Definition and Pathophysiology

In 1868, Carl Wunderlich analyzed more than 1 million axillary temperature measurements from 25,000 patients. He concluded that the average normal temperature of healthy adults was 37°C (98.6°F). However, he found a range of temperatures, with a nadir of 36.2°C between 2:00 and 8:00 am and a zenith of 37.5°C between 4:00 and 9:00 pm . A 1992 study using modern oral thermometers largely confirmed Wunderlich’s original data.

Well-regulated temperature results from hypothalamic integration of afferent thermal information from the skin, spinal cord, and other sites within the central nervous system (CNS). Hypothermia prompts vasoconstriction in peripheral tissues to decrease skin blood flow, decrease heat loss, and retain heat in the core compartment. If vasoconstriction is not adequate to prevent hypothermia, thermoregulatory shivering is triggered to increase heat production. Increased body temperature initially prompts vasodilation. It is mediated by the sympathetic nervous system, and it is observed in unanesthetized adults exposed to a hot environment before any significant change in central temperature occurs. If vasodilation is not adequate to prevent hyperthermia, thermoregulatory sweating occurs, which increases evaporative heat loss.

An abnormal body temperature can result from drugs or diseases that either change thermoregulatory thresholds or impair thermoregulatory responses. Hypothalamic activity and fever may be triggered by endogenous pyrogens released from immune effector cells in response to invasion by microorganisms ( Fig. 36.1 ). Although no single endogenous pyrogen has been conclusively identified as the mediator of the febrile response, tumor necrosis factor seems capable of reproducing many components of the febrile response. Endogenous pyrogen activity appears to depend largely on increased endothelial cell production of prostaglandins. Of interest, many of these substances help mediate uterine activity and parturition.

Chronology of events required for induction of fever. AMP, adenosine-5′-monophosphate; IFN, interferon; IL, interleukin; TNF, tumor necrosis factor; PGE ₂ , prostaglandin E ₂ .

(From Kasper DL, Fauci AS, Hauser SL, et al., eds. Harrison’s Principles of Internal Medicine . 19th ed. New York, NY: McGraw-Hill; 2016.)

Clinically, temperature measurements greater than 38°C represent fever. During episodes of fever, the thermoregulatory set point is elevated, and the normal thermoregulatory mechanisms are used to maintain the elevated temperature. However, there are circumstances in which an abnormally high temperature is measured in the absence of a change in thermoregulatory set point, such as when thermoregulatory responses to hyperthermia are prevented (e.g., block of sympathetically mediated sweating) or overwhelmed (e.g., immersion in hot water, malignant hyperthermia).

The fetus, by virtue of its intraabdominal location, has a unique problem with heat elimination. The only anatomic routes for egress of heat are the fetal skin surface (through the amniotic fluid) or the uteroplacental circulation. 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.

Neonatal Effects of Maternal Fever

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.

Early studies suggested that mild maternal intrapartum fever may not be benign. These studies focused only on the presence or absence of fever, and did not specifically comment on a clinical or pathologic diagnosis of chorioamnionitis. Macaulay et al. measured fetal scalp temperature in utero using a modified intrauterine pressure catheter. They concluded that maternal oral temperature is often an underestimation of fetal skin temperature. Lieberman et al. retrospectively reviewed the records of 1218 nulliparous women with singleton, term pregnancies in spontaneous labor who were afebrile on admission. They found fever (greater than 38°C) in 10% of the patients, nearly all of whom had received epidural analgesia. One-minute Apgar scores less than 7 and hypotonia were more common in the newborns of febrile mothers. Fever higher than 38.3°C was associated with more frequent requirement for bag-and-mask ventilation in the delivery room and need for supplemental oxygen in the nursery. There was also an increase in the incidence of neonatal seizures. The same group performed a case-control study of unexplained neonatal seizures in term infants and found a strong association with intrapartum fever and seizures (odds ratio [OR], 3.4). Perlman reported a high incidence of maternal fever among a cohort of infants with a 5-minute Apgar score less than or equal to 5 and those requiring resuscitation with chest compressions in the delivery room. Similarly, Greenwell et al. found an association between low-grade fever and adverse neonatal outcomes, including hypotonia and low 1-minute Apgar scores. More extreme fever (greater than 38.3°C) was also associated with low 5-minute Apgar scores and assisted ventilation. Lastly, a statistically significant association has been observed between maternal fever and neonatal encephalopathy.

