The normal range of temperature for adults is 36.2°C to 37.0°C (mean ± 2 standard deviations), with an average temperature of 36.6°C, according to a metaanalysis of prospectively measured temperatures. Temperature measurements greater than 38°C represent fever. The fetus, by virtue of its intraabdominal location, has a unique problem with heat elimination. Evidence suggests that the fetus relies on heat exchange across the uteroplacental circulation to dissipate most of its metabolic heat. The normal fetus maintains a temperature that is approximately 0.5°C to 0.75°C higher than the maternal temperature.

Fever produces significant maternal effects. Elevated temperature is associated with increased maternal heart rate, cardiac output, oxygen consumption, and catecholamine production. Women who develop a fever are more likely to shiver and experience uncomfortable rigors. Not surprisingly, obstetric providers, fearing infection, are more likely to treat febrile women with antibiotics.

Infection is the most common cause of fever and involves liberation of inflammatory cytokines, which are implicated in the pathogenesis of many fetal and neonatal injuries (see Chapter 10 ). The mechanism linking neonatal neurologic injuries to maternal fever likely involves the inflammatory cytokines. Animal models of chorioamnionitis suggest that fetal brain lesions can be induced by infection and blocked by antiinflammatory cytokines. Infants developing neonatal encephalopathy in the setting of maternal fever do not generally exhibit positive blood cultures, implying that it is neuroinflammation, rather than infection, that causes damage. Fever alone has a limited effect, but when combined with acidosis, inflammation, and/or infection, it appears to exacerbate neurologic injury.

Studies have suggested that maternal intrapartum fever may not be benign. Intrapartum fever is associated with neonatal morbidity. Many studies focused only on the presence or absence of fever and did not specifically comment on a clinical or pathologic diagnosis of chorioamnionitis. In studies that reported clinical or pathologic chorioamnionitis, there are high rates in all groups with fever, so it is difficult to determine whether morbidity is a result of the fever, infection, or both. Hensel et al. found a correlation with maternal fever and composite neonatal morbidity (umbilical artery pH < 7.1, mechanical ventilation, respiratory distress, meconium aspiration with pulmonary hypertension, hypoglycemia, neonatal intensive care unit (ICU) admission, and Apgar score < 7 at 5 minutes), with higher fever associated with greater odds of neonatal morbidity in a dose-dependent fashion. In this study, almost all patients with fever were diagnosed with clinical chorioamnionitis and treated accordingly.

Hot tub and sauna use in pregnancy have been linked epidemiologically to neural tube defects in the fetus. Spontaneous abortion and major structural birth defects have similarly been associated with the frequency of use of hot tubs and saunas. Neonatal hypoxic encephalopathy has been observed after prolonged immersion in 39.7°C water during otherwise uncomplicated labor.

Neuraxial labor analgesia is associated with intrapartum fever (so-called “epidural-related maternal fever”). The predominant theory is that noninfectious inflammation is responsible for epidural analgesia–associated fever (see Chapter 24 ). The incidence of fever in parturients with neuraxial analgesia ranges from 15% to 25% compared with 5% to 7% in parturients without neuraxial analgesia. Why some women with neuraxial analgesia develop fever, but others do not, is not understood. There is insufficient evidence to evaluate whether epidural analgesia–associated fever contributes to neonatal brain injury.

Clinical chorioamnionitis is primarily caused by intraamniotic infection, which is an infection of the amniotic fluid, fetal membranes, placenta, or fetus. It is a common condition encountered in the labor and delivery room, affecting 1% to 6% of term gestations, almost 40% of deliveries between 25 and 28 weeks’ gestation, and over 90% of deliveries before 24 weeks’ gestation. In 2015, an expert panel was convened by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) to review the criteria for diagnosis and management of chorioamnionitis. It proposed that the phrase “intrauterine inflammation, infection, or both” (abbreviated “Triple I”) be used instead of the term “chorioamnionitis” because of the diverse range of conditions, both infectious and inflammatory, that it was used to describe. Throughout this chapter, the phrase “clinical chorioamnionitis” is used in place of “Triple I” because most clinicians continue to use the term “chorioamnionitis” in clinical practice. The word “clinical” differentiates this diagnosis from histologic chorioamnionitis, which is diagnosed via placental pathology.

