hypothesis that patients with severe decreases in maternal blood flow to the placenta (acute abruptio placentae) have umbilical cord blood gas values that are distinctly different from those observed in patients who primarily have a From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Florida College of Medicine. Supported by the Department of Obstetricsand Gynecology, University of Florida College of Medicine. Presented at the Fifty-ninth Annual Meeting of The South Atlantic Association of Obstetricians and Gynecologists, Hot Springs, Virginia, January 25-28, 1997. Reprint requests:John W. C.Johnson, MD, Departmentof Obstetricsand Gynecology, University of Florida College of Medicine, P.O. Box 100294, Gainesville, FL 32610-0294. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/6/82719 274
reduction in the fetal perfusion of the placenta (acute umbilical cord compression). Over the years, a n u m b e r of investigators have observed that u n d e r circumstances of severe umbilical cord compression umbilical arterial blood gas values indicate fetal acidosis, whereas umbilical venous blood gas values tend to remain near normal. 4' ~ There have been animal studies demonstrating that umbilical cord occlusion is associated with significant umbilical arterial acidemia but relatively normal blood gas values in the umbilical venous blood. 6 By contrast, the general clinical observation has been that, when maternal blood flow to the placenta is reduced, both umbilical arterial and umbilical venous blood display acidosis. ~'7 These observations have not been documented in a rigorous way in h u m a n pregnancies. Methods
With use of a previously described computerized database that included all deliveries at our institution from Jan. 1, 1987, through Dec. 31, 1995, 8 we identified those patients with a discharge diagnosis of acute abruptio placentae or acute cord prolapse. Only those patients with severe acidosis, defined as an umbilical arterial pH <7.13, were included in the study. An umbilical arterial pH of <7.13 constitutes the mean value minus 2 SDs for term deliveries analyzed at this institution.9 Among these patients with severe acidosis at delivery, only those delivered by cesarean section with convincing diagnostic criteria for abruptio placentae or cord prolapse were
Johnson and Richards
Volume 177, Number 2 Am J Obstet Gynecol
included. In the case of abruptio placentae, only cases with retroplacental clots n o t e d at the time of cesarean section delivery were acceptable for inclusion in this study. In the case of prolapsed cord, only those cases in which m a n u a l elevation of the presenting part was req u i r e d before e m e r g e n c y delivery were included. Cases without umbilical arterial and umbilical venous blood gas values at delivery were excluded. Umbilical b l o o d gases were collected and analyzed as previously described, a° In an effort to exclude cases in which anesthesia complications m i g h t have altered the cord gas values, we reviewed the specific anesthesia records for evidence of cardiovascular or respiratory complications associated with the anesthesia. W h e n such complications were identified, those cases were e x c l u d e d f r o m the analysis. Electronic fetal m o n i t o r i n g interpretations were available through the obstetric data system and these were e x a m i n e d for differences between the two study groups. Statistical analysis was p e r f o r m e d with the Statgraphics Plus (Statistical Graphics, Princeton, N.J.) p r o g r a m for m i c r o c o m p u t e r . Differences between groups were tested with use of the Student t test for normally distributed data. T h e X2 test was used for categoric data analysis, unless the sample size was small, in which case Fisher's exact test was used. T h e blood gas data were not normally distributed, so they were c o m p a r e d with the MannWhitney U test. Values that m i g h t differentiate abruptio placentae f r o m cord prolapse were evaluated with receiver-operator characteristic curves. ~a This project was reviewed by our Institutional H u m a n E x p e r i m e n t a t i o n Review Board and approved u n d e r an e x e m p t e d status. T h e study was g r a n t e d an e x e m p t e d status because it involved the analysis of existing data and the subjects were n o t identifiable.
Results During the 9 years of obstetric e x p e r i e n c e abstracted in the c o m p u t e r database, this hospital r e c o r d e d 30,888 deliveries. During these years a total of 167 patients were diagnosed with abruptio placentae, for a frequency of 0.54% or 1 in every 185 deliveries. T h e diagnosis of prolapsed Umbilical cord was m a d e 97 times, for a frequency of 0.314% or 1 every 322 deliveries. O n e h u n d r e d thirty-five (81%) of the cases diagnosed as abruptio placentae did n o t m e e t o u r inclusion criteria, leaving 32 study cases. Seventy-eight (80%) of those cases diagnosed as umbilical cord prolapse did not m e e t o u r inclusion criteria, leaving 19 cases for analysis. T h e majority of the exclusions in b o t h groups were cases in which the umbilical arterial p H was >7.12. We excluded two cases because of significant cardiorespiratory complications in the mothers, which were related to anesthesia difficulties. O n e set o f twins was included in the abruptio placentae group. After a spontaneous vaginal delivery of twin A,
275
Table I. Maternal characteristics
Maternal age (yr) Maternal race White Black Singleton pregnancy Nulliparous Prior abortion General anesthesia
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance
25 -+ 6*
25 -+ 7
NS
53.1%]46.9% 96.9% 31.3% 43.7% 84.4%
57.9% 42.1% 84.2% 36.8% 31.6% 89.5%
NS NS NS NS NS
NS, Not significant. *Mean -+ 1 SD. tPercent of total within each group.
