The risk of fetal infection hematogenously spread from the mother is much less common during labor. This is partly related to the physiologic, mechanical, and immunologic barriers provided by the placenta. However, rarely, organisms such as staphylococci, streptococci, or pneumococci may infect the pregnant woman, resulting in a significant degree of maternal bacteremia. This then reaches the placenta and occasionally crosses to the fetus. These patients may present with classical symptoms of maternal fever, tachycardia, malaise, and uterine tenderness. The fetus may show evidence of tachycardia. Prompt treatment with antibiotics should be initiated, and delivery should be planned accordingly (see section “Chorioamnionitis”). Perhaps the most relevant perinatal hematogenous infection is listeriosis. Although rare (12 per 100,000 in pregnancy), this gram-positive bacillus has severe consequences for the fetus and newborn. Maternal listeriosis is associated with increased risks of fetal demise, preterm delivery, neonatal sepsis, meningitis, pneumonia, and death. The perinatal mortality rate varies between 27 and 33 percent.
Listeria monocytogenes has a particular predilection for pregnant women, who are 20 times more likely to become infected compared with the general population. The organism is acquired by the mother through contaminated water and food such as milk, cheese, chicken, coleslaw, undercooked meat, fruits, and vegetables. It can then spread transplacentally to the fetus. Mothers infected with Listeria are often asymptomatic or present with nonspecific flu-like symptoms. A high index of suspicion is thus necessary.
The predilection for pregnant women is well illustrated by a 1981 Canadian outbreak, which affected 100 individuals, of whom 34 were pregnant. In this group were nine stillbirths, 23 neonatal infections, and only two live healthy births.
Confirmation of diagnosis can be done reliably by cultures of amniotic fluid, meconium, membranes, placenta, blood, or spinal fluid. Placental pathologic examination may reveal the presence of acute villitis and of multiple microabscesses.
Because Listeria is an intracellular organism and can resemble diphtheroids, pneumococci, or Hemophilus, Gram stains are helpful clinically only one-third of the time. Cultures of the vagina or stools are not recommended because women can be normal carriers without being infected. Serologic test of listeriosis are also not recommended. Therefore, if a pregnant woman presents with a clinical scenario suggestive of listeriosis, blood cultures are recommended.
The antibiotics recommended for the treatment of listeriosis must be given in high dose to cross the placenta and to penetrate intracellularly. These include ampicillin as a first line and erythromycin as a second line. In women allergic to penicillins, trimethoprim–sulfamethoxazole has been effective. Therapy should continue for 7 to 14 days (Table 34-2).
TABLE 34-2:RECOMMENDED TREATMENT APPROACHES MATERNAL LISTERIOSIS ||Download (.pdf) TABLE 34-2: RECOMMENDED TREATMENT APPROACHES MATERNAL LISTERIOSIS
Group B streptococcus is a gram-positive organism responsible for infections mostly in infants and pregnant women. Maternal colonization of the lower gastrointestinal (GI) and urinary tracts with GBS occurs in 15 to 30 percent of women. As such, this organism is considered to be part of the “normal” flora of the vagina. However, GBS also represents one of the most important causes of neonatal mortality and morbidity, with a case fatality rate that can be as high as 50 percent. Two types of neonatal infection can occur: early onset or late onset. Early-onset disease (EOD) manifests itself in the first 7 days of life and is the result of transmission from mother to fetus. The incidence of this serious disease is reported as 0.3 per 1000 infants.
Risk Factors for Early-Onset Disease
Maternal colonization: The most important risk factors for EOD is maternal colonization. A pregnant woman with positive GBS vaginal or rectal culture near term has a 25-fold increased risk of having an infant with EOD. The GI tract serves as the reservoir for GBS, and it is noteworthy that colonization during pregnancy can be transient or persistent. In addition, the extent of colonization also plays a role in disease transmission, with heavy colonization representing an even higher risk to the infant. Finally, the presence of GBS in the urine at any time during pregnancy also carries a much higher risk of EOD
Gestational age less than 37 completed weeks
Prolonged duration of membrane rupture (12-18 hours)
Intrapartum temperature more than 38°C
Previous delivery of an infant with invasive GBS disease
Young maternal age, black race, and low maternal levels of GBS-specific anticapsular antibody
All pregnant women should be offered screening with a rectovaginal swab at around 36 weeks’ gestation. The negative predictive value of GBS cultures performed 5 weeks or less before delivery is 95 to 98 percent. However, because of a decrease in negative predictive value, the clinical utility decreases when a prenatal culture is performed more than 5 weeks before delivery.
