Intrapartum fever

INTRODUCTION — 

Fever 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. 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 first or second stage of labor, macrosomia, and prelabor rupture of membranes [1-3]. These characteristics are not independent and describe patients likely to receive neuraxial analgesia and/or develop clinical chorioamnionitis. In the absence of a preexisting febrile disorder (eg, known infection preceding labor), most pregnant patients who develop fever in labor are presumed to have clinical chorioamnionitis and are treated with broad-spectrum antibiotics [4].

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

DIAGNOSIS OF FEVER — 

Intrapartum fever is generally considered to be maternal temperature ≥38°C (≥100.4°F) orally. It has been defined as mild when 38 to 39°C (100.4 to 102.2°F) and severe when >39°C (>102.2°F) [5,6].

This threshold is based, in part, on a retrospective study of 502 normal parturients at term that found their temperature ranged from 34.6 to 37.6°C (94.3 to 99.7°F) upon admission to the labor unit and showed diurnal variation, with a peak from midnight to 2 AM and a nadir from 11 AM to noon [7]. Normal parturients were defined as having intact membranes on admission, spontaneous labor and subsequent birth, and no evidence of an infectious or inflammatory disease antepartum, intrapartum, or postpartum. Others have observed a slight increase in temperature within this range over the course of normal labor [8].

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 analgesia).

Intrapartum fever has become common in recent decades: occurring in 6.8 percent of laboring patients (1 in 15) in a prospective cohort study of over 6000 births from 2011 to 2014 [9]. By comparison, 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 [10]. The several-fold increase in prevalence has been associated with increased use of neuraxial analgesia. (See 'Use of neuraxial analgesia' below.)

RISK FACTORS — 

The risk factors for developing intrapartum fever are the risk factors for the various etiologies of intrapartum fever [3]:

●Longer time in the first stage of labor

●Longer time with ruptured membranes

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 [11]. 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 parturient has not consumed fluids or ice in the 15 minutes before the temperature is determined [11].

Tympanic and axillary temperature measurements are particularly susceptible to user error [12]. 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 [13]. 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 [11].

Of note, fetal/intrauterine temperature is 0.2 to 0.9°C (0.4 to 1.6°F) higher than maternal oral temperature [11,14-17].

DIAGNOSTIC EVALUATION

All patients

History and physical — History and physical examination are performed to look for potential causes of fever, infectious or noninfectious; obstetric and nonobstetric. As part of the history, the clinician should confirm the first occurrence of temperature elevation (eg, did the patient have fever prior to admission?) and ask about any associated symptoms and contact with sick individuals. In parturients, the initial focus of the physical examination is auscultation of the lungs; assessment for fundal, abdominal, or costovertebral angle tenderness; and assessment for malodorous amniotic fluid draining from the vagina. Key points to consider:

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

●Prolonged labor, prolonged membrane rupture, and exposure to intrauterine devices such as an intrauterine pressure catheter or a fetal scalp electrode are risk factors for clinical chorioamnionitis. (See '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 'Complicated urinary tract infection' below and 'Respiratory tract infection' below and "COVID-19: Clinical features" and "Seasonal influenza and pregnancy" and "Overview of community-acquired pneumonia in adults" and "Clinical manifestations and diagnosis of Listeria monocytogenes infection", section on 'Pregnant patients' and "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis" and "Acute appendicitis in pregnancy".)

●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 'Other noninfectious causes of fever' below.)

●Fetal tachycardia may occur in response to maternal fever or intrauterine infection.

Selective laboratory testing — Comprehensive laboratory testing is not routinely performed. Selective testing should be guided by the suspected diagnosis and the severity of clinical illness.

Patients who appear clinically ill or with temperature greater than or equal to 39°C (greater than or equal to 102.2°F)

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 [18,19]; the mean count increased linearly with the duration of elapsed labor [19]. However, when clinical concern about an infection rather than a noninfectious process is high, leukocytosis supports the diagnosis of infection, especially when accompanied by a left shift or bandemia.

