Relationship between placental histologic features and
umbilical cord blood gases in preterm gestations
Carolyn M. Salafia, MD, . . . . . . f Victoria K. Minior, BS," Jos~ A. L6pez-Zeno, MD, g
S. Scott Whittington, MS, c' f John C. PezzuUo, PhD, d' " and Anthony M. Vintzileos, MD b
Farmington, Connecticut, New Brunswick, New Jersey, Washington, D.C., and Ponce, Puerto Rico
OBJECTIVE: Our purpose was to test the hypothesis that placental histologic lesions reflect abnormal
placental respiratory function in preterm gestations.
STUDY DESIGN: A retrospective study of preterm deliveries from 22 to 32 weeks revealed 431 patients
with umbilical venous or arterial blood gas values. Excluded were stillbirth, multiple gestations, placenta
previa, maternal medical diseases, and fetal anomalies. Charts were reviewed for principal indication of
delivery, diagnosis of labor, and mode of delivery. Blood gases were studied within 10 minutes of delivery
on a model 178 automatic pH analyzer (Coming Med, Boston). Placental data included uteroplacental
vascular lesions and related villous lesions, lesions of acute inflammation, chronic inflammation, and
coagulation. Contingency tables and analysis of variance considered p < 0.05 as significant.
RESULTS: Mean - SD umbilical vein pH was 7.36 -+ 0.07 (range 6.94 to 7.56) and umbilical artery pH
was 7.30 +_ 0.08 (range 6.83 to 7.55). Increasing severity of uteroplacental thrombosis, villous lesions
reflective of uteroplacental vascular pathologic mechanisms, avascular villi, histologic evidence of abruptio
placentae, 'chronic villitis, and increased circulating erythrocytes were associated with decrease in
umbilical vein and artery pH, increase in umbilical vein and artery Pcoa, and decrease in umbilical vein
and artery Po2. Histologic evidence of acute infection and villous edema were associated with a higher
pH and Poa and a lower Pcoa in both umbilical vein and artery. Umbilical vein or artery base excess was
not related to placental lesions. Labor was not related to blood gas values in this data set, although a
subset of cases of extremely preterm premature rupture of membranes and preterm labor who labored
and were delivered by cesarean section had significantly poorer umbilical venous and fetal arterial blood
gas values (all p < 0.005). Lesions related to poorer blood gas values were significantly more frequent
in preterm preeclampsia and nonhypertensive abruptio placentae than in premature rupture of
membranes or preterm labor.
CONCLUSIONS: Changes in umbilical vein and artery pH, Poa, and Pcoa are significantly related to
lesions of uteroplacental vascular pathologic mechanisms and intraplacental thrombosis. Placental lesions
may be associated with chronic fetal distress by altering fetal oxygen availability and acid-base status.
Placental immaturity resulting from prematurity may be associated with inefficient placental respiratory
function and an increased likelihood of cesarean delivery in cases of premature rupture of membranes or
preterm labor. Altered fetal acid-base balance plus excess numbers of circulating nucleated erythrocytes
suggests that placental respiratory function is functionally abnormal when these lesions are present and
leads to fetal tissue hypoxia. (AM J OBSTETGYNECOL1995; 173:1058-64.)
Key words: Umbilical cord blood gases, prematurity, placental pathology, uteroplacental
vessels
From the Division of Anatomic Pathology, University of Connecticut
Health Center,=the Division of Maternal-Fetal Medicine, University
of Medicine and Dentistry of New Jersey, Robert Wood Johnson
Medical School~St. Peter's Medical Center,'the Perinatal Pathology~
and Informatics d Sections, Perinatology Research Facility, National
Institute of Child Health and Human Development, the Departments
of Obstetrics and Gynecology" and Pathology/Georgetown University Medical Center, and the Department of Obstetrics and Gynecology,
Ponce School of Medicine. g
Supported by National Institutes of Health contract No. NOI-HD
3-3198 (C.M.S., J.C.P., S.S.W.) and in part through an Interagency Personnel Agreement of the National Institutes of Health
(National Institute of Child Health and Human Development) with
the University of Connecticut (C.M.S.).
