Intrapartum fever

INTRODUCTION — Intrapartum fever (ie, fever during labor) can be due to an infectious or noninfectious etiology. The maternal and newborn consequences depend on the etiology.

Numerous risk factors for intrapartum fever have been reported, such as nulliparity, prolonged labor, and prelabor rupture of membranes [1]. These characteristics describe patients likely to develop intraamniotic infection (IAI, chorioamnionitis) and/or receive neuraxial anesthesia, which are the two most common causes of intrapartum fever. In the absence of a preexisting febrile disorder (eg, respiratory infection), most pregnant patients who develop fever in labor are presumed to have IAI and are treated with broad spectrum antibiotics.

This topic will discuss the etiologies, management, and potential consequences of intrapartum fever. IAI (a major cause of intrapartum fever) and postpartum endometritis (a major cause of postpartum fever) are reviewed separately. (See "Clinical chorioamnionitis" and "Postpartum endometritis".)

MECHANISM — The vast majority of patients with elevated body temperature have fever, which occurs when the hypothalamic thermoregulatory center is reset at a higher temperature by endogenous pyrogens produced by specific host cells in response to infection, inflammation, injury, or antigenic challenge. These pyrogenic polypeptides include the cytokines interleukin (IL)-1 alpha and IL-1 beta, IL-6, tumor necrosis factor (TNF)-alpha and TNF-beta, and interferon alpha [2,3].

There are a few instances in which an elevated temperature represents hyperthermia (body temperature rise due to insufficient heat loss; thermoregulatory center is not reset) rather than fever. As an example, some pharmacologic agents (eg, atropine, the recreational drug "ecstasy") raise core temperature by blocking sweating or vasodilation without changing the normal hypothalamic set-point. (See "Pathophysiology and treatment of fever in adults" and "Drug fever".)

For the purposes of this discussion, the term fever will generally be used to describe maternal intrapartum temperature elevation from any mechanism.

DEFINITION — Fever is defined as an elevation of body temperature above normal daily variation. The threshold for intrapartum fever has generally been considered to be a maternal temperature ≥38°C (≥100.4°F) orally. This is based, in part, on a study of temperature in normal parturients that found temperature ranged from 34.6 to 37.6°C (94.3 to 99.7°F) upon admission to the labor unit [4]. Diurnal variation was noted, with a peak from midnight to 2 AM and a nadir from 11 AM to noon.

However, an expert panel convened in 2016 to address the diagnosis and management of pregnant people with intrapartum infection (called in this report "triple I," which stands for intrauterine infection or inflammation or both) and their neonates recommended defining maternal fever as maternal temperature ≥39°C (≥102.2°F) on one reading orally or ≥38°C (≥100.4°F) and less than 39°C (102.2°F) orally on two readings 30 minutes apart [5]. Whether this definition will be widely accepted is unknown. (See "Clinical chorioamnionitis".)

PREVALENCE — The reported prevalence of intrapartum fever varies widely. This variation is due to several factors, including differences in ascertainment (prospective studies report higher rates than retrospective studies), differences in prevalence of risk factors in the populations studied, use of different diagnostic criteria, and temporal changes in obstetric practice (eg, increased use of intrapartum antibiotics and neuraxial anesthesia).

Intrapartum fever is now common: 6.8 percent (1 in 15 patients) [6]. The prevalence has increased severalfold in recent decades along with the increase in use of neuraxial anesthesia. A population-based study using data from birth and infant death certificates between 1995 and 1997 noted that intrapartum fever occurred in only 1.6 percent of over 11 million singleton births in the United States [7]. (See 'Use of neuraxial anesthesia' below.)

TEMPERATURE MEASUREMENT — We measure maternal temperature in the oral sublingual pocket with an electronic contact thermometer because it is accurate and the most convenient method for detecting intrapartum maternal fever [8]. Good technique is important because mouth breathing, hyperventilation, recent ingestion of ice or a hot beverage, and oxygen administration can affect oral temperature. A prudent approach is to ensure that the mother has not consumed fluids or ice in the 15 minutes before the temperature is determined [8].

