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The fetal biophysical profile

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The fetal biophysical profile
Author
Frank A Manning, MD

Section Editor
Charles J Lockwood, MD,
MHCM

Deputy Editor
Vanessa A Barss, MD,
FACOG

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2014. | This topic last updated: Aug 12, 2013.
INTRODUCTION The fetal biophysical profile score (BPS or BPP) refers to the sonographic assessment of
four discrete biophysical variables:
Fetal movement
Fetal tone
Fetal breathing
Amniotic fluid volume
Results of nonstress testing
Each of these five parameters is given a score of 0 or 2 points, depending upon whether specific criteria are
met (table 1). The presence of these biophysical variables implies absence of significant central nervous
system hypoxemia/acidemia at the time of testing. By comparison, a compromised fetus typically exhibits loss
of accelerations of the fetal heart rate (FHR), decreased body and breathing movements, hypotonia, and, less
acutely, decreased amniotic fluid volume.
The clinical value of the cumulative fetal BPS is that it is noninvasive, easily learned and performed, and an
accurate means for predicting the presence of significant fetal acidemia, which is the most common cause of
fetal death or damage [1]. Seventy to 90 percent of late fetal deaths display evidence of chronic or acute and
chronic compromise prior to demise [2]. Sonographic detection of signs of fetal compromise can allow
appropriate intervention that ideally will prevent adverse fetal sequelae.
Although the use of biophysical testing schemes to monitor high-risk pregnancies has become routine, this
practice pattern has evolved with limited high quality scientific data to support its use [3]. Moreover, there are
no randomized trials on which to base recommendations for the best initial testing approach for specific types
of high-risk pregnancies, the optimal timing of test initiation, the frequency of testing based on test results,
conditions that may affect test results, and the effect of gestational age.
ONTOGENY OF FETAL BIOPHYSICAL REGULATION The ontogeny of fetal biophysical development
follows a rigidly prescribed course. The initial step is cell differentiation, whereby cells acquire their unique
characteristics. Differentiation and functional capacity usually occur nearly simultaneously. Specific functional
entities develop as individual cells begin to interact with each other and come under local regulation. As they
become enervated, these functional entities progressively come under the control of local, then regional, and
finally central neuronal regulation. All biophysical activities are eventually regulated and controlled by discrete
centers within the brain. The individual neurons within a given regulatory site always retain their sensitivity to
local factors; however, they are also sensitive and responsive to feedback from peripheral sensors and to
traffic generated within the brain. Modulating brain traffic first manifests as short sleep-wake cycles, then
progresses to circadian cycles, and finally to consciousness cycles.
The following principles derive from this ontogeny and are the basis for fetal biophysical monitoring:
Any given biophysical variable reflects the integration of signals arising within the central nervous
system. The presence of normally organized biophysical activity is reliable, presumptive evidence that
the central nervous system is intact and not affected by pathological modulation.
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Neurons, with their high metabolic rate and demand, are exquisitely sensitive to local hypoxemia and
ischemia. Pathological suppression of the neurons composing a given regulatory site due to hypoxemia
results in loss of the normal features of a given biophysical activity.
However, the absence or diminution of a given biophysical variable does not necessarily mean
pathology is present. Normal suppression of a regulatory center can occur from intrinsic fetal rhythms,
such as the deep stage of quiet sleep, or the presence of circulating agents that cause general
suppression of the brain, such as transplacental passage of maternal sedatives and opiates.
Progressive loss of brain regulation of biophysical activities results in regression to regional control and
ultimately to local control (reverse ontogeny).
BIOPHYSICAL VARIABLES USED IN FETAL MONITORING The fetal BPS is derived from assessment
of five discrete biophysical variables (table 1), which are regulated by discrete higher central nervous system