Presented in part at the Fifteenth Annual Meeting of the Society of
Perinatal Obstetricians, Atlanta, Georgia, January 23-28, 1995.
Reprints not available from the authors.
6/6/67335
1058
Umbilical cord blood acid-base assessment is an objective method for the evaluation of the newborn, especially in cases of prematurity when Apgar scores may be
unreliable. Placental histologic features have not been
studied in relation to placental respiratory function.
Traditionally, changes in pH values not accompanied
by changes in base excess are considered indicators of
respiratory acidemia. It is known that certain placental
histopathologic lesions may be associated with decreased uteroplacental perfusion and fetal hypoxia.
However, it is not known whether these lesions are
"markers" for fetal hypoxia or whether their presence is
directly related to abnormal placental hemodynamic
function and abnormal placental respiratory exchange.
Volume 173, Number 4
Am J Obstet Gynecol
The current study examines placental histopathologic
mechanisms in relation to umbilical venous and arterial
cord blood gas values to test the hypothesis that
uteroplacental vascular or placental structural pathologic features are directly related to abnormal placental
respiratory function and potential fetal hypoxia and
acidemia.
Material and methods
Beginning in April 1988 all placentas delivered at the
J o h n Dempsey Hospital had pathologic examination.
This data set represents all cases delivered between
April 1988 and March 1994 that met the following
inclusion criteria: singleton delivery, live birth, gestational age between 22 and 32 weeks by accurate gestational dating (by last menstrual period or early ultrasonography with confirmation by neonatal assessment),
no maternal history of chronic hypertension, diabetes
mellitus, or placenta previa. The final data set was
composed of 431 preterm placentas (22 to 32 weeks'
gestation). The four primary indications for delivery
were (1) premature rupture of membranes (n = 182)
defined as rupture of membranes before onset of labor,
(2) preterm labor (n = 150) defined as regular uterine
contractions with cervical effacement and dilatation
with intact membranes unresponsive to tocolysis, (3)
preeclampsia (n = 72) defined as blood pressure
> 140/90 mm Hg or increases of 30 m m Hg systolic or
15 m m Hg diastolic with proteinuria or edema and
clinical symptoms or laboratory abnormalities warranting elective preterm delivery, and (4) nonhypertensive
abruptio placentae (n = 27) defined as antepartum
vaginal bleeding followed by preterm delivery. Clinical
management at this institution results in essentially all
cases of preeclampsia at < 32 weeks' gestation being
delivered by cesarean section without a trial of labor.
Subsets of this population have been previously studied.l-3 The current study derives from a master database
of 462 patients who form the basis for a number of
recent efforts examining the relationship of histologic
features to various aspects of clinical outcome?' 5 Maternal charts were reviewed for principal indication for
delivery, presence of labor, mode of delivery, and umbilical cord blood gas values. Blood samples for analysis
were collected in heparinized 1 ml syringes, capped,
and transported on ice to the laboratory for analysis.
Blood gas values were determined within 10 minutes of
delivery on a model 178 automatic pH analyzer (Corning Med, Boston).
All placentas were studied by standard protocols. 6 For
each case two samples of umbilical cord, two samples of
extraplacental membranes, and four samples of grossly
normal chorionic villi were examined. Additional tissue
samples were taken from each gross lesion. If routine
sampling of the basal plate did not contain uteroplacental arteries, several thin slices of the basal plate were
Salafia et al. 1059
taken perpendicular to the maternal surface, embedded
in a cassette, and processed. This technique increased
the frequency with which uteroplacental vessels were
identified and has been shown to identify a wide range
of uterine vascular lesions. 7 Placental data recorded
were placental weight and histopathologic lesions,
which were classified into one of four groups: (1) histologic markers of acute ascending infection, (2) uteroplacental vascular lesions and villous lesions reflecting the
effects of uteroplacental vascular pathologic mechanisms, (3) lesions of chronic inflammation, and (4)
lesions related to coagulation. Each placental lesion was
assigned to only one pathophysiologic group; therefore
the four groups were mutually exclusive.
