Pediatric emergency medicine trisk 578

Intrathoracic tuberculosis (pulmonary parenchymal disease, intrathoracic lymphadenopathy, and
pleural disease) and peripheral lymphadenopathy account for over 90% of all cases of childhood
tuberculosis.
Most children with tuberculosis have negative acid-fast sputum smears and cultures; the diagnosis is
instead based on a triad of findings: a positive TST or TB blood test (interferon gamma release
assays [IGRAs]); compatible radiographic and clinical findings; and contact with a person known to
have tuberculosis disease.
Preadolescent children with pulmonary tuberculosis without cavitary findings on radiography rarely
are contagious; however, providers should utilize airborne precautions because in many instances,
the child is brought to the ED by the person from whom they acquired tuberculosis, and that adult is
by definition contagious.
Current Evidence
The most common sites of infection are intrathoracic (pulmonary parenchymal, intrathoracic adenopathy, and/or
pleural effusions) and peripheral lymphadenopathy. Together, these account for over 90% of all childhood TB
cases. Meningeal tuberculosis comprises 1% to 2% of all childhood TB cases, and is most common in children in
the first 2 years of life.
Latent tuberculosis infection (LTBI) is defined as a positive TST ( e-Table 94.16 ) or IGRA in a child who
lacks TB symptoms and has a normal chest radiograph and physical examination. While LTBI will rarely be an
ED-based diagnosis, clinicians may see children with LTBI for nontuberculosis concerns or for medication adverse
events. Children with LTBI are not contagious and have no specific infection control considerations. As most
tuberculosis medications are hepatically metabolized, the clinician should be aware of potential hepatotoxicity if a
child receiving tuberculosis medication presents with abdominal pain, vomiting, anorexia, or icterus. Isoniazid
(INH) can also cause peripheral neuropathy and can cause benzodiazepine-refractory seizures in cases of overdose
(the antidote is pyridoxine, administered as a gram-to-gram dose based on the estimates of the INH dose ingested).
Goals of Treatment
The goal of treatment is to recognize which children with pulmonary, meningeal, or lymphadenitis may have
tuberculosis as opposed to other diagnoses.
Clinical Considerations
Clinical recognition: Tuberculosis disease ( e-Table 94.17 ) should be included in the differential diagnosis of
children with fever of unknown origin; pneumonia refractory to therapy for community-acquired pneumonia;
cavitary pneumonia/lung abscesses; hilar or mediastinal adenopathy; miliary pattern on chest radiograph; freeflowing pleural effusions with or without consolidation; chronic nontender adenopathy; chronic otorrhea or

chronic otitis media; and meningitis with an elevated CSF protein. Children with pulmonary tuberculosis often
have chest radiographs that look far worse than the child. Weight loss in combination with pneumonia should lead
the provider to broaden the differential diagnosis outside of the usual pathogens causing community-acquired
pneumonia. TB meningitis has an insidious onset, and in the early stages, children may have fever and
constitutional symptoms alone. Unexplained protracted vomiting (due to increased intracranial pressure) often is
identified only in retrospect. Given the nonspecific initial symptoms and the rarity of the diagnosis in
industrialized nations, many children with TB meningitis have had multiple healthcare encounters prior to
diagnosis.
Triage considerations: While prepubertal children with noncavitary chest radiographs rarely are contagious, the
person bringing the child to medical attention may be the person who transmitted tuberculosis to the child. As
such, airborne precautions should be used more to protect healthcare workers and other patients from the
caregivers, as opposed to from the patient him/herself.
Clinical assessment: The diagnosis of tuberculosis in a child infrequently is made based upon microbiologic
confirmation. Acid-fast cultures of respiratory secretions are positive in a minority of children; the highest culture
yield occurs in children with peripheral lymphadenopathy or skeletal disease. Instead, children usually are
diagnosed based on a triad of findings: epidemiologic links to a person with known or suspected tuberculosis
disease; a positive TST or IGRA; and compatible clinical or radiographic findings. A chest radiograph should be
performed in all children in whom TB is suspected; the most common findings include parenchymal infiltrates,


