Chest Pain - Case 14-5: 3-Year-Old Girl
I. History of Present Illness
A 3-year old girl was brought to the emergency department crying and clutching
her chest. She was extremely difficult to console. She had had poor oral intake
over the previous day, with decreased urine output. On the evening of
admission, she was found sitting in bed whimpering and holding her chest. She
did not have a history of vomiting or diarrhea. Her temperature had not been
measured, but she did not feel subjectively warm.
II. Past Medical History
She had been seen in the emergency department 3 weeks earlier, at which time she
was diagnosed with viral stomatitis. Culture of the lesions grew herpes simplex
virus I (HSV I), and the lesions had resolved since then. She had been taking
only ibuprofen at home. The remainder of her past medical history was
unremarkable.
III. Physical Examination
T, 38.2°C; RR, 30/min; HR, 130 bpm; BP, 98/60 mm Hg; SpO2, 95% in room air
Weight, 75th to 90th percentile
In general, she was crying and difficult to examine, holding her chest with both
arms. She was not in significant respiratory distress. Her chest examination
revealed no apparent bony tenderness over her sternum or ribs. She had
decreased aeration at the left base, with no wheezes or rales appreciated. Her
eyes were slightly sunken and she had some crusty nasal discharge. Her lips and
other mucous membranes were dry. The remainder of her physical examination was
normal.
IV. Diagnostic Studies
The complete blood count revealed 19,000 WBCs/mm3 (8% band forms, 81% segmented neutrophils, and 11% lymphocytes). The hemoglobin
was 12.8 g/dL, and the platelet count was 402,000/mm
3. Electrolytes and liver function tests were normal.
V. Course of Illness
She was given a 40 mL/kg normal saline fluid bolus. She refused to drink and was
given maintenance intravenous fluids. A chest roentgenogram revealed the
diagnosis (Fig. 14-4).
Discussion: Case 14-5
I. Differential Diagnosis
As with adolescents, chest pain in the school age child is very rarely a
life-threatening condition. Common causes of chest pain in this age group
include cough, asthma, pneumonia, and musculoskeletal causes (muscle strain,
trauma, costochondritis.) It is quite common as well for chest pain to be
deemed idiopathic. Less commonly, a child with gastroesophageal reflux,
pneumothorax or pneumomediastinum, and pleural effusion presents with chest
pain. As in older children, the history and physical examination are crucial in
guiding the appropriate workup.
Rarely, one sees a child with chest pain and cardiovascular disease. However,
because this is the diagnosis that most families are concerned about, it must
be addressed. Certainly, children with palpitations, syncope, or chest pain
with exertion should have a thorough evaluation. Finally, toddlers are always
at risk for foreign body ingestion. Although aspirated foreign bodies are not
likely to give chest pain, esophageal foreign bodies commonly cause chest pain.
II. Diagnosis
The chest roentgenogram revealed a right lower lobe opacity with a moderate
right pleural effusion (Fig. 14-4).
The diagnosis is pneumonia, and pleural effusion.
III. Incidence and Epidemiology
In children younger than 5 years of age, the yearly incidence of
community-acquired pneumonia is 34 to 40/1,000; in adolescents, the incidence
is 7/1,000. It is fairly difficult to develop a consensus definition of a case
of pneumonia. Some define it based on an abnormal chest roentgenogram, whereas
others will require only the presence of clinical symptoms.
A large number of organisms can cause community-acquired pneumonia in children.
The most common etiologic agents are viruses (RSV, influenza A and B,
parainfluenza, adenovirus, and rhinovirus),
Mycoplasma pneumoniae, Chlamydia spp. (Chlamydia trachomatis, Chlamydia pneumoniae), and bacteria (Streptococcus pneumoniae, M. tuberculosis, Staphylococcus aureus, Haemophilus
influenzae
type b, and nontypeable H. influenzae). Less common causes are other viruses (varicella, enteroviruses,
cytomegalovirus, EBV),
Chlamydia psittaci, less common bacteria (Streptococcus pyogenes, anaerobic mouth flora, Bordetella pertussis, Klebsiella pneumoniae,and Legionella), and fungi (Coccidioides immitis, Histoplasma capsulatum, and Blastomyces dermatitidis.)
Often, the difficulty lies in differentiating a bacterial from a nonbacterial
pneumonia. Classically, lobar infiltrates, cavitary lesions, and large pleural
effusions suggest either a bacterial or a mycobacterial etiology. Viral
pneumonias typically show diffuse radiologic involvement, but focal infiltrates
can be seen. Laboratory data have been used in an attempt to differentiate
viral from bacterial pneumonia, with C-reactive protein and WBC counts more
significantly elevated in bacterial pneumonias. Ultimately, when attempting to
determine the etiologic agent for pneumonia, one must determine the underlying
immunologic function of the patient. Certainly, immunocompromised patients are
susceptible to a whole host of other infectious etiologies that are often
life-threatening.
One must also consider that some noninfectious processes can cause a similar
clinical picture. These include gastroesophageal reflux, chemical aspiration,
asthma, hypersensitivity pneumonitis, and pulmonary hemosiderosis.
IV. Clinical Presentation
Typically, viral pneumonia commences with symptoms of upper respiratory tract
infection, fever, rhinorrhea, and cough. Respiratory symptoms may be insidious.
This is in contrast to most bacterial pneumonias, where there is often an acute
onset with fever, cough, and chest pain.
