Asian Cardiovasc Thorac Ann 2007;15:e38-e40
© 2007 Asia Publishing EXchange Ltd
Stanford Type A Aortic Dissection with Child B Liver Cirrhosis
Seiji Matsukuma, MD,
Hiroshi Yamaguchi, MD,
Masayoshi Hamawaki, MD
Department of Cardiovascular Surgery, National Hospital Organization, Nagasaki Medical Center, Nagasaki, Japan
For reprint information contact: Seiji Matsukuma, MD, Tel: 81 95 752 3121, Fax: 81 95 754 0292, Email: matsukuma{at}nmc.hosp.go.jp, Department of Cardiovascular Surgery, National Hospital Organization, Nagasaki Medical Center, 2-1001-1 Kubara, Omura City, Nagasaki 856-8562, Japan.
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ABSTRACT
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Cardiac surgery using cardiopulmonary bypass in patients with advanced liver cirrhosis has been infrequently performed, and reported to be too risky. Aortic dissection accompanied with liver cirrhosis is extremely rare. A 61-year-old woman who had aortic dissection and Child B liver cirrhosis underwent ascending aorta replacement. Liver protection during cardiopulmonary bypass was successfully accomplished by moderate hypothermia and use of an aortic occlusion balloon to maintain sufficient hepatic blood flow.
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INTRODUCTION
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Generally, a reduced prevalence of cardiovascular diseases has been reported in liver cirrhosis, as the risk factors of cardiovascular diseases, such as hypercholesterolemia and hypertension are usually absent in cirrhotic patients.1 Among other cardiovascular diseases, the incidence of aortic dissection accompanied with liver cirrhosis is extremely rare. In patients with advanced liver cirrhosis, cardiac surgery using cardiopulmonary bypass has been infrequently performed and reported to be associated with a higher rate of major postoperative complications.2,3
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CASE REPORT
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A 61-year-old woman was referred with chest-abdominal pain and episodes of syncope. Enhanced computed tomography (CT) revealed Stanford type A aortic dissection (Figure 1
). She had a past history of liver dysfunction due to hepatitis C at the age of 44. Five months previously, she was diagnosed with hepatocellular carcinoma, and underwent transcatheter arterial chemoembolization with lipiodol and mitomycin (Figure 2). Relevant preoperative laboratory test results were as follows: hemoglobin 10.8 g·dL–1, platelet count 136 K·µL–1, prothrombin time (international normalized ratio) 1.14, activated partial thromboplastin time 59.5 seconds, activated clotting time 140 seconds, serum fibrinogen 229 mg·dL–1, serum total bilirubin 34 µmol·L–1, serum albumin 22 g·L–1, serum aspartate transaminase (AST) 223 IU·L–1, alanine transaminase (ALT) 157 IU·L–1, and cholinesterase 37 IU·L–1. On the basis of all the investigations the patient was classified as having Child-Pugh class B cirrhosis.
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Figure 1. Enhanced computed tomography revealed Stanford type A aortic dissection with an ulcer-like projection at the posterior wall of the ascending aorta.
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Figure 2. Computed tomography revealed hepatotrophic right lobe and the high density of the S8 lesion due to lipiodol infused with mytomycin at the time of transcatheter arterial chemoembolization.
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The operation was performed via a median sternotomy. Cardiopulmonary bypass (CPB) was established by cannulating the right atrial, right axillary, and right femoral arteries. When the rectal temperature reached 25°C by means of core cooling, CPB flow through the right femoral artery was ceased and the brachiocephalic artery was clamped. The aorta was incised and mural thrombi were removed, and the left common carotid and left subclavian arteries were cannulated directly to establish antegrade selective cerebral perfusion. An aortic occlusion balloon was inserted into the descending thoracic aorta, and the balloon was inflated. Subsequently, perfusion to the lower half of the body was restarted through the right femoral artery. Perfusion flow via the right femoral artery was maintained between 0.3 and 0.4 L·min–1, and mean arterial pressure was maintained between 35 and 45 mm Hg in the left femoral artery.
Myocardial protection was established by intermittent direct infusion of cold crystalloid cardioplegia through both coronary ostia. An intimal tear was located on the posterior wall of the ascending aorta. The ascending aorta was replaced with a 28 mm gelatin coated woven polyester graft (Vascutek, Terumo, Inchinnan, Scotland, UK). Distal anastomosis was achieved with one suture line immediately below the brachiocephalic artery. After completing the distal anastomosis, the brachiocephalic artery was opened and the graft was clamped. Under total-body antegrade and retrograde perfusion from the right axillary artery and right femoral artery, the proximal anastomosis was accomplished. The duration of the operation and CPB were 349 minutes and 166 minutes, respectively. Two units of packed red blood cells, 10 units of fresh frozen plasma, and 10 units of platelets were transfused due to an intraoperative bleeding tendency. In addition, a total of 1 million kallikrein inhibiting units of aprotinin was infused to reduce blood loss until the end of the operation. Half a million units were infused after the induction of anesthesia and another half a million units were infused after declamping the aorta. In the first 24 hours after the operation, the drainage tube output was 245 mL. Major postoperative complications including infection, bleeding, and progressive liver dysfunction did not occur.