Intrapartum treatment of all women with a positive GBS culture or unscreened women with risk factors as described in Table 34-3 should be initiated at the onset of labor or rupture of membranes.
TABLE 34-3:RISK FACTORS REQUIRING ANTIBIOTIC TREATMENT INTRAPARTUM OR AT THE ONSET OF MEMBRANE RUPTURE FOR THE PREVENTION OF GROUP B STREPTOCOCCUS EARLY-ONSET DISEASE ||Download (.pdf) TABLE 34-3: RISK FACTORS REQUIRING ANTIBIOTIC TREATMENT INTRAPARTUM OR AT THE ONSET OF MEMBRANE RUPTURE FOR THE PREVENTION OF GROUP B STREPTOCOCCUS EARLY-ONSET DISEASE
|Women with a positive rectovaginal culture at 35 to 37 weeksa |
|Women with a previously affected infant |
|Women with GBS bacteriuria at any time during pregnancy (regardless of the amount of colony-forming units present) |
|Women at less than 37 weeks’ gestation unless a negative swab has been obtained in the 5 weeks before presentation |
|Women with intrapartum fever (>38°C) |
|Women with an unknown GBS status and either known GBS positive status in a prior pregnancy or ruptured membranes at term for greater than 18 hours or intrapartum fever |
Recommended antibiotics are listed in Table 34-4. Although both ampicillin and penicillin are efficacious against GBS, penicillin has a narrower spectrum and is the antibiotic of choice. In the case of low-risk penicillin allergy, cephazolins are considered appropriate. Otherwise, clindamycin or erythromycin is recommended for those at high risk of anaphylaxis to penicillins.
TABLE 34-4:ANTIBIOTIC DOSAGES FOR THE PREVENTION OF EARLY-ONSET DISEASE DUE TO GROUP B STREPTOCOCCUS ||Download (.pdf) TABLE 34-4: ANTIBIOTIC DOSAGES FOR THE PREVENTION OF EARLY-ONSET DISEASE DUE TO GROUP B STREPTOCOCCUS
|Penicillin G 5 million units IV; then 2.5 million every 4 hours |
|Penicillin-allergic, low risk of anaphylaxis: cefazolin 2 g IV; then 1 g every 8 hours |
|Penicillin allergic and at risk of anaphylaxis: clindamycin 900 mg IV every 8 hours or erythromycin 500 mg IV every 6 hours |
|In rare cases, GBS resistance may occur; vancomycin is then the antibiotic of choice |
Chorioamnionitis is an infection of the chorion and amnion, which can progress to involve the umbilical cord, placenta, and fetus itself. It is characterized by the infiltration of these membranes by neutrophil polymorphs, which starts at the interface between the decidua and chorion at the level of the os. The most common microorganisms involved include Ureaplasma spp., Mycoplasma spp., enterococci, streptococci, coliforms, and staphylococci.
Intrapartum risk factors for the development of chorioamnionitis include multiple examinations during labor, prolonged labor, nulliparity, bacterial vaginosis or group B streptococcal (GBS) colonization, meconium, use of internal monitoring, and epidural anesthesia. Finally, alcohol use and cigarette smoking are predisposing factors.
Frequently associated with preterm prelabor rupture of the membranes (PPROM) and preterm labor (PTL), chorioamnionitis is often suspected as playing a causative role in these pathologies. Ascension of microorganisms via the genital tract to the membranes results in the production and release of proinflammatory cytokines and chemokines, which in turn may weaken the membranes and lead to PPROM. In addition, the release of prostaglandins associated with the process of inflammation may induce cervical changes and result in preterm delivery. Inflammation of the amniotic cavity, independent of the presence of positive cultures, is associated with a higher risk of preterm delivery, chorioamnionitis, low APGAR scores, admission to the neonatal intensive care unit, and low birth weight.