centers. Four of these parameters: FHR accelerations in response to fetal movements (nonstress test), fetal
breathing movements, generalized fetal movements, and fetal tone are acute variables since they are acutely
affected by perturbations in fetal oxygenation.
Acute variables The selection of the acute variables for the fetal BPS was based upon their ease of
measurement and the ability to objectively evaluate them using universally available equipment (eg, external
FHR monitors and ultrasound imaging). Other fetal biophysical activities (eg, sucking, swallowing, micturition,
eye movements) may serve equally well as markers of fetal health, but are not included because measurement
is difficult and may be subjective.
Each of the acute variables can be viewed as an indirect assessment of the integrity of the regulatory center
since each acts as a peripheral transducer of central nervous system regulatory output. When a given variable
is observed to be normal (eg, fetal breathing movements), the integrity of the regulatory center is ensured and
the presence of a pathological factor, such as hypoxemia or acidemia, can be reliably excluded. In contrast,
when a given acute variable is not normal, a differential diagnosis is always required. The most common
innocuous cause of absence of a given acute variable is fetal state change and, most commonly, quiet sleep.
Since the sensitivity to depth and duration of quiet sleep varies by discrete regulatory center, it is unusual to
observe the absence of two or more variables as a consequence of quiet sleep alone. Extending the
observation period to encompass the usual duration of sleep state cycles minimizes the possibility of confusion
of pathological versus physiological causes of absent variable. The more variables are absent (ie, the lower the
score), the less likely the change is due to sleep state. Similarly, the longer the absence of variables, the more
likely the cause is due to a pathological influence.
The acute variables function to enhance fetal development, but are not essential to maintaining fetal life, thus
they are expendable in times of stress since they are energy dependent and increase fetal oxygen
requirements. As an example, pharmacological paralysis of sheep fetuses to prevent fetal movement results in
an abrupt fall in oxygen consumption by as much as 20 percent and a rise in fetal PO2 by as much as 15
percent [4]. Similarly in the human fetus, administration of a short acting curare (eg, pancuronium) to prevent
fetal movement produces an immediate rise in fetal venous PO2 by as much as 30 percent [5].
The degree of fall in oxygen concentration necessary to abolish a given regulatory center output varies by
center. The most oxygen sensitive centers are the cardioregulatory neurons controlling the coupling of fetal
movement and heart rate acceleration, and the fetal breathing center neurons. The centers regulating fetal
movement have a higher threshold than those for fetal breathing or FHR accelerations; the fetal tone center
has the highest threshold. Thus, the acute fetal variables respond to hypoxemia in a predictable,
physiologically based cascade: loss of fetal breathing movements and FHR acceleration, followed by
decreased fetal movement, and finally loss of fetal tone. This phenomenon is of great clinical value since it
allows for estimation of both the presence and severity of hypoxemia.
The threshold of the various regulatory centers is not absolute, but can adjust over time. This effect is likely a
result of adaptive response, which increases local oxygen supply, rather than the result of a true change in
neuron oxygen requirements. Such compensatory responses include increased oxygen extraction, elevated
fetal hemoglobin with increased oxygen carrying capacity, and redistribution of blood flow to favor brain
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perfusion. In some chronic fetal conditions, the acute biophysical variables may initially disappear and then
reappear despite a low P02.
The relationship between significant fetal acidemia and low BPS was inferred because the BPS was first
described before it was possible to obtain antepartum fetal blood. Perinatal mortality (gross and corrected) and
serious perinatal morbidity (nonreassuring FHR tracing in labor, low Apgar scores, neonatal seizures,
admission to an intensive care unit, hypoxemic-ischemic encephalopathy, intrauterine growth restriction)
increased significantly as the last BPS fell (figure 1) [6-8]. In addition, the cord blood pH of infants delivered
