1 Department of Medicine, Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL and 2 Emory University School of Medicine, Department of Medicine, Division of Nephrology, Atlanta, GA, USA
Correspondence and offprint requests to: S. W. Fineman, Department of Medicine, Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. Email: stevefineman{at}hotmail.com
Keywords: acute renal failure; acute tubular necrosis; arteriovenous fistula; congestive heart failure; surgery
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Introduction |
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Case |
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The patient had a stormy post-operative course, which was marked initially by persistent tachycardia and nausea. A pulmonary embolus was suspected. Non-invasive testing was inconclusive and her condition worsened. She developed hyponatraemia, acute renal failure, hepatic transaminitis and coagulopathy. She did not develop any frank hypotension; however, an echocardiogram at the time revealed a hyperdynamic state with ejection fraction >80%. A slow progressive decrease in haemoglobin from the pre-operative value of 14.1 to 8.5 g/dl during the first post-operative week went unrecognized. On post-operative day 6, she was transferred to our centre for liver transplant evaluation because of fulminant renal and liver failure. On arrival, she was found to be confused but haemodynamically stable. Her physical exam was notable for icterus, tachycardia and severe peripheral oedema. Laboratory studies at this time were remarkable for aspartate aminotransferase 8502 U/l, alanine aminotransferase 7080 U/l, prothrombin time 29 s, serum creatinine 3.2 mg/dl and blood urea nitrogen 91 mg/dl. Dialysis was initiated and the patient required full ventilatory support. The urinalysis revealed many course granular casts and ATN was diagnosed. Given her acute oliguric presentation, previous normal renal function and evidence of acute insult, urinary electrolytes were not obtained. After excluding viral hepatitis and portal vein thrombosis, the hepatology team diagnosed the patient with ischaemic liver injury, i.e. shock liver. Following several weeks of supportive care the patient slowly improved. The patient was weaned from the ventilator and intermittent haemodialysis was stopped with resumption of intrinsic clearance and urine output after 25 days. Her serum creatinine decreased to 2.0 mg/dl. Her liver function normalized with correction of her transaminitis and coagulopathy. On post-operative day 35, the patient was transferred to a rehabilitation hospital to continue physical therapy. At the time of discharge the serum creatinine had dropped to 1.4 mg/dl and the vital signs were noted to be normal.
During physical therapy sessions, the patient experienced episodes of nausea, vomiting, easy fatigue and severe diaphoresis. The patient was referred to the emergency department but no aetiology could be identified. Although a ventilation-perfusion nuclear scan for pulmonary embolus was low probability, a nuclear medicine venogram showed artefactual uptake in the right femoral region. A few days later, the patient was readmitted to our centre.
Upon re-evaluation, the patient was tachypnoeic. Manual blood pressure was 140/0 mmHg with a pulse rate of 94 per min. The widened pulse pressure of 140 mmHg was confirmed by the medical team. Jugular venous pressure was elevated and the heart was hyperdynamic. A harsh 4/6 systolic murmur was heard at the apex radiating to the carotids and a summation gallop was noted. The chest exam was otherwise clear. A loud abdominal bruit and pistol shot femoral pulses were present, though never noted previously. She was free of peripheral oedema. An electrocardiogram revealed sinus tachycardia and left atrial enlargement. An urgent echocardiogram showed normal valvular structures and a hyperdynamic right and left ventricle with ejection fraction of 80%. Thyroid tests were also normal. Due to the clinical development of high output heart failure, a presumed diagnosis of a vascular left to right shunt was made.
An aortic angiogram (Figure 1) confirmed an arteriovenous fistula between the right common iliac artery and left common iliac vein just below the aortic bifurcation at the L4L5 disc level. Vascular surgery successfully repaired the defect and the patient went home several days later with successful resolution of the high-output heart failure and return of serum creatinine to 1.0 mg/dl.
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Discussion |
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This case has several notable features. Although careful review of the operative record reveals a 30 mmHg drop in systolic blood pressure with concomitant tachycardia to 110 beats per min, the vascular injury went largely unrecognized at the time of surgery. Bleeding was likely limited initially due to pressure tamponade in the abdomen. Because she was young and otherwise healthy, compensatory tachycardia but no frank hypotension developed. Nevertheless, compromised tissue perfusion resulted in acute liver and renal failure in the first post-operative week. The haemodynamic changes leading to renal failure associated with this type of injury have been previously described. With the redistribution of blood flow there is marked elevation of renal venous pressure and concomitant decrease in mean arterial pressure [5,6]. After several weeks of critical illness requiring ventilatory and dialysis support the patient recovered, consistent with the natural history of acute ischaemic liver and renal failure. She then developed high-output congestive heart failure as the site of vascular injury healed and evolved into a fistula. A widening of the pulse pressure over time, documented at the rehabilitation hospital, correlates with the patients development of high-output heart failure. This case is unique in that we were able to witness the evolution of the fistula over a relatively short period of time. Moreover, we were unable to find previous case reports in which the patient suffered both acute renal and liver failure.
In summary, vascular injury during laminectomy is an uncommon but well described entity. The injury may not be clinically apparent due to positioning, but there should be a high index of suspicion in a patient with post-operative acute renal failure. In addition, any patient presenting with high-output congestive heart failure should have a thorough surgical history and examination for possible arteriovenous fistula. Recognition of this entity is critical, as surgical correction is almost always curative.
Conflict of interest statement. None declared.
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References |
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