Mechanical ventilation complication

The prevention of mechanical complications (MC) is a major concern in adult spinal deformity (ASD) correction surgery; thus, the global alignment and proportion (GAP) score was developed to assess MC risk. Numerous studies have clarified the validity of the GAP score, but their contradictory results have prevented researchers from reaching compelling conclusions. This study aimed to analyze the predictive power of the GAP score on MC via a meta-analysis.

A total of 1,617 patients were included in the meta-analysis. Studies relevant to the GAP score and MC were identified in PubMed, EMBASE, and Cochrane CENTRAL and screened according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The GAP score categories of the patients and their MC/revision surgery status were collected. The data collected for the meta-analysis of odds ratios (OR) included the number of patients in the GAP score subgroups and their MC/revision surgery status. To calculate the OR, three GAP score subgroups were combined into two groups; hence, the analysis was conducted twice (gap proportioned [GAP-P] and higher groups, and gap severely disproportioned [GAP-SD] and lower groups).

Eleven studies were collected; of them, revision surgery data were available for seven. The proportion of MC in the studies was 27.7-60.6%, while that of revision surgery was 11.7-34.9%. In the meta-analysis of the GAP-P and higher score groups, the difference in MC ratio was significant (OR = 2.83; 95% confidence interval [CI] = 1.20-6.67; P = 0.02), whereas that for revision surgery was not. For the GAP-SD and lower score groups, the GAP-SD group had significantly higher proportions of both MC (OR = 2.65; 95% CI = 1.57-4.45; P < 0.001) and revision surgery (OR = 2.27; 95% CI = 1.33-3.88; P = 0.003). Publication bias was significant only in the latter MC analysis.

The GAP score offers predictive value for the risk of mechanical complications.

To determine long-term survival of patients after cardiac arrest undergoing emergent coronary angiography and therapeutic hypothermia.

We analysed data from patients treated within the regional STEMI Network from January 2015 to December 2020. The primary endpoint was all-cause mortality at median follow-up. Secondary endpoints were periprocedural complications (arrhythmias, pulmonary edema, cardiogenic shock, mechanical complication, stent thrombosis, reinfarction, bleeding) and 6-month all-cause death. A landmark analysis was performed, studying two time periods; 0-6 months and beyond 6 months.

From a total of 24,125 patients in the regional STEMI network, 494 patients who suffered from cardiac arrest were included and divided into two groups: treated with (n = 119) and without therapeutic hypothermia (n = 375). At median follow-up (16.0 [0.2-33.3] months), there was no difference in the adjusted mortality rate between groups (51.3 % with hypothermia vs 48.0 % without hypothermia; HR_adj1.08 95%CI [0.77-1.53]; p = 0.659). There was a higher frequency of bleeding in the hypothermia group (6.7 % vs 1.1 %; OR_adj 7.99 95%CI [2.05-31.2]; p = 0.002), without difference for the rest of periprocedural complications. At 6-month follow-up, adjusted all-cause mortality rate was similar between groups (46.2 % with hypothermia vs 44.5 % without hypothermia; HR_adj1.02 95%CI [0.71-1.47]; p = 0.900). Also, no differences were observed in the adjusted mortality rate between 6 months and median follow-up (9.4 % with hypothermia vs 6.3 % without hypothermia; HR_adj2.02 95%CI [0.69-5.92]; p = 0.200).

In a large cohort of patients with cardiac arrest within a regional STEMI network, those treated with therapeutic hypothermia did not improve long-term survival compared to those without hypothermia.

Ventilator-induced lung injury (VILI) is a complex pathophysiological process leading to acute respiratory distress syndrome (ARDS) and poor outcomes in affected patients. As a form of programmed cell death, pyroptosis is proposed to play an important role in the development of ARDS. Here we investigated whether treating mice with the specific RIPK1 inhibitor Necrostatin-1 (Nec-1) before mechanical ventilation could inhibit pyroptosis and alleviate lung injury in a mouse model.

Anesthetized C57BL/6J mice received a transtracheal injection of Nec-1 (5 mg/kg) or vehicle (DMSO) 30 min before the experiment which was ventilated for up to 4 h. Lung damage was assessed macroscopically and histologically with oedema measured as the wet/dry ratio of lung tissues. The release of inflammatory mediators into bronchoalveolar lavage fluid (BALF) was assessed by ELISA measurements of TNF-α,interleukin-1β (IL-1β), and IL-6. The expression of RIPK1, ZBP1, caspase-1, and activated (cleaved) caspase-1 were analyzed using western blot and immunohistochemistry, and the levels of gasdermin-D (GSDMD) and IL-1β were analyzed by immunofluorescence staining.

High tidal ventilation produced time-dependent inflammation and lung injury in mice which could be significantly reduced by pretreatment with Nec-1. Notably, Nec-1 reduced the expression of key pyroptosis mediator proteins in lung tissues exposed to mechanical ventilation, including caspase-1, cleaved caspase-1, and GSDMD together with inhibiting the release of inflammatory cytokines.

Nec-1 pretreatment alleviates pulmonary inflammatory responses and protects the lung from mechanical ventilation damage. The beneficial effects were mediated at least in part by inhibiting caspase-1-dependent pyroptosis through the RIPK1/ZBP1 pathway.