A 7-month-old Girl With Decreased Oral Intake

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A 7-month old previously healthy fully vaccinated girl presents to the emergency department with poor oral intake. The mother reports that 3 days prior to presentation, the patient became fussier than usual and was also refusing to eat solids. She was taken to her pediatrician’s office where she was diagnosed with Coxsackie virus based on a palatal lesion and was sent home with guidance for supportive care. She continued to be very fussy at home and the mother reports on the day of presentation the patient seemed to have difficulty breastfeeding because of a poor latch. The mother has given the baby a total of 11 vials of homeopathic teething drops in various intervals over the course of the last 3 days to try to alleviate her symptoms.

There is no history of fevers, vomiting or diarrhea. She has had 2 wet diapers in the last 24 hours. On presentation to the emergency department, she is afebrile and her vital signs are stable. Her exam is notable for a tired appearing baby who is drooling intermittently and is not swallowing her saliva, though she does eventually drink breast milk given to her via a syringe. The remainder of her cardiopulmonary and neurologic exam is unremarkable. A complete blood count and comprehensive metabolic panel are within normal limits. She is given 2 normal saline boluses because of decreased urine output and is admitted to the pediatric floor for intravenous hydration and further monitoring. Later that evening, her exam markedly worsens and she develops diffuse hypotonia with a severe head lag, inability to sit up and a very weak cry. She is admitted to the intensive care unit for closer respiratory monitoring. Results from a lumbar puncture, urine drug of abuse screen and head ultrasound are all unremarkable. Further laboratory testing reveals the diagnosis.

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The differential diagnosis for hypotonia in infants is broad and includes the following etiologies:

  1. Infectious (sepsis, meningitis, encephalitis)
  2. Metabolic (eg, hypothyroidism, electrolyte disturbances, disorders of glycogen metabolism, mitochondrial myopathies)
  3. Toxins (eg, botulinum, anticholinergics, narcotics),
  4. Neuromuscular (eg, infantile spinal muscular atrophy, myasthenia gravis, guillan-barré syndrome)
  5. Anatomic (eg, hemorrhage, infarction).

In our patient, the decision was made 24 hours after admission to administer baby botulinum immunoglobulin (BabyBIG) for treatment of presumed Infant Botulism; 5 days later the New York City Department of Health confirmed the presence of Botulinum Type B in her stool.

The Condition:

Infant botulism results from colonization in the large intestine by the bacteria Clostridium botulinum, which produces a neurotoxin that blocks presynaptic acetylcholine transmission and thereby prevents skeletal and smooth muscle contraction. Clostridium species produce antigenic variant types A, B, E and F, with types A and B being responsible for the vast majority of infant botulism in the United States. Transmission occurs from the ingestion of C. botulinum spores, most commonly via inhalation of environmental dust or exposure to wild honey or canned foods. Our patient had none of these exposures that were known. Infants typically present with poor feeding and/or constipation which then progresses to dysfunction of the muscles innervated by the cranial nerves, manifesting as pupillary paralysis, ptosis, loss of eye tracking and abnormal suck. Subsequent involvement of the muscles of the trunk and extremities results in hypotonia, weakness and hyporeflexia. In addition, inhibition of cholinergic transmission can lead to hemodynamic instability.

The most dangerous complication of infant botulism is involvement of the diaphragm, which can lead to respiratory failure and death. In one study of over 100 infants affected by botulism, about 60% required mechanical ventilation. 2 Diagnosis is made by isolating both the toxin and the bacteria from the stool. Management: Management of infant botulism is aimed at stopping the damaging effects of the Clostridium neurotoxin on the muscle as well as providing hemodynamic and respiratory support in more severe cases. BabyBIG is an FDA approved orphan drug derived from pooled adult plasma of persons immunized with botulinum toxoid; the anti-botulism toxin antibodies allow motor nerve regeneration to begin. Because of the risk of progression to respiratory failure, the decision to treat with BabyBIG should not be delayed by waiting for confirmatory laboratory testing and should be based on history and clinical presentation. To obtain BabyBIG, the clinician must contact the Infant Botulism Treatment and Prevention Program on-call physician; more information can be found at infantbotulism. org. 3Patient Course: Our patient’s neurologic exam continued to worsen after transfer to the intensive care unit and she rapidly developed ptosis, dilated pupils and hyporeflexia. Further history obtained from our patient after admission revealed that her last stool was 5 days prior to presentation; she then began to present with signs of neuromuscular weakness. She luckily did not require mechanical ventilation and remained stable on room air during her hospitalization. After the administration of BabyBIG, her neurologic exam began to gradually improve and at the time of discharge her motor strength had returned to baseline and she was able to sit unsupported with appropriate head control. Our toxicology specialists were consulted at the time of admission in order to determine whether the teething drops administered at home could be playing a role in our patient’s symptomatology, particularly given recent FDA warnings about teething remedies being recalled for containing inconsistent amounts of belladonna. 4 Similar to botulinum toxin, belladonna overdose can also cause anti-cholinergic symptoms. However, given our patient was not showing signs of agitation on presentation, a feature of belladonna toxicity, her presentation was thought to be more likely secondary to botulism. She was discharged home on hospital day 11 with plans for intensive outpatient physical therapy.

Lessons for the Clinicians:

  • Decreased oral intake is a common chief complaint encountered in the pediatric setting, and while often times the cause is related to a benign, self-limiting condition, it is prudent for the clinician to be aware that in very rare cases it may be a warning sign of exposure to a neurotoxin, particularly in the setting of a prodrome of constipation.
  • Early signs of infant botulism can be nonspecific and include poor feeding, irritability and constipation with a subsequent acute to subacute onset of descending weakness; the most feared complication is progression to respiratory arrest.
  • The decision to treat with BabyBIG should be based on clinical presentation (even in the absence of a known exposure) and should not be delayed by waiting for confirmatory testing. Information on how to obtain BabyBIG can be found at infantbotulism. org.


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