Chest Pain - Case 14-3: 20-Year-Old Boy
I. History of Present Illness
A 20-year-old young man with a history of spina bifida presented to the
emergency department. Six days earlier, he had reported fatigue and was unable
to leave his house. Over the next few days, he had developed a fever, sore
throat, and myalgias. Two days before admission, he had noted increasing
shortness of breath, which was worse while lying supine. He described a
“pounding” discomfort in his chest.
II. Past Medical History
He was born at full term and noted at birth to have a meningomyelocele. He had
spina bifida at the L3 level and had surgical correction when he was 4 days
old. A ventriculoperitoneal shunt was placed during the first weeks of life.
Several shunt revisions had since been required due to obstruction; the last
revision was 6 years earlier. Four months before admission, he was diagnosed
with pelvic osteomyelitis related to extension of a gluteal ulcer. He was
treated with surgical debridement and 3 months of intravenous antibiotics.
He had bilateral club feet. He was able to walk with a brace and had only mild
mental retardation. He was not taking any medications. He had had a tattoo
placed on his arm 2 weeks before admission. There was a family history of
asthma in his mother, and his father died at age 40 years from a myocardial
infarction.
III. Physical Examination
T, 41.3°C; RR, 20/min; HR, 138 bpm; BP, 113/80 mm Hg; SpO2, 98% in room air
In general, he was an obese young man in moderate respiratory distress. His
oropharyngeal examination revealed an exudative pharyngitis. His cardiac
examination revealed a normal S1 and S2 with no murmur, rub, or gallop. His
physical examination was otherwise unremarkable.
IV. Diagnostic Studies
The complete blood count revealed 13,500 WBCs/mm3, with 42% segmented neutrophils, 26% lymphocytes, 18% atypical lymphocytes, and
1% monocytes. The hemoglobin was 11.3 g/dL, and platelets were 133,000/mm
3. Electrolytes, blood urea nitrogen, and glucose were within normal limits. The
serum creatinine concentration was slightly elevated at 1.1 mg/dL. Total
bilirubin was elevated at 4.0 mg/dL, with an unconjugated fraction of 2.3
mg/dL. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were
246 and 130 U/L, respectively. The erythrocyte sedimentation rate was mildly
elevated at 44 mm/hour. A chest roentgenogram revealed normal heart size and no
pulmonary infiltrates.
V. Course of Illness
Before arrival at the hospital, the patient was given adenosine twice for heart
rates greater than 160 bpm. This did not have any significant effect. On
arrival in the emergency department, his chest pain resolved and his ECG
abnormalities resolved. An echocardiogram demonstrated a shortening fraction of
28% and no wall motion abnormalities.
He was evaluated for a possible myocardial infarction, given his family history.
His cardiac enzymes remained normal. He developed bilious emesis, which was
believed to be secondary to his hepatitis. He had a repeat ECG (Fig. 14-2) and
echocardiogram on arrival in the intensive care unit. The ECG suggested a
diagnostic category, and the specific cause was suggested by the initial
laboratory testing and confirmed later by serologic testing.
Discussion: Case 14-3
I. Differential Diagnosis
As previously mentioned, the most common causes for chest pain in the adolescent
age group are asthma, pneumonia, cough, musculoskeletal causes, psychogenic
pain, and idiopathic causes.
The concerning factors in this patient were his positional shortness of breath,
his family history of early myocardial infarction, and his abnormal ECG
findings. On presentation, he was tachycardic and febrile. The acute nature of
his symptoms and the positional nature of his respiratory symptoms should raise
the concern for a possible cardiac etiology. Although cardiac causes are rare
among all causes of chest pain, they can be the most life-threatening and must
be evaluated.
