Decision for early tracheostomy in respiratory failure of a paralyzed myasthenia gravis patient with sepsis-induced pneumonia: A case report.

INTRODUCTION: The neuromuscular condition myasthenia gravis (MG) can make treating sepsis-induced pneumonia more challenging. Since these patients risk respiratory failure, decisions about airway treatment, including tracheostomy, can be difficult. We report a case of a patient with sepsis and concurrent MG who underwent an early tracheostomy due to acute respiratory failure. PRESENTATION OF CASE: A 44-year-old woman with a history of MG presented to the emergency department with a stiff tongue, hypersalivation, limb paralysis and a phlegmy cough causing severe respiratory distress, aggravated by community-acquired pneumonia. A chest X-ray showed extensive infiltration and consolidation in the lower lobes. The patient was transferred immediately to the intensive care unit on mechanical ventilation. Despite initial treatment with antibiotics and respiratory support, her mental and respiratory status deteriorated rapidly. Given the risk of myasthenic crisis, sepsis and impending respiratory failure, with anticipated lengthy ventilator utilization and hospitalization, a multidisciplinary team decided to perform an early tracheostomy. DISCUSSION: The early tracheostomy procedure was carried out securely on the third day of hospitalization. This allowed for better pulmonary hygiene, adequate ventilation, airway clearance and rehabilitation therapy. The family contributed to stoma care and breathing exercises. The patient's respiratory condition steadily improved over the following weeks. The cough reflex remained well, and mechanical ventilation was gradually weaned off. CONCLUSION: Early tracheostomy in a paralyzed MG patient with sepsis-induced pneumonia can improve clinical outcomes and optimize airway management.

Molecular mechanisms of lidocaine.

Lidocaine is an amide-class local anesthetic used clinically to inhibit pain sensations. Systemic administration of lidocaine has antinociceptive, antiarrhythmic, anti-inflammatory, and antithrombotic effects. Lidocaine exerts these effects under both acute and chronic pain conditions and acute respiratory distress syndrome through mechanisms that can be independent of its primary mechanism of action, sodium channel inhibition. Here we review the pathophysiological underpinnings of lidocaine's role as an anti-nociceptive, anti-inflammatory mediated by toll-like receptor (TLR) and nuclear factor kappa-ß (NF-kß) signalling pathways and downstream cytokine effectors high mobility group box 1 (HMGB1) and tumour necrosis factor-α (TNF-α).

Systemic lidocaine administration influences NF-kß gene expression, NF-kß and TNF- α protein levels on BALB/c mice with musculoskeletal injury.

BACKGROUND: The immune system can produce various inflammatory mediators to protect the body from stress and surgical trauma. However, this excessive inflammatory response will interfere with the body's immune system, causing systemic inflammatory response syndrome and multi-organ failure if allowed to continue. Lidocaine as an anti-inflammatory is used to treat surgical pain and pain arising from the disease process and treat ventricular arrhythmias. This study aims to prove the efficacy of systemic lidocaine injection as an anti-inflammatory drug in BALB/c mice with sterile musculoskeletal injuries. METHODS: This study used a prospective experimental laboratory study on experimental animals of BALB/c mice using a simple randomized design. Sixteen adult white BALB/c mice (male, healthy, 10-12 weeks old, 35-40 g body weight, and no disability) were selected and randomly divided into two groups: the group given lidocaine (2 mg/kg body weight) and a group that was given sterile distilled water. NF-kß and TNF-α protein levels were detected by ELISA, while mRNA expression of NF-kß was analyzed and determined by quantitative real-time PCR. RESULTS: Musculoskeletal injury significantly increased the expression of both mRNA and protein levels of NF-kß and TNF-α protein level. In addition, the NF-kß (protein and mRNA) and TNF-α (protein) levels in rats experiencing inflammation due to musculoskeletal injury were significantly decreased in the lidocaine group (p < 0.001). CONCLUSIONS: The administration of systemic lidocaine injection was able to inhibit the expression of mRNA NF-kß, the protein levels of NF-kß, and protein levels of TNF-α in mice with musculoskeletal injuries.