Changes in pericardial morphology and fibrinolytic activity during cardiopulmonary bypass.

The presence of pericardial adhesions at resternotomy not only increases the operation time but also increases the risk of serious damage to the heart, great vessels, and extracardiac grafts. The reported prevalence of damage is 2% to 6%. The fibrinolytic activity of pericardial tissue may be a crucial factor in determining the extent of adhesion formation following primary operation. Ten patients undergoing cardiac operations were studied to assess the plasminogen activating activity of homogenates of pericardial tissue samples. Samples were taken at three times during the operation and the plasminogen activating activity was measured by means of a standard fibrin plate technique. Tissue-type plasminogen activator, urokinase-type plasminogen activator, plasminogen activator inhibitor-1, and plasminogen activator inhibitor-2 were also measured by means of enzyme-linked immunosorbent assays. Compared with its initial levels (median 2.06 IU/cm2, range 1.28 to 6.48 IU/cm2), the plasminogen activating activity of pericardial biopsy tissue was significantly reduced at 75 minutes (median 0.64 IU/cm2, range 0.12 to 2.44 IU/cm2, p < 0.01) and at 135 minutes (median 1.45 IU/cm2, range 0.12 to 4.39 IU/cm2, p < 0.05). The major plasminogen activator present was tissue-type plasminogen activator. Compared with its initial levels (median 2.34 ng/ml, range 1.03 to 6.42 ng/ml), subsequent tissue-type plasminogen activator values were also significantly reduced at 75 minutes (median 0.83 ng/ml, range 0.75 to 5.13 ng/ml, p < 0.005) and at 135 minutes (median 1.24 ng/ml, range 0.75 to 6.67 ng/ml, p < 0.05). Low levels of urokinase-type plasminogen activator were found in 5 of 10 patients. However, neither plasminogen activator inhibitor-1 nor plasminogen activator inhibitor-2 was detected. Examination with a light microscope showed both increasing pericardial mesothelial damage and increasing features of acute inflammatory changes with time. This study shows that plasminogen activating activity is present in pericardial tissue and that tissue-type plasminogen activator is the major plasminogen activator. The observed inflammatory changes and concomitant damage to the pericardial mesothelium, and the significant reductions in pericardial tissue-type plasminogen activator and plasminogen activating activity seen during cardiac operations, may be important factors contributing to the early development of pericardial adhesions.

Perioperative histologic and ultrastructural changes in the pericardium and adhesions.

The presence of pericardial adhesions prolongs the operation time and increases the risk of serious damage to the heart and other major vascular structures during resternotomy. The reported incidence of such damage is 2% to 6%. Pericardial mesothelial cells exhibit fibrinolytic activity, and therefore have an actual or potential role in the breakdown of the fibrinous adhesions that serve as the initial scaffolding for the firm collagenous adhesions seen at reoperation. Ten patients undergoing primary cardiac procedures were studied to assess the morphologic changes that take place within the pericardium and to relate these to accompanying changes in the pericardial plasminogen activating activity. Samples were taken at 0, 75, and 135 minutes after pericardiotomy. Compared with samples obtained at the time of pericardiotomy, those taken at 75 and 135 minutes demonstrated a significant progression in the mesothelial cell damage (p < 0.01), together with increasing evidence of pericardial inflammation (p < 0.01). The findings from electron microscope studies confirmed and supplemented these findings. Furthermore, compared with its initial levels (median, 2.06 IU/cm2; range, 1.28 to 6.48 IU/cm2), the plasminogen activating activity of pericardial biopsy specimens was significantly reduced at 75 minutes (median, 0.64 IU/cm2; range, 0.12 to 2.44 IU/cm2; P < 0.05), with some recovery at 135 minutes (median, 1.45 IU/cm2; range, 0.12 to 4.39 IU/cm2; p = 0.059). This study has revealed that, during cardiac procedures, the pericardium undergoes inflammatory changes with concomitant damage to its mesothelium, together with a reduction in the pericardial mesothelial fibrinolytic potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Malignant peripheral nerve sheath tumour: a rare tumour and an unusual intrapericardial presentation.

A 62-year-old man presented with superior vena caval obstruction and was found to have a tumour in the pericardial cavity. This was diagnosed as a Malignant Peripheral Nerve Sheath Tumour (MPNST), an uncommon sarcoma that is exceedingly rare in this location. Stigmata of von Recklinghausen's disease were absent. Antibodies to a panel of immunoreactive markers were utilised to establish the diagnosis and exclude other tumours. The utility of such an approach in this kind of situation is briefly discussed.

Sleep apnoea/hypopnoea syndrome: a potential cause of graft failure following heart transplantation.

A 54-year-old man presented 54 months after a successful heart transplant with cor pulmonale secondary to obstructive sleep apnoea/hypopnoea syndrome (SAHS). This unusual cause of reversible graft failure following heart transplantation is presented in this case report.