The American College of Obstetricians and Gynecologists (ACOG) defines clinical chorioamnionitis (suspected intraamniotic infection) as a maternal temperature ≥ 39.0°C, or 38.0°C to 38.9°C with one additional clinical risk factor present (maternal leukocytosis, purulent cervical drainage, or fetal tachycardia). The NICHD expert panel defined maternal leukocytosis as a white blood cell count > 15,000/μL (15 × 10 ⁹ /L) in the absence of corticosteroids, and fetal tachycardia > 160 beats/min for at least 10 minutes. The expert workshop executive summary defined isolated maternal fever as a temperature ≥ 39°C with no other clinical risk factors. The ACOG recommends that these patients be given the diagnosis of clinical chorioamnionitis because infection is the most likely cause of markedly elevated maternal temperature.

Independent risk factors for clinical chorioamnionitis include low parity, a history of chorioamnionitis in a prior delivery, the number of vaginal examinations, duration of total labor, duration of ruptured membranes, and the use of internal monitors.

In most cases, bacteria gain access to the amniotic cavity and the fetus by ascending through the cervix after rupture of the membranes. Alternatively, infectious agents present in the maternal circulation may undergo transplacental transport and gain access to the amniotic cavity. Similar to other pelvic infections, histologic chorioamnionitis often is polymicrobial in origin, and bacteria normally present in the genital tract are most likely responsible for infections. Maternal bacteremia occurs in approximately 10% of women with clinical chorioamnionitis.

Maternal complications of clinical chorioamnionitis include preterm labor, placental abruption, postpartum infection, uterine atony, postpartum hemorrhage, peripartum hysterectomy, adult respiratory distress syndrome, sepsis, ICU admission, and death. In addition, several studies have noted an increased incidence of cesarean delivery for labor dystocia in parturients with clinical chorioamnionitis. Some investigators have suggested that infection adversely affects uterine contractility and contributes to an increased risk for cesarean delivery. However, in some cases, clinical chorioamnionitis may represent an ascending infection developing late in labor that is already prolonged and dysfunctional.

Neonatal complications of clinical chorioamnionitis include pneumonia, meningitis, sepsis, and death. Importantly, the use of intrapartum antibiotic therapy given in response to maternal Group B streptococcal colonization or in response to signs of chorioamnionitis has significantly decreased the incidence of neonatal infection and sepsis. An association between clinical chorioamnionitis and cerebral palsy has been identified. However, in a recent metaanalysis, once studies were separated by gestational age, excluded if they did not have an evaluation of postnatal causes of cerebral palsy, and potential sources of bias and confounding were accounted for, the relative risk (RR) was much lower than in previous analyses. The link between maternal infection and neurologic injury in the neonate appears to be related to intraamniotic infection or inflammation, particularly when there is evidence of fetal systemic inflammation or inflammation of the umbilical cord (funisitis).

Historically, prompt delivery was the cornerstone of obstetric management of patients with clinical chorioamnionitis. However, Gibbs et al. did not identify a correlation between poor maternal or neonatal outcome and the time interval from diagnosis of clinical chorioamnionitis to delivery. They performed cesarean delivery only for standard obstetric indications and not for the diagnosis of clinical chorioamnionitis alone. Similarly, a large prospective observational study found no relationship between the duration of suspected infection and most measures of adverse neonatal outcome among 1965 gestations complicated by clinical chorioamnionitis, although low 5-minute Apgar scores and neonatal mechanical ventilation were correlated with the duration of chorioamnionitis. Many fetuses will exhibit tachycardia during maternal fever and infection, but this pattern is not highly predictive of neonatal acidemia and, therefore by itself, is not an indication for immediate delivery. Neonatal adverse outcomes are associated with any exposure to clinical chorioamnionitis and not the length of time until delivery.