either vaginally or by cesarean birth demonstrated a direct relationship to last BPS (figure 2) [9]. An inverse
relationship between last BPS and incidence of cerebral palsy has also been observed, and may or may not be
related to antepartum asphyxia (figure 3). Long-term asphyxia leading to adverse neurologic outcomes such as
cerebral palsy and intellectual disability appears to be significantly reduced in high-risk patients managed by
fetal biophysical profile scoring compared to untested low-risk patients [10].
The advent of ultrasound guided intrauterine fetal blood sampling (cordocentesis) made it possible to measure
the direct and immediate relationship between the BPS, fetal PO2, and fetal pH [11,12]. (See "Fetal blood
sampling".) These studies, which include over 1000 paired observations, indicate a significant direct
relationship between the BPS and mean umbilical venous pH and further demonstrate that, in the individual
fetus, the BPS accurately predicts both the probability and severity of existing acidemia [13,14]. Thus, the
score is an accurate proxy for fetal acidosis. By comparison, the relationship between the BPS and fetal P02 is
less precise. This is expected since P02 varies according to fetal compensatory adaptive responses.
Chronic variable The fifth variable of the fetal BPS is amniotic fluid volume. Fetal urine is the predominant
source of amniotic fluid from approximately the mid-second trimester (16 weeks). Fetal urine production is
primarily dependent upon renal perfusion, which in turn reflects selective distribution of cardiac output. The
fetus responds to sustained hypoxemia (asphyxia) by selective redistribution of its cardiac output, with
preferential flow directed to the brain, heart, adrenals, and placenta at the expense of all other organ systems
[15]. (See "Physiology of amniotic fluid volume regulation".)
This protective mechanism is reflex in origin and is initiated by specialized chemoreceptors in the aortic arch
and carotid arteries. Hypoxemia-induced reflex redistribution of cardiac output results in diminished fetal urine
production [16]. Fetal swallowing, a major mechanism for removal of amniotic fluid, is a vegetative reflex and
very resistant to the effects of hypoxemia. Therefore, the net effect of decreased urine production is a gradual
reduction in the amount of amniotic fluid, ultimately leading to oligohydramnios and then anhydramnios.
The time course for the evolution of oligohydramnios is usually relatively long. On average, it takes
approximately 15 days for a fetus to progress from normal to reduced amniotic fluid volume (in the absence of
membrane rupture) and 23 days to develop severe oligohydramnios [16]. However, acute changes in amniotic
fluid volume with rapid deterioration of the BPS have been reported [17].
It is also important to recognize that the fetal effects of hypoxia-induced redistribution of cardiac output are not
confined to the fetal kidney. Other signs of chronic hypoxemia presenting in the fetus and newborn, such as
reduced fetal growth with brain sparing, can be attributed to effects from the compensatory cardiovascular
reflex response.
BIOPHYSICAL SCORE
Determination The composite fetal BPS is derived from five variables: four acute variables (FHR
accelerations in response to fetal movements [nonstress test], fetal breathing movements, generalized fetal
movements, fetal tone) and one chronic variable (amniotic fluid volume). Each of these five variables have
been evaluated independently and the normal characteristic defined (table 1) [18]. The scoring method used for
each variable is binary, ie, the variable is either normal or abnormal; gradations of abnormality are not used. A
normal variable is assigned a score of two and an abnormal variable a score of zero. The maximal score is
10/10 and the minimum score is 0/10.
A variable may be assigned a normal score as soon as it is observed. Since most fetuses will be normal and
will demonstrate these biophysical activities, the usual time to complete a normal fetal BPS is less than five
minutes [19]. The acute variables are subject to fetal sleep wake cycles; thus, continuous observation for at
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least 30 minutes must occur before the variable can be defined as absent (abnormal). In one ultrasound study
of fetuses from uncomplicated pregnancies at 36 to 42 weeks of gestation, the mean duration of a fetal sleep
(no somatic movements) was about 20 minutes, with an upper range of about 40 minutes [20].
