Postoperative pulmonary complications have a significant impact on perioperative morbidity and mortality and contribute substantially to health care costs. Surgical stress and anesthesia lead to changes in respiratory physiology, altering lung volumes, respiratory drive, and muscle function that can cumulatively increase the risk of postoperative pulmonary complications. Preoperative medical evaluation requires a structured approach to identify patient-, procedure-, and anesthesia-related risk factors for postoperative pulmonary complications. Validated risk prediction models can be used for risk stratification and to help tailor the preoperative investigation. Optimization of pulmonary comorbidities, smoking cessation, and correction of anemia are risk-mitigation strategies. Lung-protective ventilation, moderate PEEP application, and conservative use of neuromuscular blocking drugs are intra-operative preventive strategies. Postoperative early mobilization, chest physiotherapy, oral care, and appropriate analgesia speed up recovery. High-risk patients should receive inspiratory muscle training prior to surgery, and there should be a focus to minimize surgery time.
This was a prospective, multi-centre randomised controlled trial that involved centres in 16 countries. The trial was designed as a group sequential analysis with data analysed after randomisation of every 60 participants; stopping rules were predefined using the two triangle method. The trial could be stopped due to safety (due to excessive mortality in the ECMO arm), efficacy or futility (if unlikely to reach a definitive result). The trial was designed to have a power of 80% and alpha level of 5% to detect an absolute risk reduction of 20%. It was hypothesised that the mortality would be 60% in the conventional arm and 40% in the ECMO arm. Mortality at 60 days was the primary outcome measured.
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered variants of a disease continuum that results in a life-threatening exfoliative mucocutaneous disease. These are categorised as type IV cell-mediated delayed hypersensitivity reactions, and antibiotics are often implicated as a cause. Penicillins and other beta-lactam antibiotics are known to cause both immediate and delayed hypersensitivity reactions. While immediate IgE-mediated cross-reactivity between penicillins and carbapenems is well studied, less information on the risk of type IV delayed cell-mediated cross-reactivity between the two is available. We present a case of meropenem-induced SJS in a patient with documented history of SJS from amoxicillin. There are few cases of cross-reactivity with carbapenems reported in the literature, but based on the potential for life-threatening reaction, it is likely prudent to avoid the use of any beta-lactams in a patient with a history of SJS, TEN or any other severe cutaneous adverse reactions to another beta-lactam antibiotic.
A 24-year-old man with a history of HIV and large B cell lymphoma (currently in remission) presented with fever, dry cough and dizziness. His CD4+ count was undetectable, and the HIV viral load was 109 295 cop/mL. Physical examination revealed fever, hypotension and tachycardia with coarse breath sounds in the middle and lower chest zones bilaterally. Chest imaging showed diffuse abnormal micronodular and patchy infiltrates, without focal consolidation. A cavitary lesion was noted measuring 5×2 cm in axial dimensions within the left lower lobe and multiple small cystic lesions in the background. Bronchoalveolar lavage fluid culture grew Bordetella bronchiseptica. The patient was empirically treated with vancomycin and piperacillin–tazobactam for multifocal pneumonia with concerns for sepsis and was started on combined antiretroviral therapy (cART) with abacavir/dolutegravir/lamivudine. Symptoms improved after day 3 of therapy, and the patient was discharged home on 2 weeks of moxifloxacin, in addition to the cART and appropriate chemoprophylaxis.
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