eMedicine Specialties > Emergency Medicine > Pediatric

Fever in the Neonate and Young Child

Author: Stella C Wong, DO, Assistant Professor, Department of Emergency Medicine, Emory University School of Medicine
Coauthor(s): Richard J Scarfone, MD, Associate Professor, Department of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician and Director of Emergency Preparedness, Division of Emergency Medicine, The Children's Hospital of Philadelphia; Fred Henretig, MD, Director, Section of Clinical Toxicology, Professor, Medical Director, Delaware Valley Regional Poison Control Center, Departments of Emergency Medicine and Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital
Contributor Information and Disclosures

Updated: Aug 6, 2009

Introduction

Background

This article discusses the appropriate emergency department (ED) clinical and laboratory evaluation of young febrile children, particularly those younger than 3 years of age. Fever, the abnormal elevation of body temperature, has long been recognized by physicians as a sign of disease. Furthermore, the evaluation of the febrile child is one of the most commonly encountered emergency conditions in children, accounting for as many as 20% of pediatric emergency department (ED) visits.1
 
Fever in children may be caused by a number of common and exotic diseases, including viral systemic syndromes and focal infections, bacteremia and septicemia, focal bacterial infections, parasitic and vector-borne infections, and noninfectious etiologies such as vasculitic and hypersensitivity disorders, drug and vaccine reactions, Kawasaki syndrome, and several poisonings, including salicylism. Pinpointing the minimal temperature elevation considered to be definitely abnormal for all children under all circumstances is difficult.1  Factors such as excessive clothing, physical activity, hot weather, food digestion, and ovulation can raise temperature in the absence of disease. For the appropriately dressed child, at rest, a rectal temperature of 38o C (100.4o F) is defined as fever by most authors.2  

Optimal technique to measure rectal temperature is important for accuracy.3 This includes proper positioning and restraint in infants (prone, supine, or on the side with hips slightly flexed), depth of insertion (about 2-3 cm), and time for equilibration (2-3 minutes with glass thermometers, several seconds with electronic digital probes). Thermometer placement directly into a fecal mass should be avoided because fecal temperature may not have equilibrated with rapid fluctuations in body temperature, and thus may be falsely low as temperature rises rapidly. Oral and axillary temperatures usually are about 0.6o C (1o F) and 1.1o C (2o F) less than rectal temperatures, respectively.

Recent attempts to measure temperature with less invasive techniques include temperature‑sensitive pacifiers and forehead strips, both of which have been found to be unreliable in young children. However, one technique that has been found to be acceptable to parents and reliable in most settings is that of infrared tympanic membrane thermometry. Several studies in children have confirmed the reliability of this technique compared with rectal temperature, although others have questioned its accuracy in young infants, especially those younger than 3 months.4 The presence of otitis media or cerumen does not seem to adversely affect reliability. Temporal artery thermometry has also been utilized, but it has limited sensitivity for detecting temperatures in the lower end of the fever range.5

Since even low‑grade fever may be clinically significant in young infants and there is at least some doubt about the reliability of axillary, tympanic, or temporal artery measurements in this age group, it would seem prudent to rely on rectal temperatures in this population.3

Pediatricians have historically considered that febrile infants younger than 2-3 months of age require a more detailed and invasive diagnostic evaluation than older children. The reasons for this are several, including the relative immaturity of infantile host defenses and the potential for perinatally acquired infections, both of which result in an increased risk of bacteremia, sepsis, and significant bacterial focal infections. 

In addition, in this age group, the clinical assessment of "toxicity", or septic appearance, is difficult, as such judgment relies on observation of the child’s responsiveness and behavior, which in babies is so developmentally limited. Thus, the traditional management approach to such infants has consisted of  thorough clinical assessment, supplemented by a comprehensive laboratory evaluation (so-called sepsis workup), and followed typically by empiric parenteral antibiotic therapy and hospitalization pending culture results. Current evidence-based and consensus guidelines are reviewed in the sections to follow.

