Pediatric emergency medicine trisk 579

likely to result in neutropenia. Thrombocytopenia can be found with both diseases although severe
thrombocytopenia is more common in dengue. Fluid resuscitation may be needed due to dehydration from reduced
intake and increased insensible losses. Most children recover fully over a period of weeks but approximately 5% to
10% experience chronic joint symptoms. Severe complications include meningoencephalitis, cardiopulmonary
compromise, acute renal failure, and death; these are more common in patients with comorbidities and the elderly.
The primary diagnostic tool used is serology. PCR can be performed at state labs and the CDC. ELISA tests
identify IgM (approximately 7 days after infection, and IgM remains elevated for up to 3 months) antibodies.
Management: Treatment is supportive. Repeat episodes are more likely to be severe. NSAIDs or corticosteroids
may help to relive arthralgia. Standard isolation precautions should be used. The risk of human infection may be
reduced by utilization of insect repellant (no more than 30% DEET recommended for children >2 months),
wearing long pants and long sleeve shirts, and staying in screened or air-conditioned dwellings during peak
feeding times. Bed nets are ineffective since this mosquito genus is a daytime feeder. Standard precautions are
recommended.

Zika
CLINICAL PEARLS AND PITFALLS
Zika is endemic in the Americas and the Western Pacific.
While symptoms can mimic those of Chikungunya, symptom severity and duration are less intense
and over 80% of individuals are asymptomatic.
Transmission can occur via mosquito bite, blood transfusion, and sexual contact.
Current Evidence
The main vectors are Aedes species mosquitoes, which are daytime biters; as such, bednets are ineffective in
preventing Zika infection. While there was no documented Zika transmission in the United States in 2018, 56
countries have reported outbreaks in the last 5 years, most from the Caribbean, Mexico, Central and South
America, and the Western Pacific islands.
Goals of Treatment
The symptoms of Zika infection can mimic those of other pathogens more common in industrialized and
developing nations. Prompt recognition can guide reproductive decision making and allow emphasis on further
mosquito bite prevention to decrease local transmission.
Clinical Considerations
Clinical recognition: The incubation period is 3 to 14 days. Up to 80% of persons have asymptomatic infection.

Symptoms are mild, usually resolving in less than 1 week, and can include fever, arthralgia, conjunctival injection,
and a nonpetechial rash. Guillain-Barré syndrome has been reported. Infants with congenital Zika infection can
have microcephaly, microphthalmia or cataracts, contractures, tonal abnormalities, and intellectual disability.
Triage Considerations
Clinical assessment: The differential diagnosis includes dengue and Chikungunya (both transmitted by the same
mosquito vector), as well as measles, adenovirus, and Kawasaki disease. For nonvertically acquired infection, the
diagnosis is based on RT-PCR obtained within 14 days of illness onset. Even in patients with mild symptoms, PCR
confirmation may help guide conversations about contraception after infection. In congenital infection, RT-PCR in
serum and urine and serum IgM can confirm the diagnosis.
Management: Treatment is supportive. NSAIDs should be avoided until dengue can be ruled out. Standard
precautions are recommended, and affected children should avoid insect bites to decrease the risk of local
transmission.

Diarrheal Diseases
CLINICAL PEARLS


Diarrheal disease is a significant cause of morbidity and mortality worldwide.
Diarrhea is often accompanied by other clinical signs and symptoms including vomiting, dehydration,
fever, and electrolyte abnormalities.
There exist more than 40 different enteropathogens that can cause gastroenteritis and is neither
possible nor necessary to arrive at an etiologic diagnosis in all cases.
Current Evidence
Many children who travel to developing countries develop diarrhea. Most episodes of traveler’s diarrhea resolve
during or shortly after the travel. Five percent to 10% of travelers report diarrhea that lasts for 2 weeks or longer
and 1% to 3% have diarrhea that lasts 4 weeks or longer. In the majority of cases, the etiologic agent of traveler’s
diarrhea cannot be isolated. However, among cases in which a pathogen is isolated, 50% to 75% are identified
within 2 weeks of developing symptoms. As the duration of the diarrhea increases (typically greater than 2 weeks),
the likelihood of identifying a specific bacterial cause decreases; in contrast, the likelihood of identification of a
parasitic cause increases. The most commonly identified parasitic infections include G. lamblia, Cryptosporidium

