Abdominal Pain - Case 7-4: 9-Year-Old Girl
I. History of Present Illness
A 9-year-old girl was well until 6 days before admission, when she developed
vomiting, abdominal pain, and lethargy. Four days before admission, she was
noted to have a fever to 38.9
°C and cough. She was seen by her pediatrician 3 days before presentation and was
diagnosed with a lower lobe pneumonia with referred abdominal pain. She was
treated with amoxicillin. Over the next 2 days, she had worsening of her
abdominal pain and increased listlessness. There had been no recent symptoms of
upper respiratory tract infection and no diarrhea. Her mother reported that the
whites of her eyes had looked yellow for the past 3 weeks.
II. Past Medical History
The patient had had no major illnesses or hospitalizations. She had had four
episodes of dizziness over the past 5 months that had been evaluated with an
electroencephalogram (EEG) and an electrocardiogram (ECG), both of which were
normal. She was not taking medications except amoxicillin for her diagnosis of
pneumonia. The family history was significant only for several family members
with diabetes mellitus. The mother had required a splenectomy after blunt
abdominal trauma.
III. Physical Examination
T, 37.4°C; RR, 30/min; HR, 118 bpm; BP, 91/50 mm Hg; SpO2, 94% on room air
Weight, 27.9 kg (25th percentile)
The patient was responsive but withdrawn. Physical examination revealed mildly
icteric sclera, no oral lesions, and no pharyngeal injection. The neck was
supple with shotty lymphadenopathy. The lungs were clear, with equal breath
sounds bilaterally. Cardiac examination revealed a normal precordium, mild
tachycardia, normal S
1 and S2 sounds, no gallop, and no murmur. The abdomen was soft and nontender with normal
bowel sounds; the liver was palpated 4 cm below the right costal margin, and
the spleen tip was palpable. The extremities were warm, but there were
diminished pulses in both the upper and lower extremities. The neurologic
examination was normal, and the skin revealed no rash.
IV. Diagnostic Studies
A CBC revealed a 9,600 WBCs/mm3, with 72% segmented neutrophils and 23% lymphocytes. The hemoglobin and
platelets were normal. PT, PTT, electrolytes, blood urea nitrogen, and
creatinine were all normal. A hepatic function panel revealed a bilirubin
concentration of 3.2 mg/dL, with an unconjugated bilirubin concentration of 1.8
mg/dL. Albumin was 3.8 g/dL; alkaline phosphatase, 78 U/L; aspartate
transaminase, 54 U/L; lactate dehydrogenase, 237 U/L; and uric acid, 7.3 mg/dL.
Lipase was 168 U/L and amylase 63 U/L. An ECG revealed a sinus rhythm at 129
bpm, a PR interval of 0.144 seconds, right axis deviation, normal voltage, and
no ST-segment changes. The chest radiograph was abnormal (Fig. 7-4).
V. Course of Illness
The patient had an echocardiogram, which revealed a markedly dilated left
ventricle to 5.4 cm, moderate to severe mitral regurgitation, and a markedly
decreased shortening fraction of 10% to 18%. Furosemide and milrinone were
started. Despite increasing doses, by the fourth hospital day the patient had
distended neck veins, increasing dyspnea, cough, and lethargy. Repeat
echocardiography showed a decrease in the shortening fraction to less than 10%,
with a dilated and thin-walled left ventricle, persistent severe mitral
regurgitation, moderate tricuspid regurgitation, and a right ventricular
pressure 30 mm greater than that of the right atrium.
Discussion: Case 7-4
I. Differential Diagnosis
Myocarditis and other forms of heart disease are possible causes for abdominal
pain. Cardiomegaly on this patient
's chest radiograph gave the first indication of heart disease and heart failure.
A possible cause of this heart failure is congenital heart disease,
particularly septal lesions, which must be ruled out in the pediatric
population at any age. Other possible causes include dilated cardiomyopathy,
hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right
ventricular dysplasia, obliterative cardiomyopathy, inflammatory cardiomyopathy
(myocarditis), and giant cell myocarditis. In pediatrics, it is most helpful to
make the more broad distinction between cardiomyopathy and myocarditis.
II. Diagnosis
Chest radiography revealed dramatic cardiomegaly and prominence of the pulmonary
vasculature (Fig. 7-4). Cardiac catheterization with endomyocardial biopsy was
done, and the patient was noted to have a decreased cardiac index of 1.47 mm/m
2, a left ventricular end-diastolic pressure of 35 mm Hg, an increased pulmonary
capillary wedge pressure of 38 mm Hg, and a right atrial pressure of 18 mm Hg.
