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GASTROINTESTINAL SYSTEM

543

Signs and symproms of cirrhosis include the followingl9,52,6L

•

Recent weight loss or gain

•

Fatigability

• Jaundice

•

Lower-extremity edema

• Anorexia, nausea, or vomiting

•

Fever

• Decreased urine outpur (urine dark yellow or amber)

• Associated GI manifestations of esophageal varices, bowel habit

changes, and GI bleeding

• Altered mental status

Management of cirrhosis includes the following",6I:

• Supportive care, including i.v. fluids, whole blood and blood

products, colloid (albumin), vitamin and electrolyte replacement,

and dietary and behavioral modifications (eliminate alcohol consumption)

• Medical correction, surgical correction, or both of primary etiology or secondary complications as indicated

• Paracentesis

• Supplemental oxygen

•

Liver transplantation (see Chapter 12)

Hepatic Encephalopathy and Coma

Acute and chronic liver diseases, particularly cirrhosis, may lead to

neuropsychiatric manifestations that may progress from hepatic

encephalopathy to precoma ro coma. The majority of neuropsychiatric manifestations are linked to ammonia intoxication from faulty liver metabolisrn.39,52

Signs and symptoms of hepatic encephalopathy that may progress

to coma include the following:

544

AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS

• Altered states of consciousness (e.g., lethargy, stupor, confusion,

slowed responses)

• Neuromuscular abnormalities (e.g., tremor, dyscoordination,

slurred speech, altered reflexes, ataxia, rigidity, Babinski's sign, and

impaired handwriting)

• Altered intellectual function (decreased attention span, amnesia,

disorientation)

• Altered personality and behavioral changes (euphoria or depression, irritability, anxiety, paranoia, rage)

Management of hepatic encephalopathy and coma may consist of

any of the following.l9•52:

• Administering nonabsorbable disaccharides, such as lactulose, is

the mainstay of treatment

• Correction of fluid and electrolyte or acid-base imbalances, or

both

• Supplemental oxygen

• Removal of any precipitating substances

• Gastric lavage or enemas

• Ammonia detoxicants

• Anti-infective agents

• Surgical correction of causal or contributing factors (rare)

Clinical Tip

Hepatic encephalopathy may also be referred to as portal

systemic encephalopathy (PSE) because of the association

between portal hypertension and cirrhosis in the development of encephalopathy.

Cholecystitis with Cholelithiasis

Cholecystitis is acute or chronic inflammation of the gallbladder. It is

associated with obstruction by gallstones in 90% of cases. Gallstone

formation (cholelithiasis) is associated with three factors: gallbladder

GASTROII'ITF..5TINAl SYSTEM

545

hypomobility, supersaturation of bile with cholesterol, and crystal

formation from an increased concemration of insoluble bilirubin in

the bile. Cholelithiasis can lead to secondary bacterial infection that

further exacerbates the cholecystitis.39,,,

Signs and symptoms of cholecystitis include the following",4o.62:

• Severe abdominal pain in right upper quadrant with possible

pain referral to interscapular region

• Rebound tenderness and abdominal rigidity

• Jaundice

• Anorexia

•

ausea, vomiting, or both

• Fever

Management of cholecystitis includes any of the following39,,,:

• Laparoscopic cholecystectomy or cholecystostomy (temporary

drain placement in the gallbladder until obstruction is relieved)

• Gallstone dilution therapy with chenodeoxycholic and ursodeoxycholic acid

• Anti-infective agents

• Pain management

• i. v. fluids

• Insertion of nasogastric tube

Pallereatic Disorders

Pancreatitis

Inflammation of the pancreas can be acute or chronic. The incidence

of acute pancreatitis is rising, and the clinical sequelae are potentially fatal, including adult respiratory distress syndrome (ARDS) and shock. This section therefore focuses on acute pancreatitis.

Acute pancreatitis can be categorized as necrotizing or interstitial.

Pancreatitis involves an exaggerated release and activity of pancreatic enzymes into the peritoneal cavity, along with autodigestion of pancreatic parenchyma. The exact trigger to this process is