parvum, E. histolytica, and Cyclospora cayetanensis, although these are detected in less than one-third of travelers
with chronic diarrhea and in only 1% to 5% of travelers with acute diarrhea. Infected children are predominantly
asymptomatic, but bloody or nonbloody diarrhea, hepatobiliary symptoms, and failure to thrive may occur.
Viral hepatitis should be considered when evaluating a child with nonspecific gastrointestinal symptoms,
particularly when jaundice is present. Hepatitis A is prevalent in both developed and developing nations and is
acquired through contaminated food and water. Hepatitis A is usually asymptomatic or manifests as mild
symptoms in young children. Hepatitis E must be considered because it is a common etiology of acute hepatitis in
developing countries. Although rarely presenting acutely, hepatitis B and C are common in the developing world
and should be considered in any adolescent or young adult who is sexually active or has had a tattoo or body
piercing while traveling.
There are several common noninfectious causes of chronic diarrhea in travelers including tropical sprue,
postinfectious disaccharidase deficiency, and irritable bowel syndrome. Tropical sprue is characterized by acute or
chronic diarrhea, weight loss, and malabsorption of nutrients. It occurs in residents of or visitors to the tropics and
subtropics; the cause is unknown.
e-Table 94.20 reviews the differences between inflammatory and
noninflammatory diarrhea. Importantly, a diarrheal illness that develops more than 1 month after travel is not
likely due to travel exposure.
Goals of Treatment
The goal is for the clinician to know in which children bacterial or protozoal pathogens would be a more likely
etiology for diarrheal disease, and, therefore, which children would be more likely to benefit from antibiotic
therapy.
Clinical Considerations
Clinical recognition: Invasive or inflammatory enteropathy (e.g., dysentery) should be suspected in persons with
bloody diarrhea, fever, or leukocytes detected in the mucous portion of the stool. Invasive enteropathy has a fairly
abrupt onset (over a period of hours generally) and may be complicated by metastatic infections, reactive
arthropathy, or, in the case of infection with Campylobacter jejuni, Guillain–Barré syndrome. Amoebic dysentery,
caused by E. histolytica among other amoebae, often presents slowly over the course of days and may be
complicated by hepatic abscess formation.
Triage considerations: Early recognition of the dehydrated child, or of the child with possible electrolyte
disturbances, is essential. While most children with mild or moderate dehydration will respond to oral volume

resuscitation, parenteral resuscitation will be needed for the severely dehydrated child.
Clinical assessment: Returning travelers with diarrhea should have stool samples cultured for enteric pathogens
and examined microscopically for ova and parasites if there is evidence of an invasive enteropathy, if the diarrhea
is persistent, if the diarrhea is unresponsive to empirical therapy, or if the infected person is immunocompromised.
Assays for the detection of C. difficile toxins may also be indicated. Routine microbiologic techniques oftentimes
cannot detect many of the bacteria associated with persistent diarrhea. The sensitivity of a single stool specimen
for the detection of ova and parasites varies, depending on the parasite, but it rarely exceeds 80%. The likelihood


of identifying a parasite may be increased by examining additional stool samples (three samples obtained on
separate occasions increase the sensitivity to more than 90%).
Management: In many cases of persistent diarrhea, no causative agent can be identified. In these cases, some
experts recommend empiric antimicrobial therapy such as a macrolide for suspected bacterial enteritis.
Metronidazole (or a related agent such as nitazoxanide) is recommended for presumed giardiasis, since G. lamblia
is the most commonly identified intestinal parasite in travelers. Multiple courses of antimicrobial agents should be
avoided. For travelers whose diarrhea persists, endoscopic examination and biopsy should be considered to
exclude entities such as tropical sprue and inflammatory bowel disease. Contact precautions are recommended.

