Residual Hypoxemia Research Articles

Long-Term Clinical, Radiological, and Mortality Outcomes Following Pneumonitis in Nonsmall Cell Lung Cancer Patients Receiving Immune Checkpoint Inhibitors: A Retrospective Analysis

AimsDespite known short-term mortality risk of immune checkpoint inhibitor (ICI) pneumonitis, its impact on 1-year mortality, long-term pulmonary function, symptom persistence, and radiological resolution remains unclear. MethodsWe retrospectively analyzed 71 nonsmall cell lung cancer (NSCLC) patients treated with anti-PD(L)1 monoclonal antibodies between 2018-2021, who developed pneumonitis. Clinical and demographic covariates were collected from electronic medical record. Cox regression assessed associations with mortality, while logistic regression evaluated associations with persistent symptoms, hypoxemia, and radiological resolution. ResultsSteroid-refractory pneumonitis (hazard ratio [HR] = 15.1, 95% confidence interval [95% CI]:3.9-57.8, P < .0001) was associated with higher 1-year mortality compared to steroid-responsive cases. However, steroid-resistant (odds ratio [OR] = 1.4, 95% CI: 0.4-5.1, P = .58) and steroid-dependent (OR = 0.4, 95% CI: 0.1-1.2, P = .08) pneumonitis were not. Nonadenocarcinoma histology (OR = 6.7, 95% CI: 1.6-46.6, P = .01), grade 3+ pneumonitis (OR = 4.6, 95% CI: 1.3-22.7, P = .03), and partial radiological resolution (OR = 6.3, 95% CI: 1.8-23.8, P = .004) were linked to increased pulmonary symptoms after pneumonitis resolution. Grade 3+ pneumonitis (OR = 8.1, 95% CI: 2.3-31.5, P = .001) and partial radiological resolution (OR = 5.45, 95% CI: 1.29-37.7, P = .03) associated with residual hypoxemia. Nonadenocarcinoma histology (OR = 3.6, 95% CI: 1.01-17.6, P = .06) and pretreatment ILAs (OR = 4.8, 95% CI: 1.14-33.09, P = .05) were associated with partial radiological resolution. ConclusionsSteroid refractory pneumonitis increases 1-year mortality in NSCLC patients. Pretreatment ILAs may signal predisposition to fibrosis-related outcomes, seen as partial resolution, which in turn is associated with postresolution symptoms and residual hypoxemia. These findings offer insights for identifying patients at risk of adverse outcomes post-pneumonitis resolution.

The assessment of lung function and residual hypoxemia after balloon pulmonary angioplasty for patients with chronic thromboembolic hypertension

Abstract Background It has been reported that balloon pulmonary angioplasty (BPA) could dramatically improve hemodynamics in patients with chronic thromboembolic pulmonary hypertension (CTEPH). However, some patients have shown poor response in oxygenation and lung function even after BPA. The aim of our study was to evaluate the efficacy of BPA using clinical indicators and to investigate lung function and residual hypoxemia. Method Consecutive 103 patients who underwent BPA from September 2011 to August 2018 were enrolled. We evaluated hemodynamics with right heart catheterization, respiratory function test, arterial blood gas examination, and exercise capacity with 6 minute-walk-distance (6MWD). Result At the median 12-month follow-up after the final BPA session, following examination findings were significantly improved. Mean pulmonary artery pressure (39.0±8.2mmHg, 23.2±8.4mmHg, p&amp;lt;0.001), Pulmonary vascular resistance (782±378 dynes / sec / cm-5, 331±187 dynes / sec / cm-5, p&amp;lt;0.001), 6 MWD (310±94 m, 363±119 m, p&amp;lt;0.001), PaO2 (63.1±15.8 mmHg, 68.5±13.6 mmHg, p=0.044),%VC (88.5±17.1, 91±16.3, p=0.036). However, the following examination findings did not improve after BPA. Oxygen desaturation during 6MWD test (−11.9±6.3, 12±7.9, p=0.65), %DLCO (64.2 17.1, 61.3 16.8, p=0.147). Conclusion BPA could dramatically improve hemodynamics and exercise tolerance. However, arterial oxygenation was not normalized after BPA. Moreover, oxygen desaturation in exercise, and %DLCO were almost unchanged. These observations might suggest the remaining arteriopathy in capillary level of pulmonary artery, but further research is needed. Funding Acknowledgement Type of funding source: None

Contributions of residual hypoxemia to exercise hyperventilation in Fontan patients.

