|
|
|
Go Back | PDF Download
Early-Onset Group B Strep Infection in Newborns: Prevention and Prophylaxis
Early-Onset Group B Strep Infection in Newborns: Prevention
and Prophylaxis
Clinical Bulletin No. 2 -- January 1997
INTRODUCTION
Group B streptococcus (GBS) is a beta-hemolytic gram-positive organism commonly
found in the intestinal tract. Ten to 30% of pregnant women are colonized with
GBS vaginally and/or rectally (1,2,3,4). Vaginal colonization is usually asymptomatic,
but GBS can cause urinary tract infections, amnionitis, endometritis and/or
wound infections. GBS can also result in severe infection in newborns. Early-onset
neonatal Group B streptococcal disease is most frequently evident as sepsis,
meningitis and/or pneumonia that appears within the first seven postnatal days.
At present, GBS is the leading cause of neonatal sepsis and one of the most
common causes of infectious morbidity and mortality in neonates (5). Because
the case fatality rate of early-onset GBS infection in neonates is 5%-22% (6),
a strategy for prevention of this disease is of vital importance.
EPIDEMIOLOGY
Among women who are colonized with GBS at the time of delivery, puerperal infections
develop in 2% to 22% (7,8,9). Women who have a cesarean birth, heavy vaginal
colonization, or an impairment of host defenses are at increased risk for developing
chorioamnionitis or postpartum endometritis (10,11).
Factors That Increase the Risk for GBS Sepsis
Prematurity and/or Low Birth Weight
Heavy Genital Inoculation
GBS Preterm Premature Rupture of Membranes
ROM >18 hours
Maternal Fever in Labor
Bacteriuria During Pregnancy
Previously Delivered Infant with GBS Sepsis
|
| Table 1 |
More attention has been paid to newborn infection secondary to GBS. Although
60-70% of newborns born to maternal carriers will be colonized at birth (12),
passively acquired immunity derived from maternal antibodies protects the majority
of healthy newborns. Thus only 1% of colonized newborns will develop symptomatic
disease (13). The actual incidence of early-onset GBS sepsis in this country
is between 0.6 and 3.7 per 1,000 live births. In the U.S., approximately 7,600
episodes and 310 deaths were reported in 1990 (14). Certain factors further
increase the incidence of neonatal sepsis (Table 1). Infants born prematurely
have a risk for developing early-onset GBS that is 8 times higher than those
born at term. Those born 18 hours or more after rupture of membranes are 8.6
times more likely to develop GBS disease. A mother that develops a temperature
$ 38C (100.4F) in labor has an 11.8 fold increase, and children born to women
who have GBS bacteriuria at any point in pregnancy have a 4.3 fold increase
in risk for early-onset GBS disease (6,12,15).
Table 1
Vertical transmission during labor is the primary route of infection for newborns.
Strategies for the prevention of neonatal disease focus on identifying those
mothers at risk and administering antibiotics to the mother during labor (or
after rupture of membranes) which reduces the incidence of early-onset GBS disease
as much as 30 fold (16). Postnatal administration of antibiotics to exposed
newborns appears to decrease the incidence of early-onset neonatal disease (17)
but will not effectively treat newborns who establish infection intrapartally.
Concern that postnatal administration of penicillin to all exposed infants will
suppress rather than prevent disease, coupled with the theoretical risk of facilitating
the development of penicillin resistant pathogens, has restrained providers
from adopting this strategy.
DIAGNOSIS OF GBS COLONIZATION
Accurate culture technique is critical to making the diagnosis of GBS carrier
status. In colonized women, GBS can be isolated with equal frequency in the
distal vagina and in the perianal area. Therefore, to maximize culture yields,
a swab must be taken both from the distal vagina (introitus) and from the rectal
area. Table 2 describes appropriate collection technique
Procedure for Collecting and Processing Clinical Specimens
for GBS Culture
- Obtain one or two swabs of the vaginal introitus and rectal area.
Speculums should not be used for culture collection. Swabs can be dacron
or cotton. Higher yields of GBS are obtained by women who self collect
the specimens prior to a prenatal visit when compared to those collected
by a clinician.*
- Place swabs in transport medium. The transport medium should be kept
at room temperature or under refrigeration. Collected cultures can be
stored for up to 4 days prior to being plated.
- Swabs should be inoculated together onto selective broth media and
cultured for 18-24 hours then subcultured onto sheep blood agar plates.
