In our study we identified 13 patients with ALF caused by congestive heart failure. All patients suffered from cardiogenic shock, however patients that survived had significant higher CI on admission as compared with non-survivors. The overall hospital mortality was 54%. Patients who survived had a regular CI on day 7, which was associated with improved liver function. Ultrasound Doppler images on admission showed pathological traces of portal- and hepatic vein, which were reversed after cardiac recovery.
Heart failure is a most often accompanied by of elevated plasma concentrations of liver enzymes [10, 17]. Only Kubo et al. [9] reported a slight AST elevation (65 ± 82 U/L) in patients with a CI ≤ 1.5 L/min/m2. However, most other reports (Wiesen et al. [18]; Fussell et al. [4]) support the findings of our present study, where AST concentrations were shown to be elevated more than 2000-fold, despite a mean CI of 1.9 L/min/m2. The main difference of Kubo's report and the other studies are that Kubo described the incidence and severity of liver function abnormalities in patients with congestive heart failure, but in absence of acute decompensation. Despite a very low CI in his study, which did occur not abruptly, compensatory mechanisms may react (additional liver veins draining from diaphragmal veins or vena gastrica sinistra), if there is time enough to create this bypass.
Fulminant hepatic failure caused by congestive heart failure has rarely been documented; furthermore the exact pathophysiology remains unclear. Seeto et al. [13] stated that systemic hypotension or shock alone did not lead to liver failure in any patient. The majority of patients in their study with liver failure had severe underlying cardiac disease that had often led to passive congestion of the liver. They conclude that right-sided heart failure resulting in hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event. The most presumed causes of car diac induced ALF are hepatic congestion from venous hypertension and decreased oxygen delivery (DO) from a decreased CI [17]. Once DO underwent a critical threshold, hepatic hypoxia initiates a process that results in hemorrhage centrilobular necrosis [2]. Venous hypertension results in periventricular sinusoidal congestion, endothelial injury, replacement of hepatocytes with erythrocytes, and ultimatively, centrilobular necrosis [2, 6]. In our study patients fulfilled all criteria for cardiogenic shock with elevated CVP. Patients who survived and recovered from cardiogenic shock remained a high CVP, but showed an improvement in liver function. This led us to the conclusion that a low CI has more impact on the liver congestion than a high CVP. Indeed, a low CI induces a high CVP which ultimately may cause liver congestion. However, an association of liver failure with high CVP (> 10 mmHg) as a sign of volume overload but regular CI has never been reported.
The Doppler ultrasound pattern of reversed pulsatile flow (RPF) of the PV is strongly associated with high right atrial pressure (> 20 mmHg) [1, 12]. Tricuspid regurgitation is considered to be the main cause of RPF in patients with congestive heart failure, but the precise pathophysiological mechanism of the portal veins RPF remains unsolved. In our study the PV flow was only partially reversed, but with very severe impaired hepatopedal flow. After improvement of cardiac function the hepatopedal flow improved but remained pulsatile. A very similar RPV was reported in patients with a Budd-Chiari syndrome [16]. This syndrome leads to occlusion of the hepatic vein and/or inferior vena cava and therefore resembles the situation of elevated right atrial pressure. The venous outflow obstruction of the liver leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates with total or partial RPV flow [3].
Hepatic vein flow in healthy volunteers consists of two forward flows toward the heart; one systole, the other one in diastole, and one retrograde flow toward the liver during atrial contraction [15]. In patients with atrial fibrillation, and more pronounced in patients with congestive heart failure a systolic backward flow toward the liver is reported [19]. In our study we found a major backflow toward the liver at both cycle systolic and diastolic. After cardiac recovery the hepatic vein flow improved and was mainly directed out of the liver.
As any observational cohort study, our report has some limitations. First of all we performed a retrospective study were the findings of such an investigation carry less persuasive force than those of a prospective study. In order of our limited sample size we were not able to abbreviate special recommendation for treatment for these patients. Moreover we were not able to make any conclusions about the epidemiology of ALF caused by cardiac failure. However, what we learned form our data is that every patient with unknown cause of ALF should be evaluated with right heart catheter to exclude cardiac induced liver failure. The only curative treatment option for these patients is to improve cardiac function.
In conclusion, ALF induced by heart failure is rare and carries a high mortality rate. In case of unknown cause of ALF, despite a meticulous workup, cardiac failure should always be considered. Right heart catheter evaluation for exact assessment of CI, MPAP, and CVP is mandatory for these patients.
The authors declare that they have no competing interests.