The variables should be present and normal biophysical activities to be assigned a score of two. As an
example, monotonous picket-fence breathing or gasping should not be considered normal breathing movements
nor should seizures be counted as normal fetal limb movements [21-23].
We generally base evaluation of amniotic fluid volume on ultrasound measurement of the largest visible pocket.
To score 2 points, the selected largest pocket must have a transverse diameter of at least 1 centimeter and a
vertical pocket of at least 2 centimeters. However, other methods of amniotic fluid volume assessment can be
used (eg, normal amniotic fluid index is 5 to 25 cm, normal single deepest vertical pocket is 2.1 to 8 cm). (See
"Assessment of amniotic fluid volume".) There is a significant inverse relationship between oligohydramnios
and perinatal mortality and morbidity. (See "Oligohydramnios", section on 'Prognosis and management'.)
Modified biophysical profile The modified biophysical profile was developed to simplify the examination
and reduce the time necessary to complete testing by focusing on those components of the profile that are
most predictive of outcome. Assessment of amniotic fluid volume and nonstress testing appears to be as
reliable a predictor of long-term fetal well-being as the full BPS [24]. A normal modified biophysical profile will
occur in 90 percent of pregnancies tested, thus it is necessary to proceed with a full biophysical evaluation in
only a minority of patients [25]. The rate of stillbirth within one week of a normal test is the same as with the
full BPS, 0.8 per 1000 women tested [25].
Factors affecting test results Administration of antenatal corticosteroids can be associated with transient
FHR and behavioral changes that typically return to baseline by day four after treatment. The most consistent
FHR finding is a decrease in variability on days two and three [26-29]. Fetal breathing and body movements
are also commonly reduced, which may result in a lower biophysical profile score or nonreactive nonstress test
[30-34]. However, fetal blood flow velocity waveform patterns in the umbilical artery, middle cerebral artery,
and ductus venosus do not appear to be affected [31,34,35].
The behavioral changes may reflect a physiologic response of the brain to glucocorticoids. Alternatively, they
may be a consequence of a transient increase in fetal vascular resistance and blood pressure, which has been
demonstrated in animal studies [35-37]. These findings should be considered within the total clinical picture
when assessing a fetus for possible delivery because of a nonreassuring fetal evaluation (nonstress test or
biophysical profile) after corticosteroid administration.
The effect of subclinical infection on test results is controversial. Although the BPS is used to diagnose fetal
infection or chorioamnionitis [38], most studies have not found it to be a very sensitive test of subclinical
infection [39-42]. (See "Preterm premature (prelabor) rupture of membranes".)
Preterm labor may be associated with absence of fetal breathing movements. However, a systematic review
found that data were inadequate to recommend monitoring fetal breathing for prediction of preterm delivery
within 48 hours or seven days [43].
There are sparse data on the effect of fasting on BPS. A study that performed a BPS one hour after a meal and
10 to 12 hours after abstaining from food and drink in 30 women with uncomplicated pregnancies reported
scores of 8/10 for all postprandial tests, but two fasting tests were 4/10 and 6/10; both tests rose to 10/10
after the mother ate a meal [44]. Point reductions during fasting were primarily due to non-reactive NSTs and
inadequate fetal breathing movements. It is difficult to draw any conclusion about the effect of fasting on the
BPS in the clinical setting, given the small size of this study and the absence of indications for antepartum
fetal assessment.
Mild maternal anemia (mean hemoglobin 9.4 g/dL) did not appear to affect the BPS [45].
INTERPRETATION, MANAGEMENT, OUTCOME BPS results are interpreted as follows:
10/10 or 8/10 (includes 2 points for amniotic fluid): risk of developing fetal asphyxia within one week if
no intervention is low (about 1/1000).
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6 or 8/10 (0 points for amniotic fluid): when amniotic fluid volume is decreased, the risk of developing
fetal asphyxia within one week if no intervention is increased at 89/1000.
6/10 (includes 2 points for amniotic fluid): equivocal test, significant possibility of developing fetal