Postoperative adhesion formation and the use of adhesion preventing techniques in cardiac and general surgery.

The formation of postoperative adhesions is an inevitable sequel to surgical intervention, and, as part of the healing process, they are often beneficial. Nevertheless, the presence of adhesions may impose postoperative and reoperative surgical problems. An overview of some of the attempts to overcome such problems is presented, and the research surrounding them is discussed.

Time relationships in the diagnosis and treatment of left-atrial myxoma.

The records of 40 patients, 28 females and 12 males with a median age of 49 years (range 13-80 years), undergoing excision of left-atrial myxoma at 3 London hospitals during a 21-year period were reviewed. The urgency of treatment is discussed, and the interval between the onset of symptoms and diagnosis (median 38 weeks), and also between diagnosis and surgery (< 48 hours) is considered.

Malignant change in a chronic skin lesion induced by an intravenous cannula.

A cutaneous wound subjected to continuous irritation has an increased potential for malignant degeneration. The types of trauma that may give rise to the initial injury are diverse and have been well documented. We report a case of one such lesion in a 65-year-old man who had a persistent right forearm wound for over three years. The wound arose from the site of venous cannula puncture. Malignant transformation occurred in a manner comparable to that seen in other chronic lesions (Marjolin's ulcer).

Pleural abrasion: a new method of pleurodesis.

Sixty patients (48 male, 12 female; median age 32 (range 16-72) years) underwent pleural abrasion for persistent or recurrent pneumothorax. Fifty patients had recurrent pneumothorax and 10 persistence of a first pneumothorax despite conservative treatment; two had bilateral pneumothoraces. Pleural abrasion was carried out with a domestic nylon scouring pad and blebs or bullae were ligated or stapled and excised. Intercostal drainage was discontinued after a median time of two days, median serosanguinous loss was 250 ml, and the median postoperative stay in hospital was four days. During the median follow up period of 32 (range 19-52) months pneumothorax has recurred in one patient.

Spontaneous contralateral pneumothorax following pneumonectomy.

A case of a spontaneous pneumothorax occurring three days post-pneumonectomy is presented. Difficulties in diagnosis and management are discussed.

An expansible cannula: a new technique for chest drain insertion.

The insertion of a chest drain into the pleural space is a common procedure used by many specialties. The commonly used device is a prepacked, sterile plastic tube with its own central metal trocar. Complications may arise during its insertion, with the occasional penetration of intrathoracic and upper abdominal organs. As most chest drains are inserted by junior and relatively inexperienced doctors, it is therefore imperative that a simple, safe, and effective technique of insertion is found. A device has been developed that consists of a 5 cm conical length of an expansible cannula, made from rolled metal foil, which when inserted into the chest reaches only a few millimetres within the pleura. When an expander tube, 10 mm in diameter, is passed through the device from its proximal end the conical tube is distended into a hollow cylindrical one, through which a standard Portex chest catheter is passed. The whole appliance is then removed over the end of the tube, leaving the drain in situ. The efficacy of this unique device has been tested in a pilot study in 22 patients. There have been no complications.

Surgical management of spontaneous pneumothorax.

Despite the promising potential of video-assisted thoracoscopic pleurectomy in the treatment of pneumothoraces, conventional surgical intervention by a thoracotomy and pleurodesis with ligation/stapling of bullae remains the main form of treatment in many hospitals. It is with this in mind that we present our experience of 250 patients who have undergone surgical pleurodesis for treatment of a persistent or recurrent spontaneous pneumothorax. Of these patients, 74 had undergone parietal pleurectomy (PP), 93 pleural abrasion (PA), 60 transaxillary apical pleurectomy (TAP), and 23 had undergone apical pleurectomy via a posterolateral or submammary thoracotomy (APT). In general, there were few complications and we could show no discernible difference in the rate of complications between the groups. Despite there being no significant difference in the median period of postoperative intercostal tube drainage, there was a significant difference between the groups in the number of patients with a postoperative hospital stay equal to or greater than seven days and a postoperative serosanguinous volume loss greater than 500 ml. Those patients that had undergone parietal pleurectomy tended to remain in hospital for a longer period (> or = 7 days) and to have a heavier serosanguinous volume loss (> 500 ml). There have been no recurrent cases in the PP and APT groups. Their respective median follow up periods are 62 (range 15-83) and 32 (range 15-54) months. The median follow up period in the PA group was 42 (range 13-69) months, one recurrence occurred after 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical experience with heparin-coated cardiopulmonary bypass circuits.

