Bupropion is an atypical antidepressant that inhibits norepinephrine and dopamine reuptake. Poison control data demonstrate toxic effects at doses as low as 600 mg. Common adverse effects of overdose include tachycardia, seizures, and cardiac arrhythmias. Gastrointestinal complications are rarely described. Our case shows an 18-year-old male presented to the emergency department after witnessed seizure-like activity. Family reported ingestion of approximately thirty 300-mg sustained-release bupropion tablets 4-5 hours prior to presentation. On arrival, he required endotracheal intubation for airway protection. Sedation was initiated with propofol and fentanyl; fentanyl was rapidly discontinued. Given delayed presentation and sustained-release ingestion, whole bowel irrigation was initiated with nasogastric administration of 50 g activated charcoal followed by 6 L polyethylene glycol-electrolyte solution. Subcutaneous methylnaltrexone (12 mg) was administered to reverse potential opioid-related ileus without effect. Worsening abdominal distension prompted contrast-enhanced computed tomography of the abdomen and pelvis, which demonstrated diffuse fluid-filled colonic distension with distal small bowel dilation and no evidence of mechanical obstruction or pill bezoar. Gastroenterology performed colonoscopic decompression with rectal tube placement. This resulted in successful decompression. The patient was extubated the following day with return of bowel function on post-decompression day two. In supratherapeutic states, bupropion exhibits anticholinergic properties through poorly understood mechanisms, which may impair intestinal motility. Colonic complications remain rare, with only isolated reports describing colonic ischemia or pseudo-obstruction associated with bupropion toxicity. Clinicians should consider severe gastrointestinal dysmotility when managing sustained-release bupropion toxicity.

Diabetic autonomic neuropathy is a clinically important component of diabetic neuropathy involving the cardiovascular, gastrointestinal, genitourinary, sudomotor, pupillary, and glucose counterregulatory systems. Cardiovascular autonomic neuropathy (CAN) has been extensively studied and is clinically relevant because of its association with adverse cardiovascular and renal outcomes. Early CAN is frequently silent and may only be recognized by reduced heart rate variability or abnormal cardiovascular autonomic reflex testing. As CAN progresses, patients develop resting tachycardia, reduced exercise tolerance, orthostatic or postprandial hypotension, abnormal nocturnal blood pressure regulation, and perioperative hemodynamic instability. Non-cardiovascular manifestations include gastroparesis, bowel and bladder dysfunction, erectile dysfunction, sudomotor and pupillary abnormalities, and impaired hypoglycemic awareness. The underlying mechanisms involve chronic hyperglycemia, glycemic variability, dyslipidemia, insulin resistance, oxidative and mitochondrial stress, inflammation, microvascular injury, and impaired axon-glial support. Clinically, evaluation should begin with a systematic symptom review, neurological examination, supine and standing blood pressure measurements, and heart rate assessment, followed by organ-specific testing if indicated. Treatment was based on comprehensive risk factor control and symptom-directed management.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but serious complication of acute pulmonary embolism. It may be clinically silent and often presents with non-specific symptoms, making diagnosis challenging. We present the case of a man in his 40s who presented with shortness of breath and acute hypoxic respiratory failure. His hypoxia persisted despite pneumonia and superimposed human metapneumovirus infection treatment.Despite two negative CT pulmonary angiograms, clinical suspicion for pulmonary vascular disease remained high given the otherwise unrevealing diagnostic workup, persistent tachycardia, right ventricular dysfunction on echocardiography and persistent mosaic attenuation on CT of the chest. A ventilation-perfusion scan ultimately showed CTEPH, later confirmed by right heart catheterisation and pulmonary angiography.This case highlights the complex presentation and diagnostic challenges of CTEPH. It emphasises that CTEPH should remain on the differential in patients with persistent hypoxia and signs of pulmonary hypertension, even when CT imaging does not demonstrate pulmonary embolism.