Vomiting - Case 3-2: 9-Month-Old Girl
I. History of Present Illness
A 9-month-old girl presented with a 12-day history of poor feeding, decreased
activity, irritability, and frequent nonbloody, nonbilious emesis with feeds.
Ten days earlier she was initially diagnosed with a viral gastroenteritis, and
6 days before admission she was treated with amoxicillin for an acute otitis
media. She presented with continued emesis and decreased urine output, having
had only two wet diapers in the previous 18 hours. She had a history of poor
feeding and frequent episodic bouts of emesis lasting 2 to 3 days. The parents
denied any fever, diarrhea, cough, gagging with feeds, rash, bloody stools, ill
contacts, recent travel, or animal exposure. Her diet consisted of Nutramigen
formula and various infant foods.
II. Past Medical History
The patient was born at full term from an uncomplicated pregnancy, labor, and
delivery and was well until 3 months of age, when she developed episodic
vomiting. The emesis was nonbloody and nonbilious, lasted 1 to 3 days, and was
associated with decreased activity. It began during the transition from breast
milk- to cow
's milk-based formula and was therefore attributed to a “feeding intolerance.” At 4 months, she was changed to a soy- protein based formula, and then finally,
at 6 months, Nutramigen was started, without any relief in her symptoms. She
was treated with ranitidine starting at 7 months for suspected GER. A sweat
test performed at 8 months of age was normal. The family history was
noncontributory.
III. Physical Examination
T, 37.3°C; RR, 22 to 25/min; HR, tachycardic; BP, 85/53 mm Hg
Weight, 6.5 kg (less than 5th percentile; 50th percentile for a 5-month-old
child); length, 66.5 cm (less than 5th percentile); head circumference, 43.5 cm
(25th percentile)
The patient was fussy but not toxic-appearing, with scant nasal discharge and
dry oral mucosa. Her lungs were clear bilaterally, and she had a soft systolic
murmur at the lower left sternal border with a prominent S3 gallop. The liver
edge was palpated 1 cm below the right costal margin, and her spleen tip was
also palpable. The extremities were warm and well perfused. There were no
rashes, and her neurologic examination was normal for age.
IV. Diagnostic Studies
Laboratory analysis revealed 10,200 WBCs/mm3, with 41% segmented neutrophils, 53% lymphocytes, and 6% monocytes. The
hemoglobin was 11 g/dL, and the platelet count was 232,000 cells/mm
3. Serum electrolytes were as follows: sodium, 128 mmol/L; potassium, 4.5 mmol/L;
chloride, 100 mmol/L; and bicarbonate, 20 mEq/L. Blood urea nitrogen (BUN) was
19 mg/dL, creatinine was 0.3 mg/dL, glucose was 84 mg/dL, and calcium was 9.2
mg/dl. Her ABG analysis showed pH, 7.43; PaCO
2, 31 mm Hg; and PaO2 , 270 mm Hg.
V. Course of Illness
A chest radiograph revealed mild cardiomegaly and a small right pleural
effusion. An electrocardiogram (ECG) (Fig. 3-2) was diagnostic.
Discussion: Case 3-2
I. Differential Diagnosis
This patient presented with recurrent episodes of emesis and intermittent
asymptomatic periods, consistent with cyclic vomiting. Quantitative criteria
for the diagnosis of cyclic vomiting include at least four episodes of vomiting
per hour during the peak intensity and a frequency of no more than nine
episodes per month. In contrast, the patient with chronic vomiting has less
frequent episodes and fewer symptom-free days.
Cyclic vomiting frequently has a nongastrointestinal etiology. Common causes
include migraine headaches, abdominal migraines, metabolic disorders including
adrenal insufficiency, amino acidurias, and organic acidurias. Renal disorders
such as UPJ obstruction and renal calculi, as well as intermittent cardiac
arrhythmias, can also cause cyclic vomiting. Familial dysautonomia (Riley-Day
syndrome) and Munchausen syndrome by proxy must also be considered.