Tympanic and axillary temperature measurements are particularly susceptible to user error [9]. Noncontact tympanic temperature approximates core temperature but may be inaccurate because of incorrect placement of the sensor in the ear canal or interference by cerumen. Axillary temperature is 1.0 to 2.0°C (1.8 to 3.6°F) lower than oral temperature; an accurate measurement requires positioning the probe over the axillary artery and positioning the arms at the patient's side [10]. Rectal temperatures are generally 0.6°C (1.0°F) higher than oral readings, and bothersome to patients.

Large comparative studies of intrapartum techniques for measuring maternal temperature have not been performed. In one of the few small studies, oral temperature correlated better with intrauterine/core temperature than tympanic membrane or skin temperature on the thigh or abdomen [8].

Of note, fetal/intrauterine temperature is 0.2 to 0.9°C (0.4 to 1.6°F) higher than maternal oral temperature [8,11-14].

DIAGNOSTIC EVALUATION

History and physical — History and physical examination are performed to look for potential causes of fever, both obstetric and nonobstetric. The physical examination should include standard vital signs, auscultation of the lungs, and assessment of fundal tenderness, abdominal tenderness, costovertebral angle tenderness, and the character of amniotic fluid (eg, odor). Key points to consider:

●Neuraxial anesthesia is associated with intrapartum fever. (See 'Use of neuraxial anesthesia' below.)

●Prolonged labor, prolonged membrane rupture, multiple digital vaginal examinations (especially with ruptured membranes), and exposure to intrauterine devices such as an intrauterine pressure catheter or a fetal scalp electrode are risk factors for intraamniotic infection (IAI). (See 'Intraamniotic infection (chorioamnionitis)' below.)

●The source of fever may be an infection that began antepartum, such as a urinary tract infection, the common cold, or COVID-19, or more rarely influenza, pneumonia, listeriosis, Clostridioides difficile colitis, or appendicitis. (See 'Urinary tract infection' below and 'Respiratory tract infection' below.)

●Rarely, the source of fever is secondary to a drug the patient is taking or took recently. Drug fever can present several days after initiation of a medication. (See 'Drug fever' below.)

●Fetal tachycardia may occur in response to maternal fever or intrauterine infection. However, a category I fetal heart rate pattern (table 1) does not reliably exclude fetal/neonatal infection and no pattern is specific for intrauterine infection [15,16].

Laboratory — Laboratory testing is not routinely performed, and should be guided by the suspected diagnosis.

White blood cell (WBC) count and differential — We suggest obtaining a WBC count in patients who appear clinically ill or with a temperature ≥39°C (≥102.2°F). The value of an intrapartum WBC count is limited because high values normally occur during labor. Data from two series reported mean WBC counts in laboring patients of 10,000 to 16,000 cells/microL, with an upper level as high as 29,000 cells/microL [17,18]; the mean count increased linearly with the duration of elapsed labor [18]. However, when clinical concern about infection is high, leukocytosis supports the diagnosis, especially when accompanied by a left shift or bandemia.

Blood cultures — The usefulness of blood cultures has not been studied specifically in intrapartum patients, and there are no published standards for when to obtain intrapartum cultures. We suggest blood cultures for patients who appear clinically ill or with temperature ≥39°C (≥102.2°F). Our approach is based on the observation that the frequency of positive blood cultures increases as temperature increases [19-21], and appropriate antibiotic therapy is important in bacteremic patients because untreated bacteremia can lead to sepsis and shock, although these serious sequelae are rare in pregnant/postpartum patients in resource-rich countries, as these patients tend to be young and healthy [22].

Experts have suggested the following potential indications for blood cultures: fever ≥39°C (≥102.2°F), chills, hypothermia, leukocytosis with left shift, neutropenia, and the development of otherwise unexplained organ dysfunction (eg, renal failure, sepsis) [23-25]. In one study of peripartum patients, 63 percent of those with positive blood cultures had fevers ≥39°C (≥102.2°F) [20]. In another study of peripartum patients, laboratory-confirmed bacteremia was found in 5.1 percent of those with axillary temperature ≥38°C (≥100.4°F) and/or other clinical indications of systemic infection (eg, elevated C-reactive protein levels or leukocytosis) [26]. In a third study of peripartum patients, bacteremia was predicted by temperature >39.4°C (>103°F), respiratory rate >20 respirations/minute, maternal heart rate >110 beats/minute, and bandemia >10 percent [21]. (See "Detection of bacteremia: Blood cultures and other diagnostic tests".)