Acute ascending infection. The presence and severity of acute maternal (in amnion, chorio decidua, chorionic plate) and fetal (e.g., umbilical cord and chorionic
plate vessels) inflammation was scored on a scale of 0 to
4, as previously described. 8
Uteroplacental vascular pathologic features. The
presence of uteroplacental vascular pathologic features
can be inferred by lesions both in the uteroplacental
vasculature and within the villous parenchyma. The two
types of uteroplacental vascular lesions considered were
fibrinoid necrosis and atherosis of uteroplacental vessels 9 and absence of physiologic change of uteroplacental arteries? ° Fibrinoid necrosis and atherosis were
diagnosed when the uteroplacental vessel wall appeared
smudged and eosinophilic, with or without mural foamy
cells ("atherosis").l° Absence of a physiologic change of
uteroplacental vessels was diagnosed when normal endovascular trophoblast destruction of the muscular and
elastic components of the basal uteroplacental vessels
did not occur or was incomplete. Incompletely converted vessels retain muscle and elastic in their walls
and resemble spiral vessels of late luteal-phase endometrium? i, 12Villous lesions considered to be related to
uteroplacental vascular pathologic features include
abruptio placentae, ~3 villous infarcts, ~4 terminal villous
fibrosis, increased syncytiotrophoblast knotting, cytotrophoblast (X-cell) proliferation, ~~ and villous hypovascularity. 16-1~The diagnosis of abruptio placentae
was made by the gross finding of retroplacental hematoma with subjacent placental infarct or more commonly by microscopic evidence of placental villous infarct with decidual destruction and indentation with
decidual and parabasal hemorrhage. Histologic diagnosis was considered to be consistent with (but not diagnostic of) abruptio placentae when focal regions showed
decidual destruction and hemorrhage and an increase
in syncytiotrophoblast knotting, often with villous stromal hemorrhage. Also, the presence of circulating
nucleated erythrocytes was considered a potential
marker for uteroplacental vascular pathologic mechanisms. Nucleated erythrocytes are not generally seen in
smaller placental vessels after the early second trimes-
1060
Salafia et al.
October 1995
Am J Obstet Gynecol
Table I. Correlations of principal indications for delivery with umbilical cord blood gas values
I Preeclampsia I Abruptioplacentae I
UV pH
UA pH
UVPo~
UA Po2
UV Pco2
UA Pco2
UV base excess
UA base excess
7.30
7.26
24
15.3
47
52
-2.7
-3.9
_+ 0.07
+ 0.05
-+ 13.7
+- 7.8
__ 10.4
-+ 8.6
+_ 2.7
-+ 3.2
7.33
7.29
25.8
16.3
43.6
50
-2.3
-2.99
+ 0.07
- 0.07
+ 14
-+ 7.8
+- 10
+ 12.5
-+ 2.7
-+ 3
PROM
7.37
7.31
33.7
21.7
38.1
45.7
-2.7
-3.3
_+ 0.07*
- 0.08*
_+ 9.8*
+ 6.4",t
-+ 8*
+ 9,6"
-+ 3,2
-+ 3.5
I
PTL
7.37
7.31
32.2
22.4
38.3
43.3
-2.1
-3.5
+- 0.07*
- 0.09*
+- 11"
-+ 7.7",t
- 8*
-- 11"
-+ 3.6
+- 5.6
]Significance
p
p
p
p
p
p
<
<
<
<
<
<
0.001
0.001
0.001
0.001
0.001
0.001
NS
NS
PROM, Premature rupture of membranes; PTL, preterm labor; UV, umbilical vein; UA, umbilical artery; NS, not significant.
