60-year-old with a distended abdomen
Patient will present as → a 63-year-old white male with a chief complaint of blood in his stool. He is accompanied by his wife who also reports weight gain, abdominal distension, and swelling of his legs. Physical exam reveals a healthy-appearing male with 3+ bilateral lower extremity edema and distended abdomen with evidence of shifting dullness. You also note several skin lesions seen here. The patient is hemoccult positive and has blood on his urine dipstick. He denies tobacco and illicit drug use but admits to drinking 1-2 x per week and has about 6 beers on each occasion.
Cirrhosis is a late stage of hepatic fibrosis that has resulted in a widespread distortion of normal hepatic architecture
- Characterized by regenerative nodules surrounded by dense fibrotic tissue
- The liver is unable to regenerate due to large amounts of scar tissue
Cirrhosis is a leading cause of death worldwide and is the ninth leading cause of death among U.S. adults
Causes include:
- Chronic hepatitis C (26%)
- Alcohol abuse (21%)
- Hepatitis C with alcoholic liver disease (15%)
- Nonalcoholic steatohepatitis/obesity (~10%)
- Hepatitis B + hepatitis D infection (15%)
- WILSON'S DISEASE: ↑ Copper, ↓ Ceruloplasmin + family history
Physical exam may be normal until end-stage disease:
- Hepatomegaly (small, fibrotic liver in end-stage disease)
- Terry’s nails (white nail beds)
- Splenomegaly (if portal hypertension)
- Central obesity
- Abdominal fluid wave, shifting dullness (ascites)
- Gynecomastia
- esophageal varices
- pulmonary edema/effusion
Classical skin changes: spider angiomata, palmar erythema, jaundice, scleral icterus, ecchymoses, caput medusae, hyperpigmentation
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- Spider Angioma
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- Palmar Erythema
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- Caput Medusae
Hepatic encephalopathy:
- Asterixis (flapping tremor), dysarthria, delirium, coma
Progressive cirrhosis
- Elevated ammonia level; BUN, sodium, and potassium
- α-fetoprotein level at diagnosis to screen for hepatocellular carcinoma (HCC)
- Abdominal ultrasound every 6 months to screen for hepatocellular carcinoma
- All patients with cirrhosis should undergo esophagogastroduodenoscopy (EGD) ⇒ Exclude esophageal varices
- MRI best follow-up test for HCC if α-fetoprotein elevated and/or liver mass found on ultrasound
- Noninvasive modalities, such as elastography, are being researched as an alternative to liver biopsy
- Update necessary immunizations and focus on the treatment of the underlying cause of cirrhosis (hepatitis C, alcohol abuse, etc.)
- Fever and abdominal pain in a patient with cirrhosis think spontaneous bacterial peritonitis
- Hepatocellular carcinoma: Monitor AFP
- Budd Chiari (hepatic vein thrombosis) triad of abdominal pain, ascites, and hepatomegaly
Labs: typically, AST > ALT, ↑ the risk for hepatocellular carcinoma: monitor AFP
- AST/ALT: mildly elevated ⇒ Typically AST > ALT. Enzymes normalize as cirrhosis progresses
- ↑ ALP and ↑ GGT
- Anemia from hemolysis, folate deficiency, and splenomegaly
- Decreased platelet count from portal hypertension with splenomegaly
- Decreased bilirubin conjugation by the liver ⇒ ↑ unconjugated bilirubin ⇒ jaundice
- Decreased albumin production by the liver ⇒ hypoalbuminemia
- Decreased clotting factor production by the liver ⇒ Prolonged prothrombin (PT), international normalized ratio (INR), partial thromboplastin time (PTT). Vitamin K–dependent clotting factors
- Ultrasound: helpful to determine the liver size and evaluate for hepatocellular carcinoma
- Liver biopsy is invasive and is subject to sampling error, but it remains the gold standard for the diagnosis of cirrhosis
- All patients with cirrhosis should undergo esophagogastroduodenoscopy (EGD) ⇒ Exclude esophageal varices
Child-Pugh Score for Cirrhosis Mortality
- Class A (5–6 points): one-year survival 100%, two-year survival 85%
- Class B (7–9 points): one-year survival 81%, two-year survival 57%
- Class C (10–15 points): one-year survival 45%, two-year survival 35%
Generally scarring from cirrhosis is irreversible ⇒ prevent further damage by identifying and treating the underlying cause
- Stop alcohol
- Antiviral treatment for Hepatitis C
- Corticosteroids for autoimmune hepatitis
- Chelation therapy (e.g., penicillamine) for Wilson's disease
- Diuretics, antibiotics, laxatives, enemas, thiamine, steroids, acetylcysteine, pentoxifylline for decompensation
- Nonselective beta-blockers (nadolol and propranolol) for primary prophylaxis against variceal hemorrhage or esophageal variceal ligation (EVL)
- For advanced cirrhosis ⇒ liver transplant may be necessary
- Encephalopathy ⇒ lactulose + neomycin
- Ascites ⇒ sodium restriction, paracentesis
- Pruritus: ⇒ cholestyramine
Spontaneous bacterial peritonitis is suspected in cases of unexplained fever and abdominal pain
 Osmosis |
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Picmonic
Cirrhosis Assessment
Cirrhosis is a chronic liver disease that evolves slowly, has a prolonged course, and occurs as a result of excessive alcohol intake, nonalcoholic fatty liver disease (NFLD), or chronic hepatitis C. As a result of these disorders, cirrhosis stems from degeneration and destruction of liver cells.