abruptio placentae o c c u r r e d in twin B, necessitating e m e r g e n c y cesarean delivery. T h e r e were three sets of twins in the cord prolapse group. In o n e set twin A was delivered by spontaneous vaginal delivery and then the cord prolapsed in twin B, requiring cesarean section. In two o t h e r sets of twins, twin A was d e t e r m i n e d to have cord prolapse, necessitating e m e r g e n c y cesarean delivery. In all four cases of twins the cord b l o o d gas values of the unaffected twins were within n o r m a l limits and these cases were n o t included in the analyses. In a statistical comparison of d e m o g r a p h i c characteristics of the mothers, no significant differences were d e t e c t e d between the 32 cases of abruptio placentae and the 19 cases of cord prolapse (Table I). In b o t h groups of patients general anesthesia was most c o m m o n l y used for cesarean section and the mothers received supplemental oxygen frequently. T h e inspired oxygen concentrations varied from 21% to 100%. T h e a m o u n t of assisted respiration was n o t ascertainable. Maternal arterial Po 2 values were n o t d e t e r m i n e d at delivery. No statistically significant differences were n o t e d in the infants with regard to their gestational ages, birth weights, sexes, or Apgar scores (Table II). Most of the patients had electronic fetal m o n i t o r i n g p e r f o r m e d before delivery, although 6% of the cases of abruptio placentae did n o t and 21% of the cases of cord prolapse did not (Table III). T h e r e were m o r e decelerations in the abruptio placentae group (p < 0.03). Otherwise, no significant differences were n o t e d between the two groups with regard to the electronic fetal monitor tracing interpretations. Deceleration and bradycardia w e r e the most c o m m o n abnormalities noted. Variable decelerations were m o r e c o m m o n l y seen in the cord prolapse group, and late decelerations were m o r e commonly seen in the abruptio placentae group, but their fi'equencies within each g r o u p were not significantly different. R e d u c e d variability was very u n c o m m o n and tachycardia was n o t observed. T h e umbilical arterial b l o o d gas values of the abruptio
276 Johnson and Richards
August 1997 Am J Obstet Gynecol
Table II. N e o n a t a l characteristics
Gestational age (wk) Birth weight (gin) Neonatal sex male Apgar score --<3 at 1 rain Apgar score <7 at 1 rain Apgar score -<3 at 5 min Apgar score <7 at 5 min
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance
34.4 -+ 5* (range 25-40) 232l -+ 946 62.5% 72% 91% 16% 59%
34.2 -+ 6 (range 26-42) 2521 -+ 1234 57.9% 53% 84% 5% 47%
NS NS NS NS NS NS NS
NS, Not significant. *Mean -+ 1 SD. ~-Percent of total within each group. Table IlL Electronic F H R r e c o r d i n t e r p r e t a t i o n
Abruptio placentae (n = 32) No electronic fetal monitoring Electronic fetal monitoring No decelerations Variability Bradycardia (>10/min) Tachycardia (>10/min) Variable decelerations Late decelerations Other
2 30 0 1 22 0 2 5 3
(6%) (93.7%) (0%) (3%) (73%) (0%) (6%) (16%) (10%)
Cord pwlapse (n = 19) 4 15 3 0 10 0 2 1 0
Significance (Fisher's exact test)
(21%) (79%) (20%) (0%) (66%) (0%) (13%) (6%) (0%)
p p p p p
= 0.15 = 0.15 = 0.03 = 1.0 = 0.9 NS p = 0.5 p = 0.8 p = 0.5
Values are number and percentage. Percentages within each group exceed 100% because a few cases had several abnormalities. NS, Not significant. Table IV. Umbilical arterial a n d umbilical v e n o u s values
Umbilical arterial pH Po2(mm Hg) Pco2(mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (%) Oxygen content (vol/100 ml) Umbilical venous pH Po 2 (mm Hg) PCO2 (mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (%) Oxygen content (vol/100 ml) Hemoglobin (gm/dl)
Ab~ptio placentae (n = 32)
Cord prolapse (n = 19)
Significance (Mann-Whitney U test)
6.87 (6.78-7.05) 11 (7.5-12) 90.5 (76-105.5) 17.2 (13.9-20.6) - 13.9 ( - 17.9 to - 7.7) 5 (2.5-7.5) 0.9 (0.6-1.5)
7.05 (6.98-7.07) 16 (10-20) 83 (76-95) 20.7 (19-22.6) -7.5 (-11.6 to -6.1) 11 (5-17) 2.2 (1.1-2.9)
p = 0.01 p = 0.009 NS p = 0.005 p = 0.005 p = 0.002 p = 0.003
6.97 (6.84-7.13) 17 (14-23) 75 (66.5-92) 18.4 (14.1-20.2) -12.4 (-15.5 to -6.9) 11.4 (7.3-18.2) 2.2 (1.3-4.2) 14.6 + 1.7"
7.28 (7.24-7.33) 40 (27-46) 48 (45-51) 22.2 (20.9-23.6) -2.5 (-5.8 to -1.4) 67.6 (58.4-78.9) 12.3 (9.6-14.8) 14.3 -+ 1.9"
p p p p p p p
= = = = = = =
2.9 × 1.8 × 2.8 × 3.1 × 2.8 x 4.2 x 6.4 × NS
10 -8 10 -6 10 -v 10 -5 10 -v 10 - s 10 - s
Values are medians with lower and upper quartiles in parentheses. NS, Not significant. *Mean -+ 1 SD (hemoglobin only).