In addition, exposure of a fetus to such an environment can lead to the development of an intense inflammatory reaction in the fetal compartment itself. This is referred to as fetal inflammatory response syndrome (FIRS), which is characterized by elevated levels of interleukin-6 (IL-6) in the fetal blood and by the possibility of multiorgan damage, including effects on the hematopoietic system, lungs, brain, heart, kidneys, and adrenal glands. Long-term sequelae for these newborns include bronchopulmonary dysplasia and cerebral palsy. A meta-analysis examining the association between chorioamnionitis and cerebral palsy reported a 140 percent increased risk for fetuses exposed to clinical chorioamnionitis and an 80 percent increased risk for a histologic but asymptomatic chorioamnionitis.
Chorioamnionitis can present with maternal and fetal signs or be subclinical. Maternal fever (one reading of ≥39.0°C or two readings of ≥38.0°C) is often associated with general malaise and may present with uterine contractions. In addition, the presence of a tender uterus and a foul-smelling discharge help strengthen the diagnosis. Associated with this are maternal and fetal tachycardia (>100 and >160 beats/min, respectively) and a nonreassuring tracing. Although these symptoms and signs can raise the possibility of chorioamnionitis, they are neither sensitive nor specific, and as such, an overall evaluation of the risk factors present and the clinical presentation are both important.
Laboratory investigations in cases of suspected chorioamnionitis are based on the presence of a maternal response and the presence of inflammation and of an invading microorganism. As such, an evaluation of maternal leukocytosis or a left shift may help the clinician but remain nonspecific, particularly in the context of labor, which may be associated with increases in maternal leukocyte counts because of dehydration or the administration of steroids.
C-reactive protein (CRP), an acute phase reactant, moderately predicts histologic chorioamnionitis. In the presence of maternal fever and tachycardia, a maternal blood culture, although not useful in diagnosing chorioamnionitis itself, may be helpful in certain complex cases for selection of antibiotics.
Finally, the evaluation of amniotic fluid has been the scope of much research in the hope to uncover a specific and sensitive diagnostic strategy. Various rapid testing methodologies have been evaluated, including Gram stain (98% specificity), glucose levels (74% specificity), and white cell count. The need for an amniocentesis has severely limited their use clinically.
Although levels of cytokines (especially IL-6) and MMPs (especially MMP-8) were consistently found to be higher in the amniotic fluid of women with a chorioamnionitis and their sensitivities and specificities were acceptable, they are only currently available in research settings.
Amniotic fluid cultures remain the “gold standard” but the time required for a result is often too long in a clinical setting, where rapid decisions regarding delivery must be made. In addition, recent data are now revealing the presence of unsuspected microorganisms, which would not necessarily be identified on culture. Innovative technologies such as proteomics may assist the clinician in this context in the future.
Upon diagnosis of chorioamnionitis, supportive measures for both the mother and fetus must be put in place and a plan for delivery initiated. Given the possible maternal risks of sepsis, attention to intravenous (IV) fluids is essential. A Foley catheter may be useful to assess fluid balance. Monitoring of vital signs is crucial, with prompt attention paid to hypotension and tachycardia. Oxygen saturation should be evaluated regularly and maintained at 95 percent and above. Antipyretics should be administered to normalize maternal temperature given the association between maternal fever and adverse neonatal outcomes, including encephalopathy. Electronic fetal monitoring should be implemented.
The mode of delivery in these cases should be dictated by obstetrical determinants because cesarean delivery has not been shown to improve outcomes for either the mother or the fetus upon initiation of appropriate antibiotic use.
Parenteral antibiotics must be administered promptly and their choice based on the most commonly found microorganisms. In that context, it is suggested to treat with a combination of ampicillin 2 g IV every 6 hours (or vancomycin 1 g IV every 12 hours for those with allergy to penicillins) and gentamicin 1.5 mg/kg every 8 hours. Although this particular administration of gentamicin is widely used, a once-daily dosage approach (one dose of 5 mg/kg) has been found to be as efficacious in treating the infection.
Finally, if better anaerobic coverage is desired (e.g., if a cesarean section is planned), the addition of clindamycin (900 mg IV every 8 hours) or metronidazole (500 mg IV every 8 hours) may be wise.
The duration of treatment generally is limited. In the case of a vaginal delivery, antibiotics can usually be discontinued at delivery or after one postpartum dose has been administered. However, in the context of a cesarean delivery, most clinicians continue antibiotics until the patient has been afebrile for a period of 24 hours.