asphyxia cannot be excluded. Repeat test within 24 hours to see if one of the absent acute variables
returns to normal or deliver if at or near term.
0 to 4/10: risk of fetal asphyxia within one week if no intervention is 91 to 600/1000. Delivery is usually
indicated. The mode of delivery is an obstetric decision based on multiple variables including
presentation, cervical findings and maternal condition. In the absence of obstetric contraindication,
induction of labor with continuous intrapartum fetal heart surveillance is a reasonable management
option.
The predictive value of the four ultrasound-monitored variables for assurance of fetal well-being is equivalent to
that of a full BPS (four ultrasound variables and nonstress test) when the four variables are all normal. This
was illustrated in a prospective study in which the nonstress test (NST) was only performed if the ultrasound
score was less than 8 [46]. This modification reduced the need for NSTs in 95 percent of cases and the
average testing time per patient without reducing the predictive value of the test.
An NST should always be performed if any ultrasound monitored variable is 0. However, a BPS of 8/10 by any
combination of variables with or without the NST is as accurate as a score of 10/10 for the prediction of fetal
well-being as long as no points are deducted for amniotic fluid volume (eg, FM+FB+FT+AVF=8 or
FM+FT+AVF+NST=8, where FM=fetal movement, FB=fetal breathing, FT=fetal tone, AVF=amniotic fluid
volume).
Although outcome data from large randomized studies are lacking [47], observational studies have reported it to
be accurate for predicting the absence of significant fetal acidemia [48] and comparable to the contraction
stress test [49].
The probability of fetal acidemia is virtually nil when the score is normal (10 or 8 without oligohydramnios); the
likelihood of fetal compromise and death rises as the cumulative score falls. The false negative rate (ie, fetal
death within one week of a last test with a normal score) is not zero, but is exceedingly low (0.4 to 0.6 per
1000 live births) and is approximately 10 percent of the overall perinatal mortality for a high-risk population [50].
False-negatives are likely due to acute insults such as sudden cord prolapse, fetomaternal hemorrhage, or
abruptio placenta.
The utility of biophysical fetal monitoring was demonstrated in a study of 44,828 biophysical profile tests in
which the risk of fetal demise within one week of a normal test result (corrected for lethal congenital anomalies
and unpredictable causes of demise) was 0.8 per 1000 women tested [50]. This result compares favorably with
all other means of antepartum fetal assessment. In two large observational studies including over 18,000
women, use of the BPS was associated with a 61 to 76 percent reduction in perinatal mortality (corrected)
compared to historic controls [51].
However, the positive predictive value of the BPS for evidence of true fetal compromise (eg, a non-reassuring
fetal heart tracing during labor, neonatal acidemia, or other markers of neonatal morbidity at the time of
delivery) is only approximately 50 percent, with a negative predictive value greater than 99.9 percent.
Therefore, it is important that the a priori risk of fetal compromise be elevated to improve the performance of a
positive test result.
The fetal BPS reaches maximal clinical efficacy when interpreted within the context of fetal age and maternal
and obstetric factors. As an example, a normal score predicts no fetal compromise and allows for conservative
management in a gravida with discrete high risk factors, such as diabetes mellitus or hypertension. This
affords the fetus the advantage of continued intrauterine maturation and thereby reduces the risk of
complications from prematurity. In contrast, an abnormal score in a similar high risk patient allows for weighing
of relative fetal-to-neonatal risks and selection of delivery at a time when the balance shifts to greater fetal risk
(figure 4).
A change in maternal condition will also affect application of the fetal BPS. The decision to intervene in a
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patient with worsening hypertension, for example, may depend less on the score and more on maternal risk.
Similarly, the presence of a favorable cervix for induction may override the results of the BPS when the fetus is
mature or postterm.
Case reports and small series suggest that the BPS is less reliable in pregnancies complicated by severe