intrathoracic lymphadenopathy, and pleural effusions; miliary disease is more common in infants and
immunocompromised children. The majority of children with extrapulmonary disease (especially those with
meningitis) will have abnormal chest radiographs. CT of the brain should be obtained in children with suspected
TB meningitis, as leptomeningeal enhancement, hydrocephalus, infarcts in watershed areas (e.g., putamen,
caudate, basal ganglia), and tuberculomas (mass-occupying lesions) may be present and hydrocephaly may require
shunting. All infants in whom TB disease is suspected should undergo LP for routine studies, acid-fast culture, and
M. tuberculosis PCR. CSF profiles show a lymphocytic pleocytosis, high CSF protein, and low CSF glucose.
While TSTs and IGRAs are helpful when positive, negative tests do not rule out TB. All children in whom TB
disease is suspected should be screened for HIV and have a baseline CBC and hepatic transaminases performed.
Management: Initiation of multidrug tuberculosis therapy should be performed in consultation with ID

specialists. The management of children with drug-resistant tuberculosis is outside the scope of this chapter.
Airborne precautions should be used.

Typhoid
CLINICAL PEARLS
Typhoid fever is caused by the bacteria Salmonella enterica serotype typhi. It is a human pathogen
transmitted via the fecal–oral route and can cause local (diarrheal) or invasive disease (bacteremia,
meningitis, bowel perforation, osteomyelitis). For many children fever alone is the only presenting
symptom.
Typhoid fever is more common in the pediatric and immunocompromised hosts of any age and
should be suspected in any febrile child who has returned from Asia, Africa, or Latin America in the
preceding month.
Current Evidence
Typhoid fever is endemic in sub-Saharan Africa, the Indian subcontinent, Southeast Asia, East Asia, the Middle
East, and central and South America with an estimated incidence of 27 million/yr. It is most prevalent in
impoverished areas where sanitary conditions are poor. Approximately 350 returned travelers to the United States
are diagnosed with typhoid fever every year. In the United States, 67% of imported cases were from South Central
Asia, 10% from Southeast Asia, and 10% from sub-Saharan Africa. Increasing rates of antibiotic resistance to
cephalosporins, fluoroquinolones, and macrolides have been seen in recent years. In Southeast Asia, reduced
susceptibility to fluoroquinolones has complicated empiric therapy.
Goals of treatment: The goal of treatment is the rapid recognition that fever in a returned traveler could
represent typhoid fever, and for the PEM clinician to be cognizant of drug-resistance patterns globally that may
impact empiric antibiotic selection.
Clinical Considerations
Clinical recognition: Many patients infected with S. enterica subtype typhi are either asymptomatic or have mild
symptoms; 60% to 90% do not seek medical attention or are treated on in the outpatient setting. Patients with
typhoid fever have an insidious onset of fever and development of symptoms over a period of 5 to 21 days after the
ingestion of contaminated food or water. A majority of patients develop anorexia, abdominal pain, chills, in
addition to malaise, tender splenomegaly, marked headache, relative bradycardia (given the degree of pyrexia), and
a nonproductive cough in the early stages. Approximately 25% of Caucasian patients will develop painless,

erythematous, blanchable, subcentimeter, maculopapular “rose spots” on the trunk. Constipation is more common
than diarrhea in young children. The severity of illness is influenced by the particular strain virulence, quantity of
inoculum, the age of the patient, duration of illness before initiation of treatment, and current vaccination status.
Complications of severe disease include shock, meningitis, pneumonia (primary Salmonella pneumonia or
secondary bacterial infection), gastrointestinal perforation, or hemorrhage. Chronic carriers play an important role
in the transmission of the disease; they typically excrete a large number of organisms yet have a high level of
immunity. Carriage is uncommon in young children.
Triage considerations: Clinicians should consider typhoid fever in patients with abdominal pain, fever, and
chills, and with recent travel to developing nations.