p l a c e n t a e g r o u p were significantly less t h a n those o f the c o r d p r o l a p s e group, e x c e p t for the Pco 2 m e a n values,
e n c e s in the umbilical v e n o u s b l o o d gas values were m u c h m o r e striking t h a n t h o s e in the umbilical arterial
w h i c h were n o t significantly different (Table IV). T h e umbilical v e n o u s b l o o d gas values o f the a b r u p t i o pla-
samples. T h e differences b e t w e e n the umbilical v e n o u s a n d
c e n t a e g r o u p were significantly different f r o m those o f the c o r d p r o l a p s e g r o u p , e x c e p t for the plasma h e m o globin c o n c e n t r a t i o n (Table IV). In general, the differ-
arterial b l o o d gas values were c o m p u t e d in each case a n d the m e d i a n s o f the two p a t i e n t g r o u p s were c o m p a r e d (Table V). T h e differences b e t w e e n the umbilical v e n o u s
Volume 177, Number 2 Am J Obstet Gynecol
J o h n s o n and R i c h a r d s
277
o
.~
4--
o.. L.
D'I 0 r-
.Q
QJ
0"
QJ
C. LL
D. o
L 0. "0 L o
5
o -5
14
34
54
74
UVaUA 02 Sa~ D i ~ Fig. 1. This frequency histogram demonstrates umbilical venous (UI0 minus umbilical arterial (UA) oxygen saturation values for abruptio placentae group and cord prolapse group. Table V, Differences in umbilical v e n o u s - u m b i l i c a l arterial values
UV-UA pH UV-UA PO 2 UV-UA PCO 2 UV-UA bicarbonate UV-UA base excess UV-UA oxygen saturation UV-UA oxygen content
Abruptio placentae (n = 32)
Cord prolapse (n = 19)
Significance (Mann-Whitney U test)
0.6 (0.05-0.09) 7 (4-12) -12.5 ( - 1 5 to -6) 0.05 (-0.55 to 0.7) 1.1 (0.7-2.0) 6.2 (3.0-11.8) 1.4 (0.5-2.5)
0.25 (0.19-0.3) 25 (16-30) - 4 0 ( - 4 4 to 23) 0.2 (-1.1 to 4.4) 4.5 (2.8-7.5) 54.7 (42.2-64.8) 10.4 (7.9-12.3)
p ~ 1.5 M 10 - 7 p = 2.9 X 10 -5 p = 5.8 × 10 -6 NS p = 3.3 X 10 -5 p = 3.3 x 10 -s p = 7.5 x 10 -9
Values are medians with lower and upper quartiles in parentheses. UV, Umbilical venous; UA, umbilical arterial; NS, not significant.