Although IAI is a concern in patients with intrapartum fever, blood cultures are not routinely performed in patients with suspected IAI. The treatment of IAI is antibiotic therapy plus delivery, and empiric therapy is effective in 85 to 90 percent of these patients. (See 'Intraamniotic infection (chorioamnionitis)' below.)

For suspected pyelonephritis, blood cultures are less useful than urine cultures. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Acute pyelonephritis'.)

Urine testing — Urinary dipstick testing is fast, convenient, and low in cost. The specimen can be obtained from a clean catch midstream urine collection, via a straight catheter, or from an indwelling catheter. It is considered positive if either leukocyte esterase or nitrite is detected: positive leukocyte esterase indicates pyuria, and positive nitrite indicates the presence of enteric organisms that convert urinary nitrate to nitrite. For either finding, sensitivity and specificity for infection are 50 and 97 percent, respectively; thus, there is a high false negative rate [27]. We suggest confirmation with urine microscopy and urine culture if the patient is clinically ill or has a temperature ≥39°C (≥102.2°F).

Urine culture is not practical as a first-line diagnostic test when a patient is in labor since results may take 24 to 48 hours after collection. (See "Sampling and evaluation of voided urine in the diagnosis of urinary tract infection in adults".)

Sputum testing — Testing sputum for a microbial diagnosis in patients with suspected community-acquired pneumonia is optional. For most patients, omitting sputum testing is appropriate because empiric treatment is usually successful and the diagnosis of pneumonia is based on chest radiograph. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".)

Influenza testing — Pregnant patients in labor with a flu-like illness should undergo diagnostic testing for influenza. A rapid antigen or immunofluorescence antibody test provides results soonest. (See "Seasonal influenza and pregnancy" and "Seasonal influenza in adults: Clinical manifestations and diagnosis".)

Amniotic fluid testing — Amniocentesis is rarely performed in patients in whom delivery is expected within a few hours. It may be performed in patients in preterm labor with intact membranes to diagnose subclinical IAI, given tocolysis is generally not effective in this setting. (See "Clinical chorioamnionitis", section on 'When to perform amniocentesis to test amniotic fluid'.)

Biological markers — A systematic review of studies on intrapartum fever concluded that measurement of biological markers (eg, C-reactive protein) in maternal serum is unreliable for detecting intrauterine infection in clinical practice [28]. Although amniotic fluid IL-6 and IL-8 levels are significantly elevated with IAI, optimal threshold values for diagnosis of intrauterine infection have not been established and these diagnostic markers are also not used clinically.

COMMON ETIOLOGIES AND MANAGEMENT

Overview — The most common etiologies of intrapartum fever are intraamniotic infection (IAI) and use of neuraxial anesthesia. Because intrapartum fever is the key clinical sign of IAI and no intrapartum clinical or laboratory findings reliably distinguish between IAI and neuraxial anesthesia-related maternal temperature elevation, antibiotics for treatment of IAI are usually administered when maternal temperature is ≥38°C (≥100.4°F) orally and other infection-related sources of fever (respiratory, urinary tract, gastrointestinal, etc) have been reasonably excluded (algorithm 1). The low threshold for diagnosis and antibiotic treatment of IAI leads to overtreatment since many of these patients have been found to be culture-negative in research studies [29].

General supportive measures for febrile patients, regardless of the etiology, include acetaminophen, reduction in room temperature, reduction of clothing, and rehydration, as indicated.

Infectious etiologies

Intraamniotic infection (chorioamnionitis) — IAI (also called chorioamnionitis) refers to infection of the amniotic fluid, membranes, placenta, and/or decidua. Clinically, the essential criterion for diagnosis of IAI is just a maternal fever, which is a manifestation of systemic inflammation. Other criteria (clinical and laboratory) are insensitive. (See "Clinical chorioamnionitis", section on 'Diagnosis'.)

