Interscalene brachial plexus block (ISB) is commonly used for shoulder surgery and is associated with predictable complications such as phrenic nerve palsy due to its proximity to adjacent neural structures. While the spread of local anesthetic may involve the recurrent laryngeal nerve, resulting in vocal cord dysfunction, which is uncommon, progression to bilateral vocal cord paralysis, causing acute airway obstruction, is exceedingly rare. A 74-year-old obese female underwent elective outpatient right shoulder arthroscopy under ultrasound-guided interscalene block with bupivacaine. Within hours postoperatively, she developed progressive respiratory distress. Despite high-flow oxygen and bag-valve-mask ventilation, oxygen saturation declined into the 60s with marked resistance to ventilation. Emergent intubation resulted in immediate improvement. Point-of-care ultrasound demonstrated diffuse B-lines without right heart strain, and imaging confirmed pulmonary edema. Workup did not reveal a primary pulmonary or obstructive cardiac etiology; however, troponin elevation consistent with type 2 myocardial infarction was identified. The patient improved rapidly with ventilatory support and diuresis, was extubated within 48 hours, and was discharged without recurrence. This case demonstrates a rare complication of ISB involving sequential spread of local anesthetic, potentially facilitated by arthroscopic fluid extravasation, leading to phrenic nerve involvement and bilateral recurrent laryngeal nerve dysfunction. Resultant airway obstruction caused negative pressure pulmonary edema and secondary demand ischemia. Resistance to ventilation and refractory hypoxemia after ISB should raise concern for upper airway obstruction. Early airway management is critical to improve outcomes.

Aneurysmal subarachnoid hemorrhage (aSAH) remains associated with substantial morbidity and mortality despite best medical treatment. Increasing evidence implicates thrombo-inflammation (TI), driven by neutrophils and neutrophil extracellular traps (NETs), in the pathogenesis of delayed cerebral ischemia (DCI) and cognitive impairment. This narrative review summarizes experimental and clinical data linking neutrophil activation and NETs formation to DCI after aSAH and outlines emerging therapeutic strategies. This review was structured according to the SANRA (Scale for the Assessment of Narrative Review Articles) guidelines and followed general recommendations for narrative reviews. A comprehensive PubMed and clinicaltrials.gov search identified experimental and clinical studies published in English without time window, focusing on TI, neutrophil activation, or NETosis in the acute phase of aSAH. Past and ongoing clinical trials were classified by mechanism of action. Experimental models and human data show early and sustained neutrophil activation within cerebral and systemic compartments after aSAH. NETs promote microvascular thrombosis, blood-brain barrier disruption, microglial activation, and neuronal injury, ultimately contributing to DCI and long-term cognitive impairment. Outside the brain, NETs may also aggravate neurogenic pulmonary edema and cardiac dysfunction. In animal models, deoxyribonuclease I (DNase I) effectively degrades NETs, improving perfusion, limiting neuronal apoptosis, and enhancing recovery. Several ongoing trials target TI pathways, including the RESET trial, which evaluates the impact of IV DNase I on clinical outcome after aSAH. NETs produced after neutrophil activation may be central to DCI. Targeting NETs represents a promising translational path to improve cerebral and systemic outcomes after aSAH.

We present a unique case of spontaneous chordal rupture in a young infant with Down syndrome and unrepaired transitional atrioventricular septal defect. This resulted in abrupt onset of severe left atrioventricular valve regurgitation, cardiogenic shock, and multiorgan dysfunction. Our case highlights the need for a high index of suspicion for a ruptured chord in a young infant presenting with acute onset of pulmonary edema.

Diffuse alveolar haemorrhage (DAH) is a life-threatening pulmonary manifestation of small-vessel vasculitis, most commonly associated with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Unilateral DAH has been infrequently reported and may pose diagnostic challenges, as its radiological presentation can mimic pneumonia, pulmonary oedema, or localized haemorrhage. This atypical presentation may delay recognition of the underlying vasculitis and appropriate immunosuppressive therapy. We present a case of a woman in her thirties with previously diagnosed PR3-ANCA-associated vasculitis who presented with acute worsening of dyspnea (mMRC grade IV) and hemoptysis. Radiological assessments revealed extensive right-sided ground-glass opacities with areas of consolidation and minimal left lower lobe involvement. Bronchoscopy with sequential bronchoalveolar lavage (BAL) showed progressively haemorrhagic aliquots consistent with DAH. Laboratory investigations revealed anemia (Hb 7.1 mg/dL) and elevated serum creatinine (5.02 mg/dL). The patient developed type I respiratory failure requiring mechanical ventilation and hemodialysis. She was treated with pulse intravenous methylprednisolone followed by rituximab therapy, along with trimethoprim-sulfamethoxazole prophylaxis. The patient improved clinically, radiologically, and biochemically and was discharged on supplemental oxygen.

