Cough - Case 4-2: 7-Week-Old Boy
Cough - Case 4-2: 7-Week-Old Boy: Excerpt from Pediatric Complaints and Diagnostic Dilemmas
I. History of Present Illness
A 7-week-old boy presented to his pediatrician with a 3-week history of
rhinorrhea, congestion, and cough; previously he was in good health. He had no
history of fever. A chest roentgenogram demonstrated a left lower lobe
infiltrate, and a 10-day course of erythromycin for treatment of pneumonia was
started. At the completion of this antibiotic course, the boy
's mother felt that his respiratory status had improved to some extent, but his
work of breathing was still increased from baseline. Furthermore, his cough was
persistent in nature. One week later, a repeat chest roentgenogram revealed
persistence of the left lower lobe infiltrate, and he was referred for further
evaluation. The review of symptoms revealed good oral intake and normal urine
output.
II. Past Medical History
He was born at 41 weeks' gestation with a birth weight of 3,000 g. There were no pregnancy- or
birth-related complications. He had no history of cyanosis or feeding
difficulties. He was feeding on formula, taking 2 ounces every 2 hours. He had
two older siblings who were both healthy.
III. Physical Examination
T, 37.3°C; RR, 54/min; HR, 153 bpm; BP in right upper extremity, 93/59 mm Hg; BP in left
upper extremity, 87/62 mm Hg; BP in right lower extremity, 94/63 mm Hg; SpO
2, 95% in room air
Weight, 4.5 kg
Initial examination revealed a well-developed infant in moderate respiratory
distress. The physical examination was remarkable for nasal flaring,
intercostal retractions, and intermittent grunting. He had good aeration and
scattered rales at both lung bases. Cardiac examination revealed a normal first
heart sound (S
1) and a prominent second pulmonary sound (P2). A II-III/VI systolic murmur was appreciated at the left sternal border. The
liver edge was palpated 4 cm below the right costal margin. The remainder of
the physical examination was normal.
IV. Diagnostic Studies
Laboratory analysis revealed a peripheral blood count of 8,400 WBCs/mm3, with 35% segmented neutrophils, 60% lymphocytes, and 5% eosinophils. The
hemoglobin was 11.4 g/dL, and there were 203,000 platelets/mm
3. Electrolytes, blood urea nitrogen, and creatinine were all within normal
limits. Antigens of respiratory viruses were not detected by immunofluorescence
of nasopharyngeal washings.
V. Course of Illness
An electrocardiogram (ECG) was performed that suggested a diagnosis (Fig. 4-2).
Discussion: Case 4-2
I. Differential Diagnosis
The causes of a chronic cough in an infant are diverse, but the most common
causes are viral infections. In infants with a history of conjunctivitis,
C. trachomatis should be considered. B. pertussis can occur in infants and produce a chronic cough. Most often, infants are unable
to generate the force necessary for the classic
“whoop.” Certainly, other bacterial pneumonias should be considered with the lobar
infiltrate noted on chest roentgenogram in this case. Finally, GER must always
be considered a common cause for cough in infancy. Other, less common causes of
cough in this age group include congenital malformations including
tracheoesophageal fistulas, tracheobronchomalacia, vascular rings, lobar
emphysema, bronchogenic cyst, pulmonary sequestration, laryngeal cleft, and
airway hemangiomas.
Congestive heart failure should always be considered, with common etiologies in
infancy being volume overload (patent ductus arteriosus, truncus arteriosus,
ventricular septal defect, common atrioventricular canal, total anomalous
pulmonary venous return), myocardial dysfunction (myocarditis, Kawasaki
syndrome, anomalous left coronary artery), arrhythmias (supraventricular
tachycardia), pressure overload (coarctation of the aorta, aortic stenosis),
and secondary causes (hypertension, sepsis).
The features of this case that prompted additional evaluation were cardiomegaly
and increased vascular markings noted on the chest roentgenogram, presence of a
heart murmur, and biventricular hypertrophy seen on the ECG.
II. Diagnosis
The ECG revealed a ventricular rate of 150 bpm and dramatic biventricular
hypertrophy. An echocardiogram revealed a large perimembranous ventricular
septal defect (VSD) with left-to-right shunting. It also demonstrated
moderately depressed biventricular function, with a shortening fraction of 29%.
The diagnosis is perimembranous VSD.