and arterial b l o o d gas values were uniformly greater in the cord prolapse g r o u p than in the abruptio placentae group, with the e x c e p t i o n of the bicarbonate values, which were n o t different. T h e differences between umbilical venous and arterial b l o o d gas values were most m a r k e d in the c o r d prolapse g r o u p ' s oxygen saturation (Fig. 1), p H (Fig. 2), and oxygen c o n t e n t values. In an effort to d e t e r m i n e w h e t h e r differences in the umbilical arterial and venous values m i g h t be used to differentiate abruptio placentae from cord compression as the cause of severe fetal acidosis, receiver-operator characteristic curves were constructed for the umbilical venous minus the umbilical arterial oxygen saturation values (Fig. 3), and for umbilical venous minus umbilical arterial p H values (Fig. 4). In the receiver-operator characteristic curve analysis for the umbilical venous m i n u s umbilical arterial oxygen saturation difference, the b r e a k p o i n t o c c u r r e d at an oxygen saturation difference o f >-24%. Any value >-24% d e m o n s t r a t e d a sensitivity of 95% (95% confidence interval 74% to 100%) and a specificity of 91% (95% c o n f i d e n c e interval 75% to 98%) in the diagnosis of cord
prolapse. T h e area u n d e r the curve was 97% and the accuracy of this b r e a k p o i n t was 92% (Fig. 3). T h e receiver-operator characteristic curve analysis for umbilical vein minus umbilical artery p H differences (Fig. 4) indicated a b r e a k p o i n t at a p H difference of 0.15. Designating any case with a p H difference of -----0.15 as cord prolapse had a sensitivity of 89% (95% confidence interval 67% to 99%) and specificity of 94% (95% confidence interval 79% to 99%). The area u n d e r the curve was 92% and the accuracy of this breakpoint was 92% (Fig. 4). We also c o m p a r e d the m e a n b l o o d gas values of the two study groups to the m e a n reference values for a p r e t e r m obstetric p o p u l a t i o n ) As expected, we f o u n d the umbilical arterial blood gas values in b o t h patient groups to be significantly less than the r e f e r e n c e values for p r e m a t u r e infants, with the exception of the Pco 2 values, which were significantly higher. T h e umbilical venous b l o o d gas values of the abruptio placentae g r o u p were significantly m o r e h y p o x e m i c and acidemic than were the r e f e r e n c e values. Within the c o r d prolapse group, the umbilical venous p H and base excess were significantly less, but the umbilical venous Po 2, P c o 2 ,
August 1997 AmJ Obstet Gynecol
278 Johnson and Richards
c
0
i :
Break
O.
I7oi nt
t o
4 o c (11 D 0" O t kL
o oJ 111 IL co
4
o
t o. "o L
o t_) 0
0,1
0.2
0.3
0.4
0.5
OU-UA pH D i ~ Fig. 2. This frequency histogram demonstrates umbilical venous (UD minus umbilical arterial (UA) pH values for abruptio placentae group and cord prolapse group. 1"
A
,
¢J
•
~ ) ~ ~ O 2 Sat Diff 19 0"8 7 + - ~ ~O2 S a t D i f f 24
i;
0,6-~/
0,4" 0.2
Area Under Curve = 97% 0'~
0
01,1
01.2
01.3
01.4
I
0.5
I
0.6
017
018
019
1 - Specificity
Fig. 3. Receiver-operator characteristic curve analysis for umbilical venous-umbilical arterial oxygen saturation difference. Breakpoint is oxygen saturation difference of ->24% with sensitivity of 95%, specificity of 91%, and accuracy of 92%.
oxygen saturation, and oxygen content were all significantly greater than the reference values (Table VI). Comment
The frequencies of acute abruptio placentae and prolapsed cord for this hospital are compatible with those reported in other obstetric departments. 12 After our specific exclusions, the numbers remaining for study were small, representing only 20% of the total diagnostic group. We felt it was important to include cases that would have a high probability of adequately testing our hypothesis (i.e., cases with significant fetal acidosis and a definite clinical diagnosis). Clearly, other unsuspected pathologic events could have contributed to the blood
gas changes seen in our study cases, but we attempted to limit those by excluding cases without specified diagnostic criteria and those noted to have anesthetic complications. The two patient populations were very similar in terms of their general demographic characteristics. The umbilical arterial blood values tended to be more acidotic in the patients with abruptio placentae patients, which is probably an indication of the severity of the pathologic process. It has been suggested by others that umbilical cord compression tends to be characterized by fetal respiratory acidosis with elevated umbilical arterial Pco 2 values and near-normal bicarbonate or base deficit values. I3 Our results do not support these findings. The umbilical
Volume177,Number2
Johnson and Richards
279
Am J Obstet Gynecol
~ f f 0.125 0.8- [~-pl-IDiff0.15 pH Diff0.175 "r. e-
0.6" I 0,4-
°i!
Area
Under
Curve
= 94%
0'., 0'.2 0'.3 o'.4 .'.5 o'.6 °'.7 o'.s o; 1 - Specificity
Fig. 4. Receiver-operator characteristic curve analysis for umbilical venous-umbilical arterial pH
difference. Breakpoint is difference of ->0.15 pH units with sensitivity of 89%, specificity of 94%, and accuracy of 92%.
