Abstract

Elevated transaminase and cholestatic enzyme levels are frequently linked to congestive hepatopathy (CH) in the setting of decompensated heart failure. However, other etiologies such hepatitis and acute cholecystitis should still be considered on the differential diagnosis list. Our case describes a very common case of heart failure exacerbation where lab findings may be attributed to CH, however the ultimate diagnosis of gallbladder malignancy was surprising. Our case highlights the importance of performing the workup for elevated liver enzymes in the setting of acute heart failure exacerbation before attributing the cause to CH. Abdominal ultrasound is a cheap and safe tool that should always be considered in cases of elevated transaminases and cholestatic enzymes. It played a pivotal role in the diagnosis of our case.

1. Introduction

There has always been a close link between heart and liver diseases due to hemodynamic interactions and diseases that can affect both organs ¹. Liver cirrhosis can cause cirrhotic cardiomyopathy which occurs in about half the cases of cirrhosis. Right-sided heart failure can affect the liver acutely by ischemia or chronically by passive venous congestion, which leads to congestive hepatopathy (CH) ².

About 90% of the cases of CH are related to cardiac pathology including right-sided heart failure, tricuspid regurgitation, or constrictive pericarditis. However, CH can be also caused by diseases involving the hepatic veins and the IVC as Budd-Chiari syndrome ³. The venous congestion transmitted to the liver causes an increase in the central vein pressure leading to sinusoidal dilatation and decrease liver blood flow leading to chronic liver injury. Screening for CH is important as it can lead to cirrhosis and hepatocellular carcinoma ⁴.

Our case describes a patient with typical signs of CH in the setting of heart failure. However further investigations showed gallbladder adenocarcinoma.

2. Case Presentation

A 68-year-old male with a past medical history of diabetes mellitus, systemic hypertension, hyperlipidemia, heart failure with reduced ejection fraction secondary to non-ischemic cardiomyopathy presented to the emergency department with shortness of breath on minimal exertion and even at rest together with bilateral lower extremity swelling for one week after running out of his medications. He also complained of mild intermittent right upper quadrant abdominal pain associated with nausea that has been going on for one week as well.

On examination, vitals were significant for elevated blood pressure of 160/110 mmHg with otherwise normal pulse, temperature, and oxygen saturation. Physical exam showed jugular venous distention, bilateral basilar crackles with bilateral +2 pitting edema up till below the knees. Examination also showed slight right upper quadrant tenderness with no jaundice or palpable lymph nodes. Labs showed mild anemia with hemoglobin of 11 gm/dL. Complete metabolic panel showed normal electrolytes, low albumin of 2.7 gm/dL with slightly elevated creatinine of 1.4 mg/dL. Liver functions were found to be elevated with alanine aminotransferase (ALT) of 230 U/L and aspartate aminotransferase (AST) of 170 U/L as well as elevated alkaline phosphatase (ALP) of 250 IU/L and normal bilirubin and normal international normalized ratio (INR). Labs also showed elevated brain natriuretic peptide (BNP) of 4000 pg/mL. Patient was given intravenous (IV) Lasix in the emergency department. Echocardiography showed severely reduced left ventricular (LV) ejection fraction (15%), severe diffuse LV hypokinesis, mild right ventricular hypokinesis with severe mitral and tricuspid regurgitation. The patient was admitted to the hospital for further management of heart failure exacerbation.

Patient abdominal complaints and elevated liver functions were thought to be secondary to congestive hepatopathy. However, our differential diagnosis included other causes such as cholecystitis, biliary colic and hepatitis. Hepatitis viral panel was negative, and the patient denied alcohol use. Abdominal ultrasound Figure 1 showed distended gallbladder with luminal hyperechoic mass, which promoted further investigation with CT abdomen and pelvis with IV and oral contrast. CT abdomen and pelvis showed bilateral lower pleural effusion Figure 2, distended gallbladder with ill-defined intraluminal masses Figure 3, Figure 4, Figure 5 associated with necrotic lymphadenopathy in the porta hepatis Figure 6 likely representing gallbladder cancer with local regional spread.

During the hospital course, thoracentesis of the pleural effusion was done with the cytology showing malignant cells confirming gall bladder adenocarcinoma diagnosis. Oncology was further consulted and recommended outpatient follow up. He was discharged home after heart failure exacerbation treatment, and he was started on chemotherapy in the outpatient setting for gallbladder adenocarcinoma.

3. Discussion

Congestive hepatopathy (CH) is usually asymptomatic. Less commonly, some patients might develop mild right upper quadrant abdominal pain due to tension on the liver capsule. Ascites can also be present. However, esophageal varices and splenomegaly are usually absent because of the lack of porto-systemic venous pressure gradient. On a physical exam, hepatomegaly and hepatojugular reflux can be evident ⁵.

Labs can show moderate elevation of ALP. Also, ALT and AST are usually elevated more than 2 to 3 times the upper range of normal. Total bilirubin is usually elevated but usually does not exceed 3 mg/dL. Hypoalbuminemia can also be evident with albumin levels rarely below 2.5 gm/dL, which could be due to nutritional deficiency, protein losing enteropathy or defective synthesis ⁶. INR is usually not reliable as lots of patients are on anticoagulant treatment ⁷. Ultrasound examination of the liver vasculature can show dilatation of the hepatic veins with the loss of the normal variation of hepatic venous diameter during respiration ⁸.

To the best of our knowledge, this is the first case to discuss the presence of abdominal malignancy in the setting of CH. On reviewing the literature, we did not find information about accidental findings of abdominal malignancy in the workup of CH. Gallbladder cancer accounts for 1.2% of all cancer diagnoses worldwide and 1.7% of cancer deaths. Most of the cases are diagnosed at a late stage and the median survival for an advanced stage cancer is only about a year ⁹.

This case serves as a reminder of ruling out other causes of elevated liver enzymes in the setting of heart failure exacerbation before assuming that the cause is solely CH. Other causes of elevated liver enzymes include viral, alcoholic, and non-alcoholic hepatitis. It is essential to order hepatitis viral panel, ask about alcohol history and perform abdominal ultrasound. Abdominal ultrasound is a cheap and safe tool that should always be considered in cases of elevated transaminases and cholestatic enzymes. It played a pivotal role in the diagnosis of our case.

As the case presented above, our patient manifested with the classic picture of CH of mild right upper quadrant abdominal pain with labs showing BNP of 4000 pg/mL, ALT of 230 U/L, AST of 170 U/L, and ALP of 250 IU/L. However, right upper quadrant ultrasound showed hyperechoic structure in the gallbladder lumen, which turned out to be gallbladder adenocarcinoma.

4. Conclusions

Not all cases of elevated liver functions with heart failure exacerbation should be blamed on CH alone. It serves as a reminder that diagnosis of CH should be established after ruling out other causes of RUQ pain including viral hepatitis, alcohol abuse, autoimmune diseases, malignancy, etc.

ACKNOWLEDGEMENTS

All authors declare no funding.

Statement of Competing Interests

All authors declare no competing interests.

References