Gastrointestinal etiologies include pancreatitis, malrotation with intermittent
volvulus, and intestinal duplications.
In patients with significant tachycardia and cyclic vomiting, an intermittent
cardiac tachyarrhythmia must be strongly considered. The source of the
tachyarrhythmia may be sinus, supraventricular, or ventricular. Differentiation
of supraventricular tachycardia from sinus tachycardia may be difficult at
times. Sinus tachycardia rarely exceeds 230 bpm, has a normal P wave and P-wave
axis, and results in a varying HR due to changes in vagal and sympathetic tone.
Antidromic supraventricular tachycardia (SVT) or SVT with a preceding bundle
branch block (see later discussion) may result in a widened QRS complex that
resembles ventricular tachycardia. The absence of P waves and the presence of a
wide QRS complex that is dissimilar to the QRS complex observed during sinus
rhythm are more diagnostic of ventricular tachycardia.
II. Diagnosis
The EKG in this patient revealed a narrow-complex tachycardia of 250 bpm,
consistent with SVT (see Fig. 3-2).
After ice was applied to the patient's face without success, she was cardioverted to a normal sinus rhythm with the
use of intravenous adenosine. She was treated with digoxin and over the next 2
days had normalization of her cardiac examination and resolution of her
hepatomegaly. An echocardiogram revealed mild left ventricular dilation, mild
mitral valve regurgitation, and a small pericardial effusion but good cardiac
function without any structural defects. A repeat EKG before discharge showed
mild right atrial enlargement and a normal sinus rhythm without signs of
preexcitation (shortened PR interval and delta wave) (Fig. 3-3). After 2 months
on digoxin, her weight had increased to the 25th percentile. In retrospect, her
history of episodic feeding intolerance, with each episode lasting 1 to 2 days,
may have been episodes of supraventricular tachycardia.
III. Incidence and Epidemiology of Supraventricular Tachycardia
SVT is a generic term encompassing a group of cardiac arrhythmias that originate
above the atrioventricular (AV) node. It is the most common sustained
accelerated nonsinus tachyarrhythmia, with an incidence of 1 per 250 to 1,000
children. SVT can be diagnosed by EKG during an episode. Episodes can be
captured by means of a diagnostic EKG, a 24-hour Holter monitor, or
transtelephonic monitoring. Two mechanisms account for virtually all cases of
SVT: (a) an abnormal or enhanced normal automatic rhythm and (b) a reentrant
rhythm. Approximately 75% of patients with a reentrant rhythm exhibit findings
of preexcitation, with a shortened PR interval and initial slurred upstroke of
the QRS (delta wave). Children younger than 12 years of age are more likely to
have an accessory AV connection in adolescence, nodal reentry tachycardia
increases in frequency.
Reentrant rhythms account for 90% of all cases of SVT. Two separate conducting
pathways must be present, either AV or within the atrium, that lead to a cyclic
pattern of excitation resulting in SVT. Atrial reentry rhythms may lead to
either atrial fibrillation or atrial flutter. AV reentrant rhythms may be
either through the AV node (nodal) or associated with an accessory AV pathway
termed the bundle of Kent. Tachycardia may result from transmission of the
impulse antegrade through the AV node-His-Purkinje system, through the
myocardium retrograde, and through the accessory pathway completing the
circuit. This orthodromic reciprocating tachycardia (ORT) is the most common
pattern seen in Wolf-Parkinson-White syndrome and results in the typical
narrow-complex QRS tachycardia. Rarely, the antegrade impulse travels via the
accessory pathway and retrograde through the AV node-His-Purkinje system,
resulting in antidromic reciprocating tachycardia (ART).