Table VI. C o r d prolapse versus r e f e r e n c e umbilical venous values
Cord prolapse pH (mm Hg) Pco 2 (mm Hg) Bicarbonate (mEq/L) Base excess (mEq/L) Oxygen saturation (vol/100 ml) Oxygen content PO 2
7.28 37.8 49.2 22 -3.3 63.6 12.4
+ 0.07 + 11 +- 8 + 2.2 -+ 3 +- 20.3 -+ 4.4
Reference values 7.35 27.9 41.7 21.8 -2.1 47.9 9.2
-+ 0.08 +_ 8.5 -+ 10 -+ 2.6 -+ 2.2 +_ 18.5 -+ 3.6
Significance (t test) p < 0.005 p < 0.005 p < 0.01 NS p = 0.02 p < 0.005 p < 0.005
Values are mean + 1 SD, NS, Not significant. arterial P c o 2 values were significantly elevated in both the abruptio placentae group and the cord prolapse group but were not significantly different from each other. Metabolic acidosis was present in both groups, as reflected by umbilical arterial base excess and bicarbonate levels significantly less than noted in the reference population. The most striking differences between the two groups were in umbilical venous values. These were acidotic in the abruptio placentae group but near normal in the cord prolapse group. The individual differences between umbilical venous and umbilical arterial blood gas values were strikingly greater in the cord prolapse population. The receiver-operator characteristic curve indicated that a large difference in umbilical venous-umbilical arterial p H effectively distinguishes cord prolapse from abruptio placentae. A large umbilical venous-arterial oxygen saturation difference was a more sensitive marker for umbilical cord prolapse. However, because oxygen values may be affected by the technique of administration of oxygen to the mother and because many institutions do not measure the oxygen characteristics of umbilical blood gases, 14 we feel that the p H difference might prove to have greater clinical utility.
For obstetricians to further reduce the frequency and severity of intrapartum fetal acidosis, m o r e knowledge is n e e d e d regarding the etiologic associations. In general, there are two major mechanisms that may p r o d u c e fetal acidosis: (1) r e d u c e d m a t e r n a l placental oxygen delivery and (2) r e d u c e d fetal placental b l o o d flow. T h e determinants of umbilical v e n o u s - u m b i l i c a l arterial b l o o d gas gradients can be derived in simple terms f r o m the Fick blood flow and m e m b r a n e diffusion equations, a° Factors affecting these gradients include placental b l o o d flow, oxygen diffusion, oxygen capacity, oxygen tissue demands, etc. A l t h o u g h these o t h e r physiologic factors may influence the umbilical v e n o u s - u m b i l i c a l arterial b l o o d gas gradients, changes in either maternal or fetal placental b l o o d flow appear to be the most likely factors o p e r a t i n g intrapartum. O n the basis of these assumptions, a small umbilical v e n o u s - u m b i l i c a l arterial p H difference or oxygen saturation difference would be e x p e c t e d to characterize n o t only abruptio placentae but also o t h e r causes of r e d u c e d maternal oxygen delivery to the placenta, such as r e d u c e d maternal cardiac o u t p u t (maternal hypotension), increased uterine arterial resis-
280
Johnson and Richards
tance (maternal hypertension, uterine hypersystole), and maternal hypoxemia, a m o n g others. O n the o t h e r hand, a large umbilical v e i n - u m b i l i c a l artery p H difference or oxygen saturation difference would be e x p e c t e d to characterize r e d u c e d fetal perfusion of the placenta as in r e d u c e d umbilical arterial flow (cord prolapse), r e d u c e d fetal cardiac output (acute hypovolemia, fetal sepsis, or fetal myocarditis, etc.), and possibly increased intravillous vessel resistance. In c o m p a r i n g the umbilical venous values of the cord prolapse with our reference values, we f o u n d that the umbilical venous Po2, oxygen saturations, and oxygen contents were all significantly greater a m o n g the umbilical prolapse cases. T h e fact that the fetal tissues are markedly acidotic (low umbilical artery pH) in the face of elevated umbilical venous oxygen c o n t e n t seems paradoxical. However, the rate of umbilical venous oxygen delivery is a function n o t only of umbilical venous oxygen c o n t e n t but also of the rate of blood flow. In cord prolapse umbilical blood flow is significantly reduced. T h e r e f o r e the rate of oxygen delivery to fetal tissues is also r e d u c e d in spite of a near-normal umbilical vein oxygen content. The increased umbilical venous oxygen values in the babies with cord prolapse could be explained by increased oxygen diffusion across the placenta caused by high maternal arterial oxygen values and p r o l o n g e d transit time of fetal placental blood. T h e r e have b e e n animal studies m indicate that, especially in the case of umbilical cord obstruction, administration of oxygen to the m o t h e r has an i m p o r t a n t beneficial effect on fetal oxygenation. 6 T h e current data suggest that careful analysis of umbilical arterial and venous b l o o d gas values may enable clinicians to differentiate m a r k e d fetal acidosis resulting from maternal factors (abruptio placentae, etc.) from that resulting from fetal factors (cord prolapse, etc.). It is unlikely that umbilical cord b l o o d gas analysis will be helpful in differentiating these causes when they lead to less severe acidosis or if they occur in combination. In investigational studies of m a r k e d fetal acidosis, the analysis of umbilical arterial and venous b l o o d gas values could serve as an accurate m e t h o d of assessing cause. An i m p r o v e d u n d e r s t a n d i n g of the mechanisms of fetal c o m p r o m i s e m i g h t lead to m o r e effective diagnostic and therapeutic measures in future intrapartum care. Additional studies in o t h e r patient populations are n e e d e d to verify the cutoff values derived from this study.