preterm fetal growth restriction. As an example, in one study, 48 growth restricted fetuses less than 32 weeks
of gestation with abnormal umbilical artery Doppler results underwent BPS daily and NSTs three times daily
[52]. Ten of 27 fetuses with BPS of 8 developed nonreassuring fetal tracings 3.5 to 24 hours after the BPS and
the repeat BPS was 2 in all 10 of these fetuses; three died in utero, seven were delivered promptly and six of
these neonates had acidemic umbilical artery blood gases at birth.
INDICATIONS AND FREQUENCY OF TESTING The American College of Obstetricians and
Gynecologists (ACOG) recommends antepartum fetal surveillance of pregnancies in which the risk of
antepartum fetal demise is increased [53]. An ACOG Practice Bulletin states that women with high-risk factors
for significant fetal acidemia should undergo antepartum fetal surveillance with tests such as the BPS and
nonstress test. Specific indications for antenatal fetal assessment are reviewed separately. (See "Overview of
antepartum fetal surveillance", section on 'Indications for fetal surveillance'.)
All of the ultrasound-monitored variables for the BPS can be observed as early as the first trimester, although
characteristics of fetal behavior (breathing, tone, movement, as well as other fetal activities) change with
advancing gestational age [54,55]. The minimum gestational age for testing should reflect the lower limit that
intervention with delivery would be considered. This age has gradually decreased and is now 24 to 25 weeks in
most centers. Testing may be initiated at this gestational age if clinical conditions suggest early fetal
compromise is likely; otherwise, testing is initiated when individual clinical circumstances warrant fetal
monitoring. Initiating testing at 32 to 34 weeks of gestation is appropriate for most pregnancies at increased
risk of stillbirth.
A reassuring BPS (eg, BPS of 8 to 10) should be repeated periodically (weekly or twice weekly) until delivery
when the high-risk condition persists. Some experts recommend more frequent testing intervals, with
individualization based on the high-risk clinical setting (eg, early severe fetal growth restriction) [56]. Any
significant deterioration in the clinical status (eg, worsening preeclampsia, decreased fetal activity) requires
fetal reevaluation, regardless of the amount of time elapsed since the last test.
Normal antepartum testing does not preclude the need for intrapartum fetal monitoring. Induction of labor may
be attempted with abnormal antepartum testing as long as the FHR and contractions are monitored
continuously and are reassuring. Cesarean delivery is indicated if there are repetitive late decelerations.
Although the BPS test is typically used for antepartum fetal assessment, it can also be done intrapartum.
However, its clinical utility in the intrapartum is unclear [57,58].
SUMMARY AND RECOMMENDATIONS
Criteria for the fetal biophysical profile score (BPS) are listed in the table (table 1). (See 'Determination'
above.)
The acute variables are subject to fetal sleep wake cycles; thus, continuous observation for at least 30
minutes must occur before the variable can be defined as absent. (See 'Determination' above.)
A score of 8 to 10/10 is reassuring of fetal well-being when amniotic fluid is normal; 6 to 8/10 is
concerning when amniotic fluid volume is decreased and requires increased monitoring or delivery, 6/10
with normal amniotic fluid volume is an equivocal test result and should be repeated within 24 hours if
the patient is not delivered; and 0 to 4/10 suggests a high risk of fetal asphyxia within one week if the
patient remains undelivered or no therapeutic intervention is undertaken. (See 'Interpretation,
management, outcome' above.)
We recommend monitoring pregnancies at risk of fetal compromise (Grade 1C). We suggest using the
biophysical score for monitoring because it is a noninvasive, easily applied, accurate means for
predicting the presence of significant fetal acidemia. Testing should be performed one or more times per
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week, depending upon the clinical situation. (See 'Indications and frequency of testing' above.)
The integration of the BPS into the management of high-risk obstetric patients has been associated with
a significant reduction in perinatal mortality. The perinatal mortality in a high-risk patient managed
according to the fetal BPS is significantly lower than the rate observed in contemporary untested low
risk patients. (See 'Interpretation, management, outcome' above.)

