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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2737_Библиотеки_им_академика_М_И_Перельмана
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Diagnosis
CONFIRMING DIAGNOSIS Ultrasound and computed tomography (CT) scan with contrast
medium can accurately define intrahepatic lesions and assess intra-abdominal pathology.
Percutaneous needle aspiration and drainage of the abscess can be performed using ultrasound
or CT guidance to identify the causative organism.
Relevant laboratory values include elevated serum aspartate aminotransferase, alanine
aminotransferase, alkaline phosphatase, and bilirubin levels; increased WBC count; and
decreased serum albumin levels. A blood culture can identify the bacterial agent; in amebic
abscess, a stool culture and serologic and hemagglutination tests can assist in diagnosis.
Treatment
If the organism causing the liver abscess is unknown, long-term antibiotic therapy begins
immediately. When culture results are obtained, antibiotics are prescribed specific to treat the
organism. I.V. antibiotic therapy usually continues for 14 days and then is replaced with an oral
preparation to complete a 6-week course. Surgery is usually avoided, but it may be done for a
single pyogenic abscess or for an amebic abscess that fails to respond to antibiotics. Placement of
drains (using CT or ultrasound guidance), particularly in large abscesses, reduces the need for
abdominal surgery. In acutely toxic patients, percutaneous needle aspiration and decompression
may be needed to remove the abscess.
Special Considerations
Provide supportive care, monitor the patient’s vital signs (especially temperature), and
maintain fluid and nutritional intake.
Administer anti-infectives and antibiotics as ordered, and watch for possible adverse effects.
Stress the importance of compliance with therapy.
Explain diagnostic and surgical procedures.
Watch carefully for complications of abdominal surgery, such as hemorrhage or sepsis.
FATTY LIVER
Fatty liver, also known as steatosis or nonalcoholic steatohepatitis (NAFLD), is a common
clinical finding consisting of accumulated triglycerides and other fats in liver cells. In severe
fatty liver, fat comprises as much as 40% of the liver’s weight (as opposed to 5% in a normal
liver), and the weight of the liver may increase from 3.31 lb (1.5 kg) to as much as 11 lb (4.9 kg).
Minimal fatty changes are temporary and asymptomatic; severe or persistent changes may cause
liver dysfunction. Fatty liver is reversible by simply eliminating the cause.
Causes and Incidence
Chronic alcoholism is the most common cause of fatty liver in the United States and in Europe,
with the severity of hepatic disease directly related to the amount of alcohol consumed. (Fatty
liver can occur in people who consume as little as 10 oz of alcohol per week.)
Other causes of nonalcoholic steatohepatitis include malnutrition (especially protein
deficiency), obesity, diabetes mellitus, jejunoileal bypass surgery, Cushing syndrome, Reye
syndrome, pregnancy, large doses of hepatotoxins such as I.V. tetracycline, carbon tetrachloride
intoxication, prolonged parenteral nutrition, and DDT poisoning. Whatever the cause, fatty
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infiltration of the liver probably results from mobilization of fatty acids from adipose tissues or
altered fat metabolism.
Pathophysiology
Steatosis, the earliest response of the liver to alcohol abuse, is characterized by the accumulation
of fat (mainly triglycerides, phospholipids, and cholesterol esters) in hepatocytes. Early studies
indicated that alcohol consumption increases the ratio of reduced nicotinamide adenine
dinucleotide/oxidized nicotinamide adenine dinucleotide in hepatocytes, which disrupts
mitochondrial beta-oxidation of fatty acids and results in steatosis. Alcohol intake has also been
shown to augment the supply of lipids to the liver from the small intestine, increasing
mobilization of fatty acids from adipose tissue and uptake of fatty acids by the liver.
Nonalcoholic steatohepatitis mechanism is complex and incompletely understood; a two-hit
hypothesis has been proposed, in which the first hit involves an imbalance of fatty acid
metabolism that leads to hepatic triglyceride accumulation (steatosis). The second hit may be
oxidative or metabolic stress and dysregulated cytokine production resulting from efforts to
compensate for altered lipid homeostasis, leading to subsequent inflammation and fibrosis. Data
show that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD.