For clinical research, the diagnosis of IAI has usually been based upon the presence of maternal fever ≥38°C (≥100.4°F) orally and at least two of the following conditions [30]:

●Maternal tachycardia (greater than 100 beats/minute)

●Fetal tachycardia (greater than 160 beats/minute)

●Uterine tenderness

●Foul odor of the amniotic fluid

●Maternal leukocytosis (greater than 15,000 cells/cubic millimeter)

However, in 2016, an expert panel convened to address the diagnosis and management of pregnant people with IAI and their neonates recommended the new diagnostic term of "intrauterine inflammation or infection or both" or "triple I" with the features in the table (table 2) [5]. This approach has not been universally accepted clinically.

Common maternal complications of IAI include labor abnormalities, need for cesarean birth, uterine atony, postpartum hemorrhage, endometritis, and septic pelvic thrombophlebitis. Fetal complications include early onset neonatal sepsis, pneumonia, and meningitis. (See "Clinical chorioamnionitis", section on 'Maternal course' and "Clinical chorioamnionitis", section on 'Perinatal outcome'.)

Delivery is indicated after diagnosis of IAI. Prompt treatment with broad spectrum antibiotics with coverage for group B Streptococcus reduces maternal and neonatal morbidity. Ampicillin plus gentamicin is a common regimen. Doses and alternative regimens are reviewed separately. (See "Clinical chorioamnionitis", section on 'Maternal management'.)

Urinary tract infection — Urinary tract infections are common in pregnant people and can complicate labor at term. Signs and symptoms of upper or complicated urinary tract infections include fever, flank pain, nausea, vomiting, and costovertebral angle tenderness with or without lower urinary tract symptoms such as dysuria, frequency, urgency, suprapubic pain, and hematuria. Simple cystitis (infection confined to the bladder) is not associated with fever. Clinical manifestations, diagnosis, differential diagnosis, and antibiotic treatment are reviewed separately. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy".)

Respiratory tract infection

●Upper respiratory tract infection – Upper respiratory tract infection is common in pregnant people, especially in the winter, when the etiology is likely viral. The most common clinical manifestations are nasal congestion, rhinorrhea, and scratchy throat, but sore throat, cough, and malaise also occur frequently. Fever, if present, tends to be low grade. Supportive treatment is indicated. (See "Approach to the pregnant patient with a respiratory infection".)

●Pneumonia – Pneumonia classically presents with the sudden onset of rigors followed by fever, pleuritic chest pain, and cough productive of purulent sputum. The diagnosis of pneumonia is similar to that in nonpregnant individuals. A chest radiograph is usually required for confirmation of the diagnosis, but may be delayed until after the birth (see "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults"). Antibiotic therapy is targeted to cover the infecting organisms typically associated with community acquired pneumonia in nonpregnant patients. Pregnant patients may be treated safely with azithromycin or azithromycin and ceftriaxone. (See "Approach to the pregnant patient with a respiratory infection".)

●Influenza – Influenza characteristically begins with the abrupt onset of fever, headache, myalgia, and malaise after an incubation period of one to four days (average two days). These symptoms and signs are accompanied by manifestations of respiratory tract illness, such as nonproductive cough, sore throat, and nasal discharge. Pregnant people are more likely to have complications from influenza. In one study, influenza was the most common virus isolated in samples positive for a respiratory virus and obtained from symptomatic intrapartum patients [31]. Consideration of influenza is important because influenza antiviral treatment is available. Diagnosis, treatment, and prevention of influenza are described in detail separately. (See "Seasonal influenza and pregnancy".)

●COVID-19 – Coronavirus disease 2019 (COVID-19) must also be on the differential, given the pandemic. Similar to nonpregnant patients, common symptoms of COVID-19 in pregnant people are fever and cough. (See "COVID-19: Clinical features" and "COVID-19: Overview of pregnancy issues" and "COVID-19: Diagnosis".)

Noninfectious etiologies

Use of neuraxial anesthesia

●Overview – Randomized trials and observational studies have consistently observed a frequent and significant association between the use of neuraxial anesthesia (epidural, combined spinal epidural [CSE]) and rise in maternal temperature. In a 2018 meta-analysis of randomized trials of epidural versus opioids for labor pain management, epidural more than doubled the risk of fever >38°C (>100.4°F; risk ratio 2.51, 95% CI 1.67-3.77) [32]. In a 2021 meta-analysis of randomized trials that used ≥37.5°C (≥99.5°F) to define hyperthermia, epidural increased the risk of intrapartum hyperthermia more than fourfold (odds ratio 4.21, 95% CI 3.48-5.09) [33].