*Significant compared with preeclampsia.
tSignificant compared with nonhypertensive abruptio placentae.
ter. 19 A semiquantitative assessment described the presence of circulating nucleated erythrocytes as "occasional" if single cells were seen in rare fetal stem vessels
or as "numerous" if several nucleated erythrocytes were
seen in many fetal stem vessels and in smaller-caliber
placental vessels. T h e presence of hemosiderin in decidua of basal plate or placental membranes was identified on light microscopy and confirmed by Prussian
blue stain.
L e s i o n s of chronic inflammation. Decidual plasma
cell or eosinophil infiltrates, dense lymphocytic decidual infiltrates, chronic uteroplacental vasculitis,2° and
villitis involving anchoring villi were diagnostic of
chronic inflammation. Chronic, inflammation is reflected in the intervillous space and within placental villi
by chronic intervillositis and chronic viUitis, respectively? 1, ~
Lesions r e l a t e d to coagulation. Coagulation-related lesions in the maternal circulation included
uteroplacental vascular thrombosis and intervillous
thrombosis. A diagnosis of excessive perivillous fibrin
deposition indicated the presence of > 10% of villi
encased in perivillous fibrin. Coagulation-related lesions within the placental circulation included chorionic
and fetal stem vessel thrombi, "hemorrhagic endovasculitis, ~ and avascular terminal villi, indicating fetal
microcirculatory vasoocclusion.
Lesions such as uteroplacental vasculitis or absence of
uteroplacental physiologic adaptation were considered
as absent/solitary focus/multiple foci on a scale of 0 to 2.
Semiquantitative assessments were applied to lesions
such as villous fibrosis, hypovascularity, syncytiotrophoblast knotting, X-cell proliferation/~-~8 and perivillous
fibrin deposition. Because these features differ quantitatively across gestation, the diagnostic pathologist
(C.M.S.) was blinded to clinical data except gestational
age. All lesions were scored with the pathologist blinded
to the clinical data. Results were analyzed by contingency tables and analysis of variance, with p < 0.05
considered significant after Scheffe's corrections for
multiple comparisons.
Results
T h e umbilical blood gas characteristics of the population are presented in Table I. T h e mean gestational
age in cases of premature rupture of membranes and
preterm labor were significantly shorter than in cases of
preeclampsia (p < 0.05), with cases of nonhypertensive
abruptio placentae showing a borderline trend to
shorter gestational age c o m p a r e d with cases of preeclampsia (p = 0.058, Scheffe's test). Venous values
were available in 431 patients and arterial values in 405
patients. Decreased umbilical vein and artery p H and
Po 2 and increased Pco2 were observed in cases of
preeclampsia c o m p a r e d with cases of premature rupture of membranes and preterm labor (p < 0.05), and
decreased umbilical artery Po 2 was seen in nonhypertensive abruptio placentae c o m p a r e d with cases of premature rupture of membranes and preterm labor
(p < 0.05). Table II lists the significant relationships of
placental lesions to umbilical vein and artery pH, Po2,
and Pco 2. Uteroplacental vessels were available for
review in 414 of 431 (96%) of cases. Placental lesions
related to uteroplacental vascular pathologic features,
chronic villitis, and coagulation-related lesions demonstrated general associations with decreased umbilical
vein and artery pH, and Po2 and increased Pco~,
whereas the presence of acute infection and villous
e d e m a were generally related to increased umbilical
vein and artery p H and Po2 and decreased Pco2. Placental lesions related to uteroplacental vascular pathologic features, chronic viUitis, and coagulation-related
lesions were significantly less likely to occur in placentas
in which acute amnionitis, choriodeciduitis, chorionitis,
chorionic vasculitis, umbilical vasculitis, and moderate
or severe villous e d e m a were identified (eachp < 0.05).