Treatment for clinical chorioamnionitis prior to delivery results in decreased maternal and neonatal morbidity compared with postpartum treatment. With clinical chorioamnionitis, a combination of ampicillin and gentamicin should cover most relevant pathogens and is the recommended primary antibiotic regimen. The early use of antibiotics also may affect the anesthesia provider’s decision regarding the administration of neuraxial labor analgesia or anesthesia (see discussion below). If a cesarean delivery is performed, additional anaerobic coverage with clindamycin or metronidazole may decrease the risk for endometritis. Additionally, azithromycin is indicated during intrapartum cesarean delivery to reduce the risk of endometritis. Many providers also administer azithromycin at the time of cesarean delivery in this scenario in order to ensure Ure aplasma coverage; however, it has not been studied in patients with clinical chorioamnionitis. Continuation of antimicrobial agents postpartum should not be automatic, but rather based on risk factors for postpartum endometritis. In general, women who have a vaginal delivery are less likely to develop postpartum endometritis, and therefore may be candidates for discontinuing antimicrobial therapy after delivery. Even in women undergoing cesarean delivery, studies have shown only preoperative or one single postoperative dose appears to have the same efficacy as continuing antibiotics for a longer duration.

Urinary tract infections are common during pregnancy, although the incidence of asymptomatic bacteriuria may not be higher than in nonpregnant women. Increased concentration of progesterone causes the relaxation of ureteral smooth muscle. In addition, the gravid uterus causes partial ureteral obstruction. Both factors cause urinary stasis, which increases the risk for urinary tract infection. Furthermore, these physiologic changes increase the likelihood that asymptomatic bladder infection will ascend into the kidneys and produce pyelonephritis. Approximately 2% to 7% of pregnant women will develop symptomatic cystitis, and up to 25% of women with untreated bacteriuria in pregnancy may develop pyelonephritis.

Acute pyelonephritis is a serious threat to maternal and fetal well-being and complicates approximately 1% to 2.5% of pregnancies. Symptoms of acute pyelonephritis include fever, chills, flank pain, and other symptoms of lower urinary tract infection. Approximately 14% to 17% of pregnant women with pyelonephritis will develop bacteremia during the course of this infection. The most common causative organisms are Escherichia coli , gram-positive organisms, Klebsiella , Enterobacter , and Proteus species. Complications may also include anemia, renal insufficiency, respiratory insufficiency, sepsis, and septic shock.

Patients with pyelonephritis may also experience pulmonary injury. Cunningham et al. suggested that “this syndrome was probably caused by permeability pulmonary edema, likely mediated by endotoxin-induced alveolar-capillary membrane injury.” Towers et al. compared 11 pregnant women who had pyelonephritis and pulmonary injury with 119 women who had pyelonephritis only. They observed that fluid overload and the use of tocolytic therapy were the most significant predictive factors associated with pulmonary injury. The authors suggested that “strict management of fluids should occur so that patients do not have fluid overload.” Contemporary authors, however, have questioned fluid restriction in pyelonephritis and instead suggest fluid administration sufficient to generate urine output of 30 to 50 mL/h, while observing respiratory rate, oxygen saturation, and symptoms of dyspnea to identify impending respiratory compromise. Respiratory failure should be investigated with chest radiography and arterial blood gas analysis and managed with appropriate respiratory support.

Hospitalization is indicated to initiate aggressive parenteral antibiotic treatment of this serious maternal infection, although limited data support outpatient treatment for carefully selected patients in the first and second trimester. However, treatment failures and septic complications have been reported in patients randomized to outpatient therapy in clinical trials.

Pregnancy results in many changes that may predispose the pregnant woman to the development of serious respiratory tract infection. Hyperemia and hypersecretion are characteristic of the respiratory tract mucosa during pregnancy, and these changes may intensify the effect of the initial infection. In the case of a viral infection, the excess secretions may predispose the patient to bacterial superinfection. Immunologic modulation during pregnancy may also predispose to pulmonary infection. Furthermore, the increased oxygen consumption, elevation of the diaphragm, and decreased functional residual capacity characteristic of pregnancy may increase the likelihood that infection will result in maternal hypoxemia.