Urine testing — Urinary dipstick testing is a fast, convenient, practical, and inexpensive initial option if the labor unit has the ability to perform point-of-care testing. 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. If one of these tests is positive, sensitivity for a positive urine culture ranges from 46 to 100 percent and specificity ranges from 42 to 98 percent [20]. If the unit does not have point-of-care testing, we suggest sending a urine specimen to the laboratory for dipstick and reflex microscopy and urine culture. Urine culture is not as useful as the first-line diagnostic test when a patient is in labor since results may take 24 to 48 hours after collection, yet may guide antibiotic therapy selection. (See "Sampling and evaluation of voided urine in the diagnosis of urinary tract infection in adults".)

Blood cultures — The usefulness of blood cultures has not been studied specifically in intrapartum patients, and no consensus guidelines address when to obtain intrapartum blood 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 [21-23], most peripartum patients with bacteremia have fevers ≥39°C (≥102.2°F) [22], and the following observational data:  

●In a study of peripartum patients, bacteremia was predicted by temperature >39.4°C (>103°F), respiratory rate >20 respirations/minute, maternal heart rate >110 beats per minute, and bandemia >10 percent [23]. (See "Detection of bacteremia: Blood cultures and other diagnostic tests".)

●In another study of peripartum patients, laboratory-confirmed bacteremia was found in only 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) [24].

Bacteremia does not necessarily lead to sepsis. In a study of 135 pregnant and postpartum women who had at least one positive blood culture, only two developed sepsis and three septic shock [25,26].

Arguments for a more liberal approach to ordering blood cultures include: blood cultures sent before initiation of antibiotics will provide higher yield than those obtained after, a positive blood culture affects the choice and duration of antibiotic treatment and in some cases allows deescalation of antibiotic therapy, and early identification of more serious causes of fever such as group A Streptococcus may be beneficial.

Although clinical chorioamnionitis is a potential cause of intrapartum fever, blood cultures are not routinely performed when chorioamnionitis is the suspected diagnosis because the treatment is antibiotic therapy plus expeditious delivery, which is effective in 85 to 90 percent of these patients. (See 'Chorioamnionitis' below.)

For suspected pyelonephritis, blood cultures are less useful than urine cultures, yet may help in selection and duration of antibiotic therapy. (See "Urinary tract infections and asymptomatic bacteriuria in pregnancy", section on 'Acute pyelonephritis'.)

Lactate level — Obtaining a venous lactate level can be helpful since a raised concentration (hyperlactatemia) can be a sign of sepsis and correlates with severity of sepsis. Although the normal range increases during the course of labor, a lactate level greater than 4 mmol/L suggests tissue hypoperfusion or cellular metabolic dysfunction and should prompt immediate escalation of care [27,28].

Respiratory virus testing — Pregnant patients in labor with a flu-like illness should undergo diagnostic testing for influenza and SARS-CoV-2. Multiplex polymerase chain reaction (PCR) panels that test for a wide array of viral and bacterial pathogens can be used. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Testing for respiratory viruses'.)  

Other testing

Amniotic fluid testing — Amniocentesis is rarely performed in patients who are anticipated to give birth within a few hours. It may be performed in patients in preterm labor with intact membranes to diagnose subclinical intraamniotic infection, given tocolysis is generally not effective in this setting. Amniotic fluid is tested for Gram stain, glucose concentration, WBC concentration, and leukocyte esterase level, and send for culture. Interpretation of findings is reviewed separately. (See "Clinical chorioamnionitis", section on 'When to perform amniocentesis to test amniotic fluid'.)

Sputum testing — Testing sputum for a microbial diagnosis in patients with suspected community-acquired pneumonia is optional. The diagnosis of community acquired pneumonia may be based on clinical features alone (eg, fever, dyspnea, cough, tachycardia, crackles on chest auscultation, and oxygen saturation <95 percent); the demonstration of an opacity on chest imaging confirms the diagnosis. Empiric treatment is usually successful. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Approach to the pregnant patient with a respiratory infection", section on 'Community-acquired pneumonia'.)

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 [29]. Although amniotic fluid interleukin (IL)-6 and IL-8 levels are significantly elevated with clinical chorioamnionitis, 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

General principles

●Most common etiologies – Approximately 95 percent of cases of intrapartum fever have been attributed to epidural analgesia, and 5 to 10 percent of cases have been associated with infection based on a positive polymerase chain reaction (PCR) for bacterial products, bacteremia or placental culture with or without epidural analgesia [4]. (See 'Chorioamnionitis' below and 'Use of neuraxial analgesia' below.)