SYSTEMIC INFECTIONS IN THE RETURNED TRAVELER
There are several treatable infections that may affect travelers who have systemic manifestations, including
hemorrhage. These include meningococcemia, malaria, leptospirosis, and rickettsial infections. There are a handful
of viral infections (in addition to dengue and yellow fever) that are also associated with fever and hemorrhage;
these, however, are rarely acquired by travelers. Viral hemorrhagic fevers (such as Lassa fever and Ebola fever)
need to be considered in travelers who present with fever and hemorrhage; these diseases also have important
infection control and public health concerns. Epidemiologic clues include history of visits to rural areas or recent
contact with ill persons in areas where the viral hemorrhagic fevers are endemic. Most patients with viral
hemorrhagic fevers note the onset of fever within 3 weeks after exposure to infected persons, contaminated water,
or infected insects/vectors.
There is currently no specific treatment available for the viral hemorrhagic fevers. Supportive care with special
attention to careful fluid and electrolyte management is indicated. Endothelial dysfunction makes hydration

challenging; pulmonary edema occurs rapidly with intravenous hydration. To prevent agitation, analgesia and
sedation may be useful.

Yellow Fever
Yellow fever is a tropical zoonotic infection caused by a flavivirus transmitted from nonhuman primates to humans
by mosquitoes of the Aedes (in Africa) and Haemagogus (in Latin America) genera. Following a 3- to 6-day
incubation period, patients develop an influenza-like illness with fever, chills, headache, photophobia, back pain,
and myalgias lasting approximately 4 days, followed by spontaneous resolution in almost 80% of patients. The
remaining 15% to 20% of patients then develop fever, abdominal pain, vomiting, and jaundice. Oliguria and
hemorrhagic findings can be seen. Laboratory findings include leukopenia, thrombocytopenia, transaminitis,
disseminated intravascular coagulation, and proteinuria. Most patients experience remission of symptoms after an
initial 3- to 4-day period. Patients who continue to have symptoms or develop biphasic illness can progress to
multiorgan system dysfunction; in these cases, mortality rates range from 20% to 50%. Treatment is supportive,
often in an intensive care unit setting. A live-attenuated vaccine is available for children older than 6 to 9 months
and is required for entry into some Latin American and sub-Saharan African nations. Insecticide-impregnated bed
nets do not prevent yellow fever, as the mosquito vectors are daytime feeders. Standard precautions are
recommended.

Leptospirosis
Leptospirosis is caused by Leptospira interrogans, a spirochete transmitted in the urine or placental tissue of
rodents and other infected nonhuman animals. As organisms can remain viable under moist conditions (soil or
water) for months, the infection can also be spread via contact with bodies of water or after persons have been in
regions where flooding has occurred. Humans become infected via entry of leptospires through mucosal surfaces
or skin abrasions. While it has a global distribution, it is more common in tropical and subtropical regions. Most
cases are mild or asymptomatic. Severe cases typically are bimodal, with an initial septicemic phase and a second
immune phase. The septicemic phase can be icteric (Weil syndrome) or anicteric and is characterized by an
influenza-like illness lasting less than 1 week. Following this, a subset of patients will develop headache, nuchal
rigidity, rash (sometimes petechial), hepatomegaly, and conjunctival suffusion. Renal involvement may consist of
pyuria, hematuria, proteinuria, or acute kidney injury. The most severe form is Weil syndrome, characterized by
icterus and hepatorenal syndrome; it carries a 5% to 10% mortality rate. The diagnosis is based upon acute and

convalescent serologies. Parenteral penicillin is the treatment of choice. Clinicians should be aware of Jarisch–
Herxheimer reactions (acute febrile illness, myalgia, headache lasting less than 1 day) after initiation of therapy as


the spirochetes die. Doxycycline can be used in older patients with milder disease. Contact precautions are
recommended.