REFERENCES
1. American College of Obstetricians and Gynecologists. Fetal heart rate patterns: monitoring, interpretation, and management. Washington: The College; 1995. Technical Bulletin No.: 207. 2. Low JA, Cox MJ, Karchmar EJ, McGrath MJ, Pancham SR, Piercy WN. The prediction of intrapartum fetal metabolic
August 1997 A_mJ Obstet Gynecol
3. 4. 5.
6.
7. 8. 9. 10. 11. 12. 13. 14.
acidosis by fetal heart rate monitoring. AmJ Obstet Gynecol 1981;139:299-305. Silver RK, Dooley SL, MacGregor SN, Depp R. Fetal acidosis in prolonged pregnancy cannot be attributed to cord compression alone. A m J Obstet Gynecol 1988;159:666-9. Quilligan EJ, Katigbak E, Hofschild J. Correlation of fetal heart rate patterns and blood gas values. Am J Obstet Gynecol 1965;91:1123-32. Tejani NA, Mann LI, Sanghavi M, Bhakthavathsalan A, Weiss RR. The association of umbilical cord complications and variable decelerations with acid-base findings. Obstet Gynecol 1977;49:159-62. Edelstone DI, Peticca BB, Goldblum LJ. Effects of maternal oxygen administration on fetal oxygenation during reductions of umbilical blood flow in fetal lambs. Am ] O b s t e t Gynecol 1985;152:351-8. Gordon A, JohnsonJWC. Value of umbilical blood acid-base studies in fetal assessment. J Reprod Med 1985;30:329-36. JohnsonJWC, LongmateJA, Frentzen B. Excessive maternal weight and pregnancy outcome. Am J Obstet Gynecol 1992;167:353-72. RileyWJ,JohnsonJWC. Collecting and analyzing cord blood gases. Clin Obstet Gynecol 1993;36:13-24. Boesel RR, Olson AE, Johnson JWC. Umbilical cord blood studies help assess fetal respiratory status. Contemp O b / Gyn 1986;28:63-74. Gur D, KingJL, Rockette HE, Britton CA, Thaete FL, Hoy RJ. Practical issues of experimental ROC analysis: selection of controls. Invest Radiol 1990;25:583-6. Cunningham FG, MacDonald PC, Leveno KJ, Gant NF, Gilstrap LC, editors. Williams' obstetrics. 19th ed. Norwalk (CT): Appleton & Lange; 1993. Wible JL, Petri RH, Koons A, Perez A. The clinical use of umbilical cord acid-base determinations in perinatal surveillance and management. Clin Perinatol 1982;9:387-97. JohnsonJWC, Riley W. Cord blood gas studies: a survey. Clin Obstet Gynecol 199;336:99-101.