Fortunately, most respiratory tract infections during pregnancy are upper respiratory tract viral infections that do not pose a serious threat to the mother or fetus. Most lower respiratory tract infections are also viral and self-limiting; pneumonia occurs during pregnancy with an incidence approximating that of the nonpregnant population.

Benedetti et al. emphasized the importance of early diagnosis and treatment as well as the direct measurement of maternal oxygenation in cases of pneumonia during pregnancy. Most community-acquired pneumonias in healthy young women are bacterial in origin. Streptococcus pneumoniae is the most common pathogen. Mycoplasma pneumoniae and influenza are other common pathogens. Legionella pneumophila , Chlamydia , and varicella are less common pathogens in this population.

The most common source of postpartum infection is the genital tract . Postpartum endometritis occurs in 2% to 16% of patients who have cesarean delivery and typically presents with a combination of fever, malaise, abdominal pain, and/or purulent discharge or lochia. Although obstetric providers typically refer to postpartum uterine infection as endometritis , this infection involves the decidua, myometrium, and parametrial tissues. Bacteria that colonize the cervix and vagina gain access to the amniotic fluid during labor, and they may invade devitalized uterine tissue postpartum. Surgical site infection (SSI) is another increasingly common postpartum infection and appears to occur in 2% to 7% of patients after cesarean delivery. SSI is defined by the US Centers for Disease Control and Prevention (CDC) as infection related to an operative procedure that occurs at or near the surgical incision within 30 days of the procedure.

Cesarean delivery, prolonged rupture of membranes, and prolonged duration of labor are risk factors for postpartum endometritis. Similarly, risk factors for SSI following cesarean delivery include patient-level factors such as obesity, prior cesarean delivery, hypertension, diabetes, and tobacco use; pregnancy-related factors such as emergency delivery, labor or rupture of membranes, and chorioamnionitis; and surgical factors such as operative time and surgeon experience.

Prophylactic administration of antibiotics decreases the incidence of postpartum uterine infection and wound infection after cesarean delivery, whether performed electively or as an emergency. Antibiotic prophylaxis should be administered up to 60 minutes before skin incision for cesarean delivery. A first-generation cephalosporin is effective against gram-positive bacteria, gram-negative bacteria, and some anaerobic bacteria, and is the first-line antibiotic for cesarean delivery prophylaxis. In women with a history of cephalosporin allergy, clindamycin with an aminoglycoside is an appropriate alternative. However, it has been shown that patients receiving alternative antibiotics have higher rates of SSIs. Allergy skin testing is considered safe in pregnancy and is recommended to allow for appropriate antibiotic administration. Extended-spectrum antibiotics, such as azithromycin, used in addition to first-generation cephalosporins for cesarean delivery prophylaxis, have been shown to reduce the rates of endometritis and wound infection in women undergoing nonelective cesarean delivery during labor or after a membrane rupture.

A single intravenous dose of cefazolin is appropriate for most women undergoing cesarean delivery, as a therapeutic level is maintained for 3 to 4 hours. However, obese women may require a higher dose, although the specific appropriate dose has yet to be identified. Consistent with surgical prophylaxis principles, patients with prolonged surgical procedures or those with significant blood loss (>1500 mL) should receive an additional intraoperative dose of the antibiotic used for preincision prophylaxis.

Additional preventative measures for endometritis and SSI include the avoidance of perioperative hyperglycemia and hypothermia.