The approach to febrile children in the age group of 3 months to 3 years has also been the subject of considerable interest and research. Children this age are more readily evaluated by physical examination findings and observation of general appearance than neonates and young infants. However, since the early 1970s, concern exists that clinically significant bacterial infections manifested solely by fever, without localizing signs or symptoms, may be missed by ordinary clinical evaluation. These have included particularly occult bacteremia and occult urinary tract infection. The indications for screening laboratory tests and blood and urine cultures have evolved considerably over time in the ensuing 4 decades, particularly as further research findings and newer immunization strategies have been implemented. In the following discussion, these new developments are highlighted and an evidence-based approach to this age group of febrile children is offered.

Pathophysiology

Fever is a complex phenomenon, involving the highly coordinated interplay of autonomic, neuroendocrine, and behavioral responses to a variety of infectious and noninfectious inflammatory challenges.1 The febrile reaction is quite stereotyped and independent of precise causation.6  Various exogenous pyrogens (eg, toxins, infectious agents, antigen–antibody complexes) produce fever in humans by inducing the production of proteins, collectively termed endogenous pyrogens, by phagocytic leukocytes. These enter the circulation and interact with specialized receptor neurons in the preoptic, anterior hypothalamus. Signaling there leads to the production of prostaglandins, particularly PGE2, which is believed to be the critical mediator of the febrile response, and impacts on hypothalamic neurons that reset the thermostatic set point and result in several responses.

The major effect is on the vasomotor center and results in peripheral vasoconstriction of cutaneous beds with redirection of blood flow to deeper tissues, thus minimizing skin heat loss. Additionally, sweating is decreased; vasopressin secretion falls, resulting in lowered extracellular fluid volume that requires heating; and behavioral modifications such as shivering and seeking a warmer environment are stimulated. These effects combine to elevate body temperature. Very rarely, fever is the result of central nervous system dysfunction (eg, hypothalamic tumor, infarction) that alters the thermostatic set point directly, rather than via pyrogen induction.

There is evidence that increased body temperature impairs replication of many microbes and may aid phagocytic bactericidal activity.1  The febrile response includes additional adaptive neuroendocrine effects. Glucose metabolism is lessened in favor of that based on lipolysis and proteolysis, thereby depriving bacteria of their preferred substrate. Fever‑induced anorexia also diminishes glucose availability to microbes. Hepatic synthesis of acute‑phase reactant proteins may result in binding divalent cations, which serve as growth factors for microorganisms. These effects combine to further enhance the host's response to microbial invasion.

Frequency

United States

Stanley et al reported that infants younger than 3 months with hyperpyrexia (core temperature >40°C) had a significantly increased prevalence of serious bacterial infection (SBI).7 Since the introduction of Haemophilus influenzae type B (Hib) vaccine, the number of Hib meningitis cases in children has decreased significantly.8,9 Excluding the Pneumococcal Conjugate Vaccine (PCV7) studies, American College of Emergency Physicians (ACEP) Clinical Policies Committee reported that "The current prevalence of occult bacteremia among febrile children aged 3 to 36 months is most likely between 1.5% and 2%."10 PCV7 includes the following serotypes: 4, 6B, 9V, 14, 18C, 19F, and 23F.11,12  The rate of occult bacteremia has decreased to less than 1% since the introduction of PCV7 in 2000.13,14,15  

Whitney et al reported that the rates of invasive pneumococcal diseases (IPD) in children younger than 2 years old have declined 69% between 1998-1999 and 2001.12  In a "laboratory-based surveillance study" of children (<5 y old) in the Northern California Kaiser Permanente (NCKP) health care system, Black et al reported the average incidence of IPD decreased from 50.1 cases per 100,000 per year during pre-PCV 7 period (April 1996 to March 2000) to 4.9 cases per 100,000 per year after the introduction of PCV 7 (April 2000 to March 2005).16  

However, studies also show the incidence of other forms of bacteremia increased while the incidence of IPD decreased. In a quasi-experimental study of a cohort of children (<18 y old, n=188) at the Children's Hospital of Philadelphia (CHOP) from January 1999 to May 2005, Steenhoff et al reported the incidence of penicillin-resistance isolates increased from 25% (pre-PCV7) to 39% (post-PCV7), which was statistically significant (P<0.05). The incidence of bacteremia caused by vaccine (PCV7)-related serotypes also increased from 6% (pre-PCV7 period) to 35% (post-PCV7 period), which was also statistically significant (P<0.01). Vaccine-related serotypes was defined as "those of the same serogroup but not of the same serotype as PCV7".11  