Complications
Cirrhosis
Portal hypertension
Metabolic disturbances and insulin assistance
Renal failure
Coma
Signs and Symptoms
Clinical features of fatty liver vary with the degree of lipid infiltration, and many patients are
asymptomatic. The most typical sign is a large, tender liver (hepatomegaly). Common signs and
symptoms include right upper quadrant pain (with massive or rapid infiltration), ascites, edema,
jaundice, and fever (all with hepatic necrosis or biliary stasis). (See Signs of liver failure, page
281.) Nausea, vomiting, and anorexia are less common. Splenomegaly frequently accompanies
cirrhosis. Rarer changes are spider angiomas, varices, transient gynecomastia, and menstrual
disorders.
Signs of Liver Failure
Liver failure may be a complication of hepatitis, cirrhosis, and fatty liver. The signs of liver
failure may be visible in many areas of the body.
Diagnosis
Typical clinical features—especially in patients with chronic alcoholism, malnutrition, poorly
controlled diabetes mellitus, or obesity—suggest fatty liver.
CONFIRMING DIAGNOSIS A liver biopsy confirms excessive fat in the liver. These liver
function tests support this diagnosis:
Albumin—somewhat low
Globulin—usually elevated
Cholesterol—usually elevated
Total bilirubin—elevated
Alkaline phosphatase—elevated
Transaminase—elevated
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Prothrombin time—possibly prolonged.
Other findings may include anemia, leukocytosis, elevated WBC count, albuminuria,
hyperglycemia or hypoglycemia, and iron, folic acid, and vitamin B12 deficiencies.
Treatment
Treatment of fatty liver is essentially supportive and consists of correcting the underlying
condition or eliminating its cause. For instance, when fatty liver results from parenteral nutrition,
decreasing the rate of carbohydrate infusion may correct the disease. In alcoholic fatty liver,
abstinence from alcohol and a proper diet can begin to correct liver changes within 4 to 8 weeks.
In nonalcoholic fatty liver disease, gradual weight loss is the standard treatment.
Special Considerations
Providing support to the patient and family is an important element in the care of the patient with
steatosis.
Suggest counseling for the alcoholic patient and provide emotional support for the family.
Teach the patient with diabetes—and family—about proper care, such as the purpose of
insulin injections, diet, and exercise. Refer the patient to home health nurses or to group
classes, as necessary, to promote compliance with treatment. Emphasize the need for longterm medical supervision and urge the patient to report any changes in health immediately.
Instruct an obese patient and their family about proper diet. Warn against fad diets, which are
usually nutritionally inadequate. Recommend medical supervision for a patient who’s more
than 20% overweight. Encourage attendance at group diet and exercise programs and, if
necessary, suggest behavior modification programs to correct eating habits. Be sure to follow
up on the patient’s progress and provide positive reinforcement for any weight loss.
Assess for malnutrition, especially protein deficiency, in the patient with chronic illness.
Suggest dietary changes and refer the patient to a dietitian.
Advise patients receiving hepatotoxins and those at risk for occupational exposure to watch
for and immediately report signs of toxicity.
Inform the patient that fatty liver is reversible only if they strictly follow the therapeutic
program; otherwise, the patient risks permanent liver damage.
HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy, also known as portosystemic encephalopathy or hepatic coma, is a
neurologic syndrome that develops as a complication of chronic liver disease. It may be acute
and self-limiting or chronic and progressive. Treatment requires correction of the precipitating
cause and reduction of blood ammonia levels. In advanced stages, the prognosis is extremely
poor despite vigorous treatment.
Causes and Incidence
Hepatic encephalopathy follows rising blood ammonia levels.
Other factors that predispose to rising ammonia levels include excessive protein intake, sepsis,
excessive accumulation of nitrogenous body wastes (from constipation or GI hemorrhage), and
bacterial action on protein and urea to form ammonia. Certain other factors heighten the brain’s
sensitivity to ammonia intoxication: hypoxia, azotemia, impaired glucose metabolism, infection,
and administration of sedatives, narcotics, and general anesthetics. Depletion of the intravascular
volume, from bleeding or diuresis, reduces hepatic and renal perfusion and leads to contraction
alkalosis. In turn, hypokalemia and alkalosis increase ammonia production and impair its
excretion.
Complication
Irreversible coma
Death
Pathophysiology
Most common in patients with cirrhosis, this syndrome is due primarily to ammonia intoxication
of the brain. Normally, the ammonia produced by protein breakdown in the bowel is metabolized
to urea in the liver. When portal blood shunts past the liver, ammonia directly enters the systemic
circulation and is carried to the brain. Such shunting may result from the collateral venous
circulation that develops in portal hypertension or from surgically created portosystemic shunts
(such as a TIPS). Cirrhosis further compounds this problem because impaired hepatocellular
function prevents conversion of ammonia that reaches the liver.
