Severe Progressive Diffuse Alveolar Hemorrhage in a Patient with Systemic Lupus Erythematosus.

Diffuse alveolar hemorrhage (DAH) refers to the effusion of blood into the alveoli due to damaged pulmonary microvasculature. The ensuing alveolar collapse can lead to severe hypoxemia with poor prognosis. In these cases, it is crucial to provide respiratory care for hypoxemia in addition to treating the underlying disease. Here, we describe our experience with a case involving a 46-year-old woman with severe DAH-induced hypoxemia accompanying systemic lupus erythematosus (SLE). Mechanical ventilation was managed using airway pressure release ventilation (APRV) after intubation. Through APRV-based respiratory care and treatment of the underlying disease, hemoptysis was eliminated and oxygenation improved. The patient did not experience significant barotrauma and was successfully weaned from mechanical ventilation after 25 days in the intensive care unit. This case demonstrates that APRV-based control for respiratory management can inhibit the effusion of blood into the alveoli and achieve mechanical hemostasis, as well as mitigate alveolar collapse. APRV may be a useful method for respiratory care in patients with severe DAH-induced hypoxemia.

Use of High-Flow Nasal Cannula Oxygen Therapy in a Pregnant Woman with Dermatomyositis-Related Interstitial Pneumonia.

A 33-year-old pregnant woman was referred to our hospital with respiratory distress at 30 weeks of gestation. Chest computed tomography (CT) scans revealed pulmonary infiltrates along the bronchovascular bundles and ground-glass opacities in both lungs. Despite immediate treatment with steroid pulse therapy for suspected interstitial pneumonia, the patient's condition worsened. Respiratory distress was slightly alleviated after the initiation of high-flow nasal cannula (HFNC) oxygen therapy (40 L/min, FiO2 40%). We suspected clinically amyopathic dermatomyositis (CADM) complicating rapidly progressive refractory interstitial pneumonia. In order to save the life of the patient, the use of combination therapy with immunosuppressants was necessary. The patient underwent emergency cesarean section and was immediately treated with immunosuppressants while continuing HFNC oxygen therapy. The neonate was treated in the neonatal intensive care unit. The patient's condition improved after 7 days of hospitalization; by this time, she was positive for myositis-specific autoantibodies and was diagnosed with interstitial pneumonia preceding dermatomyositis. This condition can be potentially fatal within a few months of onset and therefore requires early combination immunosuppressive therapy. This case demonstrates the usefulness of HFNC oxygen therapy for respiratory management as it negates the need for intubation and allows for various treatments to be quickly performed.

The antioxidant N-acetyl cysteine suppresses lidocaine-induced intracellular reactive oxygen species production and cell death in neuronal SH-SY5Y cells.

BACKGROUND: The local anesthetic lidocaine can affect intra- and extra-cellular signaling pathways in both neuronal and non-neuronal cells, resulting in long-term modulation of biological functions, including cell growth and death. Indeed, lidocaine was shown to induce necrosis and apoptosis in vitro. While several studies have suggested that lidocaine-induced apoptosis is mitochondrial pathway-dependent, it remains unclear whether reactive oxygen species (ROS) are involved in this process and whether the observed cell death can be prevented by antioxidant treatment. METHODS: The effects of lidocaine and antioxidants on cell viability and death were evaluated using SH-SY5Y cells, HeLa cells, and HeLa cell derivatives. Cell viability was examined via MTS/PES ([3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt]/phenazine ethosulfate) assay. Meanwhile, cell apoptosis and necrosis were evaluated using a cell death detection assay with Annexin V-FITC and PI staining, as well as by assaying for caspase-3/7 and caspase-9 activity, and by measuring the release of lactate dehydrogenase, respectively. Mitochondrial transmembrane potential (ΔΨm) was assessed using the fluorescent probe tetramethylrhodamine ethyl ester. RESULTS: Lidocaine treatment resulted in suppression of the mitochondrial electron transport chain and subsequent attenuation of mitochondrial membrane potential, as well as enhanced ROS production, activation of caspase-3/7 and caspase-9, and induction of apoptosis and necrosis in SH-SY5Y cells in a dose- and time-dependent manner. Likewise, the anesthetics mepivacaine and bupivacaine also induced apoptosis in SH-SY5Y cells. Notably, the antioxidants N-acetyl cysteine (NAC) and Trolox successfully scavenged the mitochondria-derived ROS and suppressed local lidocaine-induced cell death. CONCLUSIONS: Our findings demonstrate that the local anesthetics lidocaine, mepivacaine, and bupivacaine inhibited the activity of mitochondria and induced apoptosis and necrosis in a dose-dependent manner. Furthermore, they demonstrate that treatment with the antioxidants NAC, Trolox, and GGA resulted in preservation of mitochondrial voltage and inhibition of apoptosis via suppression of caspase activation.