In a retrospective case series between September 1998 and August 2003 (n=352), Herz et al reported an increase in the incidence of bacteremia in children (3-36 months old) caused by Staphylococcus aureus, Escherichia coli, and Salmonella species.17 Singleton et al reported a 140% increase of nonvaccine serotypes IPD from 2001-2003 to 2004-2006 in Alaska Native children who were younger than 2 years old, and 28.3% of the cases (2004-2006) were caused by serotype 19A.18

Urinary tract infection (UTI) is the most common SBI in febrile infants and toddlers. The prevalence of UTI in children (2-24 months) with unknown source of fever is estimated to be 3-7%.10,19,20,21,22,23  UTI was also reported to be found in 2.7-3.5% of children with a possible source of fever.24,19,25

International

Richardson et al stated that "Infectious diseases remain a major cause of childhood mortality and morbidity in the United Kingdom".26  Health care deficiency may be the cause.26,27  

Mortality/Morbidity

The long-term effects of UTI can be serious if the infection is not diagnosed or treated. Untreated lower UTI can lead to upper-urinary-tract disease such as pyelonephritis. Pyelonephritis increases risk of renal scarring in children.10,28,29,30 Renal scarring can lead to hypertension and end-stage renal failure later in life.10,31 In addition to UTI, pneumonia, meningitis, bacteremia, and other SBI can also result if a serious infectious illness is not suspected or recognized.   

Race

Caucasian children are at higher risk for developing UTI.24,19,25

Sex

Girls aged 1 year old or younger are 2 times more likely than similarly aged boys to have UTI (6.5% vs 3.3%). In girls aged 1-2 years, the incidence of UTI increases to 8.1%, whereas, in boys, the incidence decreases to 1.9%. Uncircumcised boys are at increased risk for UTIs.10

Age

Age is an important factor in bacteremia and sepsis for at least the following 4 reasons. First, the immune system is not fully developed in young children. Second, the important pathogens vary with age. Third, infants are not scheduled to receive the first PCV immunization until they reach at least 6 weeks old. Fourth, young infants do not have the ability to demonstrate signs of an illness.32  

Pathogens acquired at birth are most likely to affect neonates (<1 mo). By comparison, infants aged 1-3 months are at lower risk for neonatally acquired pathogens; however, they are at higher risk for community-acquired pathogens. Children aged 3 months or older are still at risk for community-acquired pathogens; however, they have a decreased risk of SBI or bacteremia.33

Clinical

History

Children can be septic without having hyperpyrexia; therefore, history taking, physical examination, and clinical judgment are still the most important factors in caring for sick children. History taking is an important part of clinical decision making.

  • Clinicians should ask the patient's parents or caretakers about the following items when they bring in a febrile or ill-appearing child:
    • Immunization history, such as recent vaccination or a history of inadequate immunizations. See the 2008 immunization schedule.34
    • History of maternal infections such as group B Streptococcus (GBS) and/or sexually transmitted diseases
    • History of exposure to sick contacts and treatments, such as antibiotics
    • Recent travel history
    • History of previous hospitalization, prolonged ICU stay, prematurity, or immunocompromised diseases
    • History of change in mental status, change in eating and/or behavioral patterns such as irritability, lethargy, or apnea
    • History of neglect or abuse
    • Documented fever at home, the duration of any fever, and the last treatment (if any) for the fever
  • According to the 2003 clinical policy of the ACEP, "A response to antipyretic medication does not change the likelihood of a child having SBI and should not be used for clinical decision making."10
  • Environmental factors, such as being in the heat for a long time during the summer and being overdressed during the winter, may indicate a risk for hyperthermia.