Signs and Symptoms
Clinical manifestations of hepatic encephalopathy vary (depending on the severity of neurologic
involvement) and develop in four stages:
In stage I (minimal hepatic encephalopathy), early signs and symptoms are commonly
overlooked because they’re so subtle: slight personality changes (disorientation, forgetfulness,
and slurred speech) and a slight tremor.
During the stage II, tremor progresses into asterixis (liver flap and flapping tremor), the
hallmark of hepatic encephalopathy. Asterixis is characterized by quick, irregular extensions
and flexions of the wrists and fingers, when the wrists are held out straight and the hands
flexed upward. Lethargy, aberrant behavior, and apraxia also occur.
At the stage III, hyperventilation occurs; the patient is typically stuporous, but becomes noisy
and abusive when aroused.
In stage IV, the patient has hyperactive reflexes, a positive Babinski sign, fetor hepaticus
(musty, sweet odor to the breath), and coma.
Diagnosis
CONFIRMING DIAGNOSIS Clinical features, a history of liver disease, and elevated serum
ammonia levels in venous and arterial samples confirm hepatic encephalopathy.
Treatment
Effective treatment stops progression of encephalopathy by reducing blood ammonia levels.
Treatment includes eliminating ammonia-producing substances from the GI tract by
administering rifaximin to suppress bacterial flora (preventing the conversion of amino acids into
ammonia), performing sorbitol-induced catharsis to produce osmotic diarrhea and continuous
aspiration of blood from the stomach, and reducing dietary protein intake.
Lactulose, which traps ammonia in the bowel and promotes its excretion, is administered to
reduce blood ammonia levels. Bacterial enzymes change lactulose to lactic acid, thereby
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rendering the colon too acidic for bacterial growth. At the same time, the resulting increase in
free hydrogen ions prevents diffusion of ammonia through the mucosa; lactulose promotes
conversion of systemically absorbable ammonia to ammonium, which is poorly absorbed and
can be excreted. It is usually given orally. However, if the patient is in a coma, it may be
administered by retention enema.
Treatment may also include potassium supplements to correct alkalosis due to increased
ammonia levels, especially if the patient is taking diuretics. Hemodialysis may sometimes be
used to clear toxic blood temporarily. Salt-poor albumin may be used to maintain fluid and
electrolyte balance, replace depleted albumin levels, and restore plasma. Sedatives, tranquilizers,
and other medications metabolized or excreted by the liver should be avoided if possible.
Medications containing ammonium (including certain antacids) should also be avoided.
Special Considerations
Patient care includes monitoring symptoms and support.
Assess and record the patient’s level of consciousness frequently. Continually orient the
patient to place and time. Keep a daily record of the patient’s handwriting to monitor the
progression of neurologic involvement.
Monitor the patient’s intake, output, and fluid and electrolyte balance. Check daily weight and
measure abdominal girth. Watch for, and immediately report, signs of anemia (decreased
hemoglobin level), infection, alkalosis (increased serum bicarbonate), and GI bleeding
(melena and hematemesis).
If the encephalopathy is acute, ask the dietary department to provide the specified low-protein
diet, with carbohydrates supplying most of the calories.
Promote rest, comfort, and a quiet atmosphere. Prevent falls.
Use restraints, if necessary, but avoid sedatives. Protect the comatose patient’s eyes from
corneal injury by using artificial tears or eye patches.
Provide emotional support for the patient’s family in the terminal stage of encephalopathy.
Gallbladder and Duct Disorders
CHOLELITHIASIS AND RELATED DISORDERS
Diseases of the gallbladder and biliary tract are common and, in many cases, painful conditions
that frequently require surgery and may be life-threatening. They are generally associated with
deposition of calculi and inflammation. (See Understanding gallstone formation, page 284.)
PATHOPHYSIOLOGY
UNDERSTANDING GALLSTONE FORMATION
Abnormal metabolism of cholesterol and bile salts plays an important role in gallstone
formation. Bile is made continuously by the liver and is concentrated and stored in the
gallbladder until the duodenum needs it to help digest fat. Changes in the composition of bile
may allow gallstones to form. Changes to the absorptive ability of the gallbladder lining may
also contribute to gallstone formation.
Too Much Cholesterol
Certain conditions, such as age, obesity, and estrogen imbalance, cause the liver to secrete
bile that’s abnormally high in cholesterol or lacking the proper concentration of bile salts.