Antibiotic Prophylaxis to Prevent Perinatal Infections
The most important risk factor is delivery by cesarean section. Women delivered by cesarean section are 20 times more likely to suffer a postpartum infection compared with those delivered vaginally. These infections include endomyometritis, wound infection, and infection of the urinary tract, pelvic abscess, septic pelvic thrombophlebitis, pneumonia, and sepsis.
To reduce this risk, a significant number of studies have investigated the use of prophylactic antibiotics before performing a cesarean section. The evidence suggests that there was a significantly decreased risk of endometritis and wound infections when prophylactic antibiotics are administered to women undergoing emergency or elective cesarean sections. These data with others have led to recommendations by SOGC and ACOG that all women delivered by cesarean section should be offered prophylactic antibiotics (Table 34-5). Administration of antibiotics does not reduce the risk of subsequent infections in operative vaginal deliveries, and there are insufficient data to recommend for or against antibiotic prophylaxis in cases of manual removal of the placenta and postpartum dilatation and curettage. However, antibiotics may decrease perineal wound complications after a third- or fourth-degree perineal laceration.
TABLE 34-5:SUMMARY OF RECOMMENDATIONS FOR PROPHYLACTIC ANTIBIOTICS ||Download (.pdf) TABLE 34-5: SUMMARY OF RECOMMENDATIONS FOR PROPHYLACTIC ANTIBIOTICS
Most studies have examined the use of cephalosporins in the context of prophylaxis at cesarean section. With adequate coverage of gram-positive and modest coverage of gram-negative organisms, this class of agents carries a spectrum that is narrow enough to minimize the risk of developing resistance. In women with penicillin allergy, clindamycin or erythromycin has been suggested.
Finally, cefotetan or cefoxitin is recommended for women with third- or fourth-degree perineal tears. Table 34-6 summarizes the SOGC recommendations regarding antibiotic prophylaxis and obstetric procedures.
TABLE 34-6:ANTIBIOTIC PROPHYLAXIS: RECOMMENDATIONS FROM THE SOCIETY OF OBSTETRICIANS AND GYNAECOLOGISTS OF CANADA ||Download (.pdf) TABLE 34-6: ANTIBIOTIC PROPHYLAXIS: RECOMMENDATIONS FROM THE SOCIETY OF OBSTETRICIANS AND GYNAECOLOGISTS OF CANADA
Sepsis is a significant cause of maternal morbidity and mortality. The World Health Organization estimates that sepsis accounts for 10 percent of maternal deaths and is the third most common cause of direct maternal deaths globally. As with other causes of maternal mortality, these numbers represent the tip of the iceberg with many more cases resulting in severe maternal morbidity.
The UK Confidential Enquiry into Maternal Deaths and Morbidity (2009-2012) found that delayed recognition and management was a contributing factor in 63 percent of maternal deaths from sepsis. Data from other jurisdictions suggest that missed management opportunities likely contribute to maternal sepsis deaths globally. The physical, social, and opportunity costs associated with mortality from maternal sepsis, combined with the opportunities for prevention, have made the management of maternal sepsis a global priority.
The Third International Consensus (Sepsis-3) definition for sepsis is “life threatening organ dysfunction caused by a dysregulated host response to infection.” The updated consensus has not included severe sepsis as a discrete entity. Septic shock occurs when sepsis results in persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher, despite adequate volume resuscitation. The World Health Organization has used similar wording when they defined maternal sepsis as “a life-threatening condition defined as organ dysfunction caused by an infection during pregnancy, delivery, puerperium, or after an abortion.”
Organ dysfunction is identified using the sequential organ failure assessment (SOFA) score. An acute change in the SOFA score by 2 or more points consequent to infection is used. Importantly, the SOFA score was designed and validated as a predictor of mortality and not a diagnostic tool or guide for dynamic medical management.
The quick sequential organ failure assessment (qSOFA) was introduced by Sepsis-3 as a simplified version of SOFA. It was introduced as a more practical bedside assessment tool for patients with infection to predict those at high risk of a poor outcome. Only three variables are used: Glasgow Coma Score <15, a respiratory rate >22/minute, and a systolic blood pressure <100 mm Hg. A patient with two of these variables is considered higher risk for poor outcomes.