Physical

Positive findings to look for during physical examination include the following:

  • Vital signs: Rectal temperature, respiratory rate (RR), heart rate (HR), blood pressure (BP), pulse oximetry reading
    • The rectal temperature may indicate hypothermia or fever.
    • The RR may be increased (respiratory distress, respiratory tract diseases) or decreased (respiratory depression).
    • The HR may indicate tachycardia (dehydration, infection, cardiac etiology such as supraventricular tachycardia [SVT]) or bradycardia (hypoxia).
    • The BP may indicate hypotension.
    • The pulse oximetry reading (oxygen saturation) may be low (pneumonia, respiratory distress or depression, equipment malfunction).
    • Young infants are prone to hypoglycemia during illness. Blood sugar levels should be measured in an ill-appearing infant.
  • Change in general appearance (eg, toxic, lethargic)
    • Head - Bulging or sunken fontanelle in young children
    • Eyes - Discharge, pupil size
    • Ears - Signs of ear infection (loss of light reflect, bulging, red and immobile tympanic membrane)
    • Nose - Discharge
    • Mouth - Dry mucus membrane or lesions
    • Throat - Erythema, exudates, lesions
    • Neck - Meningeal irritation or adenopathy
    • Heart - Murmur, rubs, tachycardia, bradycardia
    • Lungs - Abnormal lung sounds, such as wheezing, rhonchi, or rales
    • Abdomen - Rigidity, guarding, abnormal bowel sounds
    • Genitals - Rash, discharge
    • Neurologic status - Not consolable, lethargic
    • Extremities - Signs of osteomyelitis, cellulitis, septic arthritis (pseudoparalysis)
    • Skin - Rash (especially petechial rash), cellulitis, abscess, omphalitis

Causes

Causes of SBI in children have been reported as follows33 :

  • Neonates (0-28 d) - GBS species, Escherichia coli, Listeria monocytogenes, Enterococcus species
  • Young infants (29-90 d) - Neonatal pathogens listed above and community-acquired pathogens listed below
  • Older infants and children (3-36 mo) -S pneumoniae, Neisseria meningitidis, HIB (unimmunized), group A Streptococcus species, E coli (pyelonephritis), Salmonella species (gastroenteritis), Staphylococcus aureus (osteomyelitis)
Even the incidence of IPD (serotypes in PCV7) in fully immunized children has decreased since the introduction of PCV7, the incidence of other bacteremia such as nonvaccine serotypes IPD, Salmonella species , penicillin-resistance bacteria, gram-negative enteric bacilli, group A Streptococcus, Neisseria meningitidis, and Staphylococcus aureus, has been reported to either stay the same or increase.11,17,18,35 Methicillin-resistant Staphylococcus aureus (MRSA) bacteremia has also become a concern in the pediatric population.36,37,38,39,40,41,42

More on Fever in the Neonate and Young Child

Overview: Fever in the Neonate and Young Child
Differential Diagnoses & Workup: Fever in the Neonate and Young Child
Treatment & Medication: Fever in the Neonate and Young Child
Follow-up: Fever in the Neonate and Young Child
Multimedia: Fever in the Neonate and Young Child
References
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References

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Further Reading

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Keywords

fever in babies, fever in young children, febrile infants and young children, serious bacterial infection, SBI, heptavalent pneumococcal conjugate vaccine (PCV7), children in the emergency department, bacteremia, sepsis, UTI, urinary tract infection, pneumonia, meningitis 

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Contributor Information and Disclosures

Author

Stella C Wong, DO, Assistant Professor, Department of Emergency Medicine, Emory University School of Medicine
Stella C Wong, DO is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Osteopathic Emergency Physicians, American Osteopathic Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Richard J Scarfone, MD, Associate Professor, Department of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician and Director of Emergency Preparedness, Division of Emergency Medicine, The Children's Hospital of Philadelphia
Richard J Scarfone, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Fred Henretig, MD, Director, Section of Clinical Toxicology, Professor, Medical Director, Delaware Valley Regional Poison Control Center, Departments of Emergency Medicine and Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital
Disclosure: Nothing to disclose.

Medical Editor

Kirsten A Bechtel, MD, Associate Professor, Department of Pediatrics, Yale University School of Medicine; Attending Physician, Department of Pediatric Emergency Medicine, Yale-New Haven Children's Hospital
Kirsten A Bechtel, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Wayne Wolfram, MD, MPH, 
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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