Congenital pulmonary airway malformation (CPAM) is a rare developmental lung anomaly that may present in the neonatal period with respiratory distress, and its association with dextrocardia is exceptional, potentially leading to diagnostic challenges. We report the case of a 26-day-old male neonate, born at term, admitted for cyanosis and respiratory distress. Clinical examination revealed tachypnea (68 breaths per minute), oxygen desaturation (SpO₂ 65% in room air), and signs of respiratory distress, with cardiac auscultation suggesting right-sided heart sounds. Imaging studies demonstrated a cystic lesion of the left upper lobe consistent with congenital pulmonary airway malformation, associated with cardiac dextroposition due to mediastinal shift, rather than true dextrocardia. The patient received supportive care and broad-spectrum antibiotic therapy; however, the clinical course was marked by progressive respiratory deterioration complicated by severe pulmonary infection, ultimately resulting in death before surgical intervention could be undertaken. CPAM results from abnormal airway development, and it is associated with cardiac dextroposition due to mediastinal shift, rather than true dextrocardia. This case highlights the importance of considering CPAM in neonates presenting with respiratory distress and emphasizes the crucial role of imaging, particularly computed tomography, in establishing the diagnosis and guiding management.

In this report, we describe a 19-day-old female neonate who presented with recurrent apnea, poor feeding, and cyanosis. Brain diffusion-weighted MRI revealed hyperintense lesions in the genu of the corpus callosum and bilateral frontal white matter with corresponding low apparent diffusion coefficient values. Antibiotic therapy and supportive management were initiated, and the apnea resolved by hospital day 6. A follow-up brain MRI performed on day 49 demonstrated the complete resolution of the previously observed lesions. No neurological sequelae were observed up to 11 months of age. This case illustrates a rare presentation of neonatal-onset apnea associated with reversible lesions localized in the genu of the corpus callosum on MRI. Several differential diagnoses were considered, including mild encephalitis/encephalopathy with a reversible splenial lesion (MERS)-related conditions, viral encephalitis, postictal changes, and pre-Wallerian degeneration. When reversible corpus callosum lesions are observed in neonates, a variety of underlying pathophysiological processes should be considered in the differential diagnosis.

Phlegmasia cerulea dolens (PCD) is a rare but catastrophic manifestation of venous thromboembolism characterized by near-complete iliofemoral venous occlusion, severe venous hypertension, and secondary arterial inflow compromise. Delayed intervention is associated with venous gangrene, limb loss, and high mortality rates. A 76-year-old male with active rectal malignancy on chemotherapy presented with acute left lower limb pain, swelling, coldness, and cyanosis. CT run-off demonstrated extensive iliofemoral deep venous thrombosis extending from the inferior vena cava (IVC) bifurcation to the infrapopliteal veins, accompanied by loss of distal arterial opacification without intrinsic arterial occlusion-findings diagnostic of advanced PCD with venous-induced arterial inflow collapse. The patient underwent urgent single-session pharmacomechanical thrombectomy using large-bore aspiration with adjunctive low-dose intraprocedural tissue plasminogen activator (tPA) boluses, without catheter-directed thrombolytic infusion. Rapid venous decompression resulted in immediate clinical and hemodynamic improvement, restoration of arterial Doppler signals, and limb salvage. Post-procedural follow-up confirmed sustained limb viability and complete clinical resolution of venous congestion without evidence of recurrent thrombosis. Single-session pharmacomechanical thrombectomy with limited intraprocedural thrombolytic dosing is an effective, limb-saving strategy for advanced PCD, particularly in high-risk oncologic patients.

Background: Chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVDs) are closely linked through shared inflammatory and metabolic pathways. Metabolic syndrome (MetS), shared by both conditions, may represent a key mechanistic link between systemic inflammation, cardiovascular disease, and COPD outcomes. Objective: To assess the prevalence and clinical correlates of MetS and examine whether increasing MetS burden is linked to more severe symptoms and a higher comorbidity load in patients with COPD. Methods: We analyzed cross-sectional data from a multicenter COPD registry. MetS was defined by the presence of at least three components: obesity, hypertension, hyperglycemia, or dyslipidemia based on clinical and medication data. Associations between MetS burden and COPD characteristics were evaluated using multivariable models adjusted for age, sex, smoking history, exacerbation status, lung function, inhaled therapy, and study center. Results: Among 5030 patients, MetS was present in 10.4% and was more frequent in women (11.9% vs. 9.6%, p = 0.01). Patients with MetS had greater symptom burden, and more frequent signs of cyanosis, cor pulmonale, and heart failure. MetS was most common in Global Initiative for Chronic Obstructive Lung Disease stage II-III and associated with higher forced expiratory volume in one second but lower forced vital capacity, with similar exacerbation rates between the groups. Cardiovascular, sleep, renal, and connective tissue comorbidities were more prevalent in patients with MetS. A dose-response relationship was observed, with each additional metabolic syndrome component independently associated with increased odds of respiratory symptoms and cardiometabolic comorbidities (all p < 0.01). Conclusions: Our findings suggest that metabolic syndrome is present in approximately 10% of patients with COPD and is associated with greater symptom burden and a higher prevalence of cardiovascular, renal, and sleep-related comorbidities. The observed stepwise relationship supports the presence of a clinically relevant cardiometabolic profile in COPD. However, given the cross-sectional registry-based design, causal inferences cannot be made, and prospective studies are needed to confirm these associations and evaluate targeted interventions.

Glenn shunt dysfunction in single‑ventricle palliation is multifactorial. Although aorto‑pulmonary collaterals are usually considered, systemic veno‑venous collaterals and congenital portosystemic shunts (CPSS) may be underrecognized causes (1,7). Our patient, a 30‑month‑old child with mitral valve atresia, severe hypoplastic left ventricle, large ventricular septal defect (VSD), pulmonary valve atresia, and ductus arteriosus-dependent pulmonary blood flow, who was undergone some palliation stages including patent ductus arteriosus (PDA) stenting / modified Blalock-Taussig (BT) shunt and a right‑sided bidirectional cavopulmonary anastomosis (Glenn). Despite an initially acceptable course, the child developed progressive central cyanosis.