Chest Pain - Case 14-6: 15-Year-Old Boy
I. History of Present Illness
A 15-year old boy with a history of asthma and chronic sinusitis presented with
a 2-day history of shortness of breath and chest pain. He described the pain as
an ache with an occasional squeezing feeling. He developed wheezing that
required increasing use of his albuterol inhaler. However, this did not relieve
his symptoms. He also developed a productive cough. His mother believed that he
had had increasing fatigue since the morning of his presentation, as well as a
decreased appetite. He denied fever, vomiting, or diarrhea.
II. Past Medical History
He was diagnosed with asthma at the age of 7 years and required multiple
emergency department visits and hospitalizations. Two years before
presentation, he had had one asthma admission that lasted for 1 month. He had
never needed endotracheal intubation or intensive care. He had recently been
started on a leukotriene inhibitor for his asthma. Many of his prior admissions
for asthma exacerbations included cardiology evaluations for chest pain. He
also had a history of chronic sinusitis requiring six sinus surgeries over the
last 3 years, as well as a somatization disorder diagnosed by psychiatry. His
daily medications included montelukast and inhaled fluticasone.
The patient had recently been admitted to the hospital for an asthma
exacerbation and gastroenteritis. During that admission, he was seen by
cardiology staff for bradycardia and chest pain. An echocardiogram at that time
revealed a shortening fraction of 24% and a left ventricular end-diastolic
pressure of 5.5 mm Hg. A Holter monitor and exercise test were both normal.
III. Physical Examination
T, 37.0°C; RR 26/min; HR, 110 bpm; BP, 85/60 mm Hg; SpO2, 91% in room air
In general, he was an uncomfortable boy in moderate respiratory distress. He was
short of breath and was able to speak only in fragmented sentences. He was
sitting up for comfort. His oropharynx was dry. His chest examination revealed
diffuse rales and wheezes with fair aeration throughout. His cardiac
examination indicated an active precordium and tachycardia with regular rhythm.
No murmurs or rubs were noted, but an intermittent gallop was appreciated. His
liver was palpable 3 cm below the right costal margin. His extremities were
cool, with weak pulses and slightly delayed capillary refill.
IV. Diagnostic Studies
Laboratory analysis revealed 7,500 WBCs/mm3. Electrolytes, blood urea nitrogen, creatinine, and liver function tests were
all within normal limits. ECG revealed a normal sinus rhythm at a rate of 100
bpm. There was possible right atrial enlargement and some ST-segment
depression.
V. Course of Illness
A chest roentgenogram suggested the diagnosis (Fig. 14-5).
Discussion: Case 14-6
I. Differential Diagnosis
The most common causes for chest pain in the adolescent age group are cough,
asthma, pneumonia, musculoskeletal causes, and idiopathic causes. With this
patient
's past medical history of asthma, it was natural for asthma to be the initial
focus of concern. However, because the patient
's physical examination was not consistent with an asthma exacerbation, other
diagnoses were appropriately considered. The concerning features on this
patient
's physical examination included signs of congestive heart failure: bilateral
rales, a gallop, and a palpable liver edge 3 cm below the right costal margin.
Furthermore, his shortness of breath was significantly worse while lying down.
Dyspnea with an asthma exacerbation is not usually positional in nature to this
extent.
The differential diagnosis for heart failure in this adolescent includes
congenital heart disease
—both pressure overload (e.g., aortic stenosis) and volume overload (e.g., aortic
regurgitation, arrhythmias); acquired heart disease (myocarditis,
cardiomyopathy, pericarditis, cor pulmonale, endocarditis); hypoglycemia;
storage diseases; and ingestions such as cardiac toxins (e.g., digitalis) and
arrhythmogenics (e.g., tricyclic antidepressants).
II. Diagnosis
His chest roentgenogram revealed pulmonary edema with cardiomegaly (Fig. 14-5).
An echocardiogram was performed and demonstrated a shortening fraction of less
than 20%, with left-ventricular end-diastolic pressure of 6.4 mm Hg. The left
ventricle was noted to be dilated.
The diagnosis is a dilated cardiomyopathy. He was initially treated with intravenous Lasix (furosemide). He was then
started on a milrinone infusion. Multiple laboratory studies were requested,
including infectious serologies and thyroid function tests, which did not
reveal a cause for his cardiomyopathy. Ultimately, a cardiac catheterization
was performed, which revealed a cardiac index of 2.81 and superior vena cava
saturation of 75%. A biopsy was performed which demonstrated an eosinophilic
and monocytic infiltrate.
