Pleuropulmonary pathologies in the early phase of acute pancreatitis correlate with disease severity

Abstract

Background Respiratory failure worsens the outcome of acute pancreatitis (AP) and underlying factors might be early detectable. Aims To evaluate the prevalence and prognostic relevance of early pleuropulmonary pathologies and pre-existing chronic lung diseases (CLD) in AP patients. Methods Multicentre retrospective cohort study. Caudal sections of the thorax derived from abdominal contrast enhanced computed tomography (CECT) performed in the early phase of AP were assessed. Independent predictors of severe AP were identified by binary logistic regression analysis. A one-year survival analysis using Kaplan-Meier curves and log rank test was performed. Results 358 patients were analysed, finding pleuropulmonary pathologies in 81%. CECTs were performed with a median of 2 days (IQR 1–3) after admission. Multivariable analysis identified moderate to severe or bilateral pleural effusions (PEs) (OR = 4.16, 95%CI 2.05–8.45, p<0.001) and pre-existing CLD (OR = 2.93, 95%CI 1.17–7.32, p = 0.022) as independent predictors of severe AP. Log rank test showed a significantly worse one-year survival in patients with bilateral compared to unilateral PEs in a subgroup. Conclusions Increasing awareness of the prognostic impact of large and bilateral PEs and pre-existing CLD could facilitate the identification of patients at high risk for severe AP in the early phase and thus improve their prognosis.

Incidence and prognostic role of pleural effusion in patients with acute pancreatitis: a meta-analysis

“…The sample sizes ranged from 25 to 909. Twenty-two studies [ 21 , 23 , 26–28 , 30 , 31 , 33 , 34 , 36–44 , 46–49 ] were from Asia, ten studies [ 16 , 17 , 20 , 22 , 25 , 29 , 32 , 35 , 45 , 50 ] were from Europe, and the rest [ 18 , 19 , 24 , 36 ] were from other regions. Among these studies, eleven studies [ 16–20 , 24 , 26 , 30 , 38 , 42 , 45 ] reported the location of PE, three studies [ 19 , 39 , 45 ] mentioned the size of PE, and five studies [ 20 , 23 , 32 , 35 , 42 ] provided data on mortality in AP patients with or without PE.…”

“…Twenty-two studies [ 21 , 23 , 26–28 , 30 , 31 , 33 , 34 , 36–44 , 46–49 ] were from Asia, ten studies [ 16 , 17 , 20 , 22 , 25 , 29 , 32 , 35 , 45 , 50 ] were from Europe, and the rest [ 18 , 19 , 24 , 36 ] were from other regions. Among these studies, eleven studies [ 16–20 , 24 , 26 , 30 , 38 , 42 , 45 ] reported the location of PE, three studies [ 19 , 39 , 45 ] mentioned the size of PE, and five studies [ 20 , 23 , 32 , 35 , 42 ] provided data on mortality in AP patients with or without PE. Additionally, PE was detected by chest X-ray in eight studies [ 16 , 18 , 20 , 22–24 , 41 , 50 ], by CT in 14 studies [ 19 , 21 , 25–27 , 30 , 32 , 35 , 38 , 39 , 42 , 45–47 ], by transthoracic sonography in one study [ 17 ] and by combination of above methods in four studies [ 29 , 31 , 48 , 49 ].…”

The relationship between inflammatory cytokines and in‐hospital complications of acute pancreatitis

“…Pleural effusion is one of the common pulmonary complications in AP patients. The latest data show that the incidence of AP combined with pleural effusion is as high as 34%–54.5% 6,7 . The potential mechanisms of pleural effusion accumulation in AP are diverse and can be explained by the following reasons: inflammation‐induced changes in capillary permeability, diaphragmatic lymphatic obstruction, pleural‐pancreatic fistula formation, and sinus formation between the pleural cavity and PPC 8 .…”

“…The latest data show that the incidence of AP combined with pleural effusion is as high as 34%–54.5%. 6 , 7 The potential mechanisms of pleural effusion accumulation in AP are diverse and can be explained by the following reasons: inflammation‐induced changes in capillary permeability, diaphragmatic lymphatic obstruction, pleural‐pancreatic fistula formation, and sinus formation between the pleural cavity and PPC. 8 Furthermore, up to 30%–40% of AP patients develop ascites, and a large proportion of patients develop mild to moderate ascites in the initial stage of inflammation, which may be secondary to local inflammation and subsequent transperitoneal and vascular exudation.…”

Fighting Fire with Fire: Exosomes and Acute Pancreatitis-Associated Acute Lung Injury

“…Acute lung injury (ALI) is a life-threatening condition characterized by diffuse interstitial and alveolar edema resulting from the damage of pulmonary microvascular endothelial cells (PMVECs) and alveolar epithelial cells (AECs) [ 3 , 4 ]. ALI and its severe form, acute respiratory distress syndrome (ARDS), are among the most prevalent consequences of SAP and are leading causes of mortality in SAP patients [ 5 ].…”