The coexistence of preeclampsia and uncontrolled thyrotoxicosis leading to acute respiratory failure is rare and poses significant diagnostic and therapeutic challenges, particularly with respect to safe fluid management in the obstetric intensive care setting. We report the case of a 35-year-old woman at 37-week gestation who presented with progressive dyspnea, acute pulmonary edema, and fetal distress, necessitating emergency cesarean section and subsequent intensive care admission. Point-of-care ultrasound (POCUS) demonstrated impaired left ventricular systolic function (ejection fraction 40%), reduced left ventricular outflow tract velocity time integral (LVOT VTI 10-11 cm), a dilated inferior vena cava, and diffuse pulmonary B-lines, consistent with volume overload and compromised forward cardiac output. Serial POCUS-guided assessments were used to titrate diuretic therapy and optimize mechanical ventilation, resulting in progressive improvement in LVOT VTI (up to 20 cm), resolution of pulmonary edema, achievement of negative fluid balance, and clinical recovery. The patient was successfully extubated on day 5 and discharged home on day 7. This case demonstrates the clinical utility of POCUS, particularly serial LVOT VTI measurements, in providing actionable, dynamic bedside data to safely guide fluid management when static hemodynamic indices are unreliable, highlighting the value of POCUS in complex high-risk obstetric critical care.

Current knowledge of hyperosmolar hyperglycaemic state (HHS) is drawn from case series and small observational cohorts, limiting applicability to broader clinical practice. There is a lack of robust, large-scale studies exploring triggers of HHS and associated mortality. This absence of reliable data impedes prevention strategies, tailored clinical guidelines, and equitable resource allocation. We conducted this systematic review to aggregate all relevant HHS cases, explore precipitating factors and outcomes, and how these vary by region. Searches across Ovid, PubMed, EMBASE, MEDLINE, Scopus, Web of Science, and Cochrane Library followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Studies reporting HHS cases from database inception to February 2025 were selected. Data on demographics, biochemical results, precipitants, outcomes, and complications were collected. 27 studies with a total of 63 935 cases were included. The median age was 63.8 years (IQR: 56.1-72.0). Common precipitants were non-infective illness (49.5%), infection (44.0%), and new diabetes diagnosis (31.7%). Intensive treatment unit admission was 40.8%, with the highest rate in North America (70.0%). Median hospital stay was 7.5 days, longest in Asia (17.5 days) and shortest in North and South America (4.0 days). Overall mortality was 21.1%, highest in Africa (40.0%), followed by Asia (18.2%), and lowest in North America (4.8%). Complications were acute kidney injury (7.6%), pulmonary oedema (4.8%), and acute coronary syndrome (3.9%). HHS presents with similar biochemistry globally, but outcomes vary significantly. Reducing mortality requires better diabetes diagnosis, harmonised protocols, and resource-adapted management to reduce gaps and inform prevention guidelines.PROSPERO registration numberCRD42025625923.

Neurogenic pulmonary edema is a rare but severe complication of acute central nervous system injury, such as subarachnoid hemorrhage, typically presenting with immediate onset. This report describes an uncommon case of delayed-onset neurogenic pulmonary edema following subarachnoid hemorrhage. A 68-year-old man with subarachnoid hemorrhage, caused by a ruptured left posterior communicating artery aneurysm, developed tachypnea and hypoxemia with bilateral pulmonary infiltrates 96 hours after symptom onset. Echocardiography was normal, ruling out cardiogenic causes, and neurogenic pulmonary edema was diagnosed. The patient improved rapidly with fluid restriction and diuretic therapy, and subsequently underwent successful aneurysm coil embolization. Neurogenic pulmonary edema is thought to result from an excessive sympathetic activation leading to pulmonary vasoconstriction, increased capillary pressure, and endothelial injury. Delayed cases may involve secondary sympathetic surges due to intracranial pressure fluctuations, vasospasm, or inflammatory injury. This case highlights the need for clinicians to consider delayed neurogenic pulmonary edema when respiratory deterioration occurs several days after subarachnoid hemorrhage to ensure timely diagnosis and life-saving management.

Acute lung injury (ALI) is a severe inflammatory disorder lacking effective therapeutic options. Lespedeza bicolor, a traditional medicinal plant, and its root extract (LBR) contain bioactive constituents with potential anti-inflammatory properties. This study aimed to evaluate the protective effects and underlying mechanisms of LBR against ALI. Network pharmacology combined with transcriptomic and enrichment analyses was used to identify potential targets and signaling pathways of LBR-derived active compounds. The anti-ALI efficacy of LBR was assessed in LPS-induced RAW264.7 cells and mouse models through histopathological examination, measurement of inflammatory cytokines, and immunohistochemistry. RNA sequencing, western blotting, and immunofluorescence assays were further performed to validate key signaling pathways. A total of 157 overlapping targets between LBR and ALI-associated genes were identified, mainly enriched in inflammatory and immune-related pathways, particularly the MAPK and NF-κB cascades. LBR significantly inhibited LPS-induced pro-inflammatory cytokine expression, phosphorylation of p38 MAPK and p65, and nuclear translocation of NF-κB p65 in vitro. In vivo, LBR improved lung histopathology, reduced inflammatory infiltration, and alleviated pulmonary edema. Mechanistically, LBR suppressed activation of the p38 MAPK/NF-κB axis with comparatively weaker effects on ERK and JNK pathways. In conclusion, LBR protects against LPS-induced ALI by modulating inflammatory responses via inhibition of the p38 MAPK/NF-κB signaling pathway, supporting its potential as a promising multi-target natural therapeutic for ALI.