TRIPASS XR تري باس

 

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p. 537

ASCITES

Cirrhosis is defined as the fibrosis of the hepatic parenchyma, resulting in

altered hepatic function, restricted venous outflow, and portal

hypertension. Cirrhosis results in an overall vasodilated state, activation

of the renin–angiotensin–aldosterone system, altered hepatic synthetic

function, and development of complications such as ascites and other

complications of cirrhosis.

Case 25-1 (Question 2)

Physical findings of ascites can include the presence of an enlarged

fluid-filled abdomen, increased abdominal girth, a positive fluid wave,

increased body weight and is often accompanied by peripheral edema.

The goals of treatment for ascites are to mobilize ascitic fluid, diminish

abdominal discomfort, as well as to prevent complications such as

bacterial peritonitis and respiratory distress.

Case 25-1 (Questions 1, 3)

The treatment for ascites involves sodium restriction (2 g/day), water

restriction for severe dilutional hyponatremia, and the use of

spironolactone and furosemide (100:40 mg ratio). Management and

monitoring of ascites includes ensuring adequate weight loss,

maintaining electrolyte balance, and preventing complications of diuretic

therapy.

Case 25-1 (Questions 4–8)

In cases of refractory ascites (diuretic-resistant), large-volume

paracentesis, along with albumin replacement, is often indicated.

Transjugular intrahepatic portosystemic shunt (TIPS), surgicalshunts,

and liver transplantation are the options for the treatment of refractory

ascites when paracentesis is deemed ineffective, or in patients who are

intolerant or who have a contraindication to paracentesis.

Case 25-1 (Questions 9–11)

Spontaneous bacterial peritonitis (SBP) is a common complication of

ascites. Prophylactic regimens include the long-term administration of

oral antibiotics such as fluoroquinolones (norfloxacin) or trimethoprimsulfamethoxazole to prevent the recurrence of SBP. Recommendations

also include the administration of antibiotic prophylaxis for prevention of

SBP in patients with variceal hemorrhage.

Case 25-2 (Question 4)

ESOPHAGEAL VARICES

Because esophageal varices are directly related to the severity of portal

hypertension, the treatment is aimed at primary prevention of bleeding

by reduction of portal pressure with the use of nonselective β-blockers,

and/or elimination of the varices with endoscopic variceal ligation

(EVL). Treatment approaches depend on the risk of hemorrhage.

Case 25-2 (Question 5)

Secondary prophylaxis to prevent recurrent bleeding episodes includes

the combination of nonselective β-blockers and EVL. TIPS may be an

option in patients who experience recurrent variceal hemorrhage despite

combination of pharmacologic and endoscopic therapy.

Case 25-2 (Question 6)

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p. 539

Acute variceal bleeding is considered a medical emergency and should

be treated immediately. Treatment goals include volume resuscitation,

acute treatment of bleeding, and prevention of recurrence of variceal

bleeding. For the control and management of acute hemorrhage, the

combination of pharmacologic therapy and variceal ligation is the

preferred approach. In cases of acute variceal bleeding uncontrolled by

pharmacologic and endoscopic therapy, TIPS can be an effective

option.

Case 25-2 (Questions 1–3)

HEPATIC ENCEPHALOPATHY

Hepatic encephalopathy is a metabolic disorder of the central nervous

system that occurs in patients with either advanced cirrhosis or

fulminate hepatic failure. The clinical features include altered mental

state and asterixis. Several theories exist about the pathogenesis of

hepatic encephalopathy; however, it is likely multifactorial. Precipitating

causes can include GI bleeding, diuretic-induced hypovolemia and/or

electrolyte abnormalities, metabolic alkalosis, as well as sedating drugs.

Case 25-3 (Questions 1–3)

After identifying and removing precipitating causes of hepatic

encephalopathy, therapeutic management is aimed primarily at reducing

the amount of ammonia or nitrogenous products in the circulatory

system by limiting protein intake and by the use of lactulose. Other

therapeutic options include rifaximin and neomycin.

Case 25-3 (Questions 4, 5)

Monotherapy with lactulose should be tried first. If satisfactory results

do not occur, switching to another option (rifamixin or neomycin) or

combination therapy should be considered.

Case 25-3 (Question 6)

HEPATORENAL SYNDROME

Hepatorenalsyndrome (HRS) is a complication of advanced cirrhosis

and is diagnosed by exclusion of other known causes of kidney disease.

The definitive treatment for type 1 and type 2 HRS is liver

transplantation, which is the only treatment that assures long-term

survival. The main goal of pharmacologic therapy is to reverse HRS

sufficiently so that appropriate candidates for liver transplantation can

survive untilsuitable donor organs can be procured.

Case 25-3 (Questions 7, 8)

OVERVIEW

According to the National Vital Statistics Report published by the Centers for

Disease Control and Prevention, chronic liver disease and cirrhosis is the 12th

leading cause of death in the United States, accounting for approximately 38,170

deaths each year.

1 Cirrhosis, or end-stage liver disease, can be defined as fibrosis of

the hepatic parenchyma resulting in nodule formation and altered hepatic function,

which results from a variety of causes. Although there are other common causes of

cirrhosis, most cases of cirrhosis worldwide result from chronic viral hepatitis or

chronic alcohol consumption.

2 This chapter describes the pathogenesis of cirrhosis

and the associated complications of portal hypertension (esophageal varices, gastric

varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and

hepatorenal syndrome) and their treatment.

PATHOGENESIS OF CIRRHOSIS

The liver consists of the hepatic parenchyma (hepatocytes) and a large proportion of

nonparenchymal cells, including sinusoidal endothelial cells, Ito cells, and

macrophages. Most of the liver’s role in detoxification takes place within the

hepatocytes. Also within the liver is the biliary tree in which bile drains from the

liver and some substances are actively transported into the bile.

3 The liver has a

strong capacity to regenerate; however, ethanol and hepatitis viruses can impair this.