A systematic review reported that skin preparation using chlorhexidine gluconate was slightly more effective than povidone iodine for reducing the incidence of SSI after cesarean delivery (RR, 0.72; 95% CI, 0.58 to 0.91). Vaginal preparation before cesarean delivery has been evaluated in a metaanalysis of 16 trials. These trials demonstrate an overall reduction in postcesarean endometritis, especially for women in labor or with ruptured membranes. More data are needed to evaluate the effect of this intervention on women not in labor or with intact membranes. A metaanalysis evaluating the effect of bundles of at least three evidence-based interventions (such as antibiotic prophylaxis selection or dose, hair removal with clippers, and chlorhexidine skin preparation) showed a significant reduction in SSI rates with a reduction in risk of 67%. There is insufficient evidence to recommend prophylactic antibiotics for operative vaginal delivery, dilation and curettage, placement of an indwelling intrauterine balloon, or manual removal of the placenta after vaginal delivery; however, consideration may be given to prophylactic antibiotics in the setting of complex perineal repairs.

Parenteral, broad-spectrum antibiotic therapy with a combination of gentamicin and clindamycin is recommended to treat postpartum endometritis. Ampicillin is added in refractory cases and often in cases in which the patient was colonized with group B streptococcus before delivery. Endometritis typically responds to this antibiotic therapy regimen, and outcomes are generally excellent. However, serious complications (e.g., peritonitis, abscess, septic thrombophlebitis) may rarely occur. Puerperal group A streptococcal infection has high rates of morbidity and mortality. Early wound debridement and/or hysterectomy may be lifesaving in the setting of clinical deterioration. For SSI treatment, debridement, wound exploration, wet to dry packing, or negative pressure therapy may be required for treatment. Antimicrobial treatment is also recommended. If the obstetric provider is unable to determine the depth of infection at bedside and the wound requires exploration, it is best practice to provide anesthesia in the operating room allowing use of American Society of Anesthesiologists (ASA) standard monitors and administration of regional anesthesia, if possible.

Herpes simplex virus type 2 (HSV-2) causes locally recurring disease that is characterized by asymptomatic periods interrupted by episodes of viral reactivation from sites in the sensory ganglia, resulting in painful vesicular lesions on the skin or mucous membranes of the genital tract or mouth. Primary maternal HSV-2 infection is associated with transient viremia, and up to 2% of pregnant women will be primarily infected during gestation. Patients with primary infection may have systemic symptoms, including fever, headache, and lymphadenopathy, although asymptomatic primary infection is common. Epidemiologic evidence suggests that HSV-1, formerly associated only with perioral lesions (herpes labialis), is the predominant cause of new genital herpes infections in some populations. During recurrent (i.e., secondary) infection , maternal antibodies prevent the recurrence of viremia. Thus, systemic symptoms are less severe—or do not occur at all—during episodes of recurrent infection. However, recurrent infection may result in severe symptoms localized to the site of the lesions on the external genitalia. Prodromal symptoms, including vulvar pain or burning, often precede development of recurrent lesions. Unfortunately, asymptomatic shedding of the virus also may occur in the genital tract.

Human immunodeficiency virus (HIV) is a member of the lentivirus subfamily of human retroviruses (i.e., it carries the enzyme reverse transcriptase). This enzyme converts the single-stranded viral RNA into double-stranded DNA, which subsequently can be integrated into the DNA of the infected cell. This process is error prone, leading to rapid mutation of the virus, which significantly complicates drug therapy. Immune suppression is mainly caused by infection of helper T cells, CD4 ⁺ monocytes, and macrophages. Abnormalities of these elements of the immune system render the HIV patient vulnerable to bacterial, viral, fungal, parasitic, and mycobacterial infection. In addition, for reasons that are not entirely clear, patients infected with HIV are susceptible to several malignancies (e.g., Kaposi’s sarcoma, B-cell lymphoma, invasive cervical carcinoma). Clinical manifestations can affect every organ system and result from the HIV infection itself, opportunistic infection, secondary malignancy, or long-term exposure to antiretroviral therapy (ART).