Clinical assessment: Diagnosis is made by blood culture. Stool cultures are positive in approximately 30% of
bacteremic patients. Bone marrow cultures may be useful because they remain positive long after treatment has
been initiated and are more sensitive than blood culture. Serology is not recommended as it often cross-reacts with
other Salmonella serotypes.
Management: Empiric management of children with suspected typhoid is reviewed in
e-Table 94.18 .
Historically, fluoroquinolones have been the treatment of choice. However, the recent evolution and recognition of
multidrug-resistant Salmonella isolates has complicated empiric therapy. In general, fluoroquinolones should not
be first-line therapy if typhoid fever in patient from South Asia or other regions where there is a known increase in
resistance to fluoroquinolones. For travelers to this area, use of third-generation cephalosporins and high-dose
azithromycin (1 g) is recommended. Bacteremia should be treated for a total 7- to 10-day total course, with
transition from parenteral to oral therapy after bacteremia has cleared and antibiotic susceptibilities are available.
In some sub-Saharan African nations, up to 40% of Salmonella isolates are cephalosporin. In patients with severe
systemic illness, such as typhoid-associated shock or encephalopathy, dexamethasone (3 mg/kg followed by 1
mg/kg every 6 hours for 48 hours), should be considered. The chronic carrier state can be eradicated by 4 weeks of
oral fluoroquinolones. Contact and standard precautions should be used for providers caring for children with
suspected typhoid fever.

Dengue

CLINICAL PEARLS AND PITFALLS
Dengue is the most prevalent mosquito-transmitted viral illness and should be considered in the
differential diagnosis of any febrile patient presenting in the ED within 2 weeks of return from a
tropical or subtropical region.
Clinical manifestations include self-limited dengue fever to life-threatening dengue hemorrhagic fever
with shock syndrome.
Treatment is with supportive care and fluid resuscitation, including blood transfusion.
Current Evidence
Dengue is transmitted by the Aedes aegypti mosquitoes, which are most active during the day, but can bite at any
time of day or night. The disease is endemic to central and South America, sub-Saharan Africa, the Indian
subcontinent, and Southeast Asia. Recently there has been a broadening of the geographic distribution of the
disease. In the last decade, outbreaks have been reported in Texas, Florida, and Hawaii, and the mosquito vector
already is widespread throughout the southern United States. The worldwide incidence has been increasing in the
past several decades due to a number of factors including population growth, overcrowded urban living with poor
sanitation, increasingly mobile/transient population and therefore increased mobility of the mosquitoes, virus and
infected individuals, and lack of effective mosquito control. Each year there are an estimated 50 to 100 million
dengue infections, with >500,000 cases of dengue hemorrhagic fever, and >22,000 deaths, primarily in children.
Goals of Treatment
The goal of dengue management is to identify which children are at risk for dengue based on travel history and for
the PEM clinician to be aware that rapid fluid shifts after fluid resuscitation can lead to volume overload.
Clinical Considerations
Clinical recognition: The differential diagnosis includes febrile illness with similar clinical manifestations such as
influenza, enteroviral infection, measles, and rubella. The diagnosis is typically a clinical one when treating
patients with recent travel to dengue endemic regions. Only 50% of patients infected with dengue develop
symptoms. Clinical manifestations range from self-limited dengue fever to dengue hemorrhagic with shock
syndrome. Symptoms typically develop within 3 to 14 days after the bite of an infected mosquito; the risk of
severe disease is much higher in sequential infections. In 2009, the World Health Organization (WHO) published
revised dengue case definitions ( e-Table 94.19 ). Three distinct phases exist. The first is the febrile phase. Here,
children develop pyrexia (or hyperpyrexia), vomiting, joint pain. Some develop a transient maculopapular rash,
lasting approximately 3 to 7 days. Most patients do not progress to the next phase and improve without