Discussion
DR. WILLIAMA. COOK III, Lynchburg, Virginia (Official Guest). Measurements of umbilical cord blood gases are b e c o m i n g m o r e and m o r e a standard practice. Many advocate the use of umbilical cord gases at all deliveries. Others strongly suggest umbilical cord b l o o d analysis in all high-risk or c o m p l i c a t e d deliveries. The question that many clinicians have is what is the purpose of the test and does the cost justify the information gained by the test. In this study by J o h n s o n and Richards a value of obtaining cord b l o o d gases is illustrated. In this retrospective study by Drs. J o h n s o n and Richards an effort is m a d e to show a difference in the umbilical cord blood values in cases of abruptio placentae and umbilical cord prolapse. It has previously b e e n shown that in cases of umbilical cord compression that the umbilical arterial p H was m u c h lower than the umbilical venous pH. This has led to the r e c o m m e n d a tion that the umbilical arterial gas values may be the main and most i m p o r t a n t vessel sampled and that the umbilical arterial gases reflect the true fetal acid-base status. Some have r e c o m m e n d e d that this is the only value that is necessary. This study shows that by obtaining both the arterial and venous pHs o t h e r valuable information may be gained. T h e data also show that the oxygen saturation difference may be an even m o r e sensitive d e t e r m i n a n t between umbilical cord compression and disruption of placental b l o o d flow. Could the
Johnson and Richards
Volume 177, Number 2 AmJ Obstet Gynecol
oxygen saturation difference be more predictive in less overt cases of cord compression and diminished placental exchange? Umbilical cord pH discordance has been previously studied in various ways as it is related to cord compression. Riley and Johnson 1 showed a large difference in the umbilical arterial pH (7.03) to venous pH (7.35) in a case of cord prolapse to illustrate the importance of using the arterial pH in the determination of fetal acidemia. Gordon and Johnson 2 compared groups of patients in an effort to show a difference in the acid-base values in patients with nuchal cords, representing cord compression, and patients with Apgar scores < 7 and patients having cesarean section for fetal distress, hopefully representing uteroplacental insufficiency. They did show a greater arterial to venous pH difference (0.12) in the patients with nuchal cords. The other groups had a slightly lower difference in the arterial to venous pH, but some of this may represent some crossover in these latter groups. Tejani et al. 3 showed a large arterial to venous pH difference in pregnancies with umbilical cord complications and variable decelerations. Hankins et al. 4 also compared nuchal cord pregnancies with matched controls and showed an arterial to venous pH difference. Egan et al. 5 compared discordant arterial to venous pH groups with nondiscordant groups. The discordant group had a pH difference of >0.12. Vaginal delivery was associated with a higher incidence of discordance compared with cesarean section. This was also noted in the Gordon and Johnson 2 study. Vaginal delivery would be associated with a higher degree of cord compression, thus leading to the greater incidence of discordance. In the Egan et al. 5 study comparisons were made of various intrapartum factors. Of note were abruptio placentae with 9% of the nondiscordant group compared with 5.7% of the discordant group. Mso, nuchal cords were noted in 15.8% of the nondiscordant group versus 24.5% of the discordant group. The results, however, were not statistically significant because of relatively low numbers. There are other studies 6-1° that also show an arterial to venous pH difference, but none attempt to quantify the amount of the difference as to use the results as a diagnostic tool. Drs. Johnson and Richards mention that further studies need to be performed in different patient populations to help verify this study. Thanks to larger databases that are being kept this should not be hard to do. As an example, I was able to obtain information on cord prolapse and abruptio placentae from our deliveries in Lynchburg, Virginia, thanks in large part to Dr. Harry Jarrett, who helped to establish the database in the labor and delivery department at Virginia Baptist Hospital. From 1989 through 1996 there were 19,307 deliveries. There were only 14 cases of cord prolapse for an incidence of 0.072%. There were 43 case of abruptio placentae, for an incidence of 0.22%. These numbers are relatively low, but this may reflect a lower risk area and smaller high-risk referral base population. Following the same criteria as Drs. Johnson and Richards, only two of the
281
prolapse group and five in the abruptio placentae group were acceptable. Most of the exclusions were because no cord gas values were obtained. Both of the cord prolapse values had a pH difference of ->0.15. In the abruptio placentae group the pH difference was -<0.11. I realize these numbers are extremely small but I present this data mainly to show the ease with which the results of this study might be confirmed, again with the available databases. Of note in the article by Drs. Johnson and Richards is the greater degree of acidemia in the abruptio placentae numbers (median pH 6.87) versus the cord prolapse values (median pH 7.05,). Did the pregnancies with abruptio placentae have a greater degree of chronic diseases, such maternal hypertension, which led to a lower antepartum acidemia and possibly to the abruptio placentae itself?. It has been shown that in infants with arterial cord pHs <7.00 there is a greater incidence of seizures and other signs of asphyxia. Does one group versus the other have any more long-term problems? In conclusion, this study provides us with a diagnostic tool with high sensitivity and high specificity. It further supports the role of obtaining umbilical cord gases in high-risk pregnancies. I agree with the authors that the study needs to be verified in other populations. Also, studies might be done in less obvious signs of cord compression and of diminished placental perfusion. REFERENCES
