Pediatric emergency medicine trisk 577

Hepatitis viruses

Leishmaniasis

Leptospirosis

Malaria

disseminated
other arboviruses in
intravascular coagulation
the same class)
Serology testing
Serology testing
Acute hepatitis A and B: supportive
Chronic hepatitis C: Ledipasvir, sofosub
specific antiviral agents, +/– ribavirin
Direct visualization of
Visualization of
Consultation with CDC should be perfor
protozoa from bone
protozoa from bone Standard treatment involves pentavalent
marrow aspirate
marrow or splenic
sodium stibogluconate; miltefosine an
aspiration
Serology if other diagnostic
also been used
tests unavailable
Serology not useful for
cutaneous form

Ancillary for visceral form:
marrow suppression,
elevated hepatic
transaminases,
hypoalbuminemia,
hypergammaglobulinemia
PCR, culture, or
PCR is sensitive and
Penicillin or ampicillin for severe diseas
immunohistochemical
continues to be
Doxycycline or amoxicillin for mild dise
staining (culture is
positive even after
also recommended for prophylaxis
sensitive and slow)
initiation of therapy Need to monitor for Jarisch–Herxheimer
Ancillary: can see
Serology (microscopic
initiation of therapy
lymphocytic
agglutination test,
cerebrospinal fluid
MAT)
pleocytosis with elevated If sending blood
protein and opening
cultures, need to
pressure; elevated hepatic
notify laboratory to
transaminases and

hold culture for 2–4
bilirubin; urinalysis
mo
showing pyuria,
proteinuria, and
hematuria; elevated
creatinine, creatine
kinase, and amylase
Thick, thin smear
Thick smear: quantify Check CDC site for regions
level of parasitemia
( />Anemia, thrombocytopenia,
) where parasites retain chloroquine su
hypoglycemia, metabolic Thin smear: allows for
acidosis, elevated
speciation; presence P. falciparum:
creatinine, bilirubin, and
of >1 ring form in a Atovaquone/Proguanil (Malarone) × 3 d
serum transaminases.
erythrocyte suggests Artemether-lumefantrine (Coartem) × 3
Obtain type and screen
P. falciparum, the
Quinine + (clindamycin or doxycycline)
and G6PD level (need to
species responsible Mefloquine (Larium) × 2 doses
know status before
for most deaths
Severe/complicated malaria: quinine + c
treating with primaquine
globally

exchange transfusion considered for c
for the hypnozoite form
high-grade parasitemia
seen in P. vivax and ovale
For vivax/ovale: atovaquone. Proguanil
)
If strongly suspect malaria,
do not withhold treatment
if initial smears negative,
simply repeat smears in
12–24 hrs


Measles

In a malaria-endemic
region, low-grade
parasitemia may not
explain all a child’s
symptoms
Serology for IgM antibody

Mumps

Clinical diagnosis
PCR and serology testing
Neurocysticercosis CSF serology, characteristic
neuroimaging: hypodense
cysts with well-defined
edges; can see edema as

parasites die
Ancillary: CSF eosinophilia
Polio
Culture of throat or stool
(obtain two or more for
enterovirus isolation
obtained at least 24 hrs
apart)
Rabies
Serology
Ancillary tests of minimal
value, except to exclude
other causes of
meningoencephalitis
Salmonella typhi Stool culture for
gastroenteritis
Bone marrow culture or
blood culture for those
with enteric fever
Salmonella,
nontyphi
Schistosomiasis

Shigella

Strongyloides

Tuberculosis

Serology for IgM

antibody

Supportive treatment
Vitamin A once daily for 2 days associat
morbidity and mortality (WHO recom

PCR and serology
testing

Supportive treatment

Serology in CSF
(serum serology
cross-reacts with
Echinococcus )

Utility of treatment if cysts is controvers
associated with acute inflammation
Use of albendazole or praziquantel with