ABSTRACTIt is unsettled whether increased exercise ventilation in Fontan subjects is due to increased pulmonary dead space or augmented ventilatory drive. Twenty-six Fontan patients underwent symptom-limited treadmill cardiopulmonary exercise testing. Two groups of age- and sex- matched subjects served as controls: the biventricularly repaired (Bi, n = 18), and the “true” control (C, n = 29) groups. Peak oxygen uptake (V̇O2peak) was not different among groups (41.0 +/– 8.4 ml/min/kg, 43.5 +/– 6.6 ml/min/kg, and 45.9 +/– 11.6 ml/min/kg for Fontan, Bi, and C groups, respectively, p = 0.16). Fontan subjects, however, showed steeper alveolar ventilation/carbon-dioxide (V̇A/V̇CO2) regression slope (35.5 +/– 5.3, 28.7 +/– 3.8, and 29.5 +/– 3.0 l/ml, for Fontan, Bi, and C groups, respectively, p<0.0001), and lower end-expiratory carbon-dioxide fraction (FetCO2VAT) at ventilatory threshold (VAT) (4.4 +/– 0.5%, 5.5 +/– 0.5%, and 5.5 +/– 0.4%, for Fontan, Bi, and C groups, respectively, p<0.001). The dead-space ventilation fraction at VAT was similar among groups (0.33 +/– 0.06, 0.33 +/– 0.04, 0.35 +/– 0.05 for Fontan, Bi, and C groups, respectively, p = 0.54). In Fontan subjects, arterial oxygen saturation at rest (SaO2rest) was correlated with V̇A/V̇CO2 regression slope (r = –0.41, p = 0.04) and with FetCO2VAT (p = –0.53, p<0.01). We conclude that Fontan patients show exercise hyperventilation due to augmented central and/or peripheral ventilatory drive, which is further augmented by residual hypoxemia.

P4675The utility of additional balloon pulmonary angioplasty for residual hypoxemia in normohemodynamic chronic thromboembolic pulmonary hypertension patients after invasive treatments

Abstract Background Balloon pulmonary angioplasty (BPA) improves hemodynamics, symptoms and exercise capacity in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who are ineligible for pulmonary endarterectomy (PEA). However, certain patients still have hypoxemia after BPA or PEA despite normalization of hemodynamics. In CTEPH, hypoxemia is related increased dead space ventilation caused by vascular obstruction. Purpose This study was aimed to clarify whether additional BPA can improve hypoxemia of CTEPH patients after normalization of hemodynamics. Methods A total of 335 patients who underwent initial series of BPA in our institute were followed up. Sixty-four patients with mean pulmonary artery pressure (mPAP) &lt;30mmHg and percutaneous oxygen saturation (SpO2) &lt;95% without oxygen inhalation at more than 6 months after the initial series of BPA and of patients who could reevaluate hemodynamics and oxygenation after additional BPA were enrolled. These patients were divided into two groups with or without additional BPA procedures. Change of hemodynamics and SpO2 were retrospectively investigated. Results Thirty-three of 64 patients underwent additional BPA procedures. Patients' age was older in BPA group than those in non-BPA group (71.3±10.4 vs. 66.5±9.4 years old, p=0.02). mPAP and pulmonary vascular resistance (PVR) was significantly higher in BPA group (mPAP: 23.9±3.2 vs. 20.7±3.8 mmHg, p=0.001, PVR: 4.2±1.2 vs. 3.5±1.4 wood unit, p=0.03, respectively). Among the 1.8±1.4 BPA procedures per person, total 6.6±3.8 segmental pulmonary arteries per person were treated. While no obvious improvements were observed in non-BPA group, PVR and SpO2 in BPA group were significantly improved (4.2±1.2 to 3.7±1.3 wood unit, p=0.002, 90.7±3.1% to 94.1±3.6%, p&lt;0.001, respectively). In the multivariate logistic regression analysis, additional BPA procedures were associated with further improvement of SpO2 (hazard ratio, 3.7; 95% confidence interval, 1.2–11.5; P=0.02). Conclusions Additional BPA procedure was associated with improvement of hypoxemia in CTEPH patients after normalization of hemodynamics. Treating as many lesions as possible in BPA might relieve the patients' residual dyspnea.

