Spontaneous pneumoperitoneum
A spontaneous pneumoperitoneum is a rare case that is not caused by an abdominal organ rupture. This is also called an idiopathic spontaneous pneumoperitoneum when the cause is not known. Causes of a spontaneous pneumoperitoneum, with no peritonitis include a barotrauma due to mechanical ventilation,  and a tracheal  rupture following an emergency intubation. In the ventilation case, air had passed from the chest into the abdominal cavity through the  diaphragm. In the tracheal rupture air had passed along the great vessels. Diagnosis
When present, pneumoperitoneum can often be seen on projectional radiography, but small amounts are often missed, and CT scan is nowadays regarded as a criterion standard in the assessment of a pneumoperitoneum. CT can visualize quantities as small as 5 cm³ of air or gas. Signs that can be seen on projectional radiography are shown below:
The double wall sign marks the presence of air on both sides of the intestine. However, a false double wall sign can result from two loops of bowel being in contact with one another. The sign is named after Leo George Rigler. It is not the same as Riglers triad. The football sign is when the abdomen appears as a large oval radiolucency reminiscent of an American football on a supine projectional radiograph. The football sign is most frequently seen in infants with spontaneous or iatrogenic gastric perforation causing pneumoperitoneum. It is also seen in bowel obstruction with secondary perforation, as in Hirschprung disease, midgut volvulus, meconium ileus and intestinal atresia.
Lurbinectedin inhibits transcription through a very precise mechanism. Firstly, lurbinectedin binds to specific DNA sequences. It is at these precise spots that slides down the DNA to produce RNA polymerase II that is blocked and degraded by lurbinectedin. Lurbinectedin also has important role in tumor microenvironment. The tumor cells act upon macrophages to avoid them from behaving like an activator of the immune system. Macrophages can contribute to tumor growth and progression by promoting tumor cell proliferation and invasion, fostering tumor angiogenesis and suppressing antitumor immune cells. Attracted to oxygen-starved (hypoxic) and necrotic tumor cells they promote chronic inflammation. So, not only that macrophages inhibit immune system avoiding the destruction of tumor cells, but they also create tumor tissue that allows tumor growth. However, macrophages associated with tumors are cells that are addicted to the transcription process. Lurbinectedin acts specifically on the macrophages associated with tumors in two ways: firstly, by inhibiting the transcription of macrophages that leads to cell death and secondly, inhibiting the production of tumor growth factors. In this way, lurbinectedin normalizes the tumor microenvironment. History
Lurbinectedin was approved for medical use in the United States in June 2020.Efficacy was demonstrated in the PM1183-B-005-14 trial (Study B-005; NCT02454972), a multicenter open-label, multi-cohort study enrolling 105 participants with metastatic SCLC who had disease progression on or after platinum-based chemotherapy. Participants received lurbinectedin 3.2 mg/m2 by intravenous infusion every 21 days until disease progression or unacceptable toxicity.