●General supportive measures – Administration of acetaminophen is the primary supportive intervention for febrile patients, regardless of the etiology. General supportive measures include reducing the room temperature, reducing clothing/bedding, and rehydration, as indicated.

●Use of antibiotics – Treatment of infection depends on the specific infection, if known. Because intrapartum fever is the key clinical sign of chorioamnionitis and no intrapartum clinical or laboratory findings reliably distinguish between it and neuraxial analgesia-related maternal temperature elevation, antibiotics are administered for treatment of presumptive chorioamnionitis when maternal temperature is ≥38°C (≥100.4°F) orally and other infection-related sources of fever (respiratory, urinary tract, etc) have been reasonably excluded (algorithm 1). The low threshold for diagnosis and antibiotic treatment of presumptive chorioamnionitis leads to overtreatment since many of these patients have been found to be culture-negative in research studies [30].

●Newborn care – A pediatrician should be called to attend any birth where the obstetrical provider has concerns that the newborn may be compromised. Otherwise, the pediatrician should be notified of maternal intrapartum fever and informed about other intrapartum events and any treatment.

Infectious etiologies

Chorioamnionitis — Chorioamnionitis refers to infection of the amniotic fluid, membranes, placenta, and/or decidua. Fever is the essential criterion for diagnosis and a manifestation of systemic inflammation; other criteria (clinical and laboratory) are insensitive. For diagnosis of chorioamnionitis, fever can be defined as maternal temperature ≥39°C (≥102.2°F) on one reading orally or ≥38°C (≥100.4°F) and <39°C (102.2°F) orally on two readings 30 minutes apart [31]. (See "Clinical chorioamnionitis", section on 'Diagnosis'.)

A presumptive diagnosis of clinical chorioamnionitis can be made in patients with fever without a clear source plus one or more of the following findings [31]:

●Baseline fetal tachycardia (greater than 160 beats per minute for 10 minutes or longer, excluding accelerations, decelerations, and periods of marked variability)

●Maternal white blood cell (WBC) count greater than 15,000 per mm³ in the absence of corticosteroids

●Definite purulent fluid from the cervical os

Common maternal complications 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'.)

Prompt initiation of broad-spectrum antibiotics (eg, ampicillin plus gentamicin; cefazolin plus gentamicin for patients with mild penicillin allergy; clindamycin or vancomycin plus gentamicin for patients with severe penicillin allergy) is required upon diagnosis to reduce maternal and neonatal morbidity. Antibiotic regimens are reviewed in detail separately. (See "Clinical chorioamnionitis", section on 'Maternal management'.)

Complicated 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 may include fever, chills, 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 [32]. 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 – COVID-19 must also be on the differential. 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 analgesia

●Overview – Randomized trials and observational studies have consistently observed a frequent and significant association between the use of neuraxial analgesia and rise in maternal temperature. In meta-analyses of randomized trials, the risk for intrapartum fever was approximately three- to fourfold higher in patients with versus without neuraxial analgesia (15 to 20 percent versus about 6 percent; risk ratio [RR] 2.51-4.21) [33-35].

●Etiology – The etiology of the temperature increase associated with neuraxial analgesia in laboring patients is incompletely understood. It has been associated with many factors that may not be independent or causal [36]. It is often attributed to one of the following [37]:

•Direct effects of local anesthetics on endothelial cells, trophoblastic tissue, or leukocytes to induce proinflammatory or inhibit anti-inflammatory cytokine release [38-42]. This immune-mediated process is the most likely etiology.

•Chorioamnionitis. Use of neuraxial analgesia and chorioamnionitis 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 analgesia 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 [43]. 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 [41].

Data from a seminal historical cohort study of maternal temperature before and after availability of neuraxial analgesia suggest that the neuraxial anesthetic itself is most likely the cause of the increase in maternal temperature. In this study, when neuraxial analgesia usage increased from 1 percent to 83 percent, the incidence of maternal temperature ≥38°C (≥100.4°F) abruptly increased from 0.6 percent to 11 percent [44].

