Cirrhosis decompensated

Various NSAIDs have been shown to reduce GFR in patients with cirrhosis. Decompensated cirrhotic patients with ascites have the highest risk [35, 36]. 

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

Ascites is the accumulation of fluid in the peritoneal space and is often one of the first signs of decompensated liver disease. Ascites is the most common complication of cirrhosis and portends a dire prognosis.14... 

In some cases, cirrhosis is diagnosed incidentally before the patient develops symptoms or acute complications. Other patients may have decompensated cirrhosis at initial presentation they may present with variceal bleeding, ascites, SBP, or HE. Patients may also have some of the laboratory abnormalities and/or signs and symptoms listed above that are associated with cirrhosis.28... 

Approximately 20% of patients with chronic HBV infection develop complications of decompensated cirrhosis, including hepatic insufficiency and portal hypertension. HBV is a risk factor for development of hepatocellular carcinoma. 

The most common symptom of chronic HCV infection is persistent fatigue. An estimated 20% of patients with chronic HCV infection will develop cirrhosis and half of those patients will progress to decompensated cirrhosis or hepatocellular carcinoma. 

Decompensated liver disease is complicated by jaundice, refractory ascites, bacterial peritonitis, coagulopathy, and variceal bleeding and may require liver transplantation. The number of liver transplants for decompensated cirrhosis doubled from 1990 to 2004, when 5845 cadaveric (orthotopic) liver transplants were performed (65). 

Gynecomastia Gynecomastia may develop and appears to be related to dosage and duration of therapy. It is normally reversible when therapy is discontinued. Reversible hyperchloremic metabolic acidosis Reversible hyperchloremic metabolic acidosis, usually in association with hyperkalemia, occurs in some patients with decompensated hepatic cirrhosis, even in the presence of normal renal function. 

Duration of treatment - The optimal duration of adefovir treatment and the relationship between treatment response and long-term outcomes, such as hepatocellular carcinoma or decompensated cirrhosis, are not known. 

Hepatic function impairment Chronic hepatitis C patients with cirrhosis may be at risk of hepatic decompensation and death when treated with alfa interferons. 

Cirrhosis patients are at risk for hepatic decompensation if dehydration or hyponatremia occurs. 

Azizov KhA (1998) Surgical treatment of the patients with a liver cirrhosis in conditions portal hypertension decompensation with ascite syndrome. MD Thesis (in Russian) Tashkent, Uzbekistan, p 45... 

Interferon therapy should be used with great caution in patients with decompensated cirrhosis since treatment may flare their disease, resulting in hepatic failure, and is often associated with significant cytopenia or infection [30,31]. Other ab-... 

Typical side effects are constitutional in nature, including a flu-like syndrome within 6 hours after dosing in more than 30% of patients that tends to resolve upon continued administration. Other potential adverse effects include thrombocytopenia, granulocytopenia, elevation in serum aminotransferase levels, induction of autoantibodies, nausea, fatigue, headache, arthralgias, rash, alopecia, anorexia, hypotension, and edema. Severe neuropsychiatric side effects may occur. Absolute contraindications to therapy are psychosis, severe depression, neutropenia, thrombocytopenia, symptomatic heart disease, decompensated cirrhosis, uncontrolled seizures, and a history of organ transplantation (other than liver). Alfa interferons are abortifacient in primates and should not be administered in pregnancy. 

A 43-year-old woman was admitted to hospital in December feeling unwell with a two-week history of urinary symptoms. She had decompensated cirrhosis of her liver on ultrasound and was taking pentoxifylline (oxpentifylline, Trental), co-amoxiclav, omeprazole and thiamine. She was jaundiced and confused with respiratory failure limiting speech to partial sentences. There was a marked deterioration in liver function overnight and she went into acute renal failure. 

Diagnosis (including the presence or absence of fibrosis, cirrhosis and hepatic decompensation). 

Patient 4 Alcoholic liver disease Decompensated cirrhosis... 

This is helpful because it gives you clues as to what sort of liver picture you should expect to see in your patient. For example, if they have autoimmune hepatitis they will have a hepatic picture of liver dysfunction, which could range from mild fibrosis with fairly normal liver function to cirrhosis which may be decompensated - you can look for signs and symptoms to help yon decide how advanced their liver disease is. 

Other studies have also demonstrated similar increases in half-life when comparing paracetamol pharmacokinetics in patients with decompensated chronic liver disease to normal subjects. Patients with cirrhosis who have a normal plasma albumin concentration and PT have been shown to have a similar paracetamol half-life and clearance to those of healthy subjects. However, cirrhotic patients with a low plasma albumin and an increased PT were found to have a prolonged paracetamol half-life. Despite this, no accumulation and no evidence of hepatotoxicity was demonstrated when therapeutic doses of paracetamol were given to patients with decompensated liver diseases for three to five days [21]. 

Novartis Pharmaceuticals, the manufacturers of Voltarol , state that In patients with chronic hepatitis or non-decompensated cirrhosis. 

A limited number of small single-dose studies have demonstrated that morphine metabolism is impaired in patients with decompensated cirrhosis, and half-life can be doubled. Information on multiple morphine doses in cirrhotic patients is lacking, but because of the demonstrated prolonged half-life in single-dose studies, accumulation could occur, and an increased dosing interval of approximately twofold is recommended in some reports. 

Overall, clinical trials have shown that the metabolism of single doses of morphine is significantly impaired in patients with decompensated cirrhosis, bnt possibly not in those with compensated cirrhosis. 

Advice as for Patient 3, but greater care needs to be taken because increased accumulation is likely to occur as the metabolic capacity of the liver is affected in decompensated cirrhosis. Doses at the higher end of the range given are unlikely to be tolerated. 

Cyclizine, prochlorperazine and promethazine can be used with caution in patients whose metabolic and synthetic function is unaffected, but must be avoided in encephalopathic patients or in those with cirrhosis who may decompensate. 

Despite cirrhosis, this patient is maintaining good hepatocyte function (normal albumin and bilirubin, mildly raised INR) and the metabolic and excretory capacity of the liver should not be significantly reduced. The patient has portal hypertension, so blood flow to the liver will be impaired, which will reduce the first-pass metabolism of highly extracted drugs (extraction ratio >0.7). This will result in greater bioavailability of oral doses of these drugs. It is important to note that the patient could rapidly deteriorate into a state of decompensation where liver function would be markedly affected. 

HRT (oral and transdermal) should not be initiated or continued in patients with decompensated cirrhosis. The hepatocyte damage is irreversible and can only worsen over time. The significant reduction in metabolic capacity and reduction in hepatic blood flow will lead to drug accumulation, with consequent increased risk of hepatotoxicity. There is also the potential to worsen the cholestatic picture in this patient, who is already profoundly jaundiced. 

Decompensated cirrhosis - category 4 unacceptable health risk if method is used. 

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