Play Video + QuizComplications of cirrhosis
Patients with cirrhosis are at risk of developing several major complications, such as portal hypertension. This can lead to ascites and esophageal varices. Other complications include decreased liver function, which manifests as coagulation defects. Encephalopathy can occur from ammonia buildup, and hepatorenal syndrome, leading to renal failure
Cirrhosis Interventions
Care of the patient with cirrhosis involves relieving the discomfort from ascites, excess fluid volume, skin changes, nutritional deficiencies, and preventing complications associated with hematologic problems, esophageal and gastric varices, and hepatic encephalopathy. Patients should avoid alcohol, NSAIDs, and other medications that impair liver function.
Play Video + QuizQuestion 1 |
A 65-year old man with liver cirrhosis was brought to the emergency room by his relative on account of altered sleep pattern, irritability, drowsiness and slowed slurred speech. His relative also said that he has been constipated for the past one week. Significant examination findings revealed fetor hepaticus, asterixis, and constructional apraxia. Which of the following is not applicable in the management of this patient?
Lactulose Hint: Lactulose, a nonabsorbable synthetic disaccharide syrup, is digested by bacteria in the colon to short-chain fatty acids, resulting in acidification of colon contents. This acidification favors the formation of ammonium ion in the NH4+ ↔NH3+H+ equation; NH4+ is not absorbable, whereas NH3 is absorbable and thought to be neurotoxic. Lactulose also leads to a change in bowel flora so that fewer ammonia-forming organisms are present. Lactulose will also stop the constipation which precipitated the hepatic encephalopathy. | |
Rifaximin Hint: Rifaximin, a nonabsorbable oral antibiotic is used to control ammonia-producing intestinal flora. It has been shown as well to maintain remission from and reduce the risk of re-hospitalization for hepatic encephalopathy. | |
Flumazenil Hint: Flumazenil is used to lower blood ammonia levels. | |
Midazolam |
Question 1 Explanation:
Midazolam is a sedative. Sedatives should not be given to patients with HEPATIC ENCEPHALOPATHY as they can worsen patient’s condition.
Question 2 |
The ascites associated with cirrhosis generally should be treated by which of the following?
sodium restriction | |
water restriction | |
spironolactone | |
furosemide | |
a, c, and d |
Question 2 Explanation:
The treatment of ascites and the edema associated with ascites includes the following: (1) sodium restriction to 800 mg of Na+/day (or 2 g of NaCl); (2) spironolactone (Aldactone), 25 to 100 mg four times per day (effective in 40% to 75% of cases); (3) paracentesis; (4) combination diuretic therapy with furosemide in those patients who do not respond, with either spironolactone plus hydrochlorothiazide or spironolactone plus furosemide; and (5) paracentesis with albumin (or dextran) infusion in refractory cases. There must be complete abstention from alcohol. Fluid restriction is unnecessary unless serum sodium concentration is less than 120 to 125 mEq/L.
The 1-year survival rate of patients with cirrhosis with ascites is 50%, compared with 90% in patients with uncomplicated cirrhosis. Formation of ascites results from a combination of portal hypertension, hypoalbuminemia, lymphatic leakage, and sodium retention. The management of ascites in patients with cirrhosis is complicated. Diagnostic paracentesis should be performed in any patient with cirrhosis who undergoes clinical deterioration. Defined indications for the treatment of ascites include significant patient discomfort, respiratory compromise, large umbilical hernia, and recurrent bacterial peritonitis.
Sodium restriction is considered the cornerstone of therapy for ascites. Patients with cirrhosis require significant curtailment of sodium intake (800 mg/day) to obtain clinical benefit. Approximately 10% to 20% of patients who maintain a strict low-salt diet achieve complete resolution of ascites without additional therapy. However, hyponatremia may accompany sodium restriction, and severe hyponatremia (serum sodium concentration of less than 125 mEq) is a reason to begin fluid restriction as well. The majority of patients will also require diuretics.
