Ioannis Bougioukas

Adenocarcinoma in pulmonary sequestration.

A 67-year-old male smoker presented with hemoptysis and recurrent pneumonia. Chest computed tomography showed an emphysematous cyst and air-fluid level cavities in the left lower lobe. A left lower lobectomy was performed. The intraoperative finding was intralobar sequestration. Histopathology revealed adenocarcinoma within the sequestrated lobe. Only 8 cases of lung cancer and sequestration have been reported since 1963.

Is there a correlation between late re-exploration after cardiac surgery and removal of epicardial pacemaker wires?

BackgroundRe-exploration for bleeding accounts for increased morbidity and mortality after major cardiac operations. The use of temporary epicardial pacemaker wires is a common procedure at many departments. The removal of these wires postoperatively can potentially lead to a serious bleeding necessitating intervention.MethodsFrom Jan 2011 till Dec 2015 a total of 4244 major cardiac procedures were carried out at our department. We used temporary epicardial pacemaker wires in all cases. We collected all re-explorations for bleeding and pericardial tamponade from our surgical database and then we focused on the late re-explorations, meaning on the 4th postoperative day and thereafter, trying to identify the removal of the temporary pacemaker wires as the definite cause of bleeding. Patients’ records and medication were examined.ResultsThirty-nine late re-explorations for bleeding, consisting of repeat sternotomies, thoracotomies and subxiphoid pericardial drainages, were gathered. Eight patients had an acute bleeding incidence after removal of the temporary wires (0.18%). In four of these patients, a pericardial drainage was inserted, whereas the remaining patients were re-explorated through a repeat sternotomy. Two patients died of the acute pericardial tamponade, three had a blood transfusion and one had a wound infection. Seven out of eight patients were either on dual antiplatelet therapy or on combination of aspirin and vitamin K antagonist.ConclusionsA need for re-exploration due to removal of the temporary pacemaker wires is a very rare complication, which however increases morbidity and mortality. Adjustment of the postoperative anticoagulation therapy at the time of removal of the wires could further minimize or even prevent this serious complication.

Intrapleural r-tPA in association with low-molecular heparin may cause massive hemothorax resulting in hypovolemia.

The use of intrapleural instillation of recombinant tissue plasminogen activator (r-tPA) in the treatment of pleural infection may increase pleural fluid drainage associated with a clinical and imaging improvement, leading to a faster resolution. The use of r-tPA is generally well tolerated. Here we report 2 cases of massive pleural hemorrhage resulting in life-threatening hypovolemia, in 2 patients treated with intrapleural r-tPA for a pleural infection, who were simultaneously receiving systemic anticoagulation (1 therapeutic, the second prophylactic) with low-molecular weight heparin. It appears that the decision of treating pleural infection with r-tPA in patients receiving therapeutic or prophylactic systemic anticoagulation must be well balanced and in case of association of these compounds, close monitoring is necessary.

Attenuation of Propofol Tolerance Conferred by Remifentanil Co-Administration Does Not Reduce Propofol Toxicity in Rabbits Under Prolonged Mechanical Ventilation

BACKGROUND Prolonged sedation with propofol at high doses may lead to fatal multi-organ dysfunction, know as propofol infusion syndrome. We tested the hypothesis that propofol plus remifentanil co-administration attenuates propofol tolerance to its sedative effect and assessed if such an effect has an impact on propofol toxicity in rabbits under prolonged mechanical ventilation. MATERIALS AND METHODS Eighteen healthy male rabbits were mechanically ventilated and received propofol (group P, n = 6), propofol plus remifentanil (group PR, n = 6), or remifentanil plus sevoflurane (group RS, n = 6) in order to be kept under sedation (group P) or sedation/analgesia (groups PR and RS) for up to 48 h. Initial propofol and remifentanil infusion rates (IRs) were adjusted, if needed, to maintain the desired level of sedation and analgesia, respectively (groups P and PR). In group RS, remifentanil was infused at IRs equivalent to those of group PR. Propofol IRs were recorded, propofol concentrations were measured in the arterial plasma, and blood biochemical parameters and organ histopathology were assessed. RESULTS Animals survived for 29-36 h in group P and 22-38 h in group PR (100% mortality rate). Tolerance was developed to propofols sedative effect. The onset of tolerance was delayed and its magnitude was decreased in group PR compared with group P. Propofol was accumulated in the systemic circulation. Propofol clearance rate was gradually decreased. Arterial lactate, and serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH), bilirubin, cholesterol, triglycerides, and creatine kinase (CK) levels were increased. The heart, lungs, liver, gallbladder, kidneys, urinary bladder, and skeletal muscles were seriously injured in groups P and PR. In group RS, mortality was 0%, while there was only mild injury of the lungs, liver, gallbladder, kidneys, and urinary bladder. CONCLUSIONS Although propofol tolerance is attenuated in propofol plus remifentanil receiving rabbits under prolonged mechanical ventilation, fatal multi-organ injury occurs resembling human propofol infusion syndrome.

Coronary artery bypass surgery in a patient with Kartagener syndrome: a case report and literature review

Kartagener syndrome consists of congenital bronchiectasis, sinusitis, and total situs inversus in half of the patients. A patient diagnosed with Kartagener syndrome was reffered to our department due to 3-vessel coronary disease. An off-pump coronary artery bypass operation was performed using both internal thoracic arteries and a saphenous vein graft. We performed a literature review for cases with Kartagener syndrome, coronary surgery and dextrocardia. Although a few cases of dextrocardia were found in the literature, no case of Kartagener syndrome was mentioned.

Surgical Myectomy after Failed Ablation for Hypertrophic Obstructive Cardiomyopathy

Background Hypertrophic cardiomyopathy is a genetic disease of the myocardial sarcolemma characterized by left ventricular hypertrophy. When obstruction to the left ventricular outflow tract is present and symptoms are refractory to medication, surgical myectomy or alcohol septal ablation is indicated. Case Description We report a case of a patient presented for myectomy due to recurrence only 1 year after alcohol ablation. Interesting findings were a firm subaortic membrane and a direct insertion of the papillary muscle into the mitral valve. Conclusion After myectomy and extensive papillary muscle mobilization, a significant relief of obstruction was achieved.

Extended thoracic manifestation of neurofibromatosis Type 1

A 38-year-old woman with history of multiple neurofibromatoses and surgery for an abdominal mass 4 years earlier, presented with dyspnea. Chest computed tomography showed a lesion in the right hemithorax (Figure 1) and loculated effusion in the mediastinum (Figure 2). She underwent decortication of the pleura. Biopsy of the mass revealed neurofibromatosis Type 1. Asian Cardiovascular & Thoracic Annals 20(3) 350 The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492311406607 aan.sagepub.com