We identified 13 patients (male: 8, female: 5) during the time period of May 2003 to December 2007 with acute liver failure caused by cardiac failure (Figure 1). The mean age of the patients was 48.4 ± 17.4 years. All patients suffered from cardiogenic shock at admission.
Causes of heart failure
Six patients suffered from dilatative cardiomyopathy (ejection fraction ≤ 20%) with acute decompensation. Two patients developed pericardial tamponade following cardiac surgery. One patient suffered from pulmo nary embolism and consecutive right heart failure, one patient experienced aortic valve stenosis III° (aortic root 0.4 cm2) with secondary pulmonary hypertension and right heart failure. Two patients were admitted with a myocardial infarction, and one patient with a known primary pulmonary hypertension had an acute right heart failure due to tachyarrhythmia absoluta.
The overall hospital mortality rate was 54% (7 out of 13). 7 patients died within 4 days due to heart failure and were not accompanied with liver failure.
The remaining 6 patients recovered from cardiogenic shock and improved in their clinical course. The patient with the aortic valve stenosis underwent a successful valve replacement and recovered. The patient with the pulmonary embolism was treated with fibrinolyses and recovered. All surviving patients were readmitted to the referring hospital with remarkable improved cardiac - and liver function.
AST, ALT, bilirubin, and INR did not differ statistically on admission between patients, who survived or deceased. AST was significantly lower in the surviving group on day 7 as compared with all patients at admission (1043 ± 1013 U/L vs 4029 ± 3514 U/L). Although, bilirubin, ALT decreased and INR increased, these apparent differences did not reach statistically significance (see Table 1 and Figure 2)
All patients suffered from cardiogenic shock (CI = 1.9 L/min/m2). However, patients who survived had significant higher CI as compared with non-survivors (2.1 ± 0.2 L/min/m2 vs. 1.6 ± 0.5 L/min/m2). There were no significant differences in other cardiovascular parameters between both groups on admission [CVP (17 ± 4 mmHg in survival group vs, 15 ± 6 mmHg non-survival), PCWP (20 ± 6 mmHg survival group, 20 ± 12 mmHg non-survival group), and MPAP (32 ± 10 mmHg survival group vs. 46 ± 21 mmHg non-survival group)].
Echocardiogram was performed in all patients that revealed global hypokinesis with estimated ejection fraction ≤ 20%.
Dobutamine as inotropic support was infused in 3 patients (dose 2-8 μg/kg/min), milrinone was used for 2 patients (dose 0.5-3 μg/kg/min), or adrenaline (8 patients, dose ≤ 0.1 μg/kg/min). Noradrenaline as a vasopressor was used in all patients to maintain a MAP of 70 mmHg.
Patients who survived showed a significant increase of CI at day 7 compared with all patients at admission. CVP and vasopressor support (noradrenalin) was significantly reduced at day 7 in the survival group as compared with baseline (see Table 1).
Abdominal ultrasound and doppler investigation
In all patients the doppler tracing documented severe impairment of portal vein flow with partial reversed flow without signs of a portal vein thrombosis (see Figure 3). A repeated ultrasound in the survival group on day 5 showed a remarkable improved portal vein tracing with pulsatile, but hepatopedal flow pattern.
The hepatic vein preserved its triphasic pattern, however with a remarkable increased retrograde flow (see Figure 4). After cardiac recovery the retrograde flow decreased. The hepatic artery showed a regular flow tracing despite a high dose of vasopressor treatment.