A detailed description of the pathophysiology of sepsis is beyond the scope of this chapter. It is important to appreciate however that sepsis occurs when local infection spreads beyond its initial site. A complex systemic inflammatory response acts at a molecular, cellular, and multiorgan level. Examples of organ and system dysfunction include altered mental status, hypotension, tachycardia, edema, hypoxemia, oliguria, hyperglycemia, elevated serum lactate, and coagulation abnormalities.
Infectious Causes in Pregnancy
Infectious causes of sepsis can be divided into either obstetric or nonobstetric categories. Obstetric and genital tract causes are more likely to occur in the intrapartum and postpartum period. Nonobstetric causes can occur at any time during pregnancy. Common infectious causes of sepsis can be seen in Table 34-7.
TABLE 34-7:COMMON CAUSES OF SEPSIS IN PREGNANCY ||Download (.pdf) TABLE 34-7: COMMON CAUSES OF SEPSIS IN PREGNANCY
|Obstetric Causes || |
|Nonobstetric Causes || |
The most common pathogens isolated in maternal sepsis are group A streptococcus, group B streptococcus, and Escherichia coli. However, many organisms including gram-negative bacteria and anaerobic bacteria have been reported depending on the primary site of infection. Mixed infections are also possible.
Sepsis is not a singular disease state, and, despite its prevalence, there is currently no diagnostic test to confirm a diagnosis of sepsis. One needs to rely on clinical signs and symptoms, and laboratory investigations that signify organ dysfunction when there is suspected or confirmed infection.
Early warning systems (EWS) have been used for many years in nonpregnant patients. These systems use standard patient variables such as heart rate, blood pressure, respiratory rate, temperature, urine output, level of consciousness, and oxygen saturation, which are tracked over time. The number of variables that deviate from normal, combined with the degree of abnormality for each variable, trigger the need for a detailed patient assessment and a proportional escalation in management.
Standardized EWS tools were not designed for, or validated for the pregnant population. Physiological changes of normal pregnancy and labor can overlap with those of evolving infection and sepsis. This can lead to diagnostic uncertainty and delayed management. The modified early obstetric warning system (MEOWS) was designed as a tool to overcome these limitations.
The MEOWS has been in widespread use for many years. The 2003-2005 report on the confidential enquiries into maternal deaths in the United Kingdom recommended the routine use of a national obstetric early warning chart for all obstetric patients to assist in the timely recognition, treatment, and referral of women who have, or are developing, critical illness. An example of a MEOWS chart can be seen in Table 34-8. The MEOWS is not intended to replace clinical decision-making. Rather it determines the urgency of assessment, and prompts an escalation of care proportional to the risk of critical illness.
TABLE 34-8:MODIFIED EARLY OBSTETRIC WARNING SYSTEM ||Download (.pdf) TABLE 34-8: MODIFIED EARLY OBSTETRIC WARNING SYSTEM
|Physiological Parameter ||3 ||2 ||1 ||0 ||1 ||2 ||3 |
|Respiratory Rate ||<12 || || ||12-20 || ||21-25 ||>25 |
|Oxygen Saturations ||<92 ||92-95 || ||>95 || || || |
|Any Supplemental Oxygen || ||Yes || ||No || || || |
|Temperature ||<36 || || ||36.1-37.2 || ||37.3-37.7 ||>37.7 |
|Systolic BP ||<90 || || ||90-140 ||141-150 ||151-160 ||>160 |
|Diastolic BP || || || ||60-90 ||91-100 ||101-110 ||>110 |
|Heart Rate ||<50 ||50-60 || ||61-100 ||101-110 ||111-120 ||>120 |
|Level of Consciousness || || || ||A || || ||V, P, or U |
|Pain (excluding labor) || || || ||Normal || || ||Abnormal |
|Discharge / Lochia || || || ||Normal || || ||Abnormal |
|Proteinurea || || || || || ||+ ||++ > |
Sepsis is a medical emergency. Speed of symptom recognition, initiation of appropriate investigations, fluid resuscitation, and antimicrobial therapy are the cornerstones of sepsis management. A linear relationship has been found between the risk of mortality and delays in initiation of management, particularly appropriate antimicrobial therapy. Once sepsis has progressed to septic shock, then the hospital mortality is in excess of 40 percent.