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78:768.
32. Katz M, Meizner I, Holcberg G, et al. Reduction or cessation of fetal movements after administration of
steroids for enhancement of lung maturation. I. Clinical evaluation. Isr J Med Sci 1988; 24:5.
33. Wijnberger LD, Bilardo CM, Hecher K, et al. Effect of antenatal glucocorticoid therapy on arterial and
venous blood flow velocity waveforms in severely growth-restricted fetuses. Ultrasound Obstet Gynecol
2004; 23:584.
34. Karaer C, Onderoglu L, Yigit N, et al. The effect of steroids on the biophysical profile and Doppler indices
of umbilical and middle cerebral arteries in healthy preterm fetuses. Eur J Obstet Gynecol Reprod Biol
2001; 99:72.
35. Derks JB, Giussani DA, Jenkins SL, et al. A comparative study of cardiovascular, endocrine and
behavioural effects of betamethasone and dexamethasone administration to fetal sheep. J Physiol 1997;
499 ( Pt 1):217.
36. Koenen SV, Mecenas CA, Smith GS, et al. Effects of maternal betamethasone administration on fetal
and maternal blood pressure and heart rate in the baboon at 0.7 of gestation. Am J Obstet Gynecol 2002;
186:812.
37. Smith RP, Miller SL, Igosheva N, et al. Cardiovascular and endocrine responses to cutaneous electrical
stimulation after fentanyl in the ovine fetus. Am J Obstet Gynecol 2004; 190:836.
38. Vintzileos AM. Antepartum surveillance in preterm rupture of membranes. J Perinat Med 1996; 24:319.
39. Lewis DF, Adair CD, Weeks JW, et al. A randomized clinical trial of daily nonstress testing versus
biophysical profile in the management of preterm premature rupture of membranes. Am J Obstet Gynecol
1999; 181:1495.
40. Ghidini A, Salafia CM, Kirn V, et al. Biophysical profile in predicting acute ascending infection in preterm
rupture of membranes before 32 weeks. Obstet Gynecol 2000; 96:201.
41. Del Valle GO, Joffe GM, Izquierdo LA, et al. The biophysical profile and the nonstress test: poor
predictors of chorioamnionitis and fetal infection in prolonged preterm premature rupture of membranes.
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42. Gauthier DW, Meyer WJ, Bieniarz A. Biophysical profile as a predictor of amniotic fluid culture results.
Obstet Gynecol 1992; 80:102.
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predicting preterm birth: a systematic review. Ultrasound Obstet Gynecol 2004; 24:94.
44. Tug N, Ayvaci H, Tarhan N, et al. Effects of short-term maternal fasting in the third trimester of
pregnancy on fetal biophysical profile and Doppler indices scores. Arch Gynecol Obstet 2011; 283:461.
45. Walach N. [Cancer in husband and wife--a report of 105 couples]. Harefuah 1991; 120:8.
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46. Manning FA, Morrison I, Lange IR, et al. Fetal biophysical profile scoring: selective use of the nonstress
test. Am J Obstet Gynecol 1987; 156:709.
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Database Syst Rev 2000; :CD000038.
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49. Nageotte MP, Towers CV, Asrat T, et al. The value of a negative antepartum test: contraction stress
test and modified biophysical profile. Obstet Gynecol 1994; 84:231.
50. Manning FA, Morrison I, Harman CR, et al. Fetal assessment based on fetal biophysical profile scoring:
experience in 19,221 referred high-risk pregnancies. II. An analysis of false-negative fetal deaths. Am J
Obstet Gynecol 1987; 157:880.
51. Manning FA. Fetal biophysical profile: a critical appraisal. Clin Obstet Gynecol 2002; 45:975.
52. Kaur S, Picconi JL, Chadha R, et al. Biophysical profile in the treatment of intrauterine growth-restricted
fetuses who weigh <1000 g. Am J Obstet Gynecol 2008; 199:264.e1.
53. American College of Obstetricians and Gynecologists. Antepartum fetal surveillance. ACOG practice
bulletin #9. American College of Obstetricians and Gynecologists, Washington, DC 1999.
54. Jansen AH, Chernick V. Fetal breathing and development of control of breathing. J Appl Physiol (1985)
1991; 70:1431.
55. Kurjak A, Andonotopo W, Hafner T, et al. Normal standards for fetal neurobehavioral developments-longitudinal quantification by four-dimensional sonography. J Perinat Med 2006; 34:56.
56. Manning FA. Dynamic ultrasound-based fetal assessment: the fetal biophysical profile score. Clin Obstet
Gynecol 1995; 38:26.
57. Kim SY, Khandelwal M, Gaughan JP, et al. Is the intrapartum biophysical profile useful? Obstet Gynecol
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GRAPHICS
Criteria for the biophysical profile test
Nonstress test: 2 points if reactive, defined as at least 2 episodes of FHR accelerations of at
least 15 bpm and at least 15 seconds duration from onset to return associated with fetal
movement within a 30-minute observation period.
Fetal breathing movements: 2 points if one or more episodes of rhythmic breathing
movements of 30 seconds within a 30-minute observation period.
Fetal tone: 2 points if one or more episodes of extension of a fetal extremity or fetal spine with
return to flexion.
Amniotic fluid volume: 2 points if a single pocket of fluid is present measuring at least 2 cm
by 1 cm. However, some clinicians use other criteria such as the amniotic fluid index.
Fetal movement: 2 points if three or more discrete body or limb movements within 30
minutes of observation. An episode of active continuous movement is counted as one
movement.