Acute amnionitis, choriodeciduitis, chorionitis, chorionic vasculitis, umbilical vasculitis, and moderate or
severe villous e d e m a were significantly more common
in premature rupture of membranes or p r e t e r m labor
than in preeclampsia or nonhypertensive abruptio placentae (each p < 0.05). Stepwise regression isolated
four variables that demonstrated significant indepen-
Volume 173, Number 4
Am J Obstet Gynecol
dent predictive values to umbilical cord blood gas
values (histologic evidence of abruptio placentae, villous
infarct, villous hypovascularity, and avascular villi,
R 2 = 0.10). For example, when umbilical vein p H was
considered, coefficients for these lesion variables indicated that for each change in lesion severity (see Table
II) a change in pH of approximately 0.10 would be
predicted.
Because labor was generally not permitted in cases of
preterm preeclampsia, labor was therefore separately
analyzed in the premature rupture of membranes and
preterm labor groups. Seventy-five cases in the premature rupture of membranes-preterm labor group did
not labor and showed a mean umbilical vein pH of
7.37 -+ 0.06 compared with 247 cases that labored and
demonstrated an umbilical vein pH of 7.37 + 0.08 (not
significant). Of the 247 cases of premature rupture of
membranes and preterm labor that labored, 109 were
eventually delivered by cesarean section. The mean
umbilical vein p H of this group was 7.35 -+ 0.07 compared with 7.39 -+ 0.08 for the cases delivered vaginally
(p < 0.003). These 109 patients also had significantly
decreased umbilical artery p H (7.28 -+ 0.07 vs 7.32 0.08, p = 0.003) and a mean elevation of 7 m m Hg in
umbilical vein Pco 2 (p < 0.0001), 5 mm Hg in umbilical
artery Pcoz (p < 0.0005), and a mean decrease of 3 mm
Hg in umbilical artery P o 2 (p < 0 . 0 0 2 ) compared with
those patients who labored and delivered vaginally. The
109 patients who labored but were subsequently delivered by cesarean section were also significantly younger
than those who labored and delivered vaginally
(191 -+ 16 days vs 199 -+ 18 days, p < 0.006). These
109 patients did not have significantly different incidences or severity of uteroplacental vascular lesions,
villous lesions reflective of the effects of impaired
uteroplacental perfusion, or obliterative lesions within
the placental vasculature itself (data not shown, each
p > 0.05).
Comment
Quantitative changes in umbilical venous and fetal
arterial pH, Pco2, and Po 2 are related to two categories
of uteroplacental and placental histologic lesions: (1)
uteroplacental vascular lesions (which restrict uteroplacental perfusion) and villous lesions believed to reflect
the effects of impaired uteroplacental perfusion and (2)
obliterative lesions within the placental vasculature itself. Lung function can be impaired by structural processes (e.g., reduced lung volume, increased thickness
of the tissue diffusion barrier, decreased alveolar capillary bed) or by physiologic processes (poor quality of
inspired air or decreased capillary flow rates). Lesions
affecting anatomic equivalents of each of these sites can
be observed in the placenta. An intact uteroplacental
circulation ensures adequate intervillous perfusion and
oxygen delivery to the conceptus; uteroplacental blood
Salafia et al.
1061
flow progressively increases in the last trimester of
pregnancy.
The diffusion distance across the trophoblast is
greater in preterm placentas than at term; vasculosyncytial membranes that reduce the diffusion distance
across the placenta do not develop until the late second
trimester. Our data suggest that there is a difference in
placental functional reserve or capacity to withstand the
stresses of labor that is best measured by the gestational
age of the placenta and not marked by any histologic
lesions. Our cases of premature rupture of membranes
and preterm labor that labored but required cesarean
delivery demonstrated poorer umbilical venous and
fetal arterial blood gas values, younger gestational age
at delivery, and no difference in incidence of placental
parenchymal lesions compared with cases that labored
and delivered vaginally at a significantly greater gestational age. The more preterm the placenta, the greater
may be its relative functional inefficiency-independent
of pathologic lesions.