III. Incidence and Epidemiology
By definition, cardiomyopathy is a structural or functional abnormality of the
ventricular myocardium that does not involve coronary artery disease,
hypertension, or valvular or congenital heart disease. Cardiomyopathy in
children can be divided into primary and secondary forms. Primary
cardiomyopathies are either dilated, hypertrophic, restrictive, or
arrhythmogenic. Secondary cardiomyopathies have multiple causes, including
infection, metabolic disorders, general systemic diseases, hereditary forms,
and toxic reactions.
This patient presented with a dilated cardiomyopathy of no definitive cause.
Idiopathic dilated cardiomyopathy has a prevalence of 36.5 cases per 100,000
persons and accounts for 50% of the total cases of dilated cardiomyopathy.
Idiopathic cardiomyopathy has survival rates of 63% to 90% at 1 year and 20% to
80% at 5 years.
IV. Clinical Presentation
Patients with a dilated cardiomyopathy most often have an insidious onset to
their symptoms. The most common complaints in adolescents are shortness of
breath and poor exercise tolerance, which are the result of decreased cardiac
output and pulmonary edema. Because infants are not able to complain of these
same symptoms, their presentation often includes more subtle symptoms, such as
tachypnea, irritability, and difficulty with feeding.
Patients often are tachycardiac, tachypneic, and nervous. Hypotension may be
seen with poor cardiac output, and fever may indicate an infection that has
brought the patient to medical attention. Quite often, patients have orthopnea,
preferring to remain in the upright position. With pulmonary edema, many
patients wheeze but are unresponsive to traditional asthma therapies.
On chest wall palpation, there may be a laterally displaced point of maximal
impulse. With auscultation of the cardiac sounds, a prominent pulmonic segment
of the S2 or a gallop, or both, may be appreciated. Many patients with
congestive heart failure have a liver edge that is abnormally below the right
costal margin.
V. Diagnostic Approach
Chest roentgenogram. Patients generally have an increased heart size noted. This is secondary to
left-sided dilation. Accompanying signs include pulmonary edema and possibly
pleural effusions.
Electrocardiogram. Sinus tachycardia is the most common finding, with supraventricular or
ventricular tachycardia possible as well. Signs of left ventricular hypertrophy
and nonspecific ST-segment and T-wave abnormalities may also be seen.
Echocardiogram. The left atrium and left ventricle are generally noted to be enlarged. There may
be increased end-diastolic and systolic volumes. Poor wall movement may be seen
secondary to ischemic injury. With this imaging modality, pericardial and
pleural effusions may also be noted.
Cardiac catheterization. One can obtain hemodynamic data on pressures in the aorta, left ventricle,
pulmonary capillary wedge, and pulmonary artery. The cardiac output can be
calculated and will be decreased. A endomyocardial biopsy can be performed and
may be useful to determine the cause of the cardiomyopathy.
VI. Treatment
Inotropic agents such as the sympathomimetic drugs dopamine, dobutamine, and
epinephrine are often required to support the poor cardiac output. Milrinone
and amrinone are inotropes that can be used to treat patients with signs of
congestive heart failure. Digoxin is used for long-term therapy and increased
cardiac contractility.
Because fluid overload is quite common in this clinical scenario, diuretics such
as furosemide are often necessary. Peripheral vasodilators, including
nitroprusside and hydralazine, may be used to decrease afterload and thereby
increase cardiac output. Angiotensin-converting enzyme (ACE) inhibitors can
have similar effects to reduce afterload.
With dilation of the cardiac chambers, the patient is at risk for thrombus
formation. Use of anticoagulants or antiplatelet drugs should be considered. If
the underlying cause of the cardiomyopathy is determined, a more specific
therapy may be warranted.
Finally, in severe cases, cardiac transplantation is required. It is difficult
to determine which children or adolescents should be considered for
transplantation. Certainly, this option should be explored for those children
who are still quite ill despite maximal intervention.
VII. References
1. Gewitz MH, Vetter VL. Cardiac emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of pediatric emergency medicine. Baltimore: Williams & Wilkins, 1993:533–572.
2. Olson TM, Chan DP. Dilated congestive cardiomyopathy. In: Driscoll DJ, eds. Moss and Adams' heart disease in infants, children, and adolescents, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2001:1187–1195.
3. Paquet M, Hanna BD. Cardiomyopathy. In: Oski FA, DeAngelis CD, Feigin RD, et
al., eds.
Principles and practice of pediatrics, 2nd ed. Philadelphia: JB Lippincott, 1994:1606–1614.
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.
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