The use of amphetamines can cause various adverse effects, including decreased appetite, insomnia, abdominal pain, nervousness, anxiety, and tachycardia (1). Pediatric patients who have never tried amphetamines can experience sympathomimetic toxidromes, including hypertension, tachycardia, inconsolability, hyperthermia, seizures, or death (2). From 2000 through 2011, there was a 71.2% increase in the number of cases of exposures to medications for attention-deficit/hyperactivity disorder, which were reported to the United States poison control center, with 76% of the cases involving children aged 12 years or younger. Among the exposures, amphetamines constituted 44.5%. Although a majority of the cases did not require medical treatment, 6.2% were hospitalized for treatment (3). Of those hospitalized, 3 cases (0.03%) ended in death (3). With the increasing availability of amphetamines across the U.S., there is an increased opportunity for accidental ingestion in the pediatric population. Our case report highlights the acute complications of amphetamine ingestion in an infant, while emphasizing the importance of including ingestion in the differential diagnosis when working up a patient with sympathomimetic toxidrome or seizure-like activity. The legal guardians of the patient provided informed consent to share the details of this case.

A previously healthy, 4-month-old, unvaccinated boy was brought to an outside hospital emergency department (ED) with altered mental status and seizure-like activity. After the infant’s mother had received limited prenatal care and chlamydia treatment during the pregnancy, he was born at a gestational age of 40 3/7 weeks via spontaneous vaginal delivery with a birth weight of 3.87 kg. At the time of visit, he was living with his mother and 5 other siblings at a domestic violence shelter.

The night prior to the presentation, the infant was under the supervision of his mother’s roommate for an hour and a half. Upon the mother’s return, he was noted to be having blank stare gazes, episodes of chewing on his hands, vomiting, and poor feeding. He did not show fever, diarrhea, cough, rhinorrhea, or rash. He had episodes of generalized stiffness with abnormal tongue movements lasting 1 minute at a time. These findings prompted the mother to bring him to the outside hospital.

The initial vital signs in the outside ED were as follows: blood pressure, 120/71 mmHg; heart rate, 150 beats/minute; respiratory rate, 46 breaths/minute; temperature, 37.0 °C; and oxygen saturation, 98% on room air. Physical examination was notable for irritability, white patches on his tongue, upper airway congestion, a hyperpigmented spot on his shoulder consistent with café-au-lait, and a hypopigmented spot to the right of the umbilicus. Neurologically, he was alert but irritable with appropriate responsiveness for age and no focal neurological deficits. There were no signs of trauma, signs of dehydration, cyanosis, petechiae, or rashes. Normal findings were noted in cardiovascular, pulmonary, and abdominal examinations.

During the initial evaluation, the infant began having left eye deviation and bilateral arm shaking, resolving with a single 0.05 mg/kg of lorazepam. At the outside facility, he obtained unremarkable findings from a head and neck computed tomography scan, chest radiography, and laboratory assays (Table). Electrocardiography showed sinus tachycardia. A lumbar puncture was unsuccessfully attempted, and empirical treatment with intravenous ceftriaxone and acyclovir was initiated due to concerns of central nervous system infection, such as herpes simplex virus encephalitis.

The infant was transferred to our hospital ED. The initial vital signs in our ED were as follows: blood pressure, 115/51 mmHg; heart rate, 168 beats/minute; respiratory rate, 46 breaths/minute; temperature, 37.0 °C; and oxygen saturation, 97% on room air. After initial evaluation in the ED, the differential diagnosis included meningitis, epileptic seizure, herpes simplex virus encephalitis, and non-accidental trauma. A repeat lumbar puncture was unsuccessful. He was then hospitalized to the general pediatric ward on the same day, with a pediatric neurologist’s recommendations for continuous video electroencephalogram and brain magnetic resonance imaging for investigation of his seizure-like activity, which turned out to be normal. The imaging did not require procedural sedation.

Upon hospitalization, the differential diagnosis was narrowed to infection or ingestion. A respiratory polymerase chain reaction detected no pathogens. The urine drug screen on day 1 was noted positive for amphetamine, with all negative for barbiturates, benzodiazepines, cocaine, methadone, opiates, and oxycodone. This positivity for amphetamine was confirmed by a repeat urine drug screen, as well as by a quantitative liquid chromatography-tandem mass spectrometry. Thus, it was likely that his symptoms stemmed from an amphetamine ingestion. On the abovementioned night, the mother had left the infant for 1.5 hours, which was when the ingestion occurred that resulted in the symptoms that she saw upon her return. A complete child abuse evaluation was conducted, including skeletal survey and ophthalmological examination to rule out retinal hemorrhage, which were both negative. An in-house social worker was involved in the care of the infant, coordinating with the Department of Children and Families (DCF). A DCF investigator indicated that the infant was able to be discharged to the care of his mother. DCF stated that they would meet with the mother’s family at the shelter upon her return and proceed with their interventions at that time.

On day 3, his irritability improved. His treatment consisted of lorazepam 0.05 mg/kg as needed and supportive care, including intravenous hydration and infant formula. Due to the infant being unvaccinated, he also received his 2-month vaccines prior to discharge.

Amphetamine ingestion in infants can present with symptoms that overlap those seen in meningitis or epileptic seizure, such as restlessness, irritability, and tachycardia (4). The ingestion may lead to other sympathomimetic toxidromes, such as hypertension, mydriasis, heightened arousal, hyperthermia, or diaphoresis (5). This possibility may be missed in cases where the guardian did not observe the ingestion. Therefore, unnecessary lumbar puncture, empiric antibiotics or antivirals, and hospitalization may be implemented to rule out an infectious cause of the symptoms.

As access to stimulant medications increases along with growing cases of ingestion of the medications requiring report to poison control centers, the importance of this increasing trend should be at the forefront of the medical provider’s mind (3). This case illustrates the value in ordering a urine drug screen when a child presents with acute onset seizure-like movements without fever, sympathomimetic toxidromes, and is otherwise clinically well appearing. In our case, although initially not on the differential diagnosis, the urine drug screen was ordered soon after the hospitalization, which quickly confirmed the amphetamine exposure. With the confirmation, the medical staff was able to safely discontinue ceftriaxone and acyclovir to discharge the infant on day 3.

The initial presentation with hypertension was likely attributed to the sympathomimetic toxidrome due to the amphetamine ingestion, rather than an underlying pathology. In addition, incidental findings on the physical examination included the café-au-lait macule and hypopigmented spot, which were not associated with other findings, and therefore determined to be clinically insignificant.

This case adds to the few reports showing that infant amphetamine ingestion can mimic a serious neurological condition, and highlights the importance of keeping a broad differential diagnosis and the use of a urine drug screen early when evaluating an infant with sympathomimetic toxidrome or seizure-like activity.