Spironolactone (Aldactone), an aldosterone antagonist, is the first-line diuretic of choice in the treatment of cirrhotic ascites. It is effective in controlling up to 50% of patients with cirrhosis. Other potassium-sparing diuretics may be substituted for spironolactone, including triamterene and amiloride. The addition of loop diuretics (e.g., furosemide) is sometimes needed to achieve maximum benefit. Alternatives to furosemide include bumetanide and torsemide. Watch for hypokalemia with diuretics. Up to 90% of patients with cirrhosis and ascites will respond to diuretics and salt restriction. For those who do not, periodic paracentesis with albumin replacement is an alternative, as are portacaval shunts and transjugular intrahepatic portosystemic shunts, the latter for those requiring frequent large-volume paracentesis.
Question 3 |
One of the following is not a feature of decompensated liver cirrhosis.
Jaundice | |
Hepatic encephalopathy | |
Ascites | |
Constipation |
Question 3 Explanation:
Constipation is not a feature of decompensated liver cirrhosis. All other options are.
Question 4 |
A 60-year old man presents to you on account of right hypochondrial pain, anorexia, and fatigue. On history taking, patient revealed that he has been taking excessive alcohol for over 20 years. Physical examination reveals icterus, gynecomastia, spider angioma, hepatomegaly, shifting dullness, visibly distended abdominal wall veins. Serum AST, AST, and ALP are elevated. Which of the following is the most likely diagnosis?
Liver abscess Hint: Patient with liver abscess will have same symptoms and fever. Alcohol ingestion is not a risk factor for abscess. | |
Hepatic encephalopathy Hint: Hepatic encephalopathy is a complication of cirrhosis. Patient would have presented with altered sleep pattern, mental confusion, drowsiness. | |
Liver cirrhosis | |
Acute viral hepatitis Hint: Patient with acute viral hepatitis may present with the same symptoms and hepatomegaly, but not ascites, gynecomastia, spider angioma, distended abdominal veins. |
Question 4 Explanation:
With a prolonged history of excessive alcohol ingestion and presence of peripheral stigmata of chronic liver disease(icterus, gynecomastia, spider angioma, ascites elicited by shifting dullness, distended abdominal veins , liver cirrhosis is the most likely diagnosis. Patient with acute viral hepatitis may present with the same symptoms and hepatomegaly, but not ascites, gynecomastia, spider angioma, distended abdominal veins. Hepatic encephalopathy is a complication of cirrhosis. Patient would have presented with altered sleep pattern, mental confusion, drowsiness. Patient with liver abscess will have same symptoms and fever. Alcohol ingestion is not a risk factor for abscess.
Question 5 |
Which of the following is (are) appropriate treatments for cirrhosis of the liver?
cessation of alcohol use | |
beta blockers | |
maintenance of proper nutrition | |
liver transplantation | |
all of the above |
Question 5 Explanation:
In uncomplicated cirrhosis, treatment includes cessation of alcohol use, maintenance of proper nutrition, and use of beta blockers to reduce portal hypertension. Patients with uncomplicated cirrhosis may have a relatively benign course of illness for many years. Once the patient has an episode of decompensation, such as fluid retention, variceal bleeding, encephalopathy, spontaneous bacterial peritonitis, or hepatorenal syndrome, mortality is high without transplantation.
Question 6 |
Which of the following is not a common cause of liver cirrhosis in the United States?
Alcoholic liver disease Hint: is a common cause of liver cirrhosis in the United States (21%). | |
Chronic hepatitis C infection Hint: is a common cause of liver cirrhosis in the United States (26%). | |
Wilson’s disease | |
Nonalcoholic fatty liver disease Hint: is a common cause of liver cirrhosis in the United States (18%). |
Question 6 Explanation:
Wilson's disease is a rare inherited disorder that causes too much copper to accumulate in your liver, brain and other vital organs. It is not a common cause of liver cirrhosis. Patients with Wilson's disease will have abnormal lab values: ↑ Copper, ↓ Ceruloplasmin + family history.
Question 7 |
Which of the following describes the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen seen in patients with cirrhosis?
caput medusae | |
spider angiomata Hint: Spider angioma is an abnormal collection of blood vessels near the surface of the skin. | |
palmar erythema Hint: Palmar erythema is a reddening of the skin on the palmar aspect of the hands, usually over the hypothenar eminence. It may also involve the thenar eminence and fingers. It can also be found on the soles of the feet, when it is termed plantar erythema. | |
scleral icterus Hint: The yellowing of the "white of the eye" is thus more properly termed conjunctival icterus. The term "icterus" itself is sometimes incorrectly used to refer to jaundice that is noted in the sclera of the eyes, however its more common and more correct meaning is entirely synonymous with jaundice. |
Question 7 Explanation:
Caput medusae, also known as palm tree sign, is the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen.
There are 7 questions to complete.
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References: Merck Manual · UpToDate