0 points are assigned for any criteria not met.


bpm: beats per minute; FHR: fetal heart rate.
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Relationship between biophysical profile score and perinatal


mortality and morbidity

A) The relationship betwen the fetal biophysical profile score (BPS) result and the
occurance of various perinatal morbidities. The incidence of fetal distress in labor (FD),
cesarean section for fetal distress (LSCS-FD), low 5-minute Apgar score, and venous cord
blood acidemia exhibit a very significant linear inverse relationship to test score. These
data are based on observations made in more than 26,000 high-risk fetuses. B) The
relationship betwen the fetal BPS and perinatal death (PNM), both gross and corrected for
fatal anomalies. Unlike morbidity, the mortality rate increases in an inverse exponential
fashion as the BPS score decreases.
Adapted from data published in: Manning, FA. Dynamic ultrasound-based fetal assessment: the fetal
biophysical profile score. Clin obstet Gynecol 1995; 38:26.
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The relationship between fetal umbilical venous pH


(2 SD) by cordocentesis and the fetal biophysical
profile score (BPS)

The correlation was linear, inverse, and very significant (R 2 0.912;


p<0.01).
Adapted from data published in: Manning FA. Dynamic ultrasound-based fetal
assessment: the fetal biophysical profile score. Clin obstet Gynecol 1995;
38:26.
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Inverse relationship between the last fetal


biophysical profile score (BPS) and cerebral palsy
(CP)

The relationship between the fetal biophysical profile score and CP is


inverse, exponential, and highly significant R 2 = -.096; P <.001.
Infants were followed for five years after birth.
Reproduced with permission from: Manning, FA, Harman, CR, Meticoglou, S, et
al. Fetal assessment by fetal biophysical profile score. IV: The incidence of
cerebral palsy among tested and non-tested perinates. Am J Obstet Gynecol
1998; 178:696. Copyright 1998 Mosby, Inc.
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Comparison of neonatal death rates as predicted


by gestational age and fetal death rates as
predicted by the fetal biophysical profile (BPS)

The red line represents the probability of neonatal death by


gestational age. For example, the risk of fetal death with a BPS of
2/10 is approximately 20 percent. Therefore, when the BPS is 2/10,
the risk of neonatal death is less than the risk of fetal death if the
gestational age is greater than 28 weeks. This graph should be used
for illustration only because the neonatal survival rate shown here
from the University of Manitoba may differ from other centers.
However, the predictive accuracy of the BPS is unlikely to vary among
centers.
Adapted from data published in: Manning, FA. Dynamic ultrasound-based fetal
assessment: the fetal biophysical profile score. Clin obstet Gynecol 1995;
38:26.
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Disclosures
Disclosures: Frank A Manning, MD Nothing to disclose. Charles J Lockwood, MD, MHCM Nothing
to disclose. Vanessa A Barss, MD, FACOG Employee of UpToDate, Inc. Equity Ownership/Stock
Options: Merck; Pfizer; Abbvie.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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