Jaundice following cardiopulmonary bypass

Serial liver function tests were performed in 29 adult patients following cardiopulmonary bypass for various open-heart procedures. In 22 patients there was a rise in serum bilirubin above 1·5 mg./100 ml., with clinical jaundice in 19 and bilirubinuria in 15 patients. The incidence of jaundice was related to age, the severity of pre-operative cardiac failure, and the duration of perfusion. Possible mechanisms for jaundice are discussed, and evidence is presented that liver damage may follow extracorporeal circulation.     

Carbamazepine-related hyponatremia following cardiopulmonary bypass

A 67-year-old man on long-term carbamazepine therapy underwent elective coronary artery bypass grafting. Following an initially uncomplicated recovery, he developed symptomatic hyponatremia. The symptoms and biochemical abnormality improved after gradual discontinuation of carbamazepine. We discuss the association between carbamazepine and hyponatremia and the causes of hyponatremia after cardiopulmonary bypass. Surgeons should consider stopping carbamazepine before operations with cardiopulmonary bypass.     

Occipital alopecia following cardiopulmonary bypass.

Postoperative alopecia is a minor complication of surgery but a cosmetic disaster to the patient. Over a 3 year period, 60 cases of occipital alopecia were discovered in patients following open-heart surgery and 5 cases on other surgical services. In contrast to previous reports, 29 patients had alopecia one year later, presumed to be permanent. Extensive operations, with prolonged recovery and elective overnight mechanical ventilation, were common to all. Retrospective analysis and prospective studies clearly demonstrated that localized scalp pressure was the cause of the alopecia and that the duration of pressure determined the extent of the damage. Moving the patient's head at regular intervals during operation and recovery eliminated the alopecia. The type of head rest used did not modify the development of alopecia. Electrical injury and the use of heparin, hypothermia, electrocautery, or hypotension were eliminated as possible causes. Conclusive evidence correlating periperative events with the formation of pressure sores in man has not been previously reported.     

End-tidal CO2 for prediction of cardiac output following weaning from cardiopulmonary bypass

This prospective study included 32 patients undergoing cardiopulmonary bypass (CPB) for elective coronary artery bypass grafting correlates the respiratory end-tidal CO2 (ETCO2) during partial separation from CPB with cardiac output (CO) following weaning from CPB. After induction of general anesthesia, a pulmonary artery catheter was inserted for measurement of cardiac output by thermodilution. Patients were monitored using a 5-lead ECG, pulse oximeter, invasive blood pressure monitoring, rectal temperature probe, and end-tidal capnography. At the end of surgery, patients were weaned from CPB in a stepwise fashion. Respiratory ETCO2 and in-line venous oximetry were continuously monitored during weaning. The ETCO2 was recorded at quarter pump flow and after complete weaning from CPB. Following weaning from CPB, CO was measured by thermodilution. The CO values were correlated with the ETCO2 during partial bypass and following weaning from bypass. Regression analysis of ETCO2 at quarter-flow and post-bypass CO showed significant correlation (r = 0.57, p < .001). Also, regression analysis of ETCO2 after complete weaning from bypass and post-bypass CO showed significant correlation (r = 0.6, p = .002). The correlation between ETCO2 and CO showed that an ETCO2 >30 mm Hg during partial CPB will always predict an adequate CO following weaning from CPB. An ETCO2 <30 mm Hg may denote either a low or a normal cardiac output and hence other predictive parameters such as SvO2 must be added.     

Myocardial function following cardiopulmonary bypass.

Twenty-one patients have been studied in the 48 h after valve replacement to determine the possible contribution of abnormalities of left ventricular myocardial blood flow and oxygen consumption to the impaired cardiac performance which is sometimes evident in such patients. In the 14 patients making an uneventful recovery (Group A) the mean values for blood flow and oxygen consumption were both higher than in resting man, while the arterio-coronary sinus oxygen content difference was narrowed, with a high coronary sinus oxygen tension. Five patients had a low cardiac output (Group B) and had similar levels of blood flow and oxygen consumption to Group A, while the coronary sinus oxygen content and tension were reduced. When the heart rate was increased by pacing (Group C) myocardial oxygen consumption increased but coronary blood flow failed to rise, while the arterio-coronary sinus oxygen content difference widened slightly. It is concluded that the low postoperative cardiac output is not due to low coronary blood flow or myocardial oxygen supply, but these patients have a limited ability to increase their already high coronary blood flow. Therefore any increase in oxygen demand may be met by the potentially detrimental mechanism of widening the arterio-coronary sinus difference, with lower coronary sinus and tissue oxygen tension.     