Preexcitation occurs in 75% of individuals with accessory pathways. This implies
that the accessory pathway can conduct the impulse in antegrade fashion, from
the atria to the ventricle. Bypassing the intrinsic delay of the AV node
results in a shortened PR interval and a slurred upstroke of the QRS, the
so-called delta wave. Twenty-five percent of accessory pathways transmit
impulses only in retrograde fashion, from the ventricle to the atrium,
resulting in a normal resting EKG (i.e., with no evidence of preexcitation).
SVT secondary to increased automaticity or atrial and junctional ectopic
tachycardias occurs more commonly in children with postoperative congenital
heart disease or cardiomyopathies.
IV. Clinical Presentation
Signs and symptoms of SVT depend on the age at presentation and the duration of
the tachycardia. Episodes of SVT may last only a few seconds or may persist for
hours. Many children tolerate these episodes extremely well, and it is unlikely
that short paroxysms are dangerous. Infants with SVT often present with heart
failure after the tachycardia goes unrecognized for a prolonged period.
Episodes lasting longer than 6 to 24 hours may result in an acutely ill child
with evidence of cardiopulmonary distress, with tachypnea, poor feeding,
vomiting, lethargy, ashen color, restlessness, and irritability. Physical
findings in such cases include pallor, tachypnea, diaphoresis, and
hepatomegaly.
Older children may complain of lightheadedness, chest tightness, palpitations,
and fatigue. Chest pain or discomfort is less common. The patient may become
faint, dizzy, or even syncopal. If the HR is exceptionally rapid or if the
attack is prolonged, heart failure may ensue.
V. Diagnostic Approach
Electrocardiogram. An EKG should be performed on any patient with tachycardia that is not thought
to be normal sinus tachycardia. Patients with SVT have a very rapid and regular
ventricular rate, usually about 240 bpm. The P waves are usually absent; when
present, they have an abnormal axis and may precede or follow the QRS. Pending
the results of the ECG, a chest radiograph or even an echocardiogram may need
to be performed.
VI. Treatment
Treatment of SVT depends on the etiology and the duration of symptoms. Automatic
rhythms are difficult to treat medically but respond well to ablation surgery.
Acute treatment of reentrant tachycardias depends on the age and stability of
the patient. In hemodynamically stable children, vagotonic maneuvers such as
straining, breath-holding, applying ice to the face, or adopting a particular
posture should be attempted first. For patients who do not respond to simple
vagal maneuvers, medical cardioversion should be attempted. Adenosine, a
nucleoside derivative that blocks the orthodromic conduction at the AV node, is
the medication of choice. Intravenous verapamil and propranolol can break an
SVT but are contraindicated in infants and children because of the risk of
bradycardia, hypotension, and cardiac arrest. If these modalities fail or if
the patient is hemodynamically unstable, then synchronized electrical
cardioversion should be performed immediately.
Once a patient has been successfully converted to a normal sinus rhythm,
maintenance therapy is selected depending on the age of the patient and the
cause of the SVT. In newborns and infants, digoxin remains the primary
medication for prevention of SVT, which is usually self-limited. Medications
that target the specific area of reentry (nodal or accessory) tend to work
better. In patients with a hidden accessory pathway, digoxin or
β-blockers are the mainstay of therapy. In children with evidence of
preexcitation syndrome (e.g., Wolff-Parkinson-White syndrome), digoxin and
calcium channel blockers are contraindicated, and
β-blockers are usually used.
Radiofrequency ablation of the accessory pathway is one choice for definitive
treatment. Success rates range from approximately 80% to 95%, depending on the
location of the bypass tract or tracts. Surgical ablation of bypass tracts can
also be successful in selected patients.
VII. References
1. Case CL. Diagnosis and treatment of pediatric arrhythmias. Pediatr Clin North Am 1999;46:351–352.
2. O'Connor B, Dick M. What every pediatrician should know about supraventricular
tachycardia.
Pediatr Ann 1991;20:368–376.
3. Park M, ed. Pediatric cardiology for practitioners, 3rd ed. St. Louis: Mosby, 1996.
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 Vomiting
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