Biopsy revealed no inflammatory cells. The patient was diagnosed with
idiopathic dilated cardiomyopathy and listed for cardiac transplantation.
The diagnosis is idiopathic dilated cardiomyopathy.
III. Incidence and Epidemiology
Although heart failure represents a major problem in adult medicine, it is far
less common in pediatrics and is the cause in fewer than 10% of pediatric heart
transplantations. Excluding infancy, when congenital heart disease is the most
common indication for heart transplantation, dilated cardiomyopathy is the
primary indication for pediatric heart transplantation throughout the world.
Although the majority of cases of dilated cardiomyopathy have no definitive
cause, several genetic and molecular lesions have been proposed. These include
mutations in the cytoskeleton, troponin, and other sarcomere protein genes. It
has long been known that the skeletal muscular dystrophies have cardial
involvement, but familial dilated cardiomyopathy, although poorly understood,
has been recognized more frequently.
The structural changes that occur in dilated cardiomyopathy include increased
left ventricular mass, normal or reduced left ventricular wall thickness, and
increased left ventricular cavity size. Histologic samples can show anything
from focal myocyte death, to increased interstitial macrophage, to interstitial
fibrosis.
Ten percent of cases of new-onset cardiomyopathy can be attributed to
myocarditis. Survival rates can be as high as 80% and the infections can be
either fulminant (usually with a better prognosis) or insidious. Arguably,
insidious cases may be missed and may later contribute to cases of idiopathic
cardiomyopathy. Bacterial, spirochetal, fungal, protozoal, parasitic,
rickettsial, and viral infectious agents have all been implicated. Worldwide,
infections with
Trypanosoma cruzi (Chagas disease) and with Corynebacterium diphtheriae (diphtheria) are the most common causes of myocarditis; in the United States,
viral infections are more common. The two major viral etiologies are
coxsackievirus B and adenovirus. Other causes of myocarditis include
immune-mediated mechanisms and toxins such as medications and heavy metals.
IV. Clinical Presentation
The clinical presentation of dilated cardiomyopathy encompasses that of clinical
heart failure, including fatigue, shortness of breath, cough, and abdominal
pain. However, the clinical features are varied and can range from asymptomatic
patients to those with fulminant cardiac failure. In myocarditis, there is
frequently a history of a recent flu-like syndrome and sometimes arrhythmias
secondary to the rapid ventricular dilatation.
V. Diagnostic Approach
The distinction between dilated cardiomyopathy and myocarditis is important,
because it may alter the management regimen that the child receives. Although
clinical symptoms (clinical heart failure, recent flu-like syndrome accompanied
by fever) and laboratory findings (leukocytosis, eosinophilia, elevated
creatinine kinase or troponin) can be helpful in supporting a diagnosis of
myocarditis, they are not sufficient.
Echocardiogram. All patients should have an echocardiogram to rule out structural anomalies.
Myocardial biopsy. Although other noninvasive modalities are important, myocardial biopsy is still
the gold standard for diagnosis of myocarditis.
Other studies. Testing for infectious agents (e.g., coxsackievirus, adenovirus, echoviruses,
respiratory syncytial virus, cytomegalovirus, Epstein-Barr virus, HIV) and any
other possible causes, including autoimmune disease (e.g., lupus) and
mitochondrial disease, is warranted in all new cases of pediatric heart
failure.
VI. Treatment
Supportive therapy is the mainstay of treatment. Although there is less evidence
to support specific treatment of heart disease in the pediatric population, the
therapy mirrors that of adult medicine and includes angiotensin-converting
enzyme (ACE) inhibitors. Less frequently,
β-blockers and digoxin are used. Although there is not a strong literature and
controversies persist, the standard is to treat cases of biopsy-proven
myocarditis with immunomodulators (ranging from immunoglobulin therapy and
steroids to cyclosporine and cytoxan) in an attempt to suppress the
inflammation. Patients with progressively worsening heart failure may be
candidates for mechanical assist devices (e.g., left ventricular assist device,
extracorporeal membrane oxygenation), which may provide stabilization until
cardiac transplantation can be achieved.
VII. References
1. Davies MJ. The cardiomyopathies: an overview. Heart 2000;83:469–474.
2. Burch M. Heart failure in the young. Heart 2002;88:198–202.
3. Batra AS, Lewis AB. Acute myocarditis. Curr Opin Pediatr 2001;13:234–239.
4. Feldman AM, McNamara D. Myocarditis. N Engl J Med 2000;343:1388–1398.
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 Lower abdominal pain
» Next page: Abdominal Pain - Case 7-5: 8-Year-Old Boy (Pediatric Complaints and Diagnostic Dilemmas)
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