The precise definition of a severe asthmatic exacerbation is an issue that presents difficulties. The term 'status asthmaticus' relates severity to outcome and has been used to define a severe asthmatic exacerbation that does not respond to and/or perilously delays the repetitive or continuous administration of short-acting inhaled beta(2)-adrenergic receptor agonists (SABA) in the emergency setting. However, a number of limitations exist concerning the quantification of unresponsiveness. Therefore, the term 'acute severe asthma' is widely used, relating severity mostly to a combination of the presenting signs and symptoms and the severity of the cardiorespiratory abnormalities observed, although it is well known that presentation does not foretell outcome. In an acute severe asthma episode, close observation plus aggressive administration of bronchodilators (SABAs plus ipratropium bromide via a nebulizer driven by oxygen) and oral or intravenous corticosteroids are necessary to arrest the progression to severe hypercapnic respiratory failure leading to a decrease in consciousness that requires intensive care unit (ICU) admission and, eventually, ventilatory support. Adjunctive therapies (intravenous magnesium sulfate and/or others) should be considered in order to avoid intubation. Management after admission to the hospital ward because of an incomplete response is similar. The decision to intubate is essentially based on clinical judgement. Although cardiac or respiratory arrest represents an absolute indication for intubation, the usual picture is that of a conscious patient struggling to breathe. Factors associated with the increased likelihood of intubation include exhaustion and fatigue despite maximal therapy, deteriorating mental status, refractory hypoxaemia, increasing hypercapnia, haemodynamic instability and impending coma or apnoea. To intubate, sedation is indicated in order to improve comfort, safety and patient-ventilator synchrony, while at the same time decrease oxygen consumption and carbon dioxide production. Benzodiazepines can be safely used for sedation of the asthmatic patient, but time to awakening after discontinuation is prolonged and difficult to predict. The most common alternative is propofol, which is attractive in patients with sudden-onset (near-fatal) asthma who may be eligible for extubation within a few hours, because it can be titrated rapidly to a deep sedation level and has rapid reversal after discontinuation; in addition, it possesses bronchodilatory properties. The addition of an opioid (fentanyl or remifentanil) administered by continuous infusion to benzodiazepines or propofol is often desirable in order to provide amnesia, sedation, analgesia and respiratory drive suppression. Acute severe asthma is characterized by severe pulmonary hyperinflation due to marked limitation of the expiratory flow. Therefore, the main objective of the initial ventilator management is 2-fold: to ensure adequate gas exchange and to prevent further hyperinflation and ventilator-associated lung injury. This may require hypoventilation of the patient and higher arterial carbon dioxide (PaCO(2)) levels and a more acidic pH. This does not apply to asthmatic patients intubated for cardiac or respiratory arrest. In this setting the post-anoxic brain oedema might demand more careful management of PaCO(2) levels to prevent further elevation of intracranial pressure and subsequent complications. Monitoring lung mechanics is of paramount importance for the safe ventilation of patients with status asthmaticus. The first line of specific pharmacological therapy in ventilated asthmatic patients remains bronchodilation with a SABA, typically salbutamol (albuterol). Administration techniques include nebulizers or metered-dose inhalers with spacers. Systemic corticosteroids are critical components of therapy and should be administered to all ventilated patients, although the dose of systemic corticosteroids in mechanically ventilated asthmatic patients remains controversial. Anticholinergics, inhaled corticosteroids, leukotriene receptor antagonists and methylxanthines offer little benefit, and clinical data favouring their use are lacking. In conclusion, expertise, perseverance, judicious decisions and practice of evidence-based medicine are of paramount importance for successful outcomes for patients with acute severe asthma.
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Pediatr Rheumatol Online J
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Translational Genetics Research Group, La Fe Health Research Institute (IIS La Fe), Avenida Fernando Abril Martorell nº 106 Tower A, 7th Floor, Valencia, Spain.
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December 2024
Translational Research Centre, Asian Healthcare Foundation, AIG Hospitals, Hyderabad, India. Electronic address:
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Biochim Biophys Acta Mol Basis Dis
December 2024
Department of Hepatobiliary Surgery, First Hospital of Shanxi Medical University, Taiyuan, Shanxi Province, China. Electronic address:
Liver transplantation is currently recognized as the most effective treatment for severe liver diseases. Although survival rates after liver transplantation have improved, rejection of the transplanted liver remains a significant cause of morbidity and transplant failure in patients. Our team previously discovered a close association between high GBP1 expression and acute rejection reactions following liver transplantation.
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Department of Allergology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China; Department of Allergy, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. Electronic address:
Background: Environmental pollutants have been found to contribute to the development and acute exacerbation of asthma. Microplastics (MPs) have received widespread attention as an emerging global pollutant. Airborne MPs can cause various adverse health effects.
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December 2024
Department of Burns and Cutaneous Surgery, Xijing Hospital, the Fourth Military Medical University, 127 Changle West Road, Xi'an, Shaanxi 710032, China. Electronic address:
Acute lung injury being one of the earliest and most severe complications during sepsis and macrophages play a key role in this process. To investigate the regulatory effects and potential mechanisms of adipose mesenchymal stem cell derived-exosomes (ADSC-exo) on macrophages and septic mice, ADSCs-exo was administrated to both LPS-induced macrophage and cecal ligation and puncture (CLP) induced sepsis mice. ADSCs-exo was confirmed to inhibit M1 polarization of macrophages and to reduce excessive inflammation.
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