The sheep agar plates will be inspected at 24 hours for results. If
GBS is not identified at the initial reading, the culture will be maintained
and re-inspected in another 24 hours for a final analysis. Total culture
turn around time should average 48-72 hours after initial inoculation
on the sheep agar. Final turn around time will vary depending upon transport
time to the lab and laboratory schedules.
* personal communication S Hillier, GBS Consensus Conference March 1995.
|
| Table 2 |
Cervical cultures or vaginal cultures without perianal swabs have a significantly
decreased sensitivity (2,4). Equally important is the use of selective broth
medium. Selective broth with antimicrobials to suppress competing organisms
will increase the yield of GBS by as much as 50% (3). The cost of using selective
broth is no greater than that of using standard transport medium and an agar
plate (18). Because GBS is difficult to capture and grow, correct culture collection
technique and lab procedure is an important component of any GBS prevention
program.
Limitations of using prenatal culture results to diagnose GBS carrier status
in order to identify those women who should be treated with antibiotics in labor
are twofold. First, the time required to obtain culture results prohibits the
use of culturing at the onset of labor as a means to identify those who need
treatment before delivery. Second, vaginal colonization with GBS is transitory
or intermittent, and re-colonization frequently occurs spontaneously after treatment
(11,19,20). The woman colonized at 27 weeks may not be colonized at term and
conversely, the woman with a negative culture at 27 weeks may be colonized at
the time of delivery (1,21). Of those who are culture positive during the first
or second trimester, only 67% will be culture positive at delivery. Of those
who are culture negative earlier in pregnancy, 8% will be culture positive at
delivery (12).
Screening at the onset of labor with the use of rapid diagnostic techniques
is appealing but currently impractical. The rapid antigen detection tests available
have a sensitivity of 40-60% which precludes their use as a reliable test (18).
STRATEGIES FOR GBS PREVENTION AND PROPHYLAXIS
Several strategies based on varying combinations of antenatal culturing and/or
use of risk factors in order to select candidates for intrapartum treatment
have been suggested (6,10,22,23). Until recently the clinical pathways recommended
by the American College of Obstetricians and Gynecologists (ACOG) and the American
Academy of Pediatrics (AAP) were different, a situation that posed an obvious
dilemma for clinicians. In March of 1995, a consensus conference was held under
the auspices of the Centers for Disease Control and Prevention (CDC) with participants
from several professional organizations. The recommendations published by the
CDC in May of 1996 were drafted at this meeting and approved by ACOG as an acceptable
option in a Committee Opinion issued in June of 1996 (24). The AAP has not,
at the time of this publishing, responded to the CDC guidelines with a formal
statement.
A consistent and systematically applied strategy for GBS prophylaxis should
be adopted by midwifery practices and patients should be informed of the GBS
prevention strategy that has been chosen. Factors to consider in choosing a
plan include:
- Prevalence of GBS in the population
- Continuity of prenatal care
- Neonatal protocols used by collaborating pediatricians
- Availability of appropriate lab facilities, techniques and culture results.
Two acceptable practice strategies are outlined in Table 3.
Strategies for GBS Prevention and Prophylaxis
| |
Screening-Based Strategy
(CDC Guidelines, 1996)
See Figure 1
|
Risk Factors-Based Strategy
(ACOG Guideline, 1996)
See Figure 2 |
|
Protocol
|
Culture at 35-37 weeks. Offer intrapartum prophylaxis to all women with
positive cultures regardless of obstetrical risk status and to those in
labor without culture results.
Antepartum treatment not recommended unless the client has GBS bacteriuria
or PTL. |
Offer intrapartum treatment to all patients with risk factors. |
| Expected outcome based on decision analysis (23) |
26.7% of patients will be offered chemoprophylaxis during labor; 86% of
expected early-onset of GBS disease will be prevented. |
18.3% of patients will be offered chemoprophylaxis during labor; 68% of
expected early-onset GBS disease will be prevented.
|
| Table 3 |
Either a screening based strategy of late prenatal cultures and intrapartum
treatment of all culture positive women (Figure 1), or a risk factor based strategy
with treatment determined by risk factors only without the use of cultures,
(Figure 2) are acceptable management schemes for GBS prevention programs. Prenatal
cultures collected remote from term and antepartum treatment of positive cultures,
other than GBS bacteriuria, are not recommended.