Because intrapartum fever is the most objective clinical sign of IAI and no intrapartum clinical or laboratory findings reliably distinguish between IAI and epidural-related maternal temperature elevation, antibiotics for treatment of IAI are usually administered when maternal temperature is ≥38°C (≥100.4°F) orally.

●Etiology – The etiology of the temperature increase associated with neuraxial anesthesia is incompletely understood. It has been associated with many factors that may not be independent or causal [34]. It is often attributed to one of the following [35]:

•Direct effects of local anesthetics on endothelial cells, trophoblastic tissue, or leukocytes to induce proinflammatory or inhibit anti-inflammatory cytokine release [2,36-39]. This is the most likely etiology.

•IAI. Use of neuraxial anesthesia and IAI share risk factors such as nulliparity, induction of labor, internal monitoring, more vaginal examinations, longer labor, and longer duration of rupture of membranes.

•Reduced heat loss. Laboring patients with epidural anesthesia have less pain-induced hyperventilation and less perspiration because of sympathetic block, which may reduce heat loss. On the other hand, vasodilation below the level of neuraxial blockade increases heat loss and is typically associated with a slight decrease in core temperature in nonpregnant patients.

•Abnormality in maternal thermoregulation. A temperature increase has also been reported to occur in nonpregnant patients receiving prolonged postoperative neuraxial analgesia; thus, it is not necessarily related to pregnancy and labor per se [40]. However, it is most common in laboring patients and not seen intraoperatively in nonpregnant populations, possibly because of inhibition of fever by inhaled anesthetic agents and use of opioids [38].

Data from a historical cohort study of maternal temperature before and after availability of neuraxial anesthesia suggest that the neuraxial anesthetic itself is most likely the cause of the increase in maternal temperature. In this study, when neuraxial anesthesia usage increased from 1 percent to 83 percent, the incidence of maternal temperature ≥100.4°F abruptly increased from 0.6 percent to 11 percent [41].

●Presentation – Most laboring patients do not experience an increase in temperature following neuraxial anesthesia, but for those who do, the rise in maternal temperature occurs immediately. Temperature increases average 0.18°C/hour (0.33°F) and are statistically significantly higher than baseline by one hour after catheter placement; an overall increased incidence of fever ≥38°C appears by four hours of exposure and increases with increasing duration of exposure [42,43].

●Epidemiology – Nulliparous patients are more likely to have longer labors and are more likely to have intrapartum fever than multiparas; the risk of neuraxial anesthesia related fever in nulliparas is 13 to 33 percent [29].

●Prevention – There is no proven safe and effective method for preventing neuraxial anesthesia-related temperature elevation. Reducing the overall dosage of local anesthetic reduced the incidence of intrapartum fever in some trials, but the reduction was not statistically significant when those at high risk of bias were excluded from a meta-analysis (RR 0.83, 95% CI 0.41-1.67) [44]. The choice of anesthetic drug may also play a role, but this requires further study. In one retrospective cohort study, for example, ropivacaine was associated with less intrapartum fever than levobupivacaine [45]. The specific technique may also be a factor. Although a randomized trial found no difference in mean maximum maternal temperature between laboring patients who received CSE versus epidural anesthesia, the results could have been affected by differences in timing of placement (CSE was performed before 4 cm whereas epidural was performed after 4 cm dilation) [46].

