Poor Weight Gain - Case 6-1: 16-Month-Old Boy
I. History of Present Illness
A 16-month-old African-American boy was seen in an outpatient clinic and
admitted because of concern for FTT. He had also been noted by his parents to
have lost some of his previously acquired developmental skills. Over the week
before admission, he had had tactile fever and two to three loose stools per
day. The stools were not bloody. He had no vomiting. He had a slight cough but
no rhinitis, rash, or ear pain. From a developmental standpoint, he was always
delayed, compared with his twin. He first rolled over at 10 months. He was not
walking or sitting. He recently had been noted to be smiling less and
interacting less. He had been receiving early intervention services for
occupational and physical therapy. It had been recommended to the family that
he start nutritional supplements, but the family has not been able to get any.
II. Past Medical History
He was the first born of a twin pregnancy. His birth weight was 5 pounds 10
ounces. He was delivered of a 20-year-old mother by cesarean section for breech
presentation. He had been bottle-fed and had had no previous hospitalizations.
He had pneumonia at 7 months of age that was treated in the outpatient setting.
At 9 months of age, he was treated for thrush that responded promptly to oral
nystatin. Otitis media had been recently diagnosed and treated at the clinic.
He had no allergies and was receiving no medication. He had not traveled outside
the United States. The only pet was an older cat. One month earlier, the mother
was hospitalized with a cerebrovascular accident. In process of evaluation, she
was found to be human immunodeficiency virus (HIV)-antibody positive.
III. Physical Examination
T, 37.8°C; RR, 40/min; HR 130 bpm; BP 96/60 mm Hg; RR 40/min SpO2, 100% in room air
Weight, 7.94 kg (less than 5th percentile for an 8-month-old); height, 75.5 cm
(10th percentile; 50th percentile for an 11-month-old); head circumference, 47
cm (25th percentile)
In general, the child was apathetic and irritable, but consolable in his mother's arms. Frontal prominence and bitemporal wasting were noted. The tympanic
membranes were normal in appearance and mobility. The oropharynx was clear;
there was no thrush. Multiple small cervical, occipital, axillary,
epitrochlear, and inguinal lymph nodes were palpable. The cardiac examination
revealed normal first and second heart sounds (S1 and S2, respectively), with
no murmurs, rubs, or gallops. The chest was clear to auscultation bilaterally.
The abdomen was soft without tenderness or guarding. The liver edge was
palpable 3 cm below the right costal margin, and the spleen was palpable 2 cm
below the left costal margin. The child was globally hypotonic, but deep tendon
reflexes were symmetrically increased. Plantar reflexes were downgoing.
IV. Diagnostic Studies
A complete blood count revealed the following: 37,900 white blood cels (WBCs)/mm3, including 8% segmented neutrophils, 47% lymphocytes, and 38% atypical
lymphocytes; hemoglobin, 11.0 g/dL; platelet count, 195,000/mm
3. Serum electrolytes, blood urea nitrogen, and creatinine were normal.
Additional laboratory findings included the following: lactate dehydrogenase,
1,586 U/L alanine aminotransferase (ALT), 98 IU/L; aspartate aminotransferase
(AST), 139 IU/L; alkaline phosphatase, 108 U/L; triglycerides, 212 mg/dL; and
albumin, 3.4 mg/dL.
IV. Course of Illness
HIV antibody testing was performed at the time of admission, given the mother's recent diagnosis, and was positive. Initial evaluation focused on determining
the child
's HIV status (in utero exposure versus true infection), because maternal HIV
antibodies may be present for the first 18 months of life. Additional testing
by HIV polymerase chain reaction (PCR) was positive, confirming this child
's diagnosis of HIV infection.
Given his HIV exposure, there was concern that his developmental regression
could be secondary to HIV encephalopathy. A noncontrast computed tomography
(CT) scan was done, which showed diffuse cerebral atrophy. Soon after
hospitalization, the child began to have high spiking fevers to 40.1
°, accompanied by tachycardia and tachypnea. His oxygenation remained adequate. A
few days into the fever spikes, he began to have persistent tachypnea, with
mild increased work of breathing and occasional rales at the left lower lung
field. A chest radiograph showed mild volume loss at the right upper lobe and
streaky atelectasis in the left lower and right upper lobes. An abdominal
ultrasound study was performed to look for increased retroperitoneal
adenopathy, because of the possibility that disseminated
Mycobacterium avium may have caused his fevers. The ultrasound study showed hepatomegaly with an
increase in the echotexture of the liver, without focal masses or abscess.
There was no ductal dilatation or gall bladder wall thickening. Splenomegaly
was present without focal lesions within the spleen. Also noted were several
enlarged nodes within the porta hepatis and several retroperitoneal nodes in
the paraaortic area. The kidneys were normal.
Discussion: Case 6-1
I. Differential Diagnosis
There were many possible diagnoses to consider in this case. In the general
categorization of organic versus nonorganic causes of FTT, the symptoms of
diarrhea and later fever were factors supporting an organic cause. Yet, the
family history of being noncompliant with getting the nutritional supplements
and the fact that this was an overstressed family, with an HIV-positive mother
and twin babies, raises some nonorganic factors. The possibility of mixed FTT
was very high on the list. As far as organic causes, HIV is a well-known cause
of FTT. It is sometimes difficult to distinguish between maternally acquired
antibodies and true infection. The positive (times 2) PCR result made true HIV
infection one diagnosis. The onset of high spiking fevers then prompted the
evaluation for an opportunistic infection.