In the United States, the estimated number of live births to women with diagnosed HIV decreased from approximately 4500 in 2010 to approximately 3500 in 2019. In the setting of opt-out HIV screening in pregnancy as well as risk-reducing strategies such as ART, scheduled cesarean delivery, and avoidance of breastfeeding, the number of perinatal transmissions of HIV in the United States has decreased dramatically. The number of infants who acquired HIV perinatally in the United States decreased from 216 in 2002 to 74 in 2010 to 32 in 2019.

Sepsis is defined by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine as “life-threatening organ dysfunction caused by a dysregulated host response to infection.” The term “severe sepsis” is no longer used because of redundancy. Septic shock is defined as “a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk for mortality than with sepsis alone.” It can be identified clinically in patients with a vasopressor requirement and a lactic acid level greater than 2 mmol/L despite adequate fluid resuscitation.

Sepsis remains an important cause of maternal mortality and morbidity, with an incidence that has not meaningfully changed over the past few decades. Between 2017 and 2019 in the United States, infection accounted for 14.3% of all maternal deaths, with a cause-specific mortality ratio of 2.5 deaths per 100,000 live births. In a population-based study of sepsis in delivery hospitalizations, Bauer et al. reported that the most common infections were pneumonia, genitourinary infection, and chorioamnionitis. Although only 40.4% reported a specific organism, the most common organisms were E. coli , staphylococcus, streptococcus, and gram-negative organisms. While multiple independent risk factors have been reported in the literature, authors have noted that sepsis often occurs in the absence of risk factors. Sepsis occurs more commonly with postpartum readmissions (compared with delivery hospitalization) and is a leading cause of postpartum maternal deaths.

Given the importance of early identification and treatment, prompt recognition is key. Clinically, sepsis is now defined as the combination of infection with end-organ injury. If end-organ injury is suspected, it is essential to assess for infection. If a patient has a suspected infection, it is essential to monitor closely for end-organ injury. Serial bedside evaluation is desirable to detect trends in vital signs and clinical status and to more rapidly assess and reassess for signs of sepsis.

Several screening tools exist to help in the identification of sepsis ( Table 36.1 ). Maternal Early Warning criteria were proposed by the National Partnership for Maternal Safety as a set of criteria to identify impending maternal morbidity from a variety of causes. These were then modified slightly by the Safe Motherhood Initiative. The California Maternal Quality Care Collaborative (CMQCC) and the UK Obstetric Surveillance System (UKOSS) both use modified systemic inflammatory response syndrome (SIRS) criteria. Previous diagnostic criteria using two or more abnormal values of the SIRS criteria were nonspecific; patients with noninfectious inflammatory processes exhibit these signs, including healthy pregnant patients. The Maternal Early Warning Trigger tool has been shown to reduce severe maternal morbidity when combined with protocols for treatment. A study by Bauer et al. demonstrated that using a nonpregnancy adjusted tool prior to 20 weeks’ gestation and after 3 days postpartum will have improved sensitivity to identify patients at risk for sepsis. During delivery hospitalizations, UKOSS and CMQCC criteria have sensitivity > 90% with the lowest false-positive rates for screening. Given the rarity of maternal sepsis, utilizing a screening tool to assess multiple types of morbidity at once rather than using a separate tool for each may be the best approach. It is recommended that if a patient meets any screening tool criteria, the patient should receive prompt evaluation by a physician or other practitioner to assess for end-organ injury (to make the diagnosis of sepsis) with ability to escalate care.

In two case series of maternal deaths due to sepsis in Michigan and California, the authors found that deaths were preceded by delays in seeking care, provider recognition, treatment, and escalation of care. Additionally, patient education of warning signs and provider education of the signs of sepsis should be improved. Presentation of sepsis during pregnancy and postpartum is different than in the general population; only 25% of patients who ultimately die of sepsis present with fever or hypothermia. A diagnosis of pulmonary, genital tract, or other systemic infection should prompt close monitoring for end-organ injury, and therefore sepsis.

Organ dysfunction is required for diagnosis of sepsis, characterized by a score of 2 points or more on the Sequential Organ Failure Assessment (SOFA) score ( Table 36.2 ).