However, pathologic disorders may further alter the
intrinsic respiratory capacity of the placenta at any
given gestational age. Increased amounts of perivillous
fibrin deposition would impair gas diffusion. Cytotrophoblast (X-cell) proliferation would increase the thickness of the trophoblast layer. Areas of syncytiotrophoblast knotting demonstrate "aging ''~8 or degenerative
nuclear changes and may be functionally abnormal.
Internal to the respiratory exchange surface, villous
fibrosis, hypovascularity, or frank obliteration of areas
of the villous capillary bed (in avascular villi or infarcts)
would reduce the capillary area for exchange, and may
have an impact on placental resistance and ultimately
placental blood flow through the villous capillary bed.
Areas of abruptio placentae would combine effects at
several levels (impairment of maternal perfusion, damage to the trophoblast surface, and initial compression
and eventual obliteration of the placental capillary
bed). It is important to note that the absence of physiologic changes or fibrinoid necrosis or atherosis of the
uteroplacental vascular lesions themselves was not correlated with umbilical blood gas values. Rather, blood
gas values were related to placental lesions, which are
believed to reflect their effects. Other analyses of this
data set have suggested that it is not so much uteroplacental vascular lesions but the placental response to the
pathologic anatomy and physiologic features that is
critical to fetal outcome. 23 These data further support
that hypothesis.
In our data set the actual values of umbilical vein and
artery pH, Po2, and P c o 2 a r e within the normal limits in
most cases. We even found no association of labor with
blood gas values in premature rupture of membranes
and preterm labor patients, the only groups that labored in this population. This may reflect the clinical
management at the John Dempsey Hospital, where
1062
Salafla et al.
October 1995
Am J Obstet Gynecol
Table II. Significant r e l a t i o n s h i p s o f p l a c e n t a l lesions to umbilical b l o o d gas values
UV pH
Acute inflammation
Amnionitis (maternal response)
Grade 0
Grades 1-2
Grades 3-4
Umbilical vasculitis (fetal response)
Grade 0
Grades 1-2
Grades 3-4
Uteroplacental vascular pathologic features
Fibrinoid necrosis/atherosis
None
One vessel
Multiple vessels
Placental lesions related to uteroplacental vascular
pathologic features
Histologic features related to abruptio placentae
None
Consistent with abruptio placentae
Gross abruptio placentae
Villous infarct
None
Single
Multiple
Syncytiotrophoblast knotting
Normal
Moderate increase
Severe increase
Cytotrophoblast ("X-cell") proliferation
Normal
Moderate increase
Severe increase
Villous fibrous
Normal
Moderate increase
Severe increase
Villous hypovascularity
Normal
Moderate increase
Severe increase
Circulating nucleated erythrocytes
Normal
Moderate increase
Severe increase
Chronic inflammation
Chronic villitis
Not present
Present
Coagulation-related lesions
Uteroplacental vessel thrombus
No occlusive
One occlusive
Multiple occlusive
Perivillous fibrin deposition
Normal for age
Moderate increase for age
Avascular terminal villi
None
Focal
Multifocal
Miscellaneous (unclassified) lesions
Villous edema
None
Mild/moderate
Severe
UA pH
7.35 ± 0.08*
7.38 -+ 0.06*
7.37 _+ 0.60*
UV Po2
(mm Hg)
29.7 - 13.3"
33.5 -+ 11.4"
34.8 ± 8.8*
7.35 ± 0.07*
7.38 - 0.06*
7.38 -+ 0.07*
31.57 -+ 12.355
29.09 -+ 8.745
20.03 ± 5.095
7.37 + 0.07t
7.35 ± 0.07t
7.34 _ 0.08t
7.32 ± 0.0St
7.30 ± 0.08t
7.28 - 0.09?
