Clinical Presentation And Diagnosis Diagnosis of Cirrhosis

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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. At diagnosis, patients may have some, all, or none of the laboratory abnormalities and/or

signs and symptoms that are associated with cirrhosis.

Ultrasound examination is used routinely to evaluate cirrhosis; a small, nodular liver with increased echogenicity is consistent with cirrhosis. Liver biopsy is the only way to diagnose cirrhosis definitively, but this is often deferred in lieu of a presumptive diagnosis. Because it is an invasive procedure, the decision to perform a biopsy is based on the expected clinical utility of the biopsy results. If the results have the potential to change the course of treatment, it may be advisable to perform a biopsy. The modified Child-Pugh and Model for End-Stage Liver Disease (MELD) classification systems (Table 22-1) are used to classify disease severity and evaluate the need for transplantation.

Clinical Presentation of Cirrhosis and Complications of Portal Hypertension

General

• Most signs and symptoms that bring a patient to the attention of medical personnel are specific to the complication the patient is experiencing at that time. The signs and symptoms vary with severity and suddenness of onset.

Symptoms

• Patients with cirrhosis may exhibit nonspecific symptoms such as fatigue and weakness but may be asymptomatic until acute complications develop.

• Nonspecific symptoms include anorexia, fatigue, and changes in libido and sleep patterns. Patients may also experience easy bruising and may bleed from minor injuries. Pruritus may be present, particularly with biliary involvement.

• Patients with ascites may complain of abdominal pain, nausea, increasing tightness and fullness in the abdomen, shortness of breath and early satiety.

• Hemorrhage from esophageal or gastric varices may be associated with melena, pallor, fatigue, and weakness from blood loss. Patients often present with nausea, vomiting, and hematemesis because blood in the Gl tract is nauseating. Bleeding from rectal varices may present as hematochezia.

• In patients with bleeding varices, digestion of swallowed blood represents a high protein load; this causes nausea and can precipitate symptoms of HE.

• In patients with HE, neurologic changes can be overwhelming or so subtle that they are not clinically apparent except during a targeted clinical evaluation.

• Patients with HE may complain of disruption of sleep patterns and day-to-night inversion; patients have delayed to-bed and wake times, which may progress to complete inversion of the normal diurnal cycle.

• If SBP occurs, symptoms of infection may include fever, chills, abdominal pain, and mental status changes.

Signs

• Nonspecific signs on physical exam include jaundice, scleral icterus, tea-colored urine, bruising, hepatomegaly, splenomegaly, spider angiomata, caput medusae, palmar erythema, gynecomastia, and testicular atrophy.

• Ascites can be detected by increased abdominal girth accompanied by shifting dullness and a fluid wave.

• Signs ofvariceal bleeding depend on the degree of blood loss and abruptness of onset. Rapid and massive blood loss is more likely to result in hemodynamic instability than is slow, steady bleeding. Signs of acute bleeding may include pallor, hypotension, tachycardia, mental status changes, and hematemesis.

• Markers of hepatic encephalopathy (HE) include decreased cognition, confusion, changes in behavior, and asterixis.

• Patients with SBP may present with fever, painful tympanic abdomen, and changes in mental status.

• Decreases in clotting factors may manifest as abnormal bruising and bleeding.

• Dupuytren contracture is a contraction of the palmar fascia that usually affects the

fourth and fifth digits. It is not specific to cirrhosis and can also be seen in repetitive use injuries.

Laboratory Abnormalities

• Hepatocellular damage manifests as elevated serum aminotransferases (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]). The degree of transaminase elevation does not correlate with the remaining functional metabolic capacity of the liver. An AST level two-fold higher than ALT is suggestive of alcoholic liver damage.

• Elevated alkaline phosphatase is nonspecific and may correlate with liver or bone disease; it tends to be elevated in biliary tract disease.

• y-Glutamyl transferase (GGT) is specific to the bile ducts, and in conjunction with an elevated alkaline phosphatase, suggests hepatic disease. Extremely elevated GGT levels further indicate obstructive biliary disease. GGT is also elevated in those who drink three or more alcoholic drinks daily.

• Increased total, direct, and indirect bilirubin concentrations indicate defects in transport, conjugation, or excretion of bilirubin.

• Lactate dehydrogenase (LDH) is a nonspecific marker of hepatocyte damage; disproportionate elevation of LDH indicates ischemic injury.