Neither prophylactic acetaminophen nor cefoxitin prevent the maternal temperature elevation, but prophylactic steroids appear to be effective (incidence of intrapartum fever with and without steroid prophylaxis: 2 in 109 [1.8 percent] versus 26 in 161 [16.1 percent]; RR 0.19, 95% CI 0.05-0.71 [44]) [44,47]. In a randomized trial, high-dose systemic corticosteroids (methylprednisolone 100 mg every four hours) prevented maternal temperature elevation (incidence of fever 2 versus 34 percent in untreated controls), but was associated with an increased risk of asymptomatic bacteremia in neonates (4 of 49 neonates versus 0 of 120 control neonates) [48]. In another randomized trial, the addition of low-dose dexamethasone to the epidural maintenance solution mitigated increases in both maternal temperature and interleukin (IL)-6 levels [49]. These latter two trials support the hypothesis that a catheter or drugs in the neuraxial space induces a maternal inflammatory response in laboring patients that results in fever and can be prevented by local or systemic steroids [50]. However, steroid use cannot be recommended until safety and efficacy for this indication have been established. Increasing the risk of infection is a concern.

Labor or birth in an overheated room — When the temperature of the surroundings becomes greater than that of the skin, the body is no longer able to lose heat by conduction or radiation. Instead, it gains heat from the environment by these same two mechanisms [51]. Measures to promote temperature reduction include lowering room temperature, removing blankets and clothing, hydration if the patient is dehydrated, and applying cool, wet towels to the skin.

Drug fever — Drug fever is a diagnosis of exclusion. The timing of the onset of fever in relation to beginning a drug and the pattern of fever are frequently not helpful in making a diagnosis. However, since the median time to onset is approximately eight days, drug fever would rarely account for a newly developed intrapartum temperature elevation unless the drug had been initiated antepartum. (See "Drug fever".)

CONSEQUENCES

Newborn — Composite neonatal morbidity appears to correlate with the severity of intrapartum fever (mild fever [38-39°C] as compared with severe fever [>39°C]). This correlation is independent of the duration of time between the occurrence of the maximum intrapartum temperature and delivery [52].

●Newborn consequences from infection-related maternal fever – When maternal fever is due to an infectious process, peripartum transfer of the infection to the fetus/neonate is a major concern [7]. The risk to the newborn depends on the type of infection. For intraamniotic infection (IAI) (chorioamnionitis), short-term adverse outcomes include neonatal sepsis, meningitis, and pneumonia; potential long-term outcomes include neurodevelopmental delay and cerebral palsy. (See "Clinical chorioamnionitis", section on 'Perinatal outcome'.)

Appropriate intrapartum maternal antibiotic therapy reduces the risk of fetal/neonatal infection (as well as some maternal complications) and is the basis for intrapartum treatment of patients with IAI. (See "Clinical chorioamnionitis", section on 'Maternal management'.)

●Newborn consequences neuraxial anesthesia-related maternal fever – The increase in maternal temperature associated with neuraxial anesthesia has been associated with an increased rate of neonatal sepsis investigations and antibiotic treatment [53], and possibly an increase in neonatal infection. In a 2021 propensity-scored matched cohort study comparing nearly 20,000 nulliparous patients who received neuraxial analgesia in labor with over 15,000 who did not, neuraxial anesthesia was associated with a higher incidence of maternal fever and neonatal infection [54]. However, there are many variables of labor management that could have confounded the results, including the number of cervical examinations and rates of oxytocin use and vacuum- or forceps-assisted birth. Furthermore, the overall incidence of neonatal infection was low (4.4 percent with versus 1.8 percent without neuraxial anesthesia), and the neonatal infections were not associated with increased morbidity or mortality.

The appropriate evaluation and management of the newborn following observation of maternal intrapartum fever is unclear. The decision to perform a neonatal sepsis work-up should be guided by factors in addition to maternal temperature, such as gestational age and maternal and neonatal clinical findings. Triggers for sepsis work-up in neonates include low birth weight, preterm birth, hypothermia at birth, maternal group B beta-hemolytic streptococcal colonization, preeclampsia, and maternal hypertension [55]. In addition, the clinician should note whether neuraxial anesthesia was administered for a prolonged length of time and whether a rapid fall in maternal temperature occurred after the neuraxial anesthetic was discontinued, which supports but does not prove neuraxial anesthesia was the source of maternal fever [56]. Ongoing monitoring of asymptomatic newborn infants with risk factors for infection is important so that early signs and symptoms of sepsis are identified. (See "Clinical features and diagnosis of bacterial sepsis in preterm infants <34 weeks gestation" and "Clinical features, evaluation, and diagnosis of sepsis in term and late preterm neonates".)