Jaundice, Irritation, Inflammation
If a stone lodges in the common bile duct, the bile flow into the duodenum becomes
obstructed. Bilirubin is absorbed into the blood, causing jaundice.
Biliary narrowing and swelling of the tissue around the stone can also cause irritation and
inflammation of the common bile duct.
Inside the Gallbladder
When the gallbladder concentrates this bile, inflammation may occur. Excessive water and
bile salts are reabsorbed, making the bile less soluble. Cholesterol, calcium, and bilirubin
precipitate into gallstones.
Fat entering the duodenum causes the intestinal mucosa to secrete the hormone
cholecystokinin, which stimulates the gallbladder to contract and empty. If a stone lodges in
the cystic duct, the gallbladder contracts but can’t empty.
Up The Biliary Tree
Inflammation can progress up the biliary tree and cause infection of any of the bile ducts.
This causes scar tissue, fluid accumulation, cirrhosis, portal hypertension, and bleeding.
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Causes and Incidence
Cholelithiasis, stones or calculi (gallstones) in the gallbladder, results from changes in bile
components. Gallstones are made of cholesterol, calcium bilirubinate, or a mixture of cholesterol
and bilirubin pigment. They arise during periods of sluggishness in the gallbladder due to
pregnancy, hormonal contraceptives, diabetes mellitus, celiac disease, cirrhosis of the liver, and
pancreatitis. Cholelithiasis is a common health problem, affecting about 50% of white women
and 30% of white men. The prognosis is usually good with treatment unless infection occurs, in
which case the prognosis depends on its severity and response to antibiotics.
One out of every 10 patients with gallstones develops choledocholithiasis, or gallstones in the
common bile duct (sometimes called common duct stones). This occurs when stones passed out
of the gallbladder lodge in the hepatic and common bile ducts and obstruct the flow of bile into
the duodenum. Prognosis is good unless infection occurs.
Cholangitis, infection of the bile duct, is commonly associated with choledocholithiasis and
may follow percutaneous transhepatic cholangiography or occlusion of endoscopic stents.
Predisposing factors may include bacterial or metabolic alteration of bile acids. Widespread
inflammation may cause fibrosis and stenosis of the common bile duct. The prognosis for this
condition is poor without stenting or surgery.
Cholecystitis, acute or chronic inflammation of the gallbladder, is usually associated with a
gallstone impacted in the cystic duct, causing painful distention of the gallbladder. Cholecystitis
accounts for most patients requiring gallbladder surgery. The acute form is most common during
middle age; the chronic form usually occurs among elderly patients. The prognosis is good with
treatment.
Biliary cirrhosis is a disorder whose primary cause is unknown. This condition usually leads
to obstructive jaundice and involves the portal and periportal spaces of the liver. It is nine times
more common among women 40 to 60 years old than among men. The prognosis is poor without
liver transplantation.
Gallstone ileus results from a gallstone lodging at the terminal ileum; it’s more common in the
elderly. The prognosis is good with surgery.
Postcholecystectomy syndrome is the presence of GI symptoms after cholecystectomy. It
occurs in 10% to 15% of all patients whose gallbladders have been surgically removed and may
produce right upper quadrant abdominal pain, biliary colic, fatty food intolerance, dyspepsia, and
indigestion. The prognosis is good with selected radiologic procedures, endoscopic procedures,
or surgery.
Acalculous cholecystitis is more common in critically ill patients, accounting for about 5% of
cholecystitis cases. It may result from primary infection with such organisms as Salmonella
typhi, E. coli, or Clostridium or from obstruction of the cystic duct due to lymphadenopathy or a
tumor. It appears that ischemia, usually related to a low cardiac output, also has a role in the
pathophysiology of this disease. Signs and symptoms of acalculous cholecystitis include
unexplained sepsis, right upper quadrant pain, fever, leukocytosis, and a palpable gallbladder.
Each of these disorders produces its own set of complications. Cholelithiasis may lead to any
of the disorders associated with gallstone formation: cholangitis, cholecystitis,
choledocholithiasis, and gallstone ileus. Cholecystitis can progress to gallbladder complications,
such as empyema, hydrops or mucocele, or gangrene. Gangrene may lead to perforation,
resulting in peritonitis, fistula formation, pancreatitis, limy bile, and porcelain gallbladder. Other
complications include chronic cholecystitis and cholangitis.
Choledocholithiasis may lead to cholangitis, obstructive jaundice, pancreatitis, and secondary
biliary cirrhosis. Cholangitis, especially in the suppurative form, may progress to septic shock
and death. Gallstone ileus may cause