GBS Prevention and Prophylaxis Culture-Based Strategy
|
Collect rector/vaginal swab for GBS culture at 35-37
weeks
When patient in labor:
|
| GBS negative |
Results unavailable |
GBS positive |
| No intraparum prophylaxis needed |
Offer intrapartum chemoprophylaxis: intraparum fever >38° C or
ROM >18 hours |
Offer intrapartum chemoprophylaxis |
GIVE INTRAPARTUM CHEMOPROPHYLAXIS REGARDLESS OF THIRD
TRIMESTER CULTURE RESULTS WHEN:
Previous infant with GBS disease
GBS bacteria present in pregnancy
Labor onset < 37 weeks of gestation (unless culture results are available)
Intrapartum fever ≥ 38° (100.4 °F)
Duration of ruptured membranes ≥ 18 hours
Adapted from MMWR 45 (RR-7:1-24) 1996
|
| Figure 1 |
GBS Prevention and Prophylaxis Risk Based Strategy
|
Risk Factors for GBS Disease:
Previous infant with GBS disease
GBS bacteriuria in present pregnancy
Labor < 37 weeks of gestation
ROM ≥18 hours
Intrapartum Fever ≥ 38°C
|
|
Risk Factor Not Present
Intrapartum chemoprophylaxis not needed
Adapted from MMWR 45 (RR-7:1-24)
|
1996 Risk Factors Present
Intrapartum chemoprophylaxis needed |
| Figure 2 |
|
Clinical Recommendations for all patients
- Choose one strategy and use it systematically.
- Patient education should be an integral part of the overall management
guidelines.
- Women with a prior affected infant should be offered intrapartum chemoprophylaxis.
- Women in labor prior to 37 weeks should be cultured and treated until the
culture results are available.
- Women with preterm premature rupture of membranes (PPROM) should be cultured
at the time PPROM is recognized. The decision to use presumptive treatment
until culture results are available versus expectant management followed by
antibiotic treatment when a positive culture is apparent varies between institutions.
- Women with GBS bacteriuria (regardless of culture count and regardless
of the gestational age at time of culture) should be treated at the time of
culture, considered GBS carriers at the time of labor, and offered intrapartum
chemoprophylaxis.
- Women with a fever $38EC in labor should be treated with an antibiotic
regimen that will cover both aerobic and anaerobic organisms regardless of
the GBS culture status or prophylaxis already started. Penicillin or Ampicillin
alone is not sufficient treatment for the anaerobic and gram-negative organisms
that frequently cause chorioamnionitis.
- Patient request for a GBS culture in settings that chose the risk-based
treatment should be honored following a discussion of the two available strategies,
including the risks and
benefits of treatment.
Intrapartum Chemoprophylaxis for GBS Prophylaxis*
First Choice:
Penicillin G, 5 mUs IV initially and then 2.5 mUs IV every 4 hours until
delivery
OR
Ampicillin, 2 g IV initially followed by 1 g IV every 4 hours until delivery
For patients who are allergic to PCN:
Clindamycin 900 mg IV every 8 hours until delivery
OR
Erythromycin 500 mg IV every 6 hours until delivery
* see Table 5 for a discussion of which antibiotic to choose
|
| Table 4 |
Which Antibiotic Should You Use?
| |
AMPICILLIN |
PENICILLIN |
| Route of Administration |
IV: recommended for intrapartum chemoprophylaxis
PO: If given PO for ruptured membranes without labor, Amoxicillin should
be used versus Ampicillin because absorption is greater with Amoxicillin.
Not recommended during labor. |
IV: recommended for intrapartum chemoprophylaxis
PO: Not as effective as Ampicillin via the PO route as it is broken down
easily by stomach acids and must be taken with meals to maintain efficacy.
Not recommended. |
| IV Administration during labor |
IV dose comes in pre-mixed vials in 500 mg or 1 gm or 2 gm that can be
attached (piggybacked) to existing IV. |
IV dose comes as 5 million units in powder form.
Must be diluted with at least 20 cc's of DW5% or normal saline.
Dosage desired is then withdrawn and injected into a second IV that is attached
(piggybacked) to a "main" line.
Stable shelf life (once mixed) for 1-7 days. |
| IV Dosage |
2 gms loading dose then
1 gm q 4 hours until delivery. |
5 mil units loading dose then
2.5 mil units q 4 hours until delivery. |
| Cost |
Inexpensive.
