Epinephrine is the first-line therapy for anaphylaxis, and intramuscular (IM) administration at recommended doses is essential to prevent progression to airway compromise, circulatory collapse, and death. However, epinephrine is a potent sympathomimetic that can provoke severe cardiovascular responses in susceptible patients. We report the case of a 50-year-old African-American male with a history of long-standing hypertension, end-stage renal disease on intermittent hemodialysis with poor adherence, type two diabetes mellitus, and chronic hepatitis C, who developed acute neurological deterioration shortly after receiving two doses of 0.5 mg IM epinephrine for suspected anaphylaxis. Blood pressure measurements were unobtainable in the prehospital setting. In the emergency department, the patient was noted to have severe hypertension with an initial recorded blood pressure of 213/110 mmHg prior to intubation. Due to difficulty obtaining reliable noninvasive measurements thereafter, a radial arterial line was placed, revealing a blood pressure of 326/101 mmHg. Computed tomography (CT) of the brain demonstrated a large acute intraparenchymal hemorrhage involving the pons and midbrain with intraventricular extension. CT angiography excluded aneurysm or vascular malformation. Despite intensive care management and blood pressure control, the patient had limited neurological recovery and required prolonged ventilatory support, tracheostomy, and transfer to a long-term acute care hospital. This case highlights a rare but severe complication temporally associated with epinephrine, particularly in patients with underlying cerebrovascular risk factors. This case also underscores the importance of vigilant hemodynamic monitoring after epinephrine administration and early recognition of neurological deterioration.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease and is characterized by progressive kidney enlargement and cyst growth leading to progressive loss of kidney function. The two main genes implicated are PKD1 and PKD2; however, pathogenic variants in other less frequent genes can also cause the disease. Diagnosis may be established in various clinical settings, including family screening, the investigation of arterial hypertension, urological events such as hematuria or flank pain, or incidental imaging findings. Diagnostic confirmation relies on targeted imaging studies and/or genetic testing. Extrarenal manifestations include hepatic cysts and an increased risk of intracranial aneurysms (ICA). The disease course varies considerably among individuals: while the median age at kidney failure is around 60years, some patients reach kidney failure before the age of 40 while others never require renal replacement therapy. Nephroprotective measures are central to the management of ADPKD and include blood pressure control with renin-angiotensin-aldosterone system (RAAS) blockade, sodium intake reduction, smoking cessation, maintenance of a healthy body weight, and regular physical activity. Tolvaptan is currently the only approved pharmacological therapy shown to slow disease progression. Several other promising therapies are under investigation to expand therapeutic options for patients with ADPKD.

Topiramate-induced multifocal exudative retinal detachment is a rare but potentially vision-threatening adverse effect. We report a 59-year-old woman with idiopathic intracranial hypertension who developed painless bilateral blurry vision and color desaturation 8 days after initiation of topiramate 25 mg twice daily. Fundus examination and spectral-domain optical coherence tomography demonstrated bilateral multifocal exudative retinal detachment with subretinal fluid. Extensive infectious and inflammatory investigations were unremarkable. Topiramate was discontinued, resulting in complete anatomical resolution of subretinal fluid and improvement of visual acuity to 20/30 in both eyes over 3 months of follow-up. This case highlights the importance of recognizing this uncommon ocular complication and the potential for complete recovery following prompt drug cessation.

Direct oral anticoagulants (DOACs) are frequently co-prescribed with angiotensin II receptor blockers (ARBs) in atrial fibrillation (AF). Because ARBs differ in P-glycoprotein (P-gp) inhibition, bleeding risk may vary. We compared major bleeding when DOACs were combined with telmisartan (high P-gp inhibition) versus olmesartan (low P-gp inhibition). We conducted a nationwide cohort study from 2016-2023 in Korea. We identified AF patients who started a DOAC with telmisartan or olmesartan. The primary outcome was a composite of intracranial hemorrhage and gastrointestinal bleeding. Secondary outcomes included each component of the primary outcome and ischemic stroke. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. Among DOAC-treated patients with AF, 27,851 and 20,010 patients were included in the telmisartan and olmesartan groups, respectively. The incidence rates of the primary outcome were 9.13 per 1000 person-years in the telmisartan group and 6.69 in the olmesartan group (HR 1.35, 95% CI 1.11-1.65). Concomitant use of telmisartan was associated with a higher risk of gastrointestinal bleeding (1.49, 1.17-1.89), but not with intracranial hemorrhage (1.06, 0.74-1.54) or ischemic stroke (0.94, 0.78-1.14). Among patients with AF using DOACs, concomitant use of ARBs with high P-gp inhibitory activity was associated with a significantly higher risk of major bleeding and gastrointestinal bleeding compared-ARBs with low P-gp inhibitory activity. These findings suggest that differences in P-gp inhibitory activity among ARBs may influence bleeding risk in clinical practice when co-administered with DOACs.