Diagnostic considerations in an HIV-infected child with fever are diverse.
Opportunistic diseases and pathogens to consider include
Pneumocystis carinii pneumonia, lymphoid interstitial pneumonia (LIP), and cryptococcal infection.
Viruses include hepatitis B and C, Epstein-Barr virus, and cytomegalovirus.
Other pathogens include
M. avium, cryptosporidium, Toxoplasma gondii, and Mycobacterium tuberculosis. Children with HIV are also at risk for focal bacterial infections such as
sinusitis, pneumonia, or intraabdominal abscess. A child who is HIV positive
and who is febrile requires an exhaustive search to identify an organism.
The initial evaluation should include a search for focal infection and a general
assessment of severity of illness. The absence of specific localizing signs
presents a greater diagnostic dilemma.
II. Diagnosis
Toxoplasma immunoglobulin M (IgM) was negative, but IgG was positive and the
patient was believed to have a clinical picture consistent with disseminated
toxoplasmosis. He had hepatitis, pneumonitis, and diffuse lymphadenopathy, with
an atypical lymphocytosis on smear. Ophthalmology staff were consulted to check
for evidence of retinal changes; none were present. Therapy for toxoplasmosis
was started, including pyrimethamine, sulfadiazine, and leucovorin rescue.
These medications were to be continued for at least 6 months.
The diagnosis is
Toxoplasmosis gondii, an intracellular parasite. Infection with this organism is usually asymptomatic in children, but serious
infection occurs in immunocompromised hosts and in children with congenitally
acquired infections. Infection is lifelong, with acute and chronic stages.
Acute illness involves a period of parasitemia after the initial infection.
With the chronic infection, the parasite is encysted in the host tissue. The
organism may periodically break out of the cells, resulting in local
reactivation of the disease. In those patients with immune compromise, the
reactivation of disease may result in dissemination and systemic spread.
III. Incidence and Epidemiology
The organism is distributed widely, and it is estimated that between 1 and 3
million people are affected worldwide. Human infection may be asymptomatic to
severe, or even fatal in individuals who are immunocompromised. Felines (cats)
are the only definitive host.
The routes of transmission in humans include blood transfusion; organ
transplantation; transplacental, and ingestion of chicken eggs, meat, milk, or
oocysts that contaminate water or vegetables as a result of feline fecal
matter. The life cycle of the parasite includes a sexual phase that occurs in
cats and an asexual phase that occurs in cats, humans, and other intermediate
hosts. The incidence in cats, other animals, and humans varies greatly by
location and age of the population studied.
IV. Clinical Presentation
In postnatally acquired toxoplasmosis, 80% of cases are asymptomatic. Among
those patients who are immunocompetent, the symptomatic cases involve
lymphadenopathy with either tender or nontender nodes. These children have a
mononucleosis-like picture. In children who are immunocompromised, multiple
organs may be involved. In patients with acquired immunodeficiency syndrome
(AIDS), central nervous system involvement is common. Findings include
headaches, hemiparesis, and visual disturbances. More severe presentations have
included speech abnormalities, seizures, and the syndrome of inappropriate
secretion of antidiuretic hormone (SIADH).
Congenital toxoplasmosis is most often asymptomatic and bears no significant
signs or symptoms, but 30% to 40% of affected newborns have some findings if
evaluated closely. The affected newborns may have hydrocephalus, fevers,
hepatosplenomegaly, prolonged hyperbilirubinemia, blindness, deafness, or other
manifestations including diarrhea and feeding difficulties. In this case, the
main findings were fever and poor feeding leading to FTT.
V. Diagnostic Approach
T. gondii antibodies. Serologic tests are most commonly employed and measure the host antibody
represented.
T. gondii-specific IgG serum antibody, at any titer, indicates a risk of active infection
in an immunocompromised individual. Testing that shows seroconversion or a
four-fold or greater rise in antibody titer in serum samples obtained 3 to 6
weeks apart confirms the diagnosis.
Other studies. The infection can also be confirmed by demonstration of the organism
histologically or by identification of nucleic acid (PCR) in a site in which
the encysted organism would not be present as part of a latent infection, such
as cerebrospinal fluid or bronchoalveolar fluid. When the diagnosis is made in
an individual who is thought to be immunocompetent, HIV testing should be
considered.
VI. Treatment
The mainstream of treatment is pyrimethamine, a folic acid antagonist. The
combination of pyrimethamine with sulfadiazine acts synergistically. There are
also some experimental agents under consideration. Spiramycin is a macrolide
that may be effective in treating women during pregnancy. Clindamycin may also
be effective when used alone or in combination with pyrimethamine. HIV-infected
patients with CD4+ T-lymphocyte counts lower than 100 to 200/mm
3 may require continued suppressive antimicrobial therapy.
VII. References
1. Freij B, Sever J. Toxoplasmosis. Pediatr Rev 1991;12:227–236.
2. Jackson MH, Hutchinson WM. The prevalence and source of toxoplasma infection
in the environment.
Adv Parasitol 1989;28:55–105.
3. Sever JL, Ellenberg JH, Ley AC, et al. Toxoplasmosis: maternal and pediatric
findings in 23,000 pregnancies.
Pediatrics 1988;82:181–192.
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 Weight gain
» Next page: Poor Weight Gain - Case 6-2: 7-Month-Old Boy (Pediatric Complaints and Diagnostic Dilemmas)
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