intervention. Phase 2 is called the critical or capillary leak phase and consists of clinical or radiographic evidence
of serositis, ascites, or pulmonary edema. Children in phase 2 are at risk for developing hypotension and
uncompensated shock. Patients may be refractory to fluid resuscitation and may develop abdominal pain,
persistent emesis, tender hepatomegaly, mucosal bleeding, and altered mentation. Phase 3 (the convalescence or
reabsorption phase) begins approximately 2 to 3 days after the initiation of phase 2. Patients typically experience
both clinical and laboratory rapid improvement as the body reabsorbs extravasated plasma and fluid. Some patients
develop a pruritic vasculitic rash that may desquamate during resolution of the illness (2 to 3 weeks).
Triage considerations: Dengue should be considered in every patient seen in the ED presenting with fever and
recent return (<2 weeks) from tropical or subtropical regions.
Clinical assessment: Dengue is predominantly a clinical diagnosis. Definitive diagnosis is via RT-PCR or
ELISA; IgM antibodies are detectable by day 4 to 5 after fever onset, but can cross-react with Zika and other
flaviviruses. Children with suspected dengue should get the following laboratory evaluation: complete blood count
(to evaluate for leukopenia, anemia, and thrombocytopenia), BUN and creatinine to evaluate for acute kidney
injury, type and screen, hepatic transaminases, prothrombin time, and partial thromboplastin time to evaluate for
disseminated intravascular coagulation.
Management: Treatment of dengue is supportive including fever control, and fluid resuscitation and red blood
cell transfusion. NSAIDs should be avoided. There appears to be no indication for platelet transfusion; the
consumptive coagulopathy seen in dengue appears to be refractory to transfusions. There are no antivirals that are
of use in dengue. There are some small, nonrandomized trials of corticosteroids for dengue shock syndrome that
have shown some possible benefit, but more data are lacking. Standard precautions are recommended.

Chikungunya
CLINICAL PEARLS AND PITFALLS
Chikungunya is endemic in Africa, the Indian subcontinent, and Southeast Asia.
Clinical manifestations mimic dengue and include fever and bilateral polyarthralgia. Hemorrhagic
manifestations are more common in children. Most recover fully over a period of weeks, but
approximately 5% to 10% experience chronic joint symptoms.
Current Evidence

The main vectors for chikungunya are the A. aegypti and Aedes albopictus mosquitoes, which also transmit dengue
and Zika. Chikungunya is found throughout Africa, India, China, and Southeast Asia, but cases in travelers
returning to North America, the Caribbean, France, and Italy have been reported. In late 2013, the first
transmission in the western hemisphere was reported in St. Martin and other French territories in the Caribbean. As
the incubation period is relatively short, it is most common in travelers who have recently returned from endemic
regions.
Goals of Treatment
As with other travel-related infections, it is important for the clinician to recognize that some imported infections
will present similarly to infections endemic in the United States (e.g., influenza virus). Asking about recent travel
will help broaden the differential diagnosis.
Clinical Considerations
Clinical recognition: The incubation period is 1 to 12 days and the first symptom is often rapid-onset arthralgia of
multiple joints. Subsequently, patients develop myalgia, high fever, generalized lymphadenopathy, and
conjunctivitis. Initial symptoms usually resolve over 2 to 3 days and are followed by the development of a
maculopapular rash in about 50% of patients. Fever may recur and some develop hemorrhagic manifestations
(more common in children).
Triage Considerations
Clinical assessment: Chikungunya mimics dengue in symptomatology and geographic distribution. One of the
distinguishing features between the two is that the arthralgia in Chikungunya is polyarticular, something rarely
seen with dengue. Chikungunya is more likely to present with lymphopenia than dengue, while dengue is more