Organ dysfunction after cardiopulmonary bypass. A systemic inflammatory reaction initiated by the extracorporeal circuit.
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Biomedical subjects
Publications and source records attributed to S Westaby.
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A 22-year-old woman with an irresectable tracheal cylindroma asphyxiated during radiotherapy. Extracorporeal oxygenation was used to facilitate endotracheal resection and the insertion of a tracheobronchial stent.
Cardiopulmonary bypass (CPB) is associated with activation of humoral systems, which results in the release of proteases. These proteases may affect platelets and stimulate granulocytes. In the present study, the protease inhibitor aprotinin was given in high doses to 11 patients to achieve plasma concentrations of more than 150 kallikrein inactivator units per milliliter during CPB. At such concentrations, kallikrein and plasmin are effectively inhibited. This treatment resulted in platelet preservation during CPB. Platelet numbers were virtually unaffected, and thromboxane release was prevented in the aprotinin-treated group in contrast to the control group. Postoperatively, hemostasis was significantly better preserved after aprotinin treatment (blood loss of 357 ml in the treated group versus 674 ml in the untreated group; p less than 0.01). Since tissue-plasminogen activator activity was similar in both groups, the improved hemostasis most likely should be attributed to platelet preservation. Furthermore, aprotinin lessened neutrophilic elastase release, which might contribute to decreased pulmonary dysfunction in patients at risk.
One hundred consecutive patients undergoing coronary artery bypass surgery were randomly allocated to a preoperative (24 h) intravenous infusion of isosorbide dinitrate (1.5-15 mg/hr) (50 patients) or to placebo (50 patients). The characteristics of the two groups were similar. Evidence of acute myocardial ischaemia was sought by continuous electrocardiographic Holter recordings and acute myocardial infarction by the appearance of new Q waves and increased activity of the creatine kinase MB isoenzyme. Episodes of acute myocardial ischaemia were found in 18% of patients in the control group and in none of those who received isosorbide dinitrate. None the less, the frequency of perioperative myocardial infarction was similar (22% and 18% respectively) in the two groups. Perioperative infarction was significantly more common in women, in patients with unstable angina or poor left ventricular function, in those who had coronary endarterectomy, and in those in whom the aortic clamping time was greater than 50 minutes. These factors may have obscured any effect that prevention of preoperative ischaemia had on perioperative infarction. Preoperative infusion of isosorbide dinitrate eliminated preoperative ischaemia but did not influence the occurrence of perioperative infarction. The probable benefits of prevention of preoperative ischaemia on postoperative left ventricular function, which is a determinant of long term survival, remain to be established.
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The clinical features of Dressler's syndrome which developed in a patient following a third myocardial infarction responded to a short course of prednisolone. However, angina at rest precipitated urgent coronary artery bypass surgery and pericardectomy.
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Detection of perioperative myocardial infarction following coronary artery bypass graft surgery may be difficult. To assess the value of cross-sectional echocardiography in detecting perioperative infarction, 45 patients were studied by this technique to assess left ventricular regional wall motion before and eight to ten days after cardiac surgery. Deterioration in septal, antero-lateral, apical, inferior and posterior segments was correlated with Q-wave change in the ECG and with CK-MB taken at pre, 4, 7, 21, 48 and 72 hours post surgery. Echocardiographic regional wall motion was assessed semiquantitatively by a point score system (3 = normal, 2 = hypokinetic, 1 = akinetic, 0 = dyskinetic). Sixteen patients showed deterioration in regional wall motion greater than or equal to 1 point. Eleven of these patients had new hypokinetic abnormalities of 1 point in the previously normal septal segment, but no ECG infarction. Three of the 11 had raised CK-MB and only one fulfilled the CK-MB criteria for perioperative infarction. Four other patients showed new akinetic segments (deterioration of two points). All four had CK-MB criteria for perioperative infarction and three had new ECG Q-wave. Three other patients showed ECG infarction without echo or CK-MB changes. Thus the development of a new akinetic segment on cross-sectional echocardiographic analysis of regional wall motion is a good marker of perioperative myocardial infarction. However, the great majority of new septal hypokinetic segments do not result from this operative complication.
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A four month old infant was investigated for heart failure was found to have mitral incompetence and severe subvalvar aortic stenosis. The left ventricular outflow tract obstruction was found to be due to an anatomically anomalous mitral valve. The obstruction could only be relieved by removal of the mitral valve and its replacement with a St Jude's prosthesis. Two years after operation the child is fit and active. There have been no difficulties with anticoagulant treatment.
We investigated the degree and time course of neutrophil sequestration into human lungs during cardiac operations. At the same time, measurement of the concentration of peroxidation products in the plasma was used as an index of oxidant free radical activity. The study was performed in two groups of patients. Group A (n = 11) had studies extending over the entire operative period and showed a highly significant sequestration of neutrophils into the lung, together with a highly significant (p less than 0.001) rise in peroxidation products from 2.8 +/- 0.12 nmol/ml(mean +/- standard error of the mean)before bypass to a peak of 5.05 +/- 0.13 nmol/ml at the end of bypass. As these changes occurred only during the time after release of the aortic cross-clamp, we investigated this period in more detail in a second group of patients (Group B, n = 7). Results from this group showed that significant release of peroxidation products occurred at the same time as pulmonary neutrophil sequestration. This study has produced evidence of increased oxidant activity in the lung associated with cardiac operations. Nevertheless, it is not known whether the neutrophils sequestered into the lung alone induced the increased activity. Similarly, whether neutrophil-derived oxidant species are the sole cause of lung tissue injury remains unproved.