Tick-borne Diseases
Rickettsial diseases in the returned traveler may include Rickettsia africae (African tick typhus), Rickettsia conorii
(causing varying clinical syndromes in different geographic regions, and called by a number of names:
Boutonneuse fever; or Mediterranean, Israeli, Kenyan, or Indian tick typhus), and Orientia tsutsugamushi (scrub or
bush typhus in Japan and Russia). These are all arthropod transmitted from game and cattle ticks, dog ticks, and
mites (“chiggers”), respectively. Symptoms are similar to endemic rickettsial diseases: fever, headaches, myalgia,
and rashes. A painless eschar can sometimes be found at the site of the bite. Risk factors include hiking, camping,
or traveling on safari in grassy or scrubby regions. Examination findings may include localized lymphadenopathy
and a petechial or nonpetechial rash (African tick typhus typically presents without rash, or with a few macular or
vesicular lesions). Laboratory findings include leukopenia and thrombocytopenia. The diagnosis is usually clinical
and treatment with doxycycline should not await confirmatory serologies or PCR-based diagnostics. Standard
precautions are recommended.

Plague
Plague is caused by a gram-negative coccobacillus, Yersinia pestis, a zoonotic infection of rodents and fleas. It can
be transmitted by respiratory droplet from person-to-person. Plague cases are consistently recorded throughout
several countries in Africa, Asia, and the Americas with a vast majority of these cases occurring in Africa. In the
United States, the main risk factor is contact with prairie dogs, and it is most common in the upper Midwestern
states. The most common form is bubonic plague, characterized by an initial brief prodrome of fever, anorexia, and
headache followed by the development of tender regional adenopathy (often in the inguinal area after flea bites to
the lower extremities). These nodes develop a reddish discoloration and proceed to necrosis. More severe forms
include pneumonic and septicemic plague. Most patients have a rapidly progressive course characterized by fever;
initial symptoms mimic influenza. If untreated, pneumonic and septicemic plague is almost uniformly fatal and

bubonic plague has a mortality rate approaching 50%. The proximate causes of death are disseminated
intravascular coagulation, respiratory failure, and renal failure. The diagnosis is made by culture; Gram stain
demonstrates a bipolar appearance to the bacillus that appears like a safety pin with clustering of the stain at the
poles with relative central clearing. The treatment of choice is an aminoglycoside. Alternative agents include
fluoroquinolones or chloramphenicol for plague meningitis, tetracyclines, or doxycycline. Cephalosporins are not
effective. TMP-SMZ is not recommended as monotherapy. The disease must be reported to public health
authorities. Droplet precautions should be used for patients with pneumonic plague.

CENTRAL/PERIPHERAL NERVOUS SYSTEM
There are numerous processes that may cause fever and neurologic manifestations; however, special consideration
should be given to specific etiologies in the returning traveler. Malaria, tuberculosis, typhoid fever, rickettsial
infections, leptospirosis, poliomyelitis, rabies, and the viral encephalitides (including Japanese encephalitis, West
Nile encephalitis, and tick-borne encephalitis) are possible infections that affect the CNS. Travelers to the
“meningitis belt” regions in Africa (during the months of December to June) and those who travel to the Arab
world around the time of the annual pilgrimage to Mecca for the Hajj are at increased risk for developing
meningococcal meningitis. CNS involvement with eosinophilia should also raise the possibility of
coccidioidomycosis and angiostrongyliasis (the latter caused by the rat lungworm Angiostrongylus cantonensis ).

Neurocysticercosis
Cysticercosis is caused by the pork tapeworm, Taenia solium, commonly found throughout central and South
America, South Asia, and China. Human cysticercosis is acquired via fecal–oral transmission by ingestion of
tapeworm eggs from a human tapeworm carrier or by autoinfection. The incubation period may be several years.
Morbidity is almost entirely due to infection of the CNS; most commonly, seizures (partial seizures with or
without secondary generalization) due to larval cysts in the brain parenchyma serving as a seizure focus. Other
manifestations can include gait dysfunction from cerebellar involvement, ocular disease with visual loss, or
encephalitis. One study in Chicago found that neurocysticercosis was a common cause of new-onset afebrile
seizures in Latino children. Subcutaneous cysts are primarily only of cosmetic significance and produce painless
palpable nodules.