INTRODUCTION: Fulminant liver failure often requires transplant for successful treatment. Causes include viral, toxins, metabolic, autoimmune, and vascular causes. We report a rare, but potentially treatable case of fulminant liver failure, due to a vascular cause.
CASE PRESENTATION: A 59-year-old female with end stage renal disease was admitted with shortness of breath, mild chest and back pain that had progressed over 24 hours. She was afebrile with a blood pressure of 200/104. A non-contrast CT of the chest abdomen & pelvis revealed atherosclerotic changes of the aorta. Laboratory values, including liver panel were normal, except for an elevated creatinine. She treated with antihypertensives, dialyzed and given several percocets for pain control. Her blood pressure stabilized and her dyspnea and pain improved. Three days after admission, she developed acute mental status changes, temp. of 103.1F, and a WBC of 16.5. She was started on empiric antibiotics. Fever work up was negative. Then, she developed right upper quadrant abdominal pain. A repeat liver panel revealed the following values: AST 2711, ALT 4855 and an alkaline phosphatase of 183. The patient was transferred to a tertiary care center for further management. On arrival, she had stable vital signs with equal blood pressures and pulses bilateral upper extremities. Cardiovascular exam was significant for equal pulses with a regular rhythm. Her lungs revealed rales at bilateral bases. Abdominal exam revealed moderate right upper quadrant tenderness, but was otherwise normal with guaiac negative stool. Neurologically, her mental status waxed and waned, intermittently answering questions. She also had asterixis, and was otherwise non-focal. Her laboratory values revealed a WBC of 14.5, PT of 25.3 seconds, PTT of 34.2 seconds, total bilirubin 2.2 mg/dL, AST 6789 iu/L, ALT 7482 iu/L, alkaline phosphatase 299 iu/L, with a lactate of 7.8. Her pH was 7.23. She was started on intravenous acetylcysteine, continued on empiric antiobiotics. A CT of her chest, abdomen, and pelvis which showed a Type III dissection arising distal to the left subclavian artery, proximal false lumen partially thrombosed with prominent flow in false channel in distal thoracic and proximal abdominal aorta with narrowing in true lumen. A liver ultrasound showed an enlarged heterogeneous liver with patent portal veins and left hepatic artery. Patency was not not confirmed in right hepatic artery.Vascular surgery was consulted. The patient's mental status deteriorated, along with her ability to protect her airway and she developed respiratory distress. We discussed further management options with her family, who decided that the patient would not want invasive interventions, and the goals of care were changed to comfort. The patient expired within 8 hours of arrival to the hospital.
DISCUSSIONS: Aortic Dissection has a 15-25% in hospital mortality and 33% have a branch artery occlusion. (1) However, our case is different from other published cases, in that she developed fulminant liver failure from decreased flow due to that flow from the false channel compressed the true lumen, along with the branches to the celiac trunk and superior mesenteric artery. However, our patient is unique due to the fact that she only showed signs of liver failure without mesenteric ischemia.
CONCLUSION: It is important to recognize that a potentially treatable cause of fulminant liver failure, without mesenteric ischemia can be related to a descending aortic dissection. This is a potential treatable cause of liver failure, by either surgical or by endovascular stent placement. (2).
DISCLOSURE: Howard Saft, None.