During follow-up, AST and ALT levels declined gradually but continued to fluctuate between 70 and 125 IU·L–1, and between 65 and 101 IU·L–1, respectively. The maximum postoperative serum total bilirubin level was 106 µmol·L–1 on day 2 after the operation, but returned to normal 3 weeks after the operation.
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DISCUSSION
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Aortic dissection accompanied with liver cirrhosis is rare, and literature concerning successful surgical treatment of aortic dissection accompanied with advanced liver cirrhosis is scarce. Only one case of a patient with aortic dissection and liver cirrhosis who underwent replacement of the ascending aorta has been reported.3 However, the patient suffered severe postoperative morbidity (infection and bleeding) and died.
In patients with advanced liver cirrhosis, cardiac surgery using cardiopulmonary bypass has been infrequently performed until now, and has been reported as too risky.2,3 On the other hand, acute Stanford type A dissection is generally associated with a bleeding tendency, and acute massive consumption coagulopathy in the false lumen is thought to be one of the contributors to the bleeding tendency.4 For aortic dissection with severe liver cirrhosis, in particular, problems with hemostasis can be highly expected because of thrombocytopenia, platelet dysfunction, and decreased hepatic production of coagulation factors. Previous reports have shown that the higher mortality of cardiac patients with cirrhosis was not attributable to impaired cardiac function, but to an increased susceptibility to infections due to poor nutrition, gastrointestinal complications, and bleeding.2 In addition it has been well documented that the use of cardiopulmonary bypass triggers the production and release of numerous vasoactive substances and cytotoxic chemicals that affect coagulopathy, vascular resistance, and major organ function.5 Hypothermia, hemodilution, and hypoperfusion to major organs during cardiopulmonary bypass may also be responsible for postoperative morbidity and mortality. Moreover circulatory arrest is thought to induce the formation of microvascular thromboses which may cause further end-organ damage.6
Okano et al7 reported that hepatosplanchnic oxygenation is better preserved during mild hypothermic rather than normothermic cardiopulmonary bypass. Normothermic cardiopulmonary bypass further exacerbates the imbalance of oxygen demand and supply. Qing et al8 reported that induction of moderate hypothermia by stimulating interleukin-10 (IL10) synthesis and suppressing tumor necrosis factor-alpha production during cardiopulmonary bypass might provide organ protection. We hypothesized that moderate hypothermia, use of an aortic occlusion balloon, decreased circulatory arrest time, and maintenance of sufficient hepatic blood flow during cardiopulmonary bypass would protect the already compromised liver.
Transesophageal echocardiography (TEE) is valuable in the diagnosis of aortic dissection. However, the development of esophageal varices is recognized as a contraindication to TEE, adding to bleeding diathesis. We believe that patients with liver cirrhosis should undergo endoscopic analysis before TEE is performed to preclude the presence of esophageal varices.
In conclusion, based on this case, patients with aortic dissection and advanced liver cirrhosis can be safely operated on by using moderate hypothermic cardiopulmonary bypass and an aortic occlusion balloon to maintain hepatic blood flow.
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REFERENCES
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- Hayashida N, Shoujima T, Teshima H, Yokokura Y, Takagi K, Tomoeda H, et al. Clinical outcome after cardiac operations in patients with cirrhosis. Ann Thorac Surg 2004;77:500–5.[Abstract/Free Full Text]
- Tanaka M, Kawahito K, Adachi H, Ino T. Platelet dysfunction in acute type A aortic dissection evaluated by the laser light-scattering method. J Thorac Cardiovasc Surg 2003;126:837–41.[Abstract/Free Full Text]
- Downing SW, Edmunds LH Jr. Release of vasoactive substances during cardiopulmonary bypass. Ann Thorac Surg 1992;54:1236–43.[Abstract]
- Wilde J. Hematological consequences of profound hypothermic circulatory arrest and aortic dissection. J Card Surg 1997;12(2 Suppl):201–6.[Medline]
- Okano N, Hiraoka H, Owada R, Fujita N, Kadoi Y, Saito S, et al. Hepatosplanchnic oxygenation is better preserved during mild hypothermic than during normothermic cardiopulmonary bypass. Can J Anaesth 2001;48:1011–4.[Medline]
- Qing M, Vazquez-Jimenez JF, Klosterhalfen B, Sigler M, Schumacher K, Duchateau J, et al. Influence of temperature during cardiopulmonary bypass on leukocyte activation, cytokine balance, and post-operative organ damage. Shock 2001;15:372–7.[Medline]
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ABSTRACT
INTRODUCTION