Hyperthermia

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.

Noninfectious Inflammatory Fever

Neuraxial labor analgesia is associated with intrapartum fever (so-called “epidural fever”). The predominant theory is that noninfectious inflammation is responsible for epidural analgesia–associated fever (see Chapter 23 ). The incidence of fever in parturients with neuraxial analgesia ranges from 20% to 30% 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. It is not known whether epidural fever is associated with an increased risk for adverse maternal and fetal outcomes.

Fever Secondary to Infection

Maternal fever from chorioamnionitis that leads to neonatal infection is associated with both short- and long-term neonatal morbidity. In an observational evaluation of women with clinical chorioamnionitis, there was a higher incidence of prolonged positive-pressure ventilation in the delivery room, tracheal intubation, admission to a neonatal intensive care unit, and 5-minute Apgar score less than 6 in febrile versus afebrile newborns. Additional acute neonatal morbidity associated with chorioamnionitis includes neonatal 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. Clinical or pathologically diagnosed chorioamnionitis may also correlate with neonatal brain injury. In several large epidemiologic studies, there was an increased incidence of cerebral palsy in infants born to mothers with intrapartum fever (greater than 38°C) diagnosed with chorioamnionitis compared with those born to afebrile mothers.

Maternal Effects of Fever

Fever also produces significant maternal effects. Elevated temperature is associated with increased maternal heart rate, cardiac output, oxygen consumption, and catecholamine production. Women who develop fever are more likely to shiver and experience uncomfortable rigors. Not surprisingly, obstetricians fearing infection are more likely to treat febrile women with antibiotics. While suspected chorioamnionitis in the setting of maternal fever is not an indication for immediate delivery, low-grade fever may prompt obstetricians to choose instrumental vaginal or cesarean delivery over expectant labor management.

Chorioamnionitis (Intrauterine Inflammation and/or Infection)

In January 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. They 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. Triple I can be diagnosed when fever (diagnosed as maternal temperature greater than or equal to 39.0°C on one reading or greater than or equal to 38.0°C on two occasions separated by 30 minutes) is present with one or more of the following: (1) fetal tachycardia (greater than 160 bpm for 10 minutes or longer), (2) maternal white blood cell count greater than 15,000 × 10 ⁶ cells/L in the absence of corticosteroids, (3) purulent fluid from the cervical os (cloudy or yellowish thick discharge confirmed visually on speculum examination to be coming from the cervical canal), and (4) biochemical or microbiologic amniotic fluid results consistent with microbial invasion of the amniotic cavity. It is stressed that maternal fever in the absence of other criteria should be categorized as “isolated maternal fever.” The new nomenclature of “intrauterine inflammation, infection, or both” (Triple-I) is in the process of being incorporated into practice to replace the term “clinical chorioamnionitis.”

Previously, the diagnosis of chorioamnionitis was made when any combination of the following elements was noted: maternal fever, maternal or fetal tachycardia or both, elevated maternal white blood cell count, uterine tenderness, and purulent fluid or discharge from the cervical os. Using this definition, it occurs with variable frequency in the literature with reported event rates ranging from 0.5% to 10%, depending on the means of ascertainment and the demographic and obstetric characteristics of the population. It may be seen in over 90% of deliveries before 24 weeks’ gestation, in almost 40% of women who deliver between 25 and 28 weeks, and in approximately 5% of deliveries at term. Independent risk factors 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 use of internal monitors. Unfortunately, the laboratory diagnosis of chorioamnionitis is neither sensitive nor specific and may not correlate with the clinical presentation. Moreover, the classic clinical signs of chorioamnionitis are often absent. Goodman et al. reviewed the records of 531 women with pathologically proven chorioamnionitis. They found that only 10% of the patients had abdominal tenderness and only 1% had foul-smelling amniotic fluid.

