An 11-year-old boy develops vomiting, weakness, weight loss and a neck mass

Fred Henretig
Childrens Hospital of Philadelphia
Philadelphia, PA

Int J Med Toxicol 1998; 1(1): 13

These case conferences are supported by a grant from Orphan Medical, Inc.

See also NEW CASE - DISCUSSION - 1998; 1(2): 14, NEW CASE - FURTHER DISCUSSION - 1998; 1(2): 15

An 11-year-old boy with blindness and mental retardation was brought to the hospital for evaluation of vomiting, weight loss and a neck mass. He had been in his usual state of health until three weeks prior to admission, when he began vomiting several times each day. The vomitus was described as neither bloody nor bilious. He was seen by a local physician who prescribed antiemetics and dietary manipulation, which resulted in some amelioration of his symptoms, but occasional vomiting persisted. Two weeks prior to admission a midline neck mass appeared, and the child became easily fatigued and anorexic. Over the three days immediately prior to admission severe vomiting recurred and the neck mass became larger. At the time of admission, the mother estimated that a 5 to 10 lb. weight loss had occurred over the preceding 3 weeks.

The child was the product of a twin gestation, complicated by a breech delivery and perinatal hypoxia with low Apgar scores. His mother remembered her doctors saying that they "almost lost him". His early developmental milestones were very delayed, and he had proven to be severely visually handicapped and developmentally retarded with autistic features. He lived at home with his family and attended a special school for the blind. There were no other known medical conditions and he was on no medications.

On initial evaluation in the emergency department, he appeared to be a thin, quiet male who was obviously functionally blind. Vital signs were: heart rate, 120/minute; blood pressure, 110/70 mm Hg; temperature, 37ÂșC; respirations, 24/minute. The child appeared moderately dehydrated with dry mucous membranes and slightly sunken eyes. The examination was further notable for a 5 X 6 cm, firm, nontender, anterior, midline, butterfly-shaped neck mass, mild hepatomegaly and roving eye movements. Cardiac, abdominal and neurologic findings were otherwise unremarkable.

Stat laboratory values revealed the following: CBC with Hgb 19.2 g/dL (Hct 54.6%), WBC 6,600 (normal differential) and platelets 288,000; chemistries with Na 134, mEq/L; K, 4.1 mEq/L; Cl, 104 mEq/L; bicarbonate, 13 mEq/L; BUN, 8 mg/dL; creatinine, 0.3 mg/dL; venous blood gas with pH 7.36, PCO2 27 mm Hg, PO2 44 mm Hg; urine specific gravity 1.025, pH 5.0, negative blood, protein, glucose. Thyroid function tests were ordered.

The child was admitted with the tentative diagnoses of thyroid disorder and dehydration with pseudo-polycythemia, and begun on intravenous fluid therapy. The following morning his vomiting worsened, and he developed a gallop rhythm. His serum bicarbonate fell to 11 mEq/L, and the hemoglobin remained 19 g/dL. Chest radiograph revealed cardiomegaly, and an abdominal ultrasound noted slight hepatomegaly. ECG was notable for sinus tachycardia and an axis of - 77, with normal intervals. Echocardiogram demonstrated normal anatomy, with mildly dilated left ventricle and decreased shortening fraction of 25%. Endocrine consultation was sought while thyroid function tests remained pending, and the complex of findings including thyromegaly, cardiomegaly and persistent tachycardia was interpreted as possible mild congestive heart failure secondary to hyperthyroidism. Thus, the patient was cautiously begun on propranolol.

Unfortunately, the child's condition failed to improve. He continued to vomit, his metabolic acidosis persisted, and his CHF seemed to worsen. The staff were further surprised when thyroid function tests returned with thyroxine 2.4 mcg/dL and TSH 26 mcU/mL. Propranolol was discontinued, and several more consultations were obtained.

Int J Med Toxicol 1998; 1(1): 13

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