The extensive area of contact between blood and synthetic surfaces during cardiopulmonary bypass results in the activation of the kallikrein, the complement and the clotting and fibrinolytic systems. This results in white cell activation and a whole body inflammatory response. Pulmonary neutrophil sequestration is also known to occur during cardiopulmonary bypass and has been associated with pulmonary damage. This has been previously demonstrated using the technique of differential neutrophil counts in simultaneous venous and left atrial samples. The efficacy of retinal fluorescein angiography as an indicator of cerebral microembolism has also been proved in previous studies. The objectives of this study were to determine whether heparin precoating with Duraflo II reduced pulmonary neutrophil sequestration, retinal microembolism and postoperative blood loss. Fourteen patients were randomized into two groups using either heparin-coated or nonheparin-coated cardiopulmonary bypass circuits. The preliminary results suggest a reduction in pulmonary neutrophil sequestration (p greater than 0.05) and the generation of thrombin antithrombin complexes (p less than 0.05). Retinal microembolism was not significantly different in the two groups nor was the postoperative blood loss. Thus, heparin-coated cardiopulmonary bypass circuits do not reduce pulmonary neutrophil sequestration, retinal microembolism or postoperative blood loss.

Pericardial substitution after cardiopulmonary bypass surgery: a trial of an absorbable patch.

Primary closure of the pericardium affords some protection against adhesion formation and the consequent hazards of resternotomy. However, its completion may be impractical and hazardous, and therefore the pursuit of an ideal pericardial substitute has prompted much research. Twenty calves were divided into 3 groups for the study. All animals underwent right posterolateral thoracotomy. The test group (group X), consisting of 6 animals, received a poly-beta-hydroxybutyrate patch (PHB) to close the pericardium following cardiopulmonary bypass (CPB). In group Y (9 animals) the pericardium was left open following CPB. Group Z (5 animals) also had their pericardium left open but did not undergo CPB (non-CPB). The plasminogen activating activity (PAA) of homogenates of pericardial tissue samples were measured in 5 animals in group X, and 5 in group Z. Samples were taken at three time points from the time of pericardiotomy, and at reoperation 4 weeks later. In group X (CPB) there was a significant reduction in the PAA during the operation with some recovery at reoperation. The reduction in the pericardial PAA of group Z (non-CPB) animals did not reach significance. For both group X and group Z the progress of mesothelial damage, compared with that at zero time, showed a significant increase. In addition, their pericardial inflammatory features became more apparent in the later samples but more significantly in group Z. This study demonstrated no significant short-term differences in adhesion formation or postoperative coronary anatomy visibility between any of the groups. At reoperation the patch material contained pronounced macrophage activity but no regenerative mesothelium. There were no infective episodes in any of the animals studied. Furthermore, this study suggests that CPB in comparison to non-CPB has a significant affect on pericardial PAA.

Pericardial trauma and adhesions in relation to reoperative cardiac surgery.

In an attempt to appreciate the changes that favour adhesion formation we compared the morphological and fibrinolytic changes that occur in human primary and reoperative pericardium. Ten patients undergoing primary elective open heart surgery and ten undergoing first time reoperative open heart surgery were studied. Pericardial samples were taken at four time points. At 0 (time A) and 30 (time B) minutes from the time of pericardiotomy (before the commencement of CPB), 30-50 minutes (time C) after the commencement of CPB, and then finally 10 minutes (time D) after the patient had been rewarmed. The fibrinolytic activity, as measured by the plasminogen activating activity (PAA), in the pericardial samples of the ten primary cases was compared with that in 5 of the reoperative cases. For the primary group, the PAA after 30 minutes of exposure (median 6.65 IU/cm2, range 3.85-11.89 IU/cm2, p = 0.14, n = 10) was not significantly reduced when compared to the initial activity (median 8.74 IU/cm2, range 2.22-17.68 IU/cm2, n = 10). After 30-50 minutes CPB the PAA was significantly reduced (median 3.93 IU/cm2, range 1.5-13.24 IU/cm2, p = 0.028, n = 10) and still reduced after rewarming for 10 minutes (median 3.12 IU/cm2, range 0.88-19.93 IU/cm2, p = 0.047, n = 10). The simultaneous plasma tissue-type plasminogen activator activity showed a significant (p < 0.05) increase after 30-50 minutes bypass with a later decline. The changes in the reoperative pericardial PAA were similar. In addition, the degree of PAA in reoperative pericardium was consistently lower than that observed in primary tissue. The extent of primary pericardial mesothelial damage at times B, C, and D compared with that at time A showed a significant (p < 0.01 for times B, C, and D) increase. Similarly there was a significant worsening of the degree of inflammation. Compared with primary pericardium, the reoperative samples showed a significant (p < 0.01 for times A, B, and C) preponderance of damaged mesothelium at the earlier stages of the operation. It appears that, following the initial bypass surgery, the processes that cause pericardial and mesothelial healing with recovery of PAA compete with those leading to pericardial adhesions and fibrosis. The histological and biochemical outcome seen in reoperative pericardium is the result of these competitive actions.