7.37 _+ 0.07t
7.33 - 0.07t
7.31 ± 0.08t
7.31 ± 0.0St
7.27 ± 0.08t
7.26 - 0.06t
32.55 + 11.17t
27.90 -+ 17.72t
23.92 - 12.70t
7.37 -+ 0.07t
7.35 ± 0.0St
7.32 + 0.06
7.31 _+ 0.08t
7.29 - 0.08t
7.27 ± 0.07t
33.5 - 11.4t
30.2 -+ 12.7t
24.9 ± 13.3t
7.36 -+ 0.07t
7.35 - 0.07t
7.32 +- 0.08t
32.3 ± 10.4t
31.4 + 17.2t
24.5 ± 10t
7.36 - 0.08*
7.35 _ 0.07*
7.32 ± 0.06*
7.36 -+ 0.07t
7.34 - 0.07t
7.30 + 0.09t
7.30 _+ 0.08*
7.30 ± 0.06*
7.25 ± 0.10"
32.0 -+ 11.0"
30.8 - 15.5'
24.3 -+ 12.9"
7.31 ± 0.07t
7.29 - 0.09t
7.26 +- 0.0St
32.2 ± 10.0"
31.4 +-_ 14.8"
23.3 - 8.2*
7.36 ± 0.07*
7.32 -+ 0.06*
7.30 -+ 0.085
7.27 +_ 0.065
7.36 ± 0.07t
7.33 -+ 0.08t
7.33 ± 0.0St
7.31 - 0.08*
7.28 -+ 0.10"
7.28 ± 0.06*
7.34 -+ 0.07*
7.37 ± 0.07*
7.35 ± 0.09*
7.28 -+ 0.08*
7.31 _+ 0.07*
7.30 ± 0.12"
All empty cells indicate nonsignificant results. UV, Umbilical vein; UA, umbilical artery.
*p < 0.01.
tp < 0.001.
Sp < 0.05.
Salafia et al.
Volume 173, Number 4
Am J Obstet Gynecol
UA Poa
(ram Hg)
19.7 -+ 7.7*
21.4 +- 6.6*
23.0 ± 7.3*
UV Pco2
(mm Hg)
1063
UA Pco2
(ram Hg)
41.6 + 9.5t
37.3 -+ 6.7t
37.4 _+ 6.6t
47.1 ± 10.7"
46.2 -+ 8.5*
42.7 + 11.2"
38.32 ± 8.38t
40.00 -+ 7.89t
42.64 ± 9.86t
43.78 -+ 9.76t
46.72 +- 10.03t
49.04 -+ 11.55t
21.5 -+ 7.1t
18.3 -+ 9.5t
14.7 +- 6.5t
38.58 + 8.02t
45.47 ± 10.29t
46.2 -+ 9.17t
44.69 -+ 10.29#
52.55 -+ 10.14t
52.10 -+ 9.11t
21.8 -+ 7.3t
20.37 ± 7.5t
15.9 ± 7.7t
38.20 -+ 8.14t
40.89 ± 9.25t
45.36 -+ 8.10t
44.80 -+ 0.19"
46.92 -+ 11.26"
50.06 -+ 8.60*
21.5 ± 6.8t
20.6 ± 8.9t
15.3 ± 7.7t
38.87 -+ 8.36t
40.80 ± 9.15~
45.45 -+ 9.16t
45.28 -+ 0.15"
46.51 -+ 10.40"
51.00 -+ 12.40"
21.4 -+ 7.0t
20.4 -+ 8.4t
15.8 -+ 5.7t
38.74 ± 8.45t
41.00 ± 9.23t
45.08 -+ 7.99t
44.95 -+ 10.78"
46.93 ± 10.48"
51.52 + 7.59*
21.5 -+ 7.4t
19.5 -+ 7.5t
14.l ± 6.3t
38.89 -+ 8.36t
41.39 _+ 9.007
47.58 ± 9.55t
44.95 ± 10.26t
47.24 + 10.01t
55.79 ± l l . 1 5 t
21.5 -+ 7.0*
20.3 - 7.9*
15.5 +- 8.0*
39.16 + 7.91++
40.45 -+ 9.51++
43.51 -+ 10.105
45.39 -+ 10.025
46.38 -+ 10.855
50.80 ± 2.18++
21.0 - 7.4t
13.6 -+ 6.6t
39.73 -+ 8.86*
44.29 + 7.90*
45.88 -+ 10.51++
50.79 -+ 10.93++
21.3 -+ 7.85
20.6 ± 6.15
19.0 -+ 6.75
39.1 ± 8.25
39.9 -+ 6.9++
41.8 + 0.45
19.8 ± 7.7*
21.6 -+ 6.6*
22.8 -+ 7.0*
20.8 + 7.5++
21.6 + 6.75
13.6 -+ 4.7++
20.79 -+ 7.50 +
21.63 - 6.705
21.42 + 7.10t
18.22 +- 8 .75t
16.68 -+ 7 . 11t
39.08 - 8.73t
42.82 -+ 9.64t
43.39 -+- 5.71t
45.21 -+ 10.13"
48.93 -+ 12.60"
50.34 -+ 8.36*
19.25 -+ 7.62++
21.15 ± 7.20++
21.93 -+ 8.805
42.81 -+ 8.917
38.43 -+ 8.38t
39.72 -+ 9.25t
49.51 -+ 10.18t
44.46 -+ 10.13t
44.72 + 12.18t
1064
Salafia et al.
each p r e t e r m presentation is extensively evaluated by