Thrombocytopenia may occur because of decreased platelet production and splenic platelet sequestration.

• Anemia (decreased hemoglobin and hematocrit) occurs as a result ofvariceal bleeding, decreased erythrocyte production, and hypersplenism.

• Elevated prothrombin time (PT) and international normalized ratio (INR) are coagulation derangements that indicate loss of synthetic capacity in the liver and correlate with functional loss of hepatocytes.

• Decreased serum albumin and total protein occur in chronic liver damage due to loss of synthetic capacity within the liver.

• The serum albumin-to-ascites gradient is 1.1 g/dL (11 g/L) or greater caused by portal hypertension.

• Increased blood ammonia concentration is characteristic of HE, but levels do not correlate well with the degree of impairment.

• Increased serum creatinine signaling a decline in renal function may be seen with hepatorenal syndrome.

• Signs and symptoms of SBP in a patient with cirrhosis and ascites should prompt a diagnostic paracentesis (Fig. 22-5). In SBP, there is decreased total serum protein, elevated white blood cell count (with left shift), and the ascitic fluid contains at least 250/mm3 (250 x 106/L) neutrophils. Bacterial culture of ascitic fluid may be positive, but lack of growth does not exclude the diagnosis.

Patients with ascites or known varices must be assumed to have portal hypertension and are treated as such, even if direct measurements of portal pressure have not been made.29

Table 22-1 Child-Pugh and MELD Classifications for Determining Severity of Liver Damage

Child-Pugh Classification"

Variable

1 Point

2 Points

3 Points

Bilirubin (mg/dL)

Less than 2

2-3

Greater than 3

0imol/L)

Less than 34

34-51

Greater than 51

Albumin (g/dL)

Greater than 3.5

2.8-3.5

Less than 2.8

(g/L)

Greater than 35

28-35

Less than 28

Prothrombin

1-3

4-6

Greater than 6

time (seconds

prolonged) or

INR

Less than 1.8

1.8-2.3

Greater than 2.3

Ascites

None

Slight

Moderate

Encephalopathy

None

Stages

Stages 3-4

1-2

The formula for the MELD score is 3.8 x Ln (bilirubin Img/dL]) + 11.2 x Ln(INR) + 9.6 x Ln(creatinine [mg/dL]) + 64 x (etiology: 0 if cholestatic or alcoholic, 1 otherwise) Using SI units, the MELD score is 3.8 x Ln(bilirubin [pmol/l] / 17.1) + 11.2 X Ln(INR) + 9.6 Ln(creatinine [pmol/L] /88.4) + 6.4 x (etiology: 0 if cholestatc or alcoholic, 1 otherwise)

INR, International Normalized Ratio; MELD, Model for Fnd-Stage Liver Disease; Ln, natural logarithm.

"Class A: 1 to 6 total points; B: 7 to 9 points; C: 10 to 15 points.

Pom Lucey MR, Brown KA, Everson GT, et al. Minimal criteria for placement of adults on the liver transplant waiting list: A report of a national conference organized by the American Society of T'ansplant Physicians and :he American Association for the Study of Liver Diseases. Liver Transpl Surq 1997;3:628-637; and Kamath

Diagnosis of Ascites

In obese patients or those with only small amounts of fluid accumulation, ultrasound evaluation may be necessary to detect ascites with certainty. Analysis of ascitic fluid obtained during paracentesis provides diagnostic clues to the etiology of the ascites. Diagnostic evaluation should include cell count with differential, albumin, total protein, Gram stain, and bacterial cultures. In patients without an established diagnosis of liver disease, the serum ascites-albumin gradient (SAAG) is sensitive in determining

if the ascites is caused by portal hypertension. SAAG compares the serum albumin concentration to the ascitic fluid albumin concentration:

Albserum - Albascites = SAAG A value of 1.1 g/dL or greater (11 g/L or greater) identifies portal hypertension

22 30

as the cause of the ascites with 97% accuracy. ' In portal hypertension, the ascitic fluid is low in albumin; this balances the oncotic pressure gradient with the hydrostatic pressure gradient of portal hypertension. The differential diagnoses for SAAG values less than 1.1 g/dL (less than 11 g/L) include peritoneal carcinoma, peritoneal infection (tuberculosis, fungal, or cytomegalovirus), and nephrotic syndrome. Serum albumin measurements should be made at the same time ascitic fluid is obtained for

an accurate comparison.

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