Pulmonary lactate release following cardiopulmonary bypass

Objective: The etiology of lung injury following cardiopulmonary bypass (CPB) is multifactorial. Our study focused on quantifying the lactate release from the lungs precipitated by extracorporeal circulation at different time points after the insult. This was complemented by an evaluation of the gas exchange at the level of the alveolar–capillary membrane. Methods: Forty consecutive patients (age 61 ± 11 years, EuroScore 4.7 ± 2.7) undergoing CABG were prospectively analyzed. The data are presented as medians and the interquartile range. Results: The pulmonary lactate release (PLR) increased from a baseline value of 0.033 (range −0.077 to 0.170) to 0.465 mmol/min/m² (range 0.113–0.922), which was seen 6 h postoperatively (P < 0.001). The A-a O₂ gradient increased from 12.7 (range 8.8–15) to 39.1 kPa (range 30.3–46.5) upon discontinuation of CPB (P < 0.001). The systemic arterial lactate (L_S) concentration increased from 1.22 (range 1–1.44) to 3.03 mmol/l (range 2.29–4.76) 6 h after surgery (P < 0.001). The veno-arterial pCO₂ difference (V-A dpCO₂) rose from 0.6 (range 0.5–0.9) to 0.9 kPa (range 0.7–1) (P = 0.014). The mortality in the studied group was 5% (2/40). Conclusions: The lungs were found to be a significant source of lactate, and this pulmonary lactate flux was accentuated by CPB. The PLR correlated with systemic hyperlactatemia as well as the A-a O₂ gradient, and was found to be higher in patients requiring prolonged mechanical ventilatory support. The duration of CPB had a significant impact on the systemic lactate concentrations, V-A dpCO₂ and the A-a O₂ gradient, but not on the PLR.     

Postoperative microcirculatory perfusion and endothelial glycocalyx shedding following cardiac surgery with cardiopulmonary bypass

We investigated microcirculatory perfusion disturbances following cardiopulmonary bypass in the early postoperative period and whether the course of these disturbances mirrored restoration of endothelial glycocalyx integrity. We performed sublingual sidestream dark field imaging of the microcirculation during the first three postoperative days in patients who had undergone on-pump coronary artery bypass graft surgery. We calculated the perfused vessel density, proportion of perfused vessels and perfused boundary region. Plasma was obtained to measure heparan sulphate and syndecan-1 levels as glycocalyx shedding markers. We recruited 17 patients; the mean (SD) duration of non-pulsatile cardiopulmonary bypass was 103 (18) min, following which 491 (29) ml autologous blood was transfused through cell salvage. Cardiopulmonary bypass immediately decreased both microcirculatory perfused vessel density; 11 (3) vs. 16 (4) mm.mm⁻², p = 0.052 and the proportion of perfused vessels; 92 (5) vs. 69 (9) %, p < 0.0001. The proportion of perfused vessels did not increase after transfusion of autologous salvaged blood following cardiopulmonary bypass; 72 (7) %, p = 0.19 or during the first three postoperative days; 71 (5) %, p < 0.0001. The perfused boundary region increased after cardiopulmonary bypass; 2.2 (0.3) vs. 1.9 (0.3) μm, p = 0.037 and during the first three postoperative days; 2.4 (0.3) vs. 1.9 (0.3) μm, p = 0.003. Increased plasma heparan sulphate levels were inversely associated with the proportion of perfused vessels during cardiopulmonary bypass; R = −0.49, p = 0.02. Plasma syndecan-1 levels were inversely associated with the proportion of perfused vessels during the entire study period; R = −0.51, p < 0.0001. Our study shows that cardiopulmonary bypass-induced acute microcirculatory perfusion disturbances persist in the first three postoperative days, and are associated with prolonged endothelial glycocalyx shedding. This suggests prolonged impairment and delayed recovery of both microcirculatory perfusion and function after on-pump cardiac surgery.     

Emergency reinstitution of cardiopulmonary bypass following cardiac surgery: outcome justifies the cost