Culture of throat or
stool

Supportive

Serology
Supportive care, but prognosis dismal on
Visualization of Negri
bodies on cerebellar
or nape of neck

biopsies
Stool culture
Supportive if asymptomatic or uncompli
gastroenteritis
Ampicillin, amoxicillin, or trimethoprim
susceptible strains
For invasive disease, empiric treatment w
spectrum cephalosporin, azithromycin
Conventional stool culture Stool culture
Ceftriaxone or azithromycin if need trea
mo old, immunocompromised host (in
hemoglobinopathies)
Identification of eggs in
Identification of eggs Praziquantel (most effective against adul
stool (S. mansoni or
immature stages, so retreatment after
Serology does not
japonicum ) or urine (S.
differentiate acute
hematobium )
and chronic
Eosinophilia
infection
Conventional stool culture Stool culture
Fluid resuscitation
Ancillary: leukocytosis with
Azithromycin or Ceftriaxone daily for 3
bandemia is common
Stool to detect larvae (often Visualization of larvae Ivermectin is treatment of choice by WH
need to obtain multiple

in stool
Also used: mebendazole
stool samples)
Watch for anaphylaxis during treatment
patients
Respiratory specimen
(expectorated sputum,
induced sputum, or

Most children will
have negative
cultures, and

Multidrug therapy (isoniazid, rifampin, p
ethambutol) administered via directly


gastric aspirate) for acidfast culture; additional
cultures if
extrapulmonary TB is
suspected
Ancillary: tuberculin skin
test, interferon gamma
release assay (IGRA),
chest radiograph; check
for HIV

Yellow fever

Serology

Ancillary:
thrombocytopenia,
elevated PT, PTT,
hyperbilirubinemia,
prolonged elevation of
hepatic transaminases

diagnosis is made on Consultation with specialists in pediatric
the basis of (1)
given infrequency of diagnosis in chil
consistent clinical
States
and radiographic
findings, (2)
epidemiologic link
to a source case, (3)
immunologic
evidence of TB
(skin test, IGRA),
and exclusion of
other diagnoses
Serology
Supportive
Patients who received Avoid nonsteroidal anti-inflammatories
yellow fever vaccine
can have an elevated
IgM for several
years; cross-reaction
with other
flaviviruses can be

seen

CDC, Centers for Disease Control and Prevention; PCR, polymerase chain reaction; ELISA, enzyme-linked immunosorbent assay; CSF, cerebrospinal
fluid; EKG, electrocardiogram; TB, tuberculosis; HIV, human immunodeficiency virus; DIC, disseminated intravascular coagulation; G6PD, glucose-6phosphate dehydrogenase; WHO, World Health Organization.

In the next section, six major diseases or syndromes will be reviewed: malaria, tuberculosis, typhoid, dengue,
chikungunya, and diarrheal diseases. Other infections will then be organized based on the primary organ system
involved. HIV will be covered at the end of this chapter.

Malaria
CLINICAL PEARLS AND PITFALLS
Persons returning to their native countries (VFRs) are at particular risk for malaria, since many fail to
take the necessary precautions either to avoid insect exposure or to take prophylaxis.
Malaria should be considered in the differential diagnosis of any febrile child who has returned from a
malaria-endemic region in the preceding month; one negative blood smear should not lead the PEM
provider to rule out malaria.
Chloroquine resistance is widespread, and this drug should not be used as empiric therapy for the ill
child with suspected malaria.
Current Evidence
Malaria is the most important parasitic disease of man with prevalence estimated to be over 200 million with
almost 500,000 deaths each year, most of whom are children. The majority of morbidity and mortality is due to
Plasmodium falciparum. Malaria is endemic throughout tropical regions worldwide; in 2017, 90 countries were
malaria-endemic, and over 3 billion persons were at risk of malaria. The most common species worldwide are
Plasmodium vivax, prevalent on the Indian subcontinent and in Central America, and P. falciparum, prevalent in
Africa and in Papua New Guinea. High-risk regions include sub-Saharan Africa, Papua New Guinea, the Solomon
Islands, and Vanuatu.
Approximately 40% of the reported cases of malaria in the United States are from foreign travelers. Infections
with P. falciparum can progress rapidly, some fatally, and must be considered in the differential diagnosis in all
febrile children who have recently visited an endemic region. Approximately 90% of P. falciparum infections are
acquired in sub-Saharan Africa, and up to 90% of travelers who are infected begin to have symptoms within 1

