Cytoreductive surgery plus bicavitary chemohyperthermia as treatment of pseudomixoma peritonei with pleural extension. A case report and review of the literature.

AIM: Intrathoracic extension in patients with pseudomixoma peritonei is a rare event, but spread of the tumour beyond the abdomen in to pleuropulmonary cavity has been reported. MATERIALS AND METHODS: We report a case of a 50-years-old woman with synchronous pleural manifestation of pseudomixoma peritonei by a mucinous ovarian cancer. During the abdominal cytoreductive surgery an extensive disease under the right hemidiaphragm was noted, requiring partial diaphragmatic resection. Once the pleural space was entered,mucinous neoplastic implants on the pleural surface was observed. The diaphragmatic defect was left open during the hyperthermic chemoperfusion to treat both the pleural and peritoneal surfaces. After a postoperative course uneventful she died after 6 months for a myocardial infarction, in presence of a left side pleural effusion with a positive cytology for high-grade malignant cells with a smear background contained wispy mucin. DISCUSSION: Despite the aggressive spread of the pseudomixoma peritonei within the peritoneal cavity, lymphatic and hematogenous metastasis are rare. However, extension of disease into pleuropolmonary cavity has been well described as pleural effusion or pleuropulmonary metastases. This is the first report in literature, to our knowledge, in which the thoracic extension is due to a mucinous ovarian cancer, and is the second case in which a simultaneous bicavitary hyperthermic chemoperfusion was done as a management option for thoracic extension of pseudomixoma peritonei. CONCLUSION: Due to the rarity of the thoracic involvement by pseudomixoma peritonei, its correct treatment is still unclear. Simultaneous cytoreductive surgery associated to intraoperative intraperitoneal and intrathoracic chemohyperthermia can be a potential therapeutic option for these patients.

Effects of anesthetics on mitochondrial signaling and function.

Mitochondria are considered the powerhouses of the cell playing an important role in energy metabolism. However, they are highly vulnerable to inhibition or uncoupling of the energy harnessing process and run a high risk of causing catastrophic damage to the cell. Several anesthetics or drugs commonly given during anesthesia interact with mitochondria and affect their structure or impair respiratory chain functioning with decreased ATP production. Mitochondria, in fact, are a potential site of action of general and local anesthetics. The purpose of this review is to update present knowledge and describe the effects and molecular mechanisms of the action of the most used drugs of anesthesia on mitochondria.

Propofol infusion syndrome: an overview of a perplexing disease.

Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent that is widely used in adults and children for sedation and the induction and maintenance of anaesthesia. Propofol has gained popularity for its rapid onset and rapid recovery even after prolonged use, and for the neuroprotection conferred. However, a review of the literature reveals multiple instances in which prolonged propofol administration (>48 hours) at high doses (>4 mg/kg/h) may cause a rare, but frequently fatal complication known as propofol infusion syndrome (PRIS). PRIS is characterized by metabolic acidosis, rhabdomyolysis of both skeletal and cardiac muscle, arrhythmias (bradycardia, atrial fibrillation, ventricular and supraventricular tachycardia, bundle branch block and asystole), myocardial failure, renal failure, hepatomegaly and death. PRIS has been described as an 'all or none' syndrome with sudden onset and probable death. The literature does not provide evidence of degrees of symptoms, nor of mildness or severity of signs in the clinical course of the syndrome. Recently, a fatal case of PRIS at a low infusion rate (1.9-2.6 mg/kg/h) has been reported. Common laboratory and instrumental findings in PRIS are myoglobinuria, downsloping ST-segment elevation, an increase in plasma creatine kinase, troponin I, potassium, creatinine, azotaemia, malonylcarnitine and C5-acylcarnitine, whereas in the mitochondrial respiratory electron transport chain, the activity of complex IV and cytochrome oxidase ratio is reduced. Propofol should be used with caution for sedation in critically ill children and adults, as well as for long-term anesthesia in otherwise healthy patients, and doses exceeding 4-5 mg/kg/h for long periods (>48 h) should be avoided. If PRIS is suspected, propofol must be stopped immediately and cardiocirculatory stabilization and correction of metabolic acidosis initiated. So, PRIS must be kept in mind as a rare, but highly lethal, complication of propofol use, not necessarily confined to its prolonged use. Furthermore, the safe dosage of propofol may need re-evaluation, and new studies are needed.