Objective: Crash back on bypass (crash-BOB) is occasionally required in the resuscitation of patients developing life-threatening complications following cardiac surgery. This study aims to determine the incidence, aetiology and cost-effectiveness of such intervention. Methods: Retrospective review of all crash-BOB patients over 5.5 years at one hospital. Results: The incidence of crash-BOB was 0.8% and occurred at a mean of 7 h post-operatively (range 1 h–20 days). Pre-operative Parsonnet scores were similar to the overall population of patients undergoing surgery in our institution (mean score 10; range 0–45). The original cardiac operations were coronary revascularization (39), valve surgery (12) and others (4). Indications for crash-BOB were cardiac arrest (23), bleeding (20), hypotension (7), ischaemia (1) and others (4). Of the 55 patients, 20 died on the operating table. Of the remaining 35, a further 12 died in hospital. Overall survival was therefore 42%. Where crash-BOB was for bleeding, 17 of 20 patients (85%) survived to leave theatre, of whom 11 patients (55%) left hospital alive. In the 35 non-bleeders, only 18 (51%) survived crash-BOB and 12 (34%) left hospital alive. Sixteen patients required a second period of aortic cross-clamping of whom 13 (81%) survived to leave theatre, and 11 (69%) left hospital alive. Conversely, of nine patients in whom no specific diagnosis was found during crash-BOB, only two (22%) survived the procedure and none survived to hospital discharge. Multiple logistic regression identified pre-operative Parsonnet score (P=0.045) and the need for aortic cross-clamping to deal with an identified surgical problem (P=0.03) as significant predictors of hospital survival. Indication for crash-BOB (bleeder/non-bleeder) failed to reach significance (P=0.08). Age, sex, intra-aortic balloon pump use at the primary procedure, and time following the primary procedure to crash-BOB were not identified as predictors of hospital survival. Of the 23 hospital survivors, three patients suffered a stroke post-operatively and made a good functional recovery prior to discharge. Two patients developed sternal wound dehiscence requiring surgical rewiring. At follow-up (mean 3 years, range 1–6 years), 19 patients were in NYHA class I and four were in class II. Crash-BOB patients required an average of 8 extra intensive care days and 2 extra ward days. The total cost of these resources was £164 900 (including theatre time, cardiopulmonary bypass and intra-aortic balloon pump use). This was equivalent to £7170 per life saved. Conclusions: Crash-BOB occurred in 0.8% of cases and was associated with a survival to discharge of 42%, and a justifiable cost of only £7170 per life saved. Establishing an accurate diagnosis for the cause of clinical deterioration resulting in crash-BOB intervention was important, and the need for a further period of aortic cross-clamping did not preclude a favourable outcome.     

The effects of cardiopulmonary bypass temperature on inflammatory response following cardiopulmonary bypass.

OBJECTIVES: The inflammatory response to cardiopulmonary bypass is believed to play an important role in end organ dysfunction after open heart surgery and may be more profound after normothermic systemic perfusion. The aim of the present study was to investigate the effects of cardiopulmonary bypass temperature on the production of markers of inflammatory activity after coronary artery surgery. METHODS: Forty-five low risk patients undergoing elective coronary artery surgery were prospectively randomized into three groups: hypothermia (28 degrees C, n = 15), moderate hypothermia (32 degrees C, n = 15), and normothermia (37 degrees C, n = 15). All patients received cold antegrade crystalloid cardioplegia and topical myocardial cooling with saline at 4 degrees C. Serum samples were collected for the estimation of neutrophil elastase, interleukin 8, C3d, and IgG under ice preoperatively, 5 min after heparinisation, 30 min following start of CPB, at the end of CPB, 5 min after protamine administration, and 4, 12 and 24 h postoperatively. RESULTS: Patients were similar with regard to preoperative and intraoperative characteristics (age, sex, severity of symptoms, number of grafts performed, aortic cross clamp time, cardiopulmonary bypass time). Neutrophil elastase concentration increased markedly as early as 30 min after the onset of cardiopulmonary bypass and peaked 5 min after protamine administration. Levels were not significantly different between the three groups. A similar finding was apparent for C3d release. Interleukin 8 concentrations also demonstrated a considerable increase related to cardiopulmonary bypass in all groups, but there was a significantly more rapid decline in interleukin 8 concentrations in the normothermic group in the postoperative period. Eluted IgG fraction showed a much earlier peak concentration than the other markers, occurring within 30 min of the start of cardiopulmonary bypass. Levels reached a plateau, before declining soon after the end of bypass and remained higher than preoperative values at 24 h. There was no difference between the three groups. The cumulative release of all markers was calculated from the concentration-time curves, and was not statistically different between groups. CONCLUSION: Normothermic systemic perfusion was not shown to produce a more profound inflammatory response compared to hypothermic and moderately hypothermic cardiopulmonary bypass.     

Treatment of cardiac compression after cardiopulmonary bypass

A diversity of techniques for delayed closure of the sternum have been advocated for management of hypotension due to cardiac compression after cardiopulmonary bypass. A simple technique utilizing materials readily available in any operating room has been described. It provides for expansion of the cardiac space and sterile coverage of the mediastinum when the skin cannot be approximated.