Inflammatory Myofibroblastic Tumor: A Rare Case Report.

Inflammatory myofibroblastic tumors (IMTs) are rare benign tumors that can occur anywhere in the body, most commonly in the pediatric and young adult populations. The gold standard treatment is surgical resection, possibly along with chemotherapy and/or radiotherapy. IMTs have a high recurrence rate and may present with secondary symptoms, such as hemoptysis, fever, and stridor. We present a 13-year-old male patient with hemoptysis for one month who was subsequently diagnosed with an obstructing IMT of the trachea. The preoperative assessment showed the patient was not in acute distress and could protect his airway, even when lying flat. The treatment plan was discussed with the otolaryngologist, to keep the patient spontaneously breathing throughout the case. Anesthesia was induced with boluses of midazolam, remifentanil, propofol, and dexmedetomidine. Doses were adjusted as needed. Glycopyrrolate was also given to limit the patient's secretions before initiating the surgical procedure. The FiO2 was kept under 30% as tolerated to reduce the risk of airway fire. During surgical resection, the patient was kept spontaneously breathing, and paralytics were avoided. Due to high tumor vascularity and inability to obtain hemostasis, the patient was kept intubated and on ventilation post-operatively until definitive treatment could be performed. On postoperative day 3, the patient returned to the operating room due to a worsening condition. He was found to have a partial obstruction of the right mainstem bronchus by the tumor. More of the tumor was debulked, and he remained intubated above the level of the debulked mass. The patient was then transferred to a higher acuity institution for advanced care. After the transfer, the patient underwent a carinal resection on cardiopulmonary bypass. This case provides insight into successfully sharing the airway during tracheal tumor resection, emphasizing minimizing the risk of airway fire and constant communication with the surgeon.

Minimally invasive management of de Garengeot hernia with staged robotic hernia repair.

De Garengeot hernia is a rare phenomenon describing the migration of the appendix into a femoral hernia sac. Many repair strategies have been described although an open inguinal approach with suture repair is the most common technique. Despite strong evidence that mesh limits recurrence, most forgo mesh use in the presence of appendicitis for fear of contamination. We report a case in a 68-year-old man managed completely with minimally invasive strategies. We performed a staged laparoscopic appendectomy followed by robotic hernia repair with polypropylene mesh. This is the first described two-stage minimally invasive approach and the first report demonstrating the feasibility of robotic hernia repair in the setting of de Garengeot hernia. It is our opinion that using a staged approach may encourage mesh repair by minimising the risk of implant contamination. Furthermore, we believe a fully minimally invasive technique may result in improved outcomes.

High mobility group box I (HMGB1) release from tumor cells after treatment: implications for development of targeted chemoimmunotherapy.

We have recently demonstrated that cytolysis of human melanoma cells by immune effectors (both NK and T cells) is associated with release of the nuclear chromatin protein, high mobility group box I (HMGB1). Extracellular HMGB1 mediates a number of important functions including endothelial cell activation, stromagenesis, recruitment and activation of innate immune cells, and also dendritic cell maturation that, in the setting of cancer, lead to a chronic inflammatory response. This reparative inflammatory response promotes tumor cell survival, expansion, and metastases. Release of HMGB1 after chemotherapy-induced cytotoxicity has not been well characterized. We measured the release of HMGB1 after chemotherapy or immune cytolysis and demonstrated that this did not correlate with conventional markers of apoptosis and necrosis in several human colorectal, pancreatic, and melanoma tumor cell lines. Rather, we observed that tumor cells incubated with the platinating agent oxaliplatin, retained HMGB1 within the nucleus for significantly longer periods than other agents used at comparable cytotoxic concentrations or even with potent cytolytic cells. Thus, release of HMGB1 from dying tumor cells treated with chemotherapy or cells with lymphokine activated killer cell activity is not dependent solely on the mode of cell death. Sequestration of the damage associated molecular pattern molecule, HMGB1, may play a role in the clinical efficacy of platinating agents and suggests this as a superior agent for coupling with immunotherapeutic strategies, possibly enhancing their effectiveness.