Background: Previous studies have shown that 20% of all patients admitted to the hospital abuse alcohol and have increased morbidity after surgery. Long-term alcoholic patients are shown to suffer from immune alterations, which might be critical for adequate postoperative performance. Cardiac surgery with cardiopulmonary bypass (CPB) also leads to pronounced immune alteration, which might be linked with patients' ability to combat infections. Therefore, the aim of our study was to investigate the perioperative levels of TNF-alpha, interleukin-6, interleukin-10, and cortisol in long-term alcoholic and nonalcoholic patients undergoing cardiac surgery to elucidate a possible association with postoperative infections.
Methods: Forty-four patients undergoing elective cardiac surgery were included in this prospective study. Long-term alcoholic patients (n=10) were defined as having a daily ethanol consumption of at least 60 g and fulfilling the Diagnostic and Statistical Manual of Mental Disorders for alcohol abuse. The nonalcoholic patients (n=34) were defined as drinking less than 20 g ethanol per day. Blood samples were obtained to analyze the immune status upon admission to hospital, the morning before surgery and on admission to the ICU, the morning of days one and three after surgery.
Results: Basic characteristics of patients did not differ between groups. Long-term alcoholics had a fourfold increase in postsurgery infection rate and prolonged need for ICU treatment and mechanical ventilation. Postoperative levels of interleukin-10 and cortisol were significantly increased in long-term alcoholic patients compared with nonalcoholic patients. These observations were in line with postoperative interleukin-10 being predictive for postoperative infectious complications.
Conclusions: The increased infection rate in long-term alcoholics strengthens the urgent need for interventional approaches providing modulation of the perioperative immune and HPA response in these high-risk patients to counteract their postoperative immune suppression.