●Presentation – Most laboring patients do not experience an increase in temperature following neuraxial analgesia, but for those who do, the rise in maternal temperature occurs soon after catheter placement and drug infusion. Temperature increases average 0.18°C/hour (0.33°F) and are statistically significantly higher than baseline by one hour of exposure; an overall increased incidence of fever ≥38°C (100.4°F) appears by four hours of exposure and increases with increasing duration of exposure [45,46].

The maximum temperature associated with intrapartum neuraxial anesthesia alone is unclear. One author stated that temperature typically does not exceed 39.5°C (103.1°F) [43]. Others have defined epidural related maternal fever as "any temperature recorded between 38°C (100.4°F) and 38.9°C (102.02°F) with no other clinical criteria indicating intraamniotic infection and with or without persistent temperature elevation" [47].

●Epidemiology – Nulliparous patients are more likely to have longer labors and are more likely to have intrapartum fever than multiparas; the risk of neuraxial analgesia related fever in nulliparas ranges from 13 to 33 percent [30].

●Course – Data are limited, but fever resolved within a few hours of giving birth in 90 percent of patients in one study [48]. The etiology of postpartum fever in the remaining patients was unclear and may have been related to infection.

●Treatment – Because intrapartum fever is the most objective clinical sign of clinical chorioamnionitis and no intrapartum clinical or laboratory findings reliably distinguish between it and epidural-related maternal temperature elevation, antibiotics for treatment of presumptive chorioamnionitis are usually administered when maternal temperature is ≥39°C (≥102.2°F) on one reading orally or ≥38°C (≥100.4°F) and <39°C (102.2°F) orally on two readings 30 minutes apart and other causes of fever have been reasonably excluded.

●Prevention – There is no proven safe and effective method for preventing neuraxial analgesia-related temperature elevation.

•Procedural factors – 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) [49]. The choice of anesthetic drug may also play a role, but this requires further study. While two randomized trials comparing combined spinal-epidural (CSE) with epidural analgesia in laboring patients found no difference in the incidence of intrapartum fever or mean maximum maternal temperature [50,51], another found that CSE resulted in a lower incidence of intrapartum fever [52]. The latter trial also found that CSE used a lower dose of epidural local anesthetic and resulted in a shorter duration of analgesia to delivery, which may have accounted for the lower incidence of intrapartum fever.

•Prophylactic medication – 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 [49]) [49,53].

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) [54]. 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 [55]. 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 [56]. However, steroid use cannot be recommended until safety and efficacy for this indication have been established. Increasing the risk of neonatal infection is a concern.

Other noninfectious causes of fever

●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 [57]. 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.

●Exposure to prostaglandins for cervical ripening/labor induction – Prostaglandins are commonly used for cervical ripening before labor induction. The frequency of prostaglandin-related fever is low in this setting. Fever appears to be related to both dose and route of administration [58,59]. It occurs at cumulative doses exceeding 600 micrograms, which are commonly used for pregnancy termination and management of atony not cervical ripening/induction [60]. (See "Induction of labor: Techniques for preinduction cervical ripening", section on 'Side effects'.)

●Thyroid storm – Thyroid storm is rare. When it occurs, hyperpyrexia to 40 to 41.1°C (104 to 106°F) is common, along with agitation, anxiety, delirium, psychosis, stupor, or coma. (See "Thyroid storm".)

●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".)

Anticholinergic drugs (eg, atropine) can raise core temperature by inhibiting sweating or vasodilatation without changing the normal hypothalamic set point.

CONSEQUENCES

Newborn — Several studies have observed an increase in composite neonatal morbidity as maternal intrapartum temperature increases (in one study: <38°C: 5.4 percent, 38°C to 39°C: 18 percent, >39°C: 29.7 percent [5]) [5,6,61,62]. In one of these studies, the relationship appeared to be independent of whether the maximum temperature occurred early or late in the course of labor, suggesting that shortening the duration of labor after the peak might not alter neonatal outcome [5].

●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 [10]. The risk to the newborn depends on the type of infection. For clinical chorioamnionitis (intraamniotic infection), 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 clinical chorioamnionitis. (See "Clinical chorioamnionitis", section on 'Maternal management'.)