Neuraxial anesthesia-related maternal temperature elevation may be associated with adverse neonatal outcome, even in the absence of documented infection; however, this is controversial, in part, because it is difficult to exclude the presence of infection conclusively. The purported mechanism is induction of the fetal inflammatory response syndrome, which has been linked to subsequent neurodevelopmental delay [57-61]. In one study, newborns of parturients with temperature elevation were at increased risk of hypotonia and having a low Apgar score and requiring bag and mask resuscitation, receiving oxygen therapy, and developing unexplained neonatal seizures [62]. A follow-up study from the same institution noted that the frequency of adverse neonatal outcomes increased with increasing maternal intrapartum temperature [58]. The long-term significance of these observations is unknown.

Maternal — Maternal outcome depends on the cause of intrapartum fever. Patients who develop intrapartum fever are more likely to receive antibiotics for presumed or documented infection [42]. One study observed that low risk nulliparous patients who developed intrapartum fever were twice as likely to require a cesarean or assisted vaginal birth than those without intrapartum fever, regardless of whether they received or did not receive neuraxial anesthesia [63].

In contrast to the neonate, composite maternal morbidity does not appear to correlate with the severity of intrapartum fever [52] .

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Group B streptococcal infection in pregnant women and neonates" and "Society guideline links: Labor".)

SUMMARY AND RECOMMENDATIONS

●Diagnosis – Intrapartum fever is generally defined as maternal temperature ≥38°C (≥100.4°F) orally. (See 'Definition' above.)

●Etiology

•The most common infection-related etiologies of intrapartum fever are intraamniotic infection (IAI), urinary tract infection, and respiratory infection. (See 'Infectious etiologies' above.)

•Use of neuraxial anesthesia is the most common cause of intrapartum fever at term. The rise in maternal temperature correlates with the duration of neuraxial anesthesia, particularly after four hours. The maternal temperature elevation in these patients is unrelated to infection. (See 'Use of neuraxial anesthesia' above.)

●Diagnostic evaluation

•Laboratory testing is not routinely performed in patients with intrapartum fever, but should be guided by the suspected diagnosis (eg, pyelonephritis, influenza). (See 'Laboratory' above.)

•The value of an intrapartum white blood cell (WBC) count is limited because high values normally occur during labor. However, when clinical concern about infection is high (eg, patient appears ill, temperature ≥39°C [≥102.2°F]), leukocytosis accompanied by a left shift or bandemia supports a diagnosis of infection. (See 'White blood cell (WBC) count and differential' above.)

•Potential indications for blood cultures include fever ≥39°C (≥102.2°F), chills, hypothermia, leukocytosis with left shift, neutropenia, and the development of otherwise unexplained organ dysfunction. (See 'Blood cultures' above.)

•We perform urinary dipstick testing to screen for urinary tract infection. We obtain confirmation with urine microscopy and urine culture if the patient is clinically ill or with temperature ≥39°C (≥102.2°F). (See 'Urine testing' above.)

●Treatment – Because intrapartum fever is key clinical sign of IAI and no intrapartum clinical or laboratory findings reliably distinguish between IAI and neuraxial anesthesia-related maternal temperature elevation, broad spectrum antibiotics for treatment of IAI are usually administered when maternal temperature is ≥38°C (≥100.4°F) orally (algorithm 1); however, this results in overtreatment of mothers. (See 'Use of neuraxial anesthesia' above.)

●Consequences – When maternal fever is due to an infectious process, peripartum transfer of the infection to the fetus/neonate is a major concern because of the potential for neonatal morbidity/mortality. Appropriate intrapartum maternal antibiotic therapy reduces the risk of fetal/neonatal infection, as well as maternal complications. (See 'Maternal' above.)

Neuraxial anesthesia-related maternal temperature elevation may be associated with adverse neonatal outcome, even in the absence of documented infection; however, this is controversial, in part, because it is difficult to exclude the presence of infection conclusively. The decision to perform a septic work-up in neonates of patients who had neuraxial anesthesia and fever should be guided by factors in addition to maternal temperature, such as gestational age and maternal and neonatal clinical findings. (See 'Newborn' above.)