III. Incidence and Epidemiology
VSDs are the most common cardiac malformation seen in children. Recent studies
have shown the incidence of VSD in newborns to be 5 to 50 per 1,000 children,
with a slight female predominance. VSDs are the most common form of congenital
heart disease associated with chromosomal disorders.
VSDs are classified into four types: perimembranous (80%), outlet (5% to 7%),
inlet (5% to 8%), and muscular (5% to 20%). Muscular defects have the greatest
likelihood of undergoing spontaneous closure. Approximately 75% to 80% of all
VSDs close spontaneously, most often by 2 years of age.
IV. Clinical Presentation
Pulmonary vascular resistance determines the extent of the left-to-right shunt.
Pulmonary vascular resistance is elevated at birth and declines to adult levels
over the first week of life. Therefore, with small VSDs, usually no heart
murmur is heard at birth. Most often, the murmur is heard at about 1 to 6 weeks
of age; it is usually holosystolic, harsh, and located along the left sternal
border. Most infants with small VSDs have no significant symptoms and thrive.
In those infants with moderate or large VSDs, symptoms may develop at about 2
weeks of age and can include tachypnea, irritability, diaphoresis or fatigue
with feeding, and failure to thrive. These symptoms develop secondary to
progressive heart failure and pulmonary edema. Not uncommonly, symptoms come to
attention immediately after a respiratory infection, which stresses the infant
's small reserve. With large defects, infants often have a hyperactive precordium
with a palpable thrill. Large VSDs, like small ones, produce an associated
harsh, holosystolic murmur located along the left sternal border.
V. Diagnostic Approach
Chest roentgenogram. With small VSDs, the chest roentgenogram may be normal. In contrast, a large VSD
may lead to significant cardiomegaly and increased vascular markings.
Electrocardiography. The ECG, like the chest roentgenogram, may be normal with small VSDs. However,
with moderate-sized VSDs, left ventricular hypertrophy is likely to be present
secondary to volume overload of the left ventricle, and right ventricular
hypertrophy secondary to pressure overload of the right ventricle. Importantly,
these changes are not always evident on the ECG of infants with moderate-sized
VSDs.
Echocardiography. Doppler echocardiography is essential to pinpoint the size and location of a
VSD. Ventricular, pulmonary artery, and interventricular pressure differences
can be determined. Echocardiography also identifies associated cardiac defects.
Magnetic resonance imaging. Cardiac MRI can be used if echocardiography does not reveal sufficient detail.
On occasion, MRI may be needed to evaluate extracardiac vascular anomalies.
Cardiac catheterization. Cardiac catheterization is necessary only for patients with complicated
cardiovascular anatomy or physiology and need not be performed in all cases of
VSD. Pulmonary blood flow and vascular resistance may be evaluated in more
detail with this procedure than with Doppler echocardiography.
VI. Treatment
As mentioned, infants with small VSDs usually do not require any intervention.
They do require careful surveillance during the first 6 months of life, to
assess growth and respiratory status. Many of these small VSDs close
spontaneously. Importantly, these patients still require endocarditis
prophylaxis.
Usually, those infants with moderate or large VSDs develop some degree of
congestive heart failure. Medical management is often the initial therapy and
may include furosemide, chlorothiazide, spironolactone, and digoxin. On
occasion, afterload reduction with captopril is also required. In those
patients with persistent failure to thrive, caloric augmentation may be
required. If the patient
's congestive heart failure and growth failure are not controlled with medical
management, surgical intervention is required.
VII. References
1. Fink BW. Ventricular septal defect. In: Fink BW, ed. Congenital heart disease: a deductive approach to its diagnosis, 3rd ed. St. Louis: Mosby, 1991:13–30.
2. Gersony WM. Ventricular septal defect and left sided obstructive lesions in
infants.
Curr Opin Pediatr 1994;6:596–599.
3. Gumbiner CH. Ventricular septal defect. In: Oski FA, DeAngelis CD, Feigin
RD, et al., eds.
Principles and practice of pediatrics, 2nd ed. Philadelphia: JB Lippincott, 1994:1561–1564.
4. Lee HR. Congestive heart failure. In: Schwartz MW, ed. The 5 minute pediatric consult, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2000:276–277.
5. McDaniel NL, Gutgesell HP. Ventricular septal defects. 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, 2001:636–650.
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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