Drug Therapy Problems in the Treatment of Decompensated Liver Cirrhosis Associated with Systolic Heart Failure


We review a case of an 18 year old lady with decompensated liver cirrhosis and systolic heart failure. In this case, we describe the pathophysiologic basis of the disease processes and describe the drug therapy modules and drug therapy problems. The article goes ahead to present data demonstrating the drug therapy problems that had occurred during the patient management and provides a resolve based on the most recent pharmaceutical and medical information.

Corresponding Author: Micheal Obia- Department of Pharmacy, Makerere University College of Health Sciences (MakCHS). Email michealobia@gmail.com Tel +256(0)788398773

Article Details: Received February 24, 2014 Reviewed March 12, 2014 Accepted March 27, 2014

Conflicting Interests: The authors have no conflicting interests to declare

Citation: Obia Micheal, Semuyaba S Andrew and Bogere Naghib. Drug Therapy Problems in the treatment of decompensated liver cirrhosis associated with Systolic Heart Failure (Review Article). MPJ 2014. 12 (1). e3-5





Decompensated liver cirrhosis is an end-stage liver disease state that is characterized by the development of pathological co-morbidities which include; ascites, jaundice, acute gastro-esophageal variceal hemorrhage, hepatic encephalopathy, spontaneous bacterial peritonitis and hepato-renal syndrome. Decompensated liver cirrhosis is a result of long-standing compensated liver cirrhosis which in Africa is commonly caused by chronic alcohol consumption, hepatocellular carcinoma and hepatitis B infection. [1, 2, 3]

Two major syndromes result from cirrhosis namely portal hypertension and hepatic insufficiency. In addition to these, peripheral and splanchnic vasodilation with resulting hyper-dynamic circulatory state is equally typical. The hyper-dynamic state is characterized by low arterial pressure, high cardiac output and decreased peripheral vascular resistance.

Jaundice results from hepatic insufficiency while the other complications of liver cirrhosis mainly culminate from portal hypertension and a hyper-dynamic circulatory state. Gastro-esophageal varices arise solely from portal hypertension although hyper-dynamic circulation may contribute to its growth and hemorrhage.  Ascites results from sodium retention and sinusoidal hypertension which in turn, is secondary to vasodilation and activation of the neuro-hormonal pathway. Hepato-renal syndrome results from severe peripheral vasodilation which leads to renal vasoconstriction. Hepatic encephalopathy is a result of blood shunting through porto-systemic collaterals, brain edema and nitrogenous imbalance caused by hepatic insufficiency. Drug therapy management of decompensated liver cirrhosis consists of individually treating the co-morbid pathologies so as to slow disease progression and prolong and improve on the quality of the patients├ö├ç├û lives. This is done by systematically selecting appropriate regimens and carefully designing a plan that maximizes their effects. This drug therapy plan is supplemented using other therapy models such as dietary modifications and change in life style. [1]

Heart failure is the inability of the heart to pump blood efficiently to tissues. Common causes of heart failure include; diseases of the peripheral vasculature, diseases of the myocardium, and diseases of the valves of the endomyocardium. Systolic heart failure accounts for 75% of all heart failure cases and is characterized by a longstanding pressure overload, chronic volume overload (congestive heart failure), loss of myocardium and loss of contractility. [4]

Endomyocardial fibrosis is a congenital anomaly associated with deposition of fibrous tissue on the endomyocardium. This affects the contractile properties of the heart muscle leading to heart failure.

A drug therapy problem is any undesirable event experienced by a patient which involves, or is suspected to involve, drug therapy, and that interferes with achieving the desired goals of therapy. [5]


The patient presented complaining of generalized body swelling, easy fatigability and vomiting. Her more recent complaints included chest discomfort and abdominal pain. Patient had been unwell for the past two years; she had had progressive abdominal swelling which has been occurring for the past two years, the patient also reported that she was experiencing abdominal pain and chest discomfort and this had started one week ago. She also complained of difficulty in breathing and occasional swelling of the lower limbs

The current admission is her third; the previous ones were due to similar symptoms. She was managed for decompensated liver cirrhosis. Patient also suffered from schistosomiasis, Tuberculosis and nephrotic syndrome in the past which were treated from private health care facilities in Nebbi district.

Patient had had Paracentesis done in the past, several times. There was nothing significant in her family and social history. Patient had used the following medicines: Spironolactone, Furosemide, Carvedilol, Dopamine, and Oral morphine, Cetirizine, Lactulose and Omeprazole.

