Transplant recipients have an increased risk of complications, including graft dysfunction and infections, which can be life-threatening if not recognized early. Pneumonia ranks as one of the most frequent complications in both solid organ and hematopoietic stem cell transplants. Clinical symptoms manifest late during infections in immunocompromised patients. An aggressive approach centered on early confirmatory diagnosis and a low threshold for empiric therapy is often the most effective strategy. The isolation of a pathogen in an upper airway sample does not necessarily mean the same organism is responsible for pneumonia. Viruses such as CMV (cytomegalovirus virus) may function as co-pathogens for opportunistic infections in transplant recipients in addition to causing their own primary infectious syndrome. Furthermore, some viruses exhibit immunomodulatory effects that can affect the graft function. Given the exhaustive list of causative pathogens responsible for pneumonia, the best approach to the diagnosis is to have a conceptual framework that includes a detailed history, such as the type of transplant, degree of immunosuppression, antimicrobial prophylaxis, risk factors, time of presentation since transplantation and the radiographic pattern on the CT chest (computer tomography of the chest). Management depends predominantly on the degree of antimicrobial resistance, drug-to-drug interaction, and adjustments to the immunosuppression.

We present a case report of a 72-year-old female with a history of stage III rectal adenocarcinoma undergoing chemotherapy who developed neutropenic sepsis and acute respiratory failure. The patient was admitted to the intensive care unit (ICU) due to worsening respiratory status and was subsequently diagnosed with disseminated herpes simplex virus (HSV) infection including acute respiratory distress syndrome (ARDS). This case highlights the challenges in diagnosing and managing HSV infection in critically ill patients and emphasizes the importance of early recognition and appropriate treatment in improving patient outcomes. This case underscores the significance of considering viral etiologies, such as HSV, in patients with unexplained respiratory symptoms presenting as ARDS.

Background: Pulmonary hypertension (PH) is a frequent and serious complication of advanced chronic obstructive pulmonary disease (COPD) and is associated with poor prognosis and limited treatment options. Current management focuses on optimizing COPD care, while the role of pulmonary vasodilators remains controversial. Ensifentrine, a dual phosphodiesterase (PDE) 3/4 inhibitor with bronchodilatory and anti-inflammatory properties, may offer therapeutic benefit in COPD-associated PH. Objective: To retrospectively evaluate the effects of 6 months of nebulized ensifentrine on pulmonary hemodynamics and functional outcomes in patients with severe COPD and associated pre-capillary PH. Methods: We conducted a single-center, retrospective chart review of patients with GOLD stage III and IV COPD and confirmed pre-capillary PH (mean pulmonary artery pressure [mPAP] ≥20 mmHg, pulmonary vascular resistance [PVR] > 2 Wood Units, pulmonary capillary wedge pressure ≤15 mmHg). Five patients treated with nebulized ensifentrine (3 mg twice daily) between September 2024 and May 2025 were analyzed. Hemodynamics via right heart catheterization (RHC) and 6-minute walk distance (6MWD) were assessed at baseline and at 6 months. Results: The cohort (mean age 76 years, 60% male, mean FEV₁ 33.4% predicted) demonstrated severe emphysema and PH (baseline mPAP 53.2 mmHg, PVR 9.5 WU, cardiac index 2.5 L/min/m²). After 6 months, mean changes were: mPAP: decrease by 1.6 mmHg Cardiac index: increase by 0.1 L/min/m² PVR: decrease by 1.0 WU 6MWD: Improved by 31 m mMRC dyspnea score improved from 3.6 to 3.2, CAT score from 23 to 21.6, and DLCO increased modestly (29%→31.2% predicted). No adverse events, exacerbations, or hospitalizations were observed during this period. The combination of ensifentrine with roflumilast was well tolerated. Conclusions: In this retrospective study, ensifentrine was safe and associated with modest improvements in pulmonary hemodynamics and functional status in severe COPD with pre-capillary PH. These preliminary findings warrant confirmation in larger, prospective controlled trials.

Background: Acute respiratory distress syndrome (ARDS) is a severe form of hypoxemic respiratory failure with high morbidity and mortality. Mechanical ventilation is essential for supportive care, but the heterogeneity of lung and chest wall mechanics limits the effectiveness of standardized approaches. Esophageal pressure (Pes) monitoring, as a surrogate of pleural pressure, provides insight into patient-specific physiology and may enable individualized ventilation strategies to minimize ventilator-associated lung injury (VALI).Objective: To determine whether esophageal pressure monitoring improves personalization of mechanical ventilation in patients with ARDS and heterogeneous lung–chest wall mechanics.Methods: A comprehensive PubMed search of English-language literature was conducted. Experimental, physiologic, and clinical studies addressing esophageal manometry in mechanically ventilated patients were reviewed, with emphasis on ARDS. Evidence was synthesized regarding PEEP titration, assessment of patient effort, and applications in complex scenarios such as obesity and COPD overlap. Data extraction focused on proposed physiologic targets, validation techniques, clinical outcomes, and bedside feasibility.Findings: Esophageal manometry enables partitioning of lung and chest wall mechanics, accurate estimation of transpulmonary pressure, and optimization of PEEP settings. Across studies, consistent target ranges were identified: expiratory transpulmonary pressure (Plexp) 0–2 cmH₂O, end-inspiratory transpulmonary pressure (Plinsp) ≤15–20 cmH₂O, and tidal transpulmonary pressure change (ΔPL) ≤10–12 cmH₂O. In assisted ventilation, diaphragmatic-protective thresholds included ΔPes 3–8 cmH₂O, ΔPdi 5–15 cmH₂O, and PTPes 60–150 cmH₂O·s/min. Technique requires careful balloon inflation (Vbest) and confirmation of placement using an occlusion test. Additional clinical uses include detection of intrinsic PEEP, assessment of hemodynamics via transmural pressure measurements, and monitoring of patient–ventilator synchrony. Collectively, these applications support lung- and diaphragm-protective ventilation strategies tailored to individual physiology.Conclusions: Esophageal pressure monitoring represents a promising adjunct for personalizing mechanical ventilation in ARDS, particularly in patients with altered chest wall mechanics such as obesity. Although technical expertise and proper calibration are required, this tool allows more precise adjustment of PEEP, tidal volume, and inspiratory effort. Integration of Pes monitoring into practice may help balance lung- and diaphragm-protective strategies, thereby reducing VALI and improving patient-specific outcomes.