A 35-year-old white woman with anomalous origin of the left coronary artery from the pulmonary artery had infective endocarditis and severe mitral regurgitation. She survived mitral valve replacement and occlusion of the anomalous left main stem, but subsequently deterioration of her condition necessitated urgent saphenous vein bypass grafts to the left anterior descending and circumflex coronary arteries. Pulmonary hypertension with raised right ventricular end-diastolic pressure probably compromised collateral flow from the right to the left coronary systems.
The potent anaphylatoxin C3a was measured in the peripheral blood of eleven patients receiving radiocontrast agents whilst undergoing coronary angiography. In seven patients C3a levels were raised during this procedure and in three of these the anaphylatoxin was increased between four and tenfold. In four patients C3a levels remained within the normal range. In vitro tests of five contrast agents revealed marked heterogeneity in their ability to generate C3a from serum.
In 120 patients subjected to coronary artery surgery we have investigated employment status and work capability in relation to age, pre-operative ventricular function and extent of coronary artery disease, peri-operative infarction and post-operative angina. The patients were followed up for 6 to 23 months (mean 10 months). Fifty-three out of 74 patients (72%) employed before the onset of angina, returned to work after operation. Return to work was more likely in patients working immediately prior to surgery and in patients less than 45 years old (P less than 0.05). Sixty patients (50%) reported a return to normal work capability, the most striking changes occurring in those less than 45 years old (P less than 0.02). Pre-operative left ventricular (LV) function and extent of coronary disease and mode of employment did not correlate with post-operative employment status but normal LV function was related to improvement in work capability (P less than 0.02). Return to work after coronary bypass surgery is mainly due to angina relief but is also related to age and pre-operative work status.
One hundred and six patients were analysed in order to assess the effect of a more aggressive surgical policy in relation to the delays in diagnosis of infective endocarditis. The average duration of symptoms before diagnosis was 9.7 weeks, even though the patients had sought medical advice at a relatively early stage of their illness (2.2 weeks). Three of the 29 (10.3%) patients who were treated surgically died and all three were operated upon five weeks or later after diagnosis. Seventy-seven patients did not have surgery and 15 died (19.5%). The outcome of surgical treatment for prosthetic valve endocarditis was no worse than for native valve endocarditis. The mortality of prosthetic valve endocarditis including early infections was 32% with medical but only 10% with surgical management compared with 14.5% and 10.5% in native valve endocarditis. Endocarditis cannot always be prevented but earlier diagnosis would reduce mortality and prevent complications. When medical treatment is failing then surgery should be considered early and urgently particularly in staphylococcal infection or when large mobile vegetations are recognized; surgery is mandatory in fungal endocarditis. Earlier diagnosis would greatly reduce the current high incidence of surgery, but that depends on a much heightened index of suspicion amongst both general practitioners and hospital physicians.
A case is presented of a 36-year old female who presented with signs of mitral regurgitation due to infective endocarditis. Investigation revealed an anomolous left coronary artery arising from pulmonary artery. She successfully underwent mitral valve replacement. Survival following mitral valve replacement and presentation with endocarditis have never been reported in this rare condition.
A 2 1/2 year old boy had a sudden, severe, and unexpected anaphylactoid reaction after an otherwise uncomplicated repair of a partial atrioventricular septal defect. The reaction, comprising haemorrhagic pulmonary oedema and peripheral circulatory collapse, followed neutralisation of heparin by protamine. Measurements of serum complement (C3 and C4) concentrations suggested that a pronounced consumption of complement occurred during the adverse response.
To evaluate the role of ischaemia in the genesis of new septal wall motion abnormalities after coronary artery bypass surgery 45 patients were studied by cross sectional echocardiography before and 8-10 days after operation. Regional left ventricular wall motion was classified as normal, hypokinetic, akinetic, or dyskinetic. Septal wall motion abnormalities were correlated with electrocardiographic Q wave changes and serial serum MB creatine kinase measured before and 4, 7, 21, 48, and 72 hours after operation. Of the 14 patients who developed new septal wall motion abnormalities after operation two developed septal akinesis (both had perioperative infarction) and one new dyskinesis in the previously akinetic septal segment. Of the 11 patients with new septal hypokinesis, eight had normal serial creatine kinase MB values, two had raised values peaking four and seven hours after operation, with a return to normal values at 21 hours indicating transient ischaemia, and one had enzymatic criteria for perioperative infarction. Most new echocardiographic septal wall motion abnormalities after coronary artery bypass grafting are not caused by transient ischaemia, perioperative infarction, or generalised cell necrosis.