Cirrhosis of the liver represents the final common pathway of many hepatic disorders characterized by chronic cellular destruction. An intervening stage of increased fibrosis is followed by formation of parenchymal regenerative nodules. It is the nodular distortion of the lobules and vascular network that defines cirrhosis and ultimately plays a critical part in the development of portal hypertension (Fitz, 2003). The cellular and biochemical events leading to this altered growth response and resulting architectural distortion are not well characterized (Yamada, 1998). Cirrhosis accounts for over 40,000 deaths each year in the United States and more than 228,145 years of potential life lost. The average patient with alcoholic liver disease loses 12 years of productive life, a much larger loss than that for heart disease (2 years) and cancer (4 years) (Fitz, 2003).

Clinical manifestations of end-stage liver disease follow a similar pattern despite the causative etiology. Early indications of disease are often vague and include gastrointestinal symptoms such as anorexia, indigestion, nausea, vomiting, constipation, diarrhea, and complaints of dull, diffuse abdominal pain. The major symptoms that often accompany the early manifestations of this disease occur as a result of hepatic insufficiency and portal hypertension and may lead to the following organ system abnormalities (Isselbacher & Podolsky, 2004):

Additional symptoms can include a musty (acetone) breath, enlarged superficial abdominal veins, muscle atrophy, pain in right abdominal quadrant that worsens when the patient sits up or leans forward, palpable liver or spleen, and temperature of 101° to 103° F. Bleeding from esophageal varices can occur from an increase in the portal vascularity leading to hypertension and increasing the likelihood of esophageal hemorrhage (Meyer, 2001).

Chronic liver failure caused by acetaminophen toxicity can present with varying complications. Patients may be asymptomatic, with only incidentally detected laboratory test abnormalities, or they may have obvious features of liver involvement. Typically, drug hepatotoxicity begins 1 to 2 months after initiation of a drug, but latency may be longer (Krahenbuhl & Reichen, 2000).

An extensive patient history is crucial when evaluating for liver pathologies and/or gastrointestinal complaints during any juncture of the disease. Evaluation of suspected liver disease begins with a detailed assessment of risk factors (Kamath, 2001), followed by a clear chronological account of the patient’s current situation that includes the onset of the problem, the setting in which it developed, and identification of concomitant manifestations. Identification of factors that alleviate or exacerbate the patient’s symptoms is helpful. Additional assessment should query the patient about previous surgeries; abdominal or liver traumas; alcohol ingestion; comorbid pathologies; past or present viral, bacterial, parasitic, or fungal infections; and a family history of illnesses, as this health information is valuable and may influence treatment options. In addition, it is important to include a current list of medications taken, dosages used, allergies, previous drug toxicities, illicit drug use, OTC medications, herbal products, and any drug-drug interactions previously experienced. A study by Bernard and Bruera (2000) identified patients who were admitted to palliative settings and generally prescribed six or seven medications at any given time, contributing to the risk of adverse drug reactions and to drug-to-drug interactions. Many of these patients were prescribed 10 to 20 different medications and had a 20% or greater chance of experiencing a significant adverse drug-to-drug event, which can be fatal.

The patient’s general appearance and vital signs may suggest clues to his or her overall condition and stability. Inspection, palpation, and auscultation of the abdomen may disclose signs of abdominal inflammation, scars, abdominal bulges, hernias, or distention; symmetry; and skin color. The liver and spleen are measured, and abdominal percussion identifies the amount of air in the stomach and bowel. Percussion also identifies the presence of abdominal masses and ascites. Many individuals with cirrhosis in the early stage often present with few nonspecific symptoms, making the diagnosis less obvious.

Causes of liver injury are diverse, ranging from isolated and clinically silent laboratory abnormalities to dramatic and rapidly progressive liver failure. This spectrum relates in part to the broad range of pathophysiologic processes that can damage the liver and in part to the reserve capacity of the organ, which is large and can mask significant injury. It is estimated that approximately 40% of patients with cirrhosis are asymptomatic. When the diagnosis of end-stage liver disease is confirmed, the diagnosis often is confirmed before the patient seeks palliative care treatment (Fitz, 2003). However, some diagnostics may be appropriate and guide interventions that enhance the patient’s diagnosis and comfort. Plasma ammonia levels are often markedly elevated in end-stage liver disease (Kichian & Bain, 2003). The diagnosis of liver injury from acetaminophen toxicity should be confirmed by a serum acetaminophen level, laboratory markers include evaluating the aspartate aminotransferase, alanine aminotransferase, bilirubin, electrolytes, and prothrombin time. The clinician can also order an abdominal ultrasound and computed tomography scan to investigate for suspected biliary obstruction or abdominal masses (Kichian & Bain, 2003).

Human illness results from a complex interplay of clinical, biologic, psychologic, and sociologic variables. The clinician’s understanding of these diverse yet interacting variables is critical for appropriate treatment of end-stage liver disease (Yamada, 1998). The clinician aids in giving realistic prognostic information and facilitating exchange of information with every patient when discussing appropriate diagnostics in relationship to the goals of care. Skilled, compassionate palliative care clinicians should continue to use their expertise in maintaining safe prescribing practices by reviewing individual patients’ medication profiles on a routine basis, which will assist in avoiding adverse drug reactions and toxicities. Some adverse drug events can be minimized by reducing the number of drugs prescribed and by use of a dose interval and route based on known drug pharmacodynamics and pharmacokinetics (Bernard & Bruera, 2000).