Neonates have distinctive anatomic and physiologic features that predispose them to obstructive sleep apnea (OSA). The overall prevalence of neonatal OSA is unknown, although an increase in prevalence has been reported in neonates with craniofacial malformations, neurological disorders, and airway malformations. If remained unrecognized and untreated, neonatal OSA can lead to impaired growth and development, cardiovascular morbidity, and can even be life threatening. Polysomnography and direct visualization of the airway are essential diagnostic modalities in neonatal OSA. Treatment of neonatal OSA is based on the severity of OSA and associated co-morbidities. This may include medical and surgical interventions individualized for the affected neonate. Based on this, it is expected that infants with OSA have more significant healthcare utilization.

Children with Down syndrome (DS) are at high risk for developing obstructive sleep apnea (OSA) compared to children without DS. The negative impact of OSA on health, behavior, and cognitive development in children with DS highlights the importance of timely and effective treatment. Due to the higher prevalence of craniofacial and airway abnormalities, obesity, and hypotonia in patients with DS, residual OSA can still occur after exhausting first-line options. While treatment commonly includes adenotonsillectomy (AT) and continuous positive airway pressure (CPAP) therapy, additional therapy such as medical management and/or adjuvant surgical procedures need to be considered in refractory OSA. Given the significant comorbidities secondary to untreated OSA in children with DS, such as cardiovascular and neurobehavioral consequences, more robust randomized trials in this patient population are needed to produce treatment guidelines separate from those for the general pediatric population of otherwise healthy children with OSA. Further studies are also needed to look at desensitization and optimization of CPAP use in patients with DS and OSA.

Lactic acidosis is a common finding in the intensive care unit and is associated with increased mortality. We present the case of a 42-year-old male with alcohol use disorder and cirrhosis who developed sudden onset shortness of breath while smoking marijuana. He was found to have a lactic acid level of 25.6 mmol/L with a significant anion gap metabolic acidosis requiring emergent dialysis. He was hypertensive without evidence of tissue hypoperfusion. His profound type B lactic acidosis was primarily attributed to a rare manifestation of cannabinoid toxicity. At a clinic visit 3 months later, he was doing well and had not smoked marijuana since his discharge.