It is not known how SOFA performs in the identification of sepsis in pregnant patients. Parameters have not been adjusted for pregnancy. Pregnancy-adjusted changes such as lower creatinine levels, lower blood pressure (which nadirs at 20 weeks’ gestation), and lower platelet count are not accounted for in the SOFA criteria; no standardized pregnancy-adjusted criteria to indicate end-organ injury are available. Any change in markers for end-organ injury should prompt concern for sepsis and the need for escalation of care.

The Sepsis in Obstetrics Score (SOS) may be useful for assessing the severity of illness, and to identify patients requiring ICU admission ( Table 36.3 ). In a retrospective cohort of 850 women with clinical suspicion of sepsis, an SOS ≥ 6 was independently associated with ICU admission. A prospective validation study confirmed the threshold score of 6, making it the first score derived and validated in an obstetric population. The specificity of the score was 88%, but the sensitivity was only 64%. Additionally, given the low incidence of ICU admission, the negative predictive value of the score was excellent (98.6%), but the positive predictive value was poor (15%). It did not perform statistically better than other validated sepsis scoring systems. A screening tool that consistently facilitates rapid diagnosis of sepsis as well as the need for escalation of care in pregnancy remains an unmet need.

Once diagnosis has been established, prompt treatment is of paramount importance. In nonobstetric patients, there is an increase in mortality of 7.6% for each hour delay in appropriate antibiotic administration. Similarly, a multicenter case control study demonstrated a mortality rate of 8% in pregnant patients who received antibiotics within 1 hour and a mortality rate of 20% in patients who received antibiotics after 1 hour. Care should be escalated to accommodate the resources and requirements to treat critically ill patients. Surviving Sepsis Campaign (SSC) Guidelines were created to define best practice in the management of sepsis based on available evidence, with strong recommendations worded as “recommended” and weak recommendations as “suggested.” The SSC guidelines recommend IV antimicrobial administration as soon as possible, ideally within 1 hour for patients with septic shock or a high likelihood for sepsis. The antibiotic regimen chosen should provide empiric coverage for common obstetric infections; a combination of vancomycin and pipercillin/tazobactam should be considered if the cause is unknown or in cases of septic shock. Both the CMQCC sepsis toolkit and the Society for Maternal-Fetal Medicine Consult Series for Maternal Sepsis provide first-line antimicrobial selection for pregnant and postpartum common conditions. Within the first 3 hours it is suggested to give 30 mL/kg (ideal body weight) of IV crystalloid fluid to treat sepsis-induced hypotension or septic shock. It is recommended to set an initial target mean arterial blood pressure of 65 mm Hg, with norepinephrine used as the first-line vasopressor, and the suggested addition of vasopressin to achieve hemodynamic goals. It is suggested that trends in serum lactate may be used to guide resuscitation. In the Confidential Enquiries into Maternal Deaths and Morbidity in the United Kingdom and Ireland 2009 to 2012 report, it was also recommended to consult with an infectious disease specialist. Further discussion of sepsis management is found in Chapter 53 .

Although the effects of maternal therapy on the fetus should be considered, treatment of the mother has first priority. Fetal status is best optimized by meeting maternal treatment goals. For nonreassuring fetal heart rate patterns in the setting of maternal sepsis, fetal resuscitation in utero and maternal medical therapy are frequently successful in delaying delivery. Nevertheless, in some cases, maternal sepsis may require delivery, even before viability, particularly if chorioamnionitis is present. In a 2013 series of maternal admissions for sepsis, 40% of women diagnosed with severe sepsis and all with septic shock required delivery during the same hospitalization and most required emergency delivery for worsening maternal respiratory status. Maternal sepsis also increases the risk for perinatal mortality, with the rate of stillbirth approaching 33% when maternal sepsis requires ICU admission. A multidisciplinary team should consider the mother’s response to initial therapeutic interventions; vasopressor, oxygen, and ventilatory requirements; and the gestational age and fetal well-being when considering the optimal timing and route of delivery.