Obstructive sleep apnea (OSA) is a disease process involving recurrent pharyngeal collapse during sleep, resulting in apneic episodes. Clinically, symptoms can include snoring, sudden awakening with a chokinglike sensation, excessive somnolence, non-restorative sleep, difficulty in starting or maintaining sleep, and fatigue. It results in impaired gas exchange, subsequently causing various cardiovascular, metabolic, and neurocognitive pathologies. Historically, OSA has been underdiagnosed and undertreated, especially in women.OSA is associated with WHO (World Health Organization) class III pulmonary hypertension (PH) or PH due to lung disease. PH is a concerning complication of OSA and thought to occur in roughly 20% of individuals with OSA. The pathogenesis of PH in OSA can include pulmonary artery vasoconstriction and remodeling. Patients suffering from OSA who develop PH tend to have worse cardiovascular and pulmonary changes. We present a thorough review of the literature examining the interplay between OSA and PH.

Wernicke encephalopathy has traditionally been associated with chronic alcohol abuse leading to thiamine deficiency. Clinical symptoms include mentation change, gait ataxia, and oculomotor abnormalities. However, it is often an underdiagnosed condition in patients suffering from chronic malnutrition, especially in the West. We examine a unique case of non-alcoholic Wernicke encephalopathy in an elderly patient.The patient had a long history of chronic malnutrition due to her atypical diet, consuming an unbalanced diet deprived of thiamine, unbeknownst to her. She presented with symptoms of encephalopathy, recurrent falls, and pupillary changes. After exhausting all other therapeutic interventions, she received a thiamine infusion; her mentation and other symptoms improved dramatically.Thiamine deficiency can lead to severe complications, including Wernicke encephalopathy and cardiomyopathy. Wernicke encephalopathy can progress to Korsakoff syndrome, which is characterized by amnesia and confabulation. Case reports, such as ours, may remind clinicians to keep thiamine deficiency as a viable differential while evaluating acute encephalopathy, especially in the malnourished geriatric population.