Cardiac causes for chest pain include structural lesions such as aortic or
pulmonic stenosis, idiopathic hypertrophic subaortic stenosis (IHSS), and
mitral valve prolapse. Patients with IHSS often have a family history of sudden
death. Coronary artery disease can also lead to chest pain and may be secondary
to anomalous coronary arteries, Kawasaki disease, or long-standing diabetes
mellitus. Patients with either corrected or uncorrected congenital heart
disease may complain of chest pain, which must be carefully evaluated.
Arrhythmias such as supraventricular tachycardia and ventricular tachycardia
can also manifest with chest pain and palpitations. Finally, infectious causes
such as myocarditis and pericarditis may manifest with chest pain.
II. Diagnosis
The repeat ECG revealed sinus tachycardia at 139 bpm with 2-mm ST-segment
elevations in leads V2 and V3 (Fig. 14-2). Repeat echocardiogram revealed a
left ventricular ejection fraction of 25% and dilated left and right
ventricles. Cardiac catheterization revealed a left ventricle end-diastolic
pressure of 16 mm Hg and a cardiac index of 4.4 L/min. The patient was believed
to have myocarditis. Soon after admission, he developed congestive heart
failure with respiratory distress, diaphoresis, somnolence, and hypotension. He
was ultimately treated with dopamine and dobutamine. To help determine the
cause of his myocarditis, Epstein-Barr virus (EBV) studies were requested. His
Monospot test was positive. He also had hepatitis, thrombocytopenia, and an
atypical lymphocytosis. The EBV viral capsid antigen (VCA) IgG was 1:640; early
antigen (EA) IgG was 1:80; and Epstein-Barr nuclear antigen (EBNA) IgG was
undetectable.
The diagnosis is EBV myocarditis.
III. Incidence, Epidemiology, and Etiology
EBV is a member of the herpesvirus family. It is a relatively common infectious
organism, causing a clinical syndrome of infectious mononucleosis. This
syndrome is most frequently seen in adolescents and young adults. Males and
females are affected equally, and 90% to 95% of all adults have evidence of
past EBV infection. EBV is believed to have low contagiousness, and
transmission generally requires intimate contact between individuals. For this
reason, infectious mononucleosis has been termed,
“the kissing disease.”
The classic clinical syndrome consists of fever, sore throat, and adenopathy
developing after an incubation period of 3 to 7 weeks. Most cases of EBV
infection are self-limited, although rare complications are seen. These
complications can be multisystemic and include hematologic, hepatorenal,
splenic, dermatologic, immunologic, and cardiopulmonary symptoms.
Myocarditis in EBV infection is rare, with an incidence ranging from 0% to 6%.
Viruses are the most common etiologic agents causing myocarditis. Aside from
EBV, they include enterovirus (e.g., coxsackie B), adenovirus, cytomegalovirus,
herpesvirus, influenza A, varicella, mumps, measles, parvovirus, respiratory
syncytial virus (RSV), and HIV. Less commonly, other nonviral infectious
agents, such as rickettsiae, bacteria, parasites, fungi, and yeasts, are
responsible. Also rare are noninfectious causes such as drugs, hypersensitivity
reactions, autoimmune diseases, Kawasaki disease, and sarcoidosis.
IV. Clinical Presentation
Newborns and infants with myocarditis may present with decreased appetite,
fever, irritability, and diaphoresis. Sudden death occurs rarely in this age
group. Infants with congestive heart failure may not have signs of jugular
venous distention and rales on pulmonary examination.
Older children and adolescents typically provide a history of recent viral
illness (approximately 2 weeks earlier). Similar to infants, these children
exhibit lethargy, fever, and pallor. Diaphoresis, palpitations, rashes, and
decreased exercise tolerance may also be present. Occasionally, they complain
of abdominal pain. As the disease progresses, respiratory distress may become
more prominent. With the development of congestive heart failure, the child may
develop jugular venous distention and rales on examination. It is not uncommon
for arrhythmias to develop, including supraventricular tachycardia and
ventricular tachycardia.
V. Diagnostic Approach
Whenever a patient develops congestive heart failure or arrhythmias of unknown
cause, myocarditis should be included in the differential diagnosis.