●Newborn consequences of neuraxial analgesia-related maternal fever – The increase in maternal temperature associated with neuraxial analgesia has been associated with an increased rate of neonatal sepsis investigations and antibiotic treatment [63], 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 analgesia was associated with a higher incidence of maternal fever and neonatal infection [64]. 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 analgesia), and the neonatal infections were not associated with increased morbidity or mortality. The authors concluded that the results of their study should not be a reason to refuse epidural analgesia.

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 [65]. In addition, the clinician should note whether neuraxial analgesia 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 analgesia was the source of maternal fever [66]. Ongoing monitoring of asymptomatic newborn infants with risk factors for infection is important so that early signs and symptoms of sepsis are identified. (See "Neonatal bacterial sepsis: Clinical features and diagnosis in neonates born at less than 35 weeks gestation" and "Neonatal bacterial sepsis: Clinical features and diagnosis in neonates born at or after 35 weeks gestation".)

Neuraxial analgesia-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 [67-71]. In one study, newborns of parturients with temperature elevation were at increased risk of hypotonia, of having a low Apgar score, requiring bag and mask resuscitation, receiving oxygen therapy, and developing unexplained neonatal seizures [72]. A follow-up study from the same institution noted that the frequency of adverse neonatal outcomes increased with increasing maternal intrapartum temperature [68]. 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 [45]. One study observed that low risk nulliparous patients who developed intrapartum fever were twice as likely to require a cesarean or forceps- or vacuum-assisted vaginal birth than those without intrapartum fever, regardless of whether they received or did not receive neuraxial analgesia [73].

In contrast to the neonate, composite maternal morbidity does not appear to correlate with the severity of intrapartum fever [5].

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 people 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. It has been defined as mild when 38 to 39°C (100.4 to 102.2°F) and severe when >39°C (>102.2°F). (See 'Diagnosis of fever' above.)

●Diagnostic evaluation

•History and physical examination – These assessments are performed to look for potential causes of fever. The most common infection-related etiologies are clinical chorioamnionitis, urinary tract infection, and respiratory infection (see 'Infectious etiologies' above). Use of neuraxial analgesia is the most common noninfection-related etiology and the most common cause of intrapartum fever at term. (See 'Use of neuraxial analgesia' above.)

•Laboratory testing for patients who do not appear ill – Comprehensive laboratory testing is not routinely performed in patients with intrapartum fever who do not appear ill and have mild temperature elevation. Selective testing should be guided by the suspected diagnosis (eg, chorioamnionitis, urinary tract infection and respiratory infection). (See 'Diagnostic evaluation' above.)

The value of an intrapartum white blood cell (WBC) count is limited because high values normally occur during labor. (See 'White blood cell (WBC) count and differential' above.)

•Laboratory testing for patients who appear ill and/or have temperature ≥39°C [≥102.2°F])

-WBC count. Leukocytosis accompanied by a left shift or bandemia supports a diagnosis of infection. (See 'White blood cell (WBC) count and differential' above.)

-Urinary dipstick testing, reflex microscopy, and sending urine for culture. (See 'Urine testing' above.)

-Blood cultures (See 'Blood cultures' above.)

-Venous lactate level. An intrapartum level greater than 4 mmol/L is abnormal. (See 'Lactate level' above.)

-Diagnostic testing for influenza and SARS-CoV-2 (in patients with a flu-like illness). (See 'Respiratory virus testing' above.)

●Treatment

•Administration of acetaminophen is the primary supportive intervention for febrile patients, regardless of the etiology. (See 'General principles' above.)

•Treatment of infection depends on the specific infection, if known. (See 'General principles' above and 'Infectious etiologies' above.)

•Intrapartum fever is the most objective clinical sign of clinical chorioamnionitis and no intrapartum clinical or laboratory findings reliably distinguish between it and neuraxial analgesia-related maternal temperature elevation. Broad-spectrum antibiotics are administered to patients with a presumptive diagnosis of chorioamnionitis to minimize maternal and neonatal morbidity from infection, if present (algorithm 1). The choice of antibiotics and evidence supporting treatment of chorioamnionitis are reviewed separately. (See "Clinical chorioamnionitis".)

●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 analgesia-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 analgesia 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.)