month after their return. In contrast to P. falciparum infections, travelers infected with P. vivax and Plasmodium


ovale may show symptoms several months to years after exposure. Seventy percent of P. vivax infections are
acquired in Asia or Latin America.
Chloroquine-sensitive malaria exists in Central America as well as the Caribbean and limited parts of South
America. There are regions that have developed chloroquine and mefloquine (Lariam) resistance, specifically in
Southeast Asia. It is vital for the clinician to ask about not only if malaria prophylaxis was taken but also the
medication and how it was administered. Both chloroquine and mefloquine kill the parasite only in the
hematogenous phase; it is thus vital to take these medications for 4 weeks upon leaving the endemic region. Early
termination of these medications could result in malaria even in someone who was “taking prophylaxis.” Bed nets
are effective as the mosquito vector is a night-time feeder.
Goals of Treatment
The goal of treatment is for the clinician to rapidly recognize that the febrile child returning from a malariaendemic region should be evaluated for plasmodial infection and that empiric antimalarial therapy, even in the
absence of a positive blood smear, should be initiated for the toxic-appearing child.
Clinical Considerations
Clinical recognition: The most common symptoms of malaria are fever, malaise, headache, myalgia, vomiting, and
diarrhea. Signs include pyrexia, tachycardia, tachypnea, dehydration, pallor, splenomegaly, and icterus. While the
frequency and spectrum of complications differ among the plasmodial species ( e-Table 94.15 ), signs and
symptoms cannot differentiate between species. The malaria species and degree of parasitemia will affect the types
and degree of symptoms that are displayed. Severe malaria is defined as shock, acidosis, hypoglycemia, end-organ
involvement (e.g., CNS, renal), and/or parasitemia exceeding 5% of erythrocytes.
Triage considerations: Given the constellation of symptoms, malaria should be considered in all febrile travelers
almost regardless of their clinical presentation.
Clinical assessment: The blood smear is considered the diagnostic reference standard. Both thick and thin
smears should be obtained. Thick smears allow for a much larger volume of blood to be examined and thus for the
detection of smaller numbers of parasites (leading to increased sensitivity), while the thin smear will allow for the
identification of the species and the percentage of affected red blood cells. If the initial blood films are negative for
malaria and the disease is still clinically suspected, examination of the thick and thin smears should be repeated at
least once within 12 to 24 hours after the initial evaluation. One negative blood smear should not cause the

clinician to exclude malaria from the differential diagnosis. In malaria-endemic areas, many children have lowlevel parasitemia. It is therefore important to consider other pathogens when children are found to have low-grade
parasitemia on blood smear. Thrombocytopenia without leukocytosis is a characteristic feature of malaria, as is
splenomegaly. Rapid assays for malaria are also available. In laboratories where personnel may be less familiar
with performing blood smears, these rapid assays may be far superior to blood smears.
Management: Malaria is a reportable disease to the U.S. CDC. Empiric treatment should be decided upon in
consultation with an ID specialist. Most children with malaria treated in the United States are admitted for
treatment. Empiric therapy is based upon the disease severity, the species, and data regarding drug resistance in
different geographic regions. Children with severe malaria should be admitted to an intensive care unit for
monitoring and because some children will require exchange transfusion (if parasitemia exceeds 10% or there is
evidence of cerebral or renal involvement). These children should receive parenteral therapy (clindamycin with
either IV quinine or quinidine; artesunate is a newer parenteral regimen and is likely to be used more frequently as
IV quinidine becomes less available). Blood smears should be repeated after therapy is initiated to evaluate
response to therapy and need for additional interventions. Primaquine is needed to kill the dormant phase seen in P.
vivax and P. ovale infections to prevent relapse. Prior to use of primaquine, patients need to be screened for
glucose-6-phosphate dehydrogenase (G6PD) deficiency (primaquine can cause hemolytic anemia in patients with
G6PD); women of child-bearing age also need to be screened for pregnancy (primaquine is a potential teratogen).
Both chloroquine and quinidine are available in intravenous preparations from the CDC. Standard precautions are
used for patients with malaria.

Tuberculosis
CLINICAL PEARLS AND PITFALLS