The Surviving Sepsis Campaign introduced an update to their sepsis care bundle in 2018. The updated recommendation introduced a 1-hour bundle. Elements of this bundle can be seen in Table 34-9. This update reiterates the high degree of importance placed on prompt and comprehensive initial management. The first step, however, is thinking that sepsis may be a possibility. One cannot wait for confirmation of an infective organism or source before starting management.
TABLE 34-9:1-HOUR BUNDLE FROM SURVIVING SEPSIS CAMPAIGN ||Download (.pdf) TABLE 34-9: 1-HOUR BUNDLE FROM SURVIVING SEPSIS CAMPAIGN
Measure serum lactate level. Remeasure if initial lactate is >2 mmol/L
Obtain blood cultures prior to administration of antibiotics
Administer broad-spectrum antibiotics
Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate >4 mmol/L
Begin vasopressors if patient is hypotensive during or after fluid resuscitation to maintain mean arterial pressure >65 mm Hg
Lactate is a biproduct of anaerobic metabolism and is produced when there is a switch from using oxygen to using the glycolytic pathway for energy. Raised serum lactate can be used as a surrogate marker for tissue hypoperfusion. In patients with sepsis, a correlation has been found between increasing levels of serum lactate and mortality. Lactate levels can be used to guide fluid resuscitation and, if abnormal, should be remeasured every 2-4 hours.
Identifying the responsible pathogen is key to guiding appropriate antimicrobial therapy. As soon as infection is considered as a possible cause for organ dysfunction, blood cultures should be obtained. If an obvious source of infection is present, then samples from this site should also be collected. Sterilization of cultured organisms can occur very quickly after the first dose of an antibiotic. Ideally, cultures should be taken before the administration of an antimicrobials. However, given the increase in mortality with delaying antibiotic therapy, administration should not be delayed for blood cultures in patients suspected of sepsis.
Administer Broad-Spectrum Antibiotics
Empiric broad-spectrum antibiotic administration is the first part of infection source control. Antibiotic choice will depend on the likely source of infection, and likely organisms accounting for geographic variation in bacteria and antibiotic resistance. Hospital, health region or local specialty society guidelines can guide appropriate antibiotic choice. Initial choices should have coverage of aerobic and anaerobic gram-positive and gram-negative bacteria. Broad-spectrum carbapenem (e.g., Meropenem) or a broad-spectrum β-lactam antibiotic with combination beta-lactamase inhibitor (e.g., Piperacillin/tazobactam) are examples of possible initial therapies. Addition of antifungal and antiviral medication should also be considered based on clinical suspicion. Antibiotic coverage can be narrowed when culture and sensitivity results become available.
Intravenous fluid resuscitation should begin immediately if hypotension or evidence of tissue hypoperfusion (serum lactate >2 mmol/L) is present. The Surviving Sepsis Campaign recommend an initial bolus of 30 mL/kg of crystalloid solution to be completed within the first 3 hours. Although this recommendation is not supported by strong evidence, especially in the pregnant population, it allows a starting position while more clinical information is gathered to accurately guide therapy. Fluid responsiveness is variable in septic patients, and pregnancy related conditions or pathology may also make some patients more susceptible to fluid overload. For this reason, a recommendation of 1-2 L of crystalloid has been an alternative recommendation in the pregnant population. Ongoing reassessment of physiological parameters as well as noninvasive or invasive hemodynamic parameters, if available, will assist in guiding further fluid administration.
Administration of Vasopressors
Prolonged hypotension in patients with sepsis increases the risk of mortality. For patients, whose blood pressure is no longer fluid responsive or where further fluid administration is harmful, administration of vasopressor medication is indicated. A norepinephrine infusion is considered the first-line medication with the target mean arterial pressure of >65 mm Hg. This target pressure has not been adequately studied in the pregnant population but should be the initial target until individualized assessment of organ perfusion is possible.
Specific Pregnancy Considerations
Sepsis in pregnancy is associated with an increased risk of preterm delivery and stillbirth. The presence of sepsis in a pregnant patient is not an indication for delivery. Delivery should be for obstetric indications. The exception being sepsis from chorioamnionitis where delivery should be expedited as a means of source control. Multidisciplinary involvement of senior obstetrical staff, anesthesiology, neonatology, and critical care staff is recommended. Obstetrical management should occur concurrently with sepsis management. Corticosteroids are not contraindicated in maternal sepsis and can be used if indicated for fetal lung maturity.