On physical examination, patients may have signs suggestive of consolidation
(dullness to percussion, bronchial breath sounds, and egophony). This is more
suggestive of a bacterial process. In contrast, patients with
Mycoplasma or viral infections may have unimpressive physical examination findings but
very distinct infiltrates noted on their chest roentgenograms. Furthermore,
patients with
Mycoplasma infection may have a concurrent bullous myringitis.
V. Diagnostic Approach
Chest roentgenogram. As mentioned previously, the difficulty in diagnosing a pneumonia is
differentiating a bacterial from a viral process. Lobar consolidation,
cavitation, and large pleural effusions suggest a bacterial or mycobacterial
process. Small, bilateral pleural effusions are present in approximately 20% of
children with
M. pneumoniae pneumonia. Pneumococcal pneumonia is the most common bacterial cause of lobar
consolidation. However, approximately 10% of cases of
Mycoplasma pneumonia present with lobar consolidation. Pneumatoceles are detected in two
thirds of children with pneumonia caused by
S. aureus. Viral pneumonias typically have a diffuse appearance that may be either
interstitial or alveolar. Disease confined to the lower lobes, or to the upper
lobes in supine patients, may suggest aspiration pneumonia.
Chest computed tomography. For an uncomplicated pneumonia, chest CT is not necessary. However, it is useful
in cases of recurrent pneumonia and in recalcitrant cases. Furthermore, in the
immunocompromised patient, a chest CT may reveal subtle parenchymal disease. In
children with unilateral pleural effusion, the chest CT can detect loculations
and distinguish pleural effusions from anatomic abnormalities such as pulmonary
lobe sequestration.
Sputum examination. Sputum culture may help identify the bacterial cause of pneumonia in
adolescents, but it is not predictive of the cause of pneumonia in younger
children due to the difficulty in obtaining an adequate sputum sample.
Bronchoscopy. As with chest CT, a bronchoscopy is not necessary in uncomplicated pneumonia.
However, a pneumonia that does not respond to appropriate antibiotic therapy
may require bronchoscopy to obtain appropriate samples for culture. With this
technique, a bronchoalveolar lavage is performed, and the fluid is analyzed for
culture of causative organisms. Bronchoscopy is often indicated for
immunocompromised patients who are at risk for opportunistic infections in
addition to common bacterial and viral infections.
VI. Treatment
In the majority of cases, the causative organism is hypothesized but not
verified. Therefore, therapy must be empiric. In the newborn period, the most
common organisms are group B streptococci, gram-negative bacteria (particularly
Escherichia coli and Klebsiella spp.), and Listeria monocytogenes. Therefore, a combination of ampicillin and either gentamicin or cefotaxime is
often used. There is no consensus as to when the newborn period is over, but
after 2 to 3 months of age, the causative organisms tend to switch to
C. trachomatis, viruses, S. pneumoniae, B. pertussis, and S. aureus. Currently, the prevailing opinion is to treat these children (who are generally
in the 3- to 4-month age group) with amoxicillin, ampicillin, or cefotaxime.
From 4 months to approximately 4 years of age, the causative organisms tend to
include viruses,
S. pneumoniae, H. influenzae, M. pneumoniae, and M. tuberculosis. In a study of 3,475 S. pneumoniae isolates by Whitney and colleagues, ampicillin was effective against 98% of
isolates with intermediate sensitivity against penicillin, whereas erythromycin
and second-generation cephalosporin antibiotics were effective against only 65%
of those same isolates. For these reasons, many clinicians commence treatment
with either amoxicillin or ampicillin for lobar pneumonia and consider a switch
to a macrolide only if the child does not improve clinically, raising their
suspicion for a
Mycoplasma infection. Children with antecedent influenza infection are at higher risk for
pneumonia due to
S. aureus. An agent with activity against both S. pneumoniae and S. aureus, such as amoxicillin-clavulanate, clindamycin, or azithromycin, is preferred to
treat pneumonia in the child with influenza.
Finally, in the 5- to 15-year-age group, Mycoplasma spp. and C. pneumoniae are more common than other etiologic agents, including S. pneumoniae and M. tuberculosis. Therefore, the prevailing opinion for this age group is to commence treatment
with either macrolide or fluoroquinolone antibiotics. Certainly, in any age
range, one should pursue the diagnosis of
M. tuberculosis if it is at all clinically suspected.
VII. References
1. Campbell PW, Hazinski TA. Acute pneumonia. In: Hoekelman RA, Friedman SB,
Nelson NM, et al., eds.
Primary pediatric care, 3rd ed. St. Louis: Mosby, 1997:1521–1253.
2. Donowitz GR, Mandell GL. Acute pneumonia. In: Mandell GL, Bennett JE, Dolin
R, eds.
Mandell, Douglas, and Bennett's principles and practice of infectious diseases, 5th ed. Philadelphia: Churchill Livingstone, 2000:717–735.
3. Ferwerda A, Moll HA, de Groot R. Respiratory tract infections by Mycoplasma pneumoniae in children: a review of diagnostic and therapeutic measures. Eur J Pediatr 2001;160:483–491.
4. Franquet T. Imaging of pneumonia: trends and algorithms. Eur Respir J 2001;18:196–208.
5. McIntosh K. Community-acquired pneumonia in children. N Engl J Med 2002;346:429–437.
6. Whitney CG, Farley MM, Hadler J, et al. Increasing prevalence of
multidrug-resistant
Streptococcus pneumoniae in the United States. N Engl J Med 2000;343:1917–1924.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2008 Williams & Wilkins.
More About Causes of Chest pain
» Next page: Chest Pain - Case 14-6: 15-Year-Old Boy (Pediatric Complaints and Diagnostic Dilemmas)
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