No real difference between the cost of the drugs. |
Inexpensive .
May incur a higher cost relative to Ampicillin if time and materials necessary
to mix and dilute the drug is considered. |
| Pt Acceptance |
Readily accepted: can be given quickly. |
The potassium in Penicillin G can be irritating to the veins. It must
be given slowly over 20-30 minutes. |
Antimicrobial
Activity |
Ampicillin has a broader spectrum of antimicrobial activity. Widespread
use may lead to the development of resistant organisms. |
GBS is very sensitive to penicillin. Incidence of GBS that is resistant
to PCN is virtually negligible. Due to the narrower spectrum of activity,
this may be the preferable drug. |
| Table 5 |
COMMENTARY
Neither of the recommended strategies have been subjected to randomized controlled
trials or comparative analysis. The guidelines suggested by both the CDC and
ACOG for the prevention of GBS prophylaxis are based upon prevalence of the
organism, incidence and virulence of this disease and the assumption that either
strategy (by decreasing the incidence of neonatal illness) will lower the morbidity
and cost associated with early-onset GBS disease.
Untoward side effects of any intervention must be considered. Widespread use
of penicillin agents could lead to both the emergence of resistant organisms
and/or to an increase in maternal allergic reactions. Allergic reactions to
antibiotic agents, neonatal costs secondary to institutional policies for neonatal
care when antibiotics have been given intrapartally and the incidence of protocol
failures have not been evaluated to date.
Expectant management of premature rupture of membranes at term without labor
poses special considerations. The CDC and ACOG guidelines do not address the
issue of oral antibiotics for women not in labor. Penicillin agents achieve
blood levels quickly (25), can be found in vaginal secretions following oral
intake and are known to eradicate or suppress GBS vaginal colonization during
treatment (26). Studies evaluating the use of oral agents have shown them to
be ineffective in eradicating vaginal colonization over time, presumably because
the recolonization rates are high (27,28).
The ability of oral agents to eradicate or suppress GBS colonization within
amniotic fluid in the presence of ruptured membranes has not been evaluated.
Oral agents are commonly used for women who are not in labor but at risk for
GBS infection secondary to ROM >18 hours. If the choice is made to use oral
agents, Amoxicillin 500 mg TID will be more efficacious than Penicillin (PCN
VK) or Ampicillin because Amoxicillin is better absorbed. Pen VK is not recommended,
as this agent breaks down easily in the presence of stomach acids and must be
taken with meals to maintain efficacy. The antibiotic should be continued during
labor but changed to an intravenous route because absorption from the stomach
is not assured in laboring women (25). See Table 6 for one strategy for prophylaxis
with PROM at term. This strategy should not be used in the presence of other
known risk factors.
GBS Prophylaxis in Patients with PROM at Term and
No Labor During Expectant Management
Regardless of prophylaxis strategy used:
Start Amoxicillin PO 500 mg TID at 18 hours of ROM*
For patients allergic to PCN: Clindamycin PO 300 mg q6
hrs*
Instruct patients to take temp q 4-6 hours while awake
and report any elevation >37.8EC
Change to IV chemoprophylaxis when patient in active labor
* Plan based on presumed effectiveness in population at low risk for
invasive GBS disease as there is no data confirming the effectiveness
of oral agents in eradicating GBS colonization in the presence of ruptured
membranes
|
| Table 6 |
There are a few situations in which a woman might be at higher risk for GBS
related morbidity, yet there is insufficient data to recommend a single course
of action. The risk for GBS related morbidity in immunocompromised women or
in known GBS carriers who have an elective cesarean section is not known. Management
strategies for these women must be individualized, taking into account the general
infection profiles of the populations served.
SUMMARY
A systematically applied strategy for selecting candidates for intrapartum
chemoprophylaxis to decrease the incidence of early-onset GBS disease is an
important component of midwifery care. The strategy that an individual practice
chooses to follow will depend upon multiple factors including but not limited
to: the prevalence of GBS colonization in the prenatal population, ability of
clients to return for regular prenatal visits, availability of laboratory services,
choices made for screening and treatment by collaborating obstetric and pediatric
colleagues, place of birth and logistics required for protocol compliance.
REFERENCES
- Regan JA, Klebanoff MA, Nugent RP. The epidemiology of group B streptococcal
colonization in pregnancy. Vaginal Infections and Prematurity Study Group.
Obstetrics and Gynecology 1991;77:604-610.
- Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and vaginal carriage of
group B streptococci during pregnancy. Journal of Infectious Diseases 1982;145:794-799.
- Baker CJ, Edwards MS. Group B streptococcal infections. In: Remington JS,
Klein JO, eds. Infectious diseases of the fetus and newborn infant. 4th edition.
Philadelphia: WB Saunders, 980-1054, 1995.
- Boyer KM, Gadzala CA, Burd LI, Fisher DE, Paton JB, Gotoff SP. Selective
intrapartum chemoprophylaxis of neonatal group B streptococcal early-onset
disease. I. Epidemiologic rationale. Journal of Infectious Diseases 1983;148:795-801.
- Ohlsson A, Myhr TL. Intrapartum chemoprophylaxis of perinatal group B streptococcal
infections: a critical review of randomized controlled trials. American Journal
of Obstetrics and Gynecology 1994;170:910-917.
- Centers for Disease Control and Prevention. Prevention of perinatal group
B streptococcal disease: a public health perspective. MMWR 45 (RR-7):1-24,
1996.
- Clay, LS. Group B streptococcus in the perinatal period: a review. Journal
of Nurse-Midwifery 1996;41:355-363.
- Katz VL. Management of group B streptococcal disease in pregnancy. Clinical
Obstetrics and Gynecology 1993;36:832-842.
- Boyer KM, Gotoff SP. Prevention of early onset neonatal group B streptococcal
disease with selective intrapartum chemoprophylaxis. New England Journal of
Medicine 1986;314:1665-1669.
- American College of Obstetricians and Gynecologists. Group B streptococcal
infections in pregnancy. American College of Obstetricians and Gynecologists
Technical Bulletin no. 170, July 1992.
- Bobbitt JR, Damato JD, Sakakini J Jr. Perinatal complications in group
B streptococcal carriers: a longitudinal study of prenatal patients. American
Journal of Obstetrics and Gynecology 1985;151:711-717.
- Boyer KM, Gotoff SP. Antimicrobial prophylaxis of neonatal group B streptococcal
sepsis. Clinics in Perinatology 1988;15:831-850.
- 13. Noya FJ, Baker CJ. Prevention of group B streptococcal infection. Infectious
Disease Clinics of North America 1992;6:41-55.
- Centers for Disease Control and Prevention. Prevention of group B streptococcal
diseases: a public health perspective, notice. Federal Register, 59(240)64764-64773,
Dec. 15, 1994.
- Schuchat A, Deaver-Robinson K, Plikaylis BO, Zangwill KM, Mohle-Boetani
J, Wenger JD. Multistate case-control study of maternal risk factors for neonatal
group B streptococcal disease. Pediatric Infectious Disease Journal 1994;13:623-629.
- Allen UD, Navas L, King SM. Effectiveness of intrapartum penicillin prophylaxis
in preventing early onset group B streptococcal infection: results of a meta-analysis.
Canadian Medical Association Journal 1993;149:1659-1665.
- Siegel JD, McCracken GH Jr, Threlkeld N, Milvenan B, Rosenfeld CR. Single
dose penicillin prophylaxis against neonatal group B streptococcal infections.
A controlled trial in 18,738 newborn infants. New England Journal of Medicine
1980;303:769-775.
- Division of Communicable Disease Control. Summary proceedings of the group
B streptococcal disease prevention consensus conference. California Department
of Health Services, Berkeley, California, March 10, 1995.
- Yancey MK, Duff P, Kubilis P, Clark P, Frentzen BH. Risk factors for neonatal
sepsis. Obstetrics and Gynecology 1996;87:188-94.
- Lewin EB, Amstey MS. Natural history of group B streptococcus colonization
and its therapy during pregnancy. American Journal of Obstetrics and Gynecology
1981;139:512-515.
- Yow MD, Leeds LJ, Thompson PK, Mason ED Jr, Clark DJ, Beachler CW. The
natural history of group B streptococcal colonization in the pregnant woman
and her offspring. I. Colonization studies. American Journal of Obstetrics
and Gynecology 1980;137:34-38.
- American Academy of Pediatrics Committee on Infectious Diseases and Committee
on Fetus and Newborn. Guidelines for prevention of group B streptococcal (GBS)
infection by chemoprophylaxis. Pediatrics 1992;90:775-778.
