A previously healthy 10-month-old female was found by her mother after waking in the morning to have slow, labored breathing. She was unresponsive to voice and tactile stimulation. This prompted a call to 911. On arrival, emergency medical services personnel noted that the infant was non-arousable, bradypneic, and stridorous, with a blood oxygen saturation of 80% on room air. She was transported to the emergency department of a regional hospital, where orotracheal intubation was immediately performed. Her blood pressure on arrival was 93/53 mmHg (mean arterial pressure 66 mmHg). Neurologic examination revealed 1 mm hyporeactive pupils bilaterally, global hypertonia, and hyperreflexia. A non-contrast computed tomography (CT) scan of the head was obtained. Arterial blood gas demonstrated a combined metabolic and respiratory acidosis (pH 7.15, PaCO2 29, PaO2 103, 10). Additional laboratory evaluation revealed mild transaminitis (aspartate aminotransferase 100 IU/L, normal = 8–50 IU/L; alanine aminotransferase 55 IU/L, normal = 7–45 IU/L) and leukocytosis (31,000/mm3, normal = 6,000–11,000/mm3). A broad differential diagnosis of respiratory failure of unknown origin was proposed, and treatment was pursued for possible allergic reaction or meningitis with two doses of epinephrine (0.085 mg), methylprednisolone (2 mg/kg), diphenhydramine (2 mg/kg), and a meningitic dose of ceftriaxone. The patient was then transferred to our tertiary care center.\nOn admission, workup was expanded with a full toxicology panel, which was positive for oxycodone and its metabolite, oxymorphone. Of note, elevated transaminases raised concern for acetaminophen toxicity; however this was ruled out by a negative result on the toxicology panel. A diagnosis of respiratory failure secondary to opiate ingestion and overdose was established. A total of four doses of naloxone (0.1 mg/kg i.v. push each) were administered with improvement in level of consciousness and reduction of ventilator support that allowed extubation. Continuous naloxone infusion was administered for 5 h thereafter. Results of initial neuroimaging were reviewed and revealed extensive symmetric bilateral cerebellar hypoattenuation (Figure A). The patient was admitted to the pediatric intensive care unit and was placed under close observation with frequent neurological exams.\nOn the third day of hospitalization, she became obtunded, with hyporeactive pupillary reflexes, hypertonia, hypertension, and ocular bobbing. Emergent magnetic resonance imaging (MRI) of the brain was obtained. The MRI demonstrated a pattern of symmetric restricted diffusion in the cerebellar hemispheres (Figure A), right parietal lobule, the heads of the caudate nuclei bilaterally and the right putamen. Additionally, hydrocephalus, elevation of the tectum, cerebellar tonsillar herniation, and an area of increased susceptibility weighted imaging signal in the left perirolandic area were present which suggested hemorrhagic transformation of an infarct.\nThe patient was taken emergently to the operating room for placement of an external ventricular drain, suboccipital craniectomy, and a C1 laminectomy. A significant portion of the edematous and ischemic cerebellar hemispheres and tonsils were resected bilaterally, thereby decompressing the posterior fossa and cervicomedullary junction.\nA postoperative magnetic resonance angiography (MRA) of the head and neck showed normal anterior and posterior circulations. A full coagulopathy workup and echocardiography were unremarkable. No other visceral or musculoskeletal injuries were noted, and an investigation by the child abuse team provided no evidence for physical abuse. After an uneventful postoperative course, the patient was discharged on postoperative day 11.\nFollow-up at 33 months of age (23 months after presentation) demonstrated an active, engaged child who spoke in full sentences. She was able to ambulate, jump, and climb stairs with alternating feet but had mild spasticity and internal rotation of her left leg with gait and occasional dystonic posturing of the left upper extremity.
The patient was a 9-month-old male with a past medical history significant for in utero drug exposure and mild oral aversion, who had otherwise been reportedly well. The day prior to his initial presentation, he had been swimming with his family and was put down for a nap at 1600. Family checked on him at 2100 hours due to not waking up for dinner but found him sleeping and attributed his increased fatigue to his increased activity throughout the day. At 0700 hours the next day, family was still unable to wake the child. He was taken to the nearest emergency department, where his initial vitals were significant for hypoxemia, with oxygen saturation of 77% on room air and mild hypothermia with axillary temperature of 36.2°C. His physical exam was notable for lethargy and decreased level of arousal without external physical exam findings concerning for apparent injury or infection. Labs were significant for hypoglycemia (30 mg/dL), but his mental status did not improve with glucose supplementation. A head CT was performed, and he was found to have bilateral cerebellar hemisphere hypoattenuation with acute swelling on computed tomography (). The presumed diagnosis at the time was acute stroke of unknown etiology, with the possibility of prolonged hypoglycemia and subsequent hypoxia contributing. He was flown to the closest pediatric tertiary care center and admitted to the Pediatric Intensive Care Unit (PICU) for close neurological monitoring and further evaluation.