biophysical profile scores and r e p e a t e d tests of fetal
well-being. Any fetus that demonstrates a potential for
"decreased placental reserve" by showing an abnormality in antepartum testing is promptly delivered by
cesarean section. In cases of p r e m a t u r e rupture of
membranes and preterm labor that are allowed to
labor, clinical triage has selected those cases with placentas better able to maintain umbilical venous (and by
extension fetal artery blood gas values) at healthy levels.
However, in our data placental lesions may contribute
to as much as 10% of the variation in blood gas values.
Why not a greater percent? First, this study does not
consider potential physiologic modifiers of placental
respiratory function. None of our patients were diagnosed with sickle cell disease or other frank hemoglobinopathy; major differences in the oxygen-carrying
capacity of maternal blood delivered to the intervillous
space is not likely. Retrospective data regarding maternal smoking are frequently unreliable. We also did not
have available data regarding fetal cardiac status or
studies of Doppler velocimetry. However, the same
lesions are associated with the release of nucleated
erythrocytes (a process that is most commonly attributed to hypoxia) and to symmetric and asymmetric
intrauterine growth retardation. 23 T h e maintenance of
fetal acid-base balance on the lower end of the normal
range in the face of chronic placental parenchymal
d a m a g e may due to chronic fetal accommodations to
impaired placental function. We speculate that placental lesions play a causal role of impairing placental
respiratory function and umbilical vein blood quality,
leading to chronic fetal hypoxia and restricted fetal
metabolism and growth. These fetal compensations
restore acid-base balance within the homeostatic range
but may not be without cost to the fetus.
In any p r e t e r m population statistical relationships of
blood gas values to labor will d e p e n d on the clinical mix
of preeclampsia and spontaneous prematurity and on
the clinical m a n a g e m e n t of laboring patients. Maternal
maneuvers to increase uterine perfusion and maternal
oxygen content may have different effects of fetal oxygenation and acid-base status d e p e n d i n g on the anatomic site of impairment of the uteroplacental respiratory apparatus. Prospective studies of the fetal response
to such interventions, which include detailed placental
histopathologic study, may improve our ability to diagnose the nature of uteroplacental respiratory impairm e n t and indicate the most efficient target therapy.
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