English

We report a case of an ipsilateral re-expansion pulmonary edema occurring after the insertion of an intercostal drainage tube in a young male patient with spontaneous pneumothorax. The patient was managed with oxygen via a non-rebreathing face mask to compensate for his hypoxemia. In about 24 hours after the event, the patient gradually improved and recovered completely without any residual hypoxemia. Re expansion pulmonary edema occurring after the insertion of an intercostal drainage tube for pneumothorax or pleural effusion is a rare complication with a high mortality rate up to 20%. This condition should be considered if the patient develops cough, dyspnea and hypoxemia following the insertion of a chest tube. The exact pathophysiology leading to this complication is still unknown. The risk factors for re-expansion pulmonary edema should be evaluated and considered prior to the insertion of chest tubes. Treatment remains supportive only. INTRODUCTION: In 1853, Pinault (1) described REPE following pleural effusion in a patient who had a large volume of pleural fluid rapidly removed by thoracentesis. This is probably the first report of REPE. In 1958, re expansion pulmonary edema (REPE) was first reported following pneumothorax by Carlson and colleagues(2) and was comprehensively reviewed by Ziskind and colleagues(3) in 1965. In 1991 Matsuura in his clinical analysis of 146 patients and summarized that 21 of 146 cases of spontaneous pneumothorax which were treated by Thoracentesis and continuous low negative pressure suction drainage (- 12cm H20) of the pleural space developed REPE, The rate of REPE was higher in patients 20 to 39 years of age than in those over the age of 40. (4) REPE can occur on the ipsi- or contralateral side, can be bilateral and can even be asymptomatic.(5-9) The exact pathophysiology for this complication is unknown. Factors that have been implicated in the pathogenesis of this complication include chronicity of collapse, technique of re-expansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant and pulmonary artery pressure changes. (10) Oxygen radicals are produced during the hypoxemia in the collapsed lung. Moreover, the activity of different cytokines such as interleukin 8 and monocyte chemo attractant protein 1 (MCP-1),(11) or the activity of xanthine oxidase(12) have been implicated in the pathogenesis of REPE. Additionally, the GJP-binding protein Rho and its target Rho-Kinase (ROCK) identified by Sawafuji et al. has been implicated in permeability changes causing RPE as well. (13)

Successful Management of Fatal Paraquat Poisoning with Four Courses of Steroid and Cyclophosphamide Pulse

Although severe paraquat poisoning is fatal, intensive immunosuppression can be successful in selected patients. We report the case of a 33-yr-old patient who was poisoned by paraquat and developed multi-organ failure, progressive hypoxemia, and pulmonary fibrosis. The patient was successfully treated with four courses of immunosuppressive pulse therapy. The patient presented to the hospital 2.5 hours after ingesting 2 mouthfuls of paraquat. The serum level of paraquat was 10.40 µg/mL at 3 hours and 3.36 µg/mL at 10 hours after ingestion, which is predictive of a fatal outcome. The first course of steroid and cyclophosphamide pulse therapy was initiated after hemoperfusion. During the hospital course, the patient showed progressive hypoxemia with pulmonary fibrosis. Accordingly, three additional courses of immunosuppressive pulse therapy were administered to prevent pulmonary injury. This treatment inevitably led to bone marrow suppression, which was recovered with supportive care. The patient fully recovered after repeated immunosuppressive pulse therapy without residual hypoxemia and was successfully discharged from the hospital. (Korean J Med 2012;83:373-377)

Ipsilateral reexpansion pulmonary edema after drainage of a spontaneous pneumothorax: a case report

We report a case of ipsilateral reexpansion pulmonary edema occurring after the insertion of a chest tube in a patient with spontaneous pneumothorax. The patient received supplemental oxygen via a non-rebreather face mask to compensate for hypoxemia. 24 hours after the acute event, the patient recovered completely without residual hypoxemia. Reexpansion pulmonary edema after the insertion of a thoracic drainage for pneumothorax or pleural effusion is a rare complication with a high mortality rate up to 20%. It should be considered in case of hypoxemia following the insertion of a chest tube. The exact pathophysiology leading to this complication is not known. Risk factors for reexpansion pulmonary edema should be evaluated and considered prior to the insertion of chest tubes. Treatment is supportive.

ECMO and Inhaled Nitric Oxide for Cardiopulmonary Failure After Heart Retransplantation

Cardiopulmonary failure occurred in a 62-year-old patient a few hours after emergency cardiac retransplantation. Venoarterial extracorporeal membrane oxygenation was required to support biventricular dysfunction; thereafter, inhaled nitric oxide was given for residual hypoxemia and pulmonary hypertension. We report survival after venoarterial extracorporeal membrane oxygenation and inhaled nitric oxide treatment for both heart and lung failure in a heart recipient.(Ann Thorac Surg 1997;63:533–5)

Results Following Physiological Repair for Tricuspid Atresia

Fourteen patients underwent a physiological operation for tricuspid atresia. Seven patients survived up to 3 years after operation. Six patients underwent hemodynamic studies 2 to 34 months postoperatively (mean, 15 months). Average age at the time of operation was 14 years (range, 5 to 25 years). Postoperative studies showed 4 patients to be in sinus rhythm and 2 in junctional rhythm. Right atrial pressure was elevated an average of 17 mm Hg (range, 10 to 34 mm Hg). All patients showed good atrial transport function regardless of their rhythm. Two had a right atrium-left pulmonary artery gradient of 1.5 to 10 mm Hg across the conduit. Average arterial saturation was 92% (range, 87 to 97%), an improvement of 13% over preoperative values. Residual hypoxemia was due to pulmonary vein desaturation and to atrial right-to-left shunting early postoperatively and later, to atrial right-to-left shunting alone.