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Ann Thorac Surg 2006;82:715-716
© 2006 The Society of Thoracic Surgeons
a Department of Artificial Heart and Transplant, Royal Brompton and Harefield NHS Trust, Harefield, Middlesex
b Department of Cardiothoracics Surgery and Transplant, Royal Brompton and Harefield NHS Trust, Harefield, Middlesex
c Department of Microbiology, Royal Brompton and Harefield NHS Trust, Harefield, Middlesex
Accepted for publication November 4, 2005.
* Address correspondence to Dr Petrou, Royal Brompton and Harefield NHS Trust, Sydney St, London, SW3 6NP United Kingdom (Email: m.petrou{at}rbh.nthames.nhs.uk).
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Introduction |
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The patient is a 56-year-old man with end-stage heart failure secondary to idiopathic dilated cardiomyopathy who required mechanical support as a bridge to transplantation. In October 2003, he had a Thoratec left ventricular assist device inserted. The operation was unremarkable and he continued to do well while waiting for a donor heart.
Four months later he underwent orthotopic heart transplantation. The donor was a 31-year-old man (weighing 75 kg) who died of a subarachnoid haemorrhage. Re-sternotomy was uneventful despite dense pericardial adhesions. Bicaval cannulation was instituted, and the patient was placed on cardiopulmonary bypass. Both the inflow and outflow cannulas of the mechanical pump were mobilized and removed from the left ventricle and the aorta, respectively. The mediastinal parts of the cannulas were cut close to the inner surface of the chest wall. Orthotopic transplantation was performed using the Lower-Shumway technique. Total ischemic time was 179 minutes, and the total bypass time was 147 minutes. After full rewarming, the heart was beating in sinus rhythm. Routine decannulation was performed and the sternum was approximated using interrupted steel wires. Soft tissues were closed in layers in routine fashion. The remaining components of the left ventricular assist device cannulas were pulled out leaving the exit sites of the cannulas open to drain. The explanted components of the left ventricular assist device and the heart were sent for microbiology, and the results were negative.
The patient was transferred to the intensive care unit in a hemodynamically stable condition and was commenced on cyclosporine (10 mg/kg once daily initially, which was then reduced to maintain blood levels at 200 ng/mL), prednisolone (15 mg once daily for 3 days, which was then reduced to 7.5 mg once daily), and mycophenolate (1.25 g twice daily).
His early postoperative course was complicated by acute renal failure, coagulopathy, diarrhea secondary to clostridium difficile, infarction in the right middle cerebral artery territory causing left sided weakness and grand-mal seizures, pulmonary edema, and episodes of respiratory distress requiring a tracheostomy.
Ten days posttransplantation his sputum and sternal wound grew moderate to high growth density of Acinetobacter species. There was no evidence of over immunosuppression and he was started on tobramycin (3 mg/Kg) intravenously; his isolate of Acinetobacter baumannii was found to belong to the OXA-23 clone 2 strain, which is resistant to ß-µlactams, fluoroquinolones, and many aminoglycosides, and is susceptible to tobramycin, minocycline, and colistin only. Initially he was started on colistin (1 million units three times a day intravenously), then on minocycline (100 mg twice a day), which was added when he became septic. A few days later a collection was noted in his sternal wound; he was taken back to the operating room for wound cleaning and debridement. The sternal wound edges were necrotic and careful debridement took place. The wound was packed and drains were left in situ. Infection continued to spread and more tissue became necrotic, and extensive debridement was repeated on three different occasions within 3 days with the aim to salvage as much living tissue as possible. On the third occasion, bilateral pectoralis major flaps were used to close the sternal wound. Two weeks later his pectoralis major flaps became necrotic and foul smelling. Total sternectomy, pectoralis flap removal, and wide excision of the wound edges were done leaving a very large elliptical defect measuring 20 cm in its maximum diameter with only the transplanted heart at base. The wound was covered with vacuum dressing and was reviewed daily when it was cleaned, initially with 5% chlorohexidine and then sterile normal saline. Eventually the wound started to granulate and healed by secondary intention with a fibrous tissue replacing the sternum. He was discharged home 8 months after transplantation. His routine biopsies have shown no rejection. He is to remain on long-term minocycline (100 mg twice a day). A follow-up echocardiogram revealed good overall left ventricular function, and his outpatient sternal wound swabs have been negative for all microbiology.
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By definition, mediastinitis denotes deep mediastinal wound infection. El-Oakley and Wright [2] have classified mediastinitis into 7 different types according to the time of infection, presence or absence of risk factors, and failure or success of either medical or surgical management. According to their classification our patient had type IVB mediastinitis, and he had multiple risk factors for infection with Acinetobacter species. These ranged from previous surgery for left ventricular assist device insertion, multiple episodes of sternal wound bleeding, numerous blood transfusions, and the use of immunosuppressive drugs.
Gram positive organisms are the most common isolated organisms in mediastinitis (eg, Staphylococcus aureus and Staphylococcus epidermidis are identified in 70% to 80% of cases) [3]. Mixed infections account for 40%, and gram negative and fungal infections are infrequently found in mediastinitis [3]. Acinetobacter species has been recognized as a potentially pathogenic microorganism after thoracotomy [4]. In contrast, in their 15 years experience of mediastinitis postoperative heart and lung transplantation, Abid and colleagues [3] have failed to include Acinetobacter as one of the pathogenic organisms.
Acinetobacter species are ubiquitous in the environment and apart from human infections, food and milk are important spoilage agents. In the hospital, Acinetobacter baumannii can be recovered from bed linen, mattresses, pillows, surfaces and wet sinks, cleaning cloths, face flannels, and the air of units with colonized patients. Many strains are soap tolerant. Acinetobacter baumannii is an important nosocomial pathogen that can cause severe infections in debilitated patients. Certainly in our case the most likely source of infection was pulmonary as the sputum culture also grew Acinetobacter. The incidence of infection increases with age and is particularly marked in patients older than 45 years of age. The OXA 23 clone 2 strain has been found in 8 hospitals since July 2003 [5]. It is typically susceptible to minocycline, colistin, some of the aminoglycosides including amikacin, which is resistant to gentamicin, and the novel glycylcycline tigecycline. Since the year 2000 there has been a significant increase in resistant Acinetobacter baumannii, which are genetically related [6]. Coelho and colleagues [7] have shown that there is an increasing population of multi-resistant Acinetobacter in the United Kingdom with the majority of the increase in London, the Southeast, and the West Midlands.
Treatment of mediastinitis usually varies from simple prolonged antibiotic therapy to complete sternectomy combined with plastic surgery. In our case, bilateral pectoralis major flaps were used instead of the conventional omental flap closure. In spite of the rich vascular supply and high immunologic properties of the omental flap, there were two reasons advocating its use. Laparotomy would have lead to additional complications as the patient was critically ill with an ongoing sepsis. In addition, the omental flap does not improve sternal stability unless it is used with pectoralis major cover.
Persistent infection and total necrosis of the remaining sternum and pectoralis major flaps necessitated extensive sternal wound debridement as a method of source elimination. The wound was left to close by secondary intention with the aid of vacuum-assisted closure and regular irrigation. The use of vacuum-assisted closure has been shown to be as effective as conventional surgical management of sternal wound infections with reduced mortality and recurrence of sternal wound infections and fistulae [8].
We believe that this is the first case in the literature describing severe infection with acinetobacter after heart transplantation in which the patient has survived after radical debridement, sternectomy, prolonged vacuum dressing, and long-term antibiotics. We recommend that extensive intervention should not be withheld, and that appropriate drainage in conjunction with antibiotics is essential.
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