Studies on mechanical-medical bridging for decompensated pulmonary hypertension (PH) are limited. We analysed the outcomes for critical PH patients who underwent extracorporeal membrane oxygenation (ECMO) support using a bridge-to-recovery (BTR) strategy. This study aimed to identify prognostic factors of BTR and evaluate the outcomes of survivors. Between 2009 and 2012, 6 patients who received veno-arterial ECMO due to decompensated PH with cardiogenic shock were retrospectively reviewed. All of the patients were managed with an aggressive titration of PH therapies and the optimization of right ventricular (RV) function to wean them off of ECMO. Three of the patients survived to discharge, and the others suffered in-hospital mortality. The differences between their baseline characteristics, ECMO set-up, haemodynamic change and complications were analysed. The average age was 46.67 ± 14.07 years, with a male-to-female ratio of 1:2. The non-survival group exhibited a higher baseline systolic pulmonary artery pressure (127.67 ± 25.81 vs 67.67 ± 24.83 mmHg, P = 0.044) than the survival group before ECMO. All of the non-survivors underwent cardiopulmonary-cerebral resuscitation prior to ECMO implantation (100 vs 0%, P = 0.100). The survivors tended to have received suboptimal PH therapies before ECMO and had more readily correctable predisposing factors of right ventricular failure. The non-survivors required a longer duration of ECMO and suffered more end-organ failure or sepsis, although those differences were not statistically significant. Pneumonia developed in 3 of the survivors and caused late mortality in 2 after discharge. ECMO provides a therapeutic window for the medical stabilization of critically decompensated PH patients. Prompt ECMO intervention before haemodynamic collapse and careful patient selection are critical for successful BTR outcomes.

Esophageal perforation after external air-blast trauma is rarely presented in the emergency room. The diagnosis is often delayed more than 24 hours.

Although serious adverse events have remained uncommon, cases of myocarditis induced by messenger RNA (mRNA) COVID-19 vaccines have been reported. Here, we presented a rare but potentially fatal disorder, hemophagocytic lymphohistiocytosis, in a 14-year-old previously healthy adolescent after BNT162b2 mRNA vaccination. The initial evaluation showed splenomegaly, pancytopenia, hyperferritinemia, and hypofibrinogenemia. Further examination revealed positive blood EBV DNA, and other infectious pathogen surveys were all negative. Hemophagocytosis was observed in the bone marrow aspiration and biopsy. HLH was confirmed and intravenous immunoglobulin (IVIG) and methylprednisolone pulse therapy were given. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was set up for cardiopulmonary support for 3 days due to profound hypotension. The patient was kept on oral prednisolone treatment for 28 days with the following gradual tapering. The hemogram and inflammatory biomarkers gradually returned to normal, and the patient was discharged. The fulminant presentation of HLH in our case could be the net result of both acute immunostimulation after COVID-19 vaccination and EBV infection. Our case suggests that the immune activation after COVID-19 vaccination is likely to interfere with the adequate immune response to certain infectious pathogens, resulting in a hyperinflammatory syndrome.