- Rouse DJ, Goldenberg RL, Cliver SP, Cutter GR, Mennemeyer ST, Fargason
CA Jr. Strategies for the prevention of early-onset neonatal group B streptococcal
sepsis: a decision analysis. Obstetrics and Gynecology 1994;83:483-494.
- American College of Obstetricians and Gynecologists. Prevention of early
onset group B streptococcal disease in newborns. American College of Obstetricians
and Gynecologists Committee Opinion no. 173, June 1996.
- Sweet RL, Gibbs RS. Infectious diseases of the female genital tract. Williams
and Wilkins; Baltimore, Maryland, 1990.
- Merenstein GB. Group B beta-hemolytic streptococcus: randomized controlled
treatment study at term. Obstetrics and Gynecology 1980;55:315-318.
- Hall RT, Barnes W, Krishnan L, Harris DJ, Rhodes PG, Fayez J, Miller GL.
Antibiotic treatment of parturient women colonized with group B streptococci.
American Journal of Obstetrics and Gynecology 1976;124:630-634.
- Gardner SE. Failure of penicillin to eradicate group B streptococcal colonization
in the pregnant woman. A couple study. American Journal of Obstetrics and
Gynecology 1979;135:1062-1065.
ADDITIONAL REFERENCES
Agnoli FL. Group B streptococcus: perinatal considerations. Journal of Family
Practice 1994;39:171-177.
Capeless E. Editorial on clinical obstetrics. ACOG Current Journal Review 1994;7:16.
Coleman RT, Sherer DM, Maniscalco WM. Prevention of neonatal group B streptococcal
infections: advances in maternal vaccine development. Obstetrics and Gynecology
1992;80:301-309.
Farley MM, Harvey RC, Stull T, Smith JD, Schuchat A, Wenger JD, Stephens DS.
A population-based assessment of invasive disease due to group B streptococcus
in nonpregnant adults. New England Journal of Medicine 1993;328:1807-1811.
Garland SM, Fliegner JR. Group B streptococcus (GBS) and neonatal infections:
the case for intrapartum chemoprophylaxis. Australia and New Zealand Journal
of Obstetrics and Gynecology 1991;31:119-122.
Gigante J, Hickson GB, Entman SS, Oquist NL. Universal screening for group
B streptococcus: recommendations and obstetricians' practice decisions. Obstetrics
and Gynecology 1995;85:440-443..
Greenspoon JS, Wilcox JG, Kirschbaum TH. Group B streptococcus: the effectiveness
of screening and chemoprophylaxis. Obstetrical and Gynecological Survey 1991;46:499-508.
Hueston WJ. Preventing group B streptococcal infection in newborns. American
Family Physician 1991;43:487-492.
Landon MB, Harger J, McNellis D, Mercer B, Thom EA. Prevention of neonatal
group B streptococcal infection. Obstetrics and Gynecology 1994;84:460-462.
Mohle-Boetani JC, Schuchat A, Plikaylis BD, Smith JD, Broome CV. Comparison
of prevention strategies for neonatal group B streptococcal infection: a population-based
economic analysis. JAMA 1993;270:1442-1448.
Pylipow M, Gaddis M, Kinney JS. Selective intrapartum prophylaxis for group
B streptococcus colonization: management and outcome of newborns. Pediatrics
1994;93:631-635.
Siegel JD, Cushion NB. Prevention of early-onset group B streptococcal disease:
another look at single dose penicillin at birth. Obstetrics and Gynecology 1996;87:692-697.
Yancey MK, Duff P. An analysis of the cost-effectiveness of selected protocols
for the prevention of neonatal group B streptococcal infection. Obstetrics and
Gynecology 1994;83:367-371.
Zangwill KM, Schuchat A, Wenger JD. Group B streptococcal disease in the United
States, 1990: report from a multistate active surveillance system. CDC Surveillance
Summaries 1992; MMWR 41(SS-6):25-32.
CLINICAL BULLETIN DISCLAIMER
This Clinical Bulletin was developed under the direction of the Division of
Standards and Practice, Section on Clinical Standards and Documentation of the
American College of Nurse-Midwives as an educational aid to members of the College.
The Clinical Bulletin is not intended to define a standard of care, to dictate
an exclusive course of management, or to substitute for individual professional
judgement. It presents recognized methods and techniques of clinical practice
which nurse-midwives may consider incorporating into their practices. The needs
of an individual patient, or the resources and limitations of an institution
or type of practice may appropriately lead to variations in clinical care.
|