Chest roentgenogram. With myocarditis, the chest roentgenogram may reveal cardiomegaly with prominent
vascular markings. This generally indicates pulmonary edema.
Electrocardiogram. Patients with myocarditis may develop sinus tachycardia with low-voltage QRS
complexes. Inverted T waves may also be seen. Q waves and ST-segment elevation
indicate myocardial infarction.
Echocardiogram. A dilated, poorly functional left ventricle is seen with myocarditis. This may
be accompanied by pericardial effusion. Occasionally, other cardiac chambers
are dilated as well.
Cardiac catheterization. This may indicate low cardiac output with elevated end-diastolic pressures. With
the use of this procedure, one may obtain endomyocardial biopsies of the right
ventricle. In myocarditis, a mononuclear cell infiltrate will be present.
Because this procedure carries a relatively significant risk, it is not
performed in all cases.
Complete blood count. With EBV infection, there is usually a lymphocytosis that peaks during the
second or third week. Classically, the patient has more than 10% atypical
lymphocytes. Neutropenia and thrombocytopenia are also seen. An anemia, usually
of an autoimmune nature, may develop with EBV infection.
Monospot test. This tests for the presence of heterophile antibodies, which are found in
approximately 90% of patients with EBV infection. The heterophile antibody test
is often negative in children younger than 4 years of age.
Epstein-Barr virus-specific antibodies. Antibodies to VCA may be seen. VCA IgG antibodies develop rapidly and are
present in acute and past infections. However, the presence of VCA IgM is
considered diagnostic of acute EBV infection. One may also look for EA
antibodies, but 30% of patients do not develop them. Antibodies to EBNA do not
develop until late in the infection. The absence of EBNA in the presence of VCA
IgG and EA indicates acute EBV infection.
Liver function tests. Most patients develop a hepatitis from an EBV infection, with elevated AST, ALT,
and lactic dehydrogenase. Patients may also develop hyperbilirubinemia.
VI. Treatment
Patients who present with myocarditis may have only mild symptoms of congestive
heart failure. They can be monitored with no specific immediate intervention.
It is not uncommon for bed rest to be prescribed, because this is thought to
possibly decrease intramyocardial viral replication.
However, some patients have poor cardiac output and poor tissue perfusion. In
these cases, digitalis and diuretics may be prescribed. One should also
consider anticoagulation medications including aspirin, warfarin, and heparin
to prevent thromboembolic disease.
With EBV myocarditis, some would advocate the use of steroids and even
acyclovir. However, this combination has not been extensively studied, because
the disease entity is relatively rare.
VII. References
1. American Academy of Pediatrics. Epstein-Barr virus infections. In: Pickering
LK, Peter G, Baker CJ, et al., eds.
2000 Red Book: Report by the Committee on Infectious Diseases, 25th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2000:238–240.
2. Baykurt C, Caglar K, Ceviz N, et al. Successful treatment of Epstein-Barr
infection associated with myocarditis.
Pediatr Int 1999;41:389–391.
3. Graziano JN, Ludomirsky A, Goldberg CS. Acute myocardial ischemia in a
healthy male child: an atypical presentation of acute Epstein-Barr virus
infection.
Clin Pediatr 2001;40:277–281.
4. Schooley RT. Epstein-Barr virus (infectious mononucleosis). In: Mandell GL,
Bennett JE, Dolin R, eds.
Mandell, Douglas, and Bennett's principles and practice of infectious diseases, 5th ed. Philadelphia: Churchill Livingstone, 2000:1599–1608.
5. Towbin JA. Myocarditis. In: Allen HD, Gutgesell HP, Clark EB, et al., eds. Moss and Adams' heart disease in infants, children, and adolescents, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1197–1215.
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 14-4: 17-Year-Old Boy (Pediatric Complaints and Diagnostic Dilemmas)
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