Introduction: Boussignac CPAP has recently been considered as an alternative to mechanical ventilation for AHRF after open cardiac surgery. Objectives: The study aims to: 1) Evaluate the effectiveness of Boussignac CPAP on clinical profile and arterial blood gases in treating AHFR after cardiac surgery. 2) Identify the success rate and adverse effects of Boussignac CPAP. Subjects and method: Controlled clinical trial included 35 patients with AHRF after open cardiac surgery. Patients were treated by Boussignac APCP. Measurements of MAP, HR, RR, PaO2, PaO2/FiO2 and PaCO2 before and after procedure were compared. Duration, success rate and disadvantages of Boussignac CPAP were noted. Results: MAP, HR, RR measurements were stabilised gradually. ABGs just before, at 30, 60 minutes after and at the end of procedure revealed as following: PaO2 increased from 71.6 to 148.3 to 155.8 to 166.1mmHg; PaO2/FiO2 increased from 208.3 to 297.4 to 311.8 to 332.9mmHg. PaCO2 decreased from 52.7 to 38.6 to 37.1 to 35.3mmHg (p<0.001). The duration of Boussignac CPAP ranged from 2.09+/-0.5 to 51.2+/-14.1h, dependent on AHRF causes. The success rate was 97.1% with minor adverse effects. Conclusion: Boussignac CPAP can be considered as a safe procedure with high success rate. It can improve significantly MAP, HR, RR, oxygenation (PaO2, PaO2/FiO2) and ventilation (PaCO2). The duration of Boussignac CPAP in patients with hemodynamic-originated AHRF was significantly shorter than that in patients with nonhemodynamic-originated AHRF.
Boussignac CPAP: AHRF ; Cardiac surgery

Anaphylaxis is a life-threatening systemic allergic reaction presenting various clinical manifestations. Its prevalence has increased in almost all age groups and both sexes. Food, venom, and drugs are major causes in both children and adults; a higher prevalence of food-induced anaphylaxis is noted in children, while a higher prevalence of drug-induced anaphylaxis is noted in adults. The pathogenic mechanism is mediated by immunologic and nonimmunologic mechanisms, where mast cells and basophils are key cells that release mediators. A diagnosis of anaphylaxis is mainly based on clinical symptoms and physical findings; however, an increased serum tryptase level is a useful biomarker. Epinephrine is the first-line drug to treat acute symptoms, and an epinephrine auto-injector should be prescribed for each patient. Antihistamines and systemic corticosteroids are used to relieve symptoms. This review updates current issues in the management of anaphylaxis as well as the new guidelines for proper diagnosis and treatment.

Anaphylaxis is a life-threatening systemic allergic reaction presenting various clinical manifestations. Its prevalence has increased in almost all age groups and both sexes. Food, venom, and drugs are major causes in both children and adults; a higher prevalence of food-induced anaphylaxis is noted in children, while a higher prevalence of drug-induced anaphylaxis is noted in adults. The pathogenic mechanism is mediated by immunologic and nonimmunologic mechanisms, where mast cells and basophils are key cells that release mediators. A diagnosis of anaphylaxis is mainly based on clinical symptoms and physical findings; however, an increased serum tryptase level is a useful biomarker. Epinephrine is the first-line drug to treat acute symptoms, and an epinephrine auto-injector should be prescribed for each patient. Antihistamines and systemic corticosteroids are used to relieve symptoms. This review updates current issues in the management of anaphylaxis as well as the new guidelines for proper diagnosis and treatment.

Asthma is characterized by airway obstruction and inflammation, and presents significant diagnostic and treatment challenges. The concept of endotypes has improved understanding of the mechanisms of asthma and has stimulated the development of effective treatment strategies. Sputum profiles may be used to classify asthma into two major inflammatory types: type 2-high (T2H) and type 2-low (T2L) asthma. T2H, characterized by elevated type 2 inflammation, has been extensively studied and several effective biologic treatments have been developed. However, managing T2L is more difficult due to the lack of reliable biomarkers for accurate diagnosis and classification. Additionally, conventional anti-inflammatory therapy does not completely control the symptoms of T2L; therefore, further research is needed to identify effective biologic treatments. This review provides new insights into the clinical characteristics and underlying mechanisms of severe T2L and investigates potential therapeutic approaches to control the disease.

Severe asthma (SA) has heterogeneous inflammatory phenotypes characterized by persistent airway inflammation (eosinophilic and/or neutrophilic inflammation) and remodeling. Various immune cells (eosinophils, neutrophils, and macrophages) become more activated and release inflammatory mediators and extracellular traps, damaging the protective barrier of airway epithelial cells and further activating other immune and structural cells. These cells play a role in autoimmune responses in asthmatic airways, where the adaptive immune system generates autoantibodies, inducing immunoglobulin G-dependent airway inflammation. Recent studies have suggested that adult asthmatics had high titers of autoantibodies associated with asthma severity, although pathogenic factors or diagnostic criteria are not well-defined. This challenge is further compounded by asthmatics with the autoimmune responses showing therapy insensitivity or failure to current pharmacological and biological treatment. This review updates emerging mechanisms of autoimmune responses in asthmatic airways and provides insights into their roles, proposing potential biomarkers and therapeutic targets for SA.