1. RileyWJ,JohnsonJWC. Collecting and analyzing cordblood gases. Clin Obstet Gynecol 1993;36:13-24. 2. Gordon A, Johnson JWC. Value of umbilical acid-base studies in fetal assessment. J Reprod Med 1985;30:329. 3. Tejani NA, Mann LI, Sanghavi M, Bhakthavathsalan A, Weiss RR. The association of umbilical cord complications and variable decelerations with acid-base finding. Obstet Gynecol 1977;49:159-62. 4. Hankins GDV, Synder RR, Hauth JC, Gilstrap LC, Hammond T. Nuchal cords and neonatal outcome. Obstet Gynecol 1987;70:687. 5. Egan JFX, VintzileosAM, Campbell WA, et al. Arteriovenous cord blood pH discordancy in a high-risk population and its clinical significance. J Matern Fetal Med 1992;1:39. 6. Gilstrap LC, Cunningham GF. Umbilical cord blood acidbase analysis. In: Cunningham FG, MacDonald PC, Leveno KJ, Gant NF, Gilstrap LC, editors. Williams' obstetrics. 19th ed. Norwalk (CT): Appleton & Lange; 1993. 7. Thorp JA, Sampson DE, Parisi VM, Creasy RK. Routine umbilical cord blood determinations? Am J Obstet Gynecol 1989;161:600. 8. Johnson JWC, Richards DS, Wagaman RA. The case for routine umbilical blood acid-base studies at delivery. Am J Obstet Gynecol 1990;162:621. 9. Wible JL, Petrie RH, Koons A, Perez A. The clinical use of umbilical cord acid-base determinations in perinatal surveillance and management. Clin Perinatol 1982;9:387. 10. Boesel RR, Olson AE, Johnson JWC. Umbilical cord blood studies help assess fetal respiratory status. Contemp Ob/ Gyn 1986;28:63. DR. HERBERT G. HovwooD, Arlington, Virginia. Was the diagnosis of abruptio placentae a clinical diagnosis or a pathologic diagnosis? How many placentas actually had depressed cotyledons? How many of the cases of cord prolapse were genuine prolapse or what might be called "occult prolapse"?
282
Johnson and Richards
DR. LAWRENCED. DEvon., Augusta, Georgia. You've attacked two etiologies that at least clinically should be very obvious and easy to diagnosis at the time of their occurrence. I am puzzled by the inability to distinguish between these two entities on the basis of the electronic tracings because there are characteristic patterns associated with both. I think that there is an opportunity to look at other causes for fetal compromise that might not be as obvious as cord prolapse and abruptio placentae (i.e., the issues of fetal anemia and substance abuse). I wonder if you identified subsets of infants in your population that might give us data in this area? DR. JOHNSON (Closing). I want to thank Dr. Cook for verifying in his own hospital that their cord acid-base values seem to be in agreement with ours. The fact that our abruptio placentae cases were more acidotic than the cord prolapse cases is probably related to the more catastrophic nature of acute abruptio placentae. In the case of cord prolapse, while awaiting delivery, the physician may be able to temporarily ameliorate the condition by elevating the presenting part. But there is no ameliorative treatment for the fetus in acute abruptio placentae that I know of except delivery. Whether the umbilical venous arterial oxygen saturation difference could discriminate occult cases of cord compression from cases of diminished maternal perfusion is something we hope to study in the future. We have not investigated the long-term neurologic sequelae of our babies born
August 1997 AmJ Obstet Gynecol
with marked umbilical arterial acidemia. In reply to Dr. Hopwood's questions, we only studied cases in whom the clinical diagnoses were definite. All were delivered by cesarean section. The diagnosis of abruptio placentae required the detection of retroplacental clots. The placentas were not assessed for depressed cotyledons. The cases of cord prolapse were genuine cases of cord prolapse into the vagina, requiring manual elevation of the presenting part. I agree with Dr. Devoe that it is puzzling the electronic FHR tracings did not differentiate these two major pathologic entities, but I know of no clinical studies that assess the diagnostic accuracy of FHR tracings. It may have been that the acuity and severity of our cases resulted in deep and prolonged decelerations not interpretable as late or variable decelerations. Whatever the explanation, in this study we didn't find that FHR tracings were very helpful in establishing the diagnosis. We suspect that this may not be unusual in circumstances of severe fetal acidosis. So far, we have not studied other etiologic categories of fetal acidosis, such as fetal anemia or maternal substance abuse. The hypothesis we are presenting is that cord blood gases might provide in retrospect a more accurate analysis of the pathophysiologic mechanisms in cases of severe fetal acidosis. Refinements in our general knowledge about such mechanisms might provide improvements in prevention and treatment in the future.
Availability of Journal back issues As a service to our subscribers, copies of back issues of the American Journal of Obstetrics and Gynecology for the preceding 5 years are maintained and are available for purchase from Mosby until inventory is depleted at a cost of $15.00 per issue. The following quantity discounts are available: 25% off on quantities of 12 to 23 and one third off on quantities of 24 or more. Please write to Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318, or call (800)453-4351 or (314)453-4351 for information on availability of particular issues. If back issues are unavailable from the publisher, photocopies of complete issues may be purchased from UMI, 300 N. Zeeb Road, Ann Arbor, MI 48106-1346. Tel.: (313)761-4700.