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, chorioamnionitis often is polymicrobial in origin, and bacteria normally present in the genital tract most likely are responsible for infections. Bacteroides species, Group B streptococci, Mycoplasma and Ureaplasma species, and Escherichia coli are organisms commonly isolated from the amniotic fluid of parturients with chorioamnionitis. Maternal bacteremia occurs in 5% to 12% of women with the clinical diagnosis of chorioamnionitis.

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

Neonatal complications of chorioamnionitis include pneumonia, meningitis, sepsis, and death. An association between chorioamnionitis and cerebral palsy has been identified. A recent meta-analysis also found an association with chorioamnionitis and cerebral palsy, but the association was much weaker than in previous meta-analyses. Once the studies were separated for analysis by gestational age, exclusion of studies without evaluation of postnatal causes of cerebral palsy, and potential sources of bias and confounding, the relative risk was much lower than in previous analyses. The link between maternal infection and neurologic injury in the neonate appears related to intra-amniotic 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 chorioamnionitis. However, Gibbs et al. did not identify a correlation between poor maternal or neonatal outcome and the time interval from diagnosis of chorioamnionitis to delivery. They performed cesarean delivery only for standard obstetric indications and not for the diagnosis of chorioamnionitis alone. Similarly, a large prospective observational study found no relationship between the duration of infection and most measures of adverse neonatal outcome among 1965 gestations complicated by chorioamnionitis, although low 5-minute Apgar scores and neonatal mechanical ventilation were correlated with duration of chorioamnionitis. No recent studies have reinvestigated this practice as it relates to neonatal neurologic injuries. 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.

Early antepartum treatment for chorioamnionitis results in decreased maternal and neonatal morbidity compared with delayed postpartum treatment. With 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 later discussion). If a cesarean delivery is performed, additional anaerobic coverage with clindamycin or metronidazole may decrease the risk for endometritis. 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.

Urologic Infection

Urinary tract infections are common during pregnancy, although the incidence of asymptomatic bacteriuria may not be higher than in nonpregnant women. Increased concentrations of progesterone cause 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 1.3% 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. Complications may also include anemia, renal insufficiency, and respiratory insufficiency. The most common causative organisms are E. coli, gram-positive organisms, Klebsiella, Enterobacter, and Proteus species.

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. Nevertheless, treatment failures and septic complications have been reported in patients randomized to outpatient therapy in clinical trials.

Pyelonephritis may be associated with organ dysfunction. Nearly 20% of affected women have transient renal dysfunction, and the disease may also be complicated by 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.

Respiratory Tract Infection

Pregnancy results in a number of 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. Varicella pneumonia has been associated with maternal and fetal morbidity and up to 40% maternal mortality. Acyclovir has been used successfully to treat varicella pneumonia during pregnancy.

Because morbidity and mortality from influenza are increased in pregnancy, influenza vaccination is strongly recommended for pregnant women or those who will be pregnant during influenza season. Notably, pregnant women are disproportionately represented when evaluating mortality from influenza, and a significant number of women were treated with extracorporeal membrane oxygenation (ECMO). In the Confidential Enquiries into Maternal Deaths and Morbidity in the United Kingdom and Ireland 2009 to 2012 report, of the women who died, one in eleven died from influenza and more than one-half of the deaths could have been prevented by vaccination. The risk for fetal death is increased by maternal influenza infection and is reduced by vaccination. The infant is also passively protected for up to 20 weeks after birth. Aggressive treatment with antiviral drugs (oseltamivir, zanamivir) reduces the severity of the ensuing illness; in the 2009 to 2010 H1N1 influenza pandemic, initiation of therapy in the first 2 days of the infection reduced hospitalization and ICU admission; however, benefits have also been seen if antiviral drugs were started up to 4 days after onset of symptoms. Antiviral drugs appear to be safe in pregnancy, with no reported increase in adverse pregnancy or neonatal outcomes.

The Centers for Disease Control and Prevention (CDC) recommends the following: “droplet precautions should be implemented for patients with suspected or confirmed influenza for 7 days after illness onset or until 24 hours after the resolution of fever and respiratory symptoms, whichever is longer, while a patient is in a healthcare facility.” It is also recommended that health care providers wear a fitted N95 respirator or its equivalent when performing aerosol-generating procedures (e.g., tracheal intubation and extubation).

Postpartum and Surgical Site Infection

The most common source of postpartum infection is the genital tract. The urinary tract and less often the breasts or the lungs may also be infected. Postpartum uterine infection typically presents with a combination of fever, malaise, abdominal pain, and/or purulent discharge or lochia. Although obstetricians 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), defined by the CDC as infection related to an operative procedure that occurs at or near the surgical incision within 30 days of the procedure, is another increasingly common postpartum infection.

Cesarean delivery, prolonged rupture of membranes, and prolonged duration of labor are risk factors for postpartum endometritis. Similarly, risk factors for surgical site infection 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 in all women, whether performed electively or emergently.

Antibiotic prophylaxis should be administered 15 to 60 minutes before skin incision for cesarean delivery unless the patient is already receiving appropriate antibiotic coverage (e.g., for chorioamnionitis). 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 a significant penicillin or cephalosporin allergy, clindamycin with an aminoglycoside is an appropriate alternative. Extended-spectrum antibiotics, such as azithromycin, used in addition to first-generation cephalosporins for cesarean delivery prophylaxis, have been shown to reduce rates of endometritis and wound infection in women undergoing nonelective cesarean delivery during labor or after 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 should receive an additional intraoperative dose of the antibiotic used for preincision prophylaxis.

No important differences have been identified among various skin preparation solutions used before cesarean delivery. Vaginal preparation before cesarean delivery has been evaluated in a meta-analysis 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 meta-analysis 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 surgical site infection rates with a reduction in risk of 67%.

Systematic reviews have found insufficient evidence to recommend prophylactic antibiotics for operative vaginal delivery or for 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 the above antibiotic therapy, and outcomes are generally excellent. However, serious complications (e.g., peritonitis, abscess, septic thrombophlebitis) may rarely occur.

Definition

In 2016, the definitions for sepsis and septic shock were updated. 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.

Sepsis remains an important cause of maternal mortality and morbidity. In the United States between 2006 and 2013, infection accounted for 13% of all maternal deaths, with a cause-specific mortality ratio of 2.2 deaths per 100,000 live births. In a population-based study of sepsis in delivery hospitalizations, Bauer et al. reported 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. Independent risk factors of congestive heart failure, chronic liver disease, chronic renal disease, cerclage, and retained products of conception were identified; however, the authors noted that sepsis often occurs in the absence of risk factors, and screening tools should be developed to enhance detection in pregnant women.

In the United Kingdom and Ireland, sepsis was the reported cause of death in almost 25% of all maternal deaths in the Confidential Enquiries into Maternal Deaths and Morbidity 2009 to 2012 report owing to the large increase in maternal deaths from an H1N1 influenza epidemic. The most recent 2013 to 2015 report demonstrated a cause-specific mortality ratio of 0.6 per 100,000. In a United Kingdom case-control study, Acosta et al. reported the most common sources of infection were genital tract infection in 31.0% of cases, followed by urinary tract infection in 19.7% of cases. The most common organisms identified were E. coli, Group A streptococcus, and Group B streptococcus. No organism was identified in 36.2% of cases. Most cases of a Group A streptococcal infection were diagnosed with severe sepsis (using the previous definition) less than 9 hours from the first sign of the systemic inflammatory response syndrome (SIRS); one-half had less than 2 hours between first signs and diagnosis.

Screening and Diagnosis

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 screen 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 end-organ injury. Organ dysfunction is characterized by a score of greater than or equal to 2 points on the Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score ( Table 36.1 ). Bedside screening for end-organ injury can be accomplished using an abbreviated set of criteria called quick SOFA (qSOFA). A nonobstetric patient screens positive with two or more of the following criteria: respiratory rate greater than or equal to 22 breaths/min, altered mentation, and systolic blood pressure less than or equal to 100 mm Hg. 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 women.

TABLE 36.1

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