On physical examination, the patient did not have jaundice, anemia, fever or dehydration; however the patient was sick looking. Her blood pressure was 97/73 mmHg, she had an increased jugular venous pressure, and her pulse rate was 72 bpm. Her respiratory rate was 18/min and she had diffuse crepitations from the mid to inferior zones. Her abdomen was grossly distended, symmetrical and non-tender. Other systems were unremarkable.

At the time the patient was being managed, the physicians were using decompensated liver cirrhosis with gross ascites and right-sided heart failure as working diagnoses. Peptic ulcer disease had been confirmed and she had reported that she had been taking omeprazole tablets in the past but had stopped due to financial constraints.

Table 1: Laboratory Results







22.9 g/L




109 U/L




13.4 U/L




48.7 H u/L


Slightly high


73.99 H u/L


Very high


156 H umol/L




39 U/L




59.2 g/L




10.2 mmol/L




122 mmol/L




5.63 mmol/L


Slightly high


83.4 mmol/L





Proper management of decompensated liver cirrhosis and systolic heart failure should consist of a regimen that has been demonstrated to slow disease progression. As mentioned earlier, each of the co-morbidities will consist of a drug therapy regimen that will be instituted for a designated period of time and monitored accordingly for effectiveness and associated toxicity. [2]

Based on a systematic review of the patientÔÇÖs record, the following conclusions were made about the potential for drug therapy problems;

The patient was being treated for a systolic heart failure associated with endomyocardial fibrosis, however, the regimen consisted of dopamine, Carvedilol and captopril. Conventions and algorithms state that at this stage of heart failure, deterioration of myocardium should be halted using a diuretic (preferably a loop diuretic), or an ACEI in combination with a negative iatrogenic drug such as the beta-adrenergic blockers. Hence, it can be expected that the effect of Carvedilol will be nullified by dopamine, a beta-adrenergic drug with positive iatrogenic activity. [2]

Ascites caused by reversed oncotic pressure and hyper-filtration due to portal hypertension leads to superior extension of the diaphragm. This leads to chest congestion and disturbance of normal of breathing. Morphine, an opioid analgesic is known to cause respiratory depression which could potential complicate respiratory function hence it would be inappropriate to use morphine to treat abdominal and chest pain. Chest and abdominal pain are relieved after reduction in ascetic fluid after therapy program and Paracentesis. 1,2

Ascitic fluid in the peritoneal cavity creates a medium for the growth of specific species of bacteria including gram-negative organisms. This usually causes spontaneous bacterial peritonitis (SBP) at a later disease stage. Therefore, prophylaxis should be instituted using appropriate drugs that the organisms are susceptible to. Generally, the fluoroquinolones especially levofloxacin have been used to prevent SBP. In this patient case, the type of drug therapy problem would be the need for additional drug therapy. [1, 2]

The patient had been diagnosed with peptic ulcer disease and she was taking omeprazole. However, no definite diagnosis had been made at the facility to rationalize the use of omeprazole and also, in any case, management of PUD should consist of triple therapy consisting of two anti-bacterials (clarithromycin, amoxicillin, metronidazole) and a proton pump inhibitor (omeprazole, lansoprazole, pantoprazole). In this scenario, the drug therapy would be a drug without an apparent medical indication. [1, 2]


Because of the complex nature of disease processes and their treatment, health care providers should be vigilant about their role and practices in drug therapeutics. PharmacistsÔÇÖ clinical roles should also be extended further such having pharmacy personnel with only clinical roles so as to extend pharmaceutical skill and knowledge to help the health care team in making better medicines related decisions and improving patient welfare and life.


1.        Guadalupe Garcia-Tsao et al Management and Treatment of Patients with Cirrhosis and Portal Hypertension: Recommendations from the Department of Veterans Affairs Hepatitis C Resource Center Program and the National Hepatitis C Program. Clinical reviews, nature publishing group.

2.        Andres Cardenas, Pere Gine`s Management of complications of cirrhosis in patients awaiting liver transplantation. Journal of Hepatology 42 (2005) S124├ö├ç├┤S133.

3.        Joseph Dipiro et al, Liver Cirrhosis Pharmacotherapy, The pathophysiologic basis of disease.

4.        Robinsons├ö├ç├û textbook of pathology.

5.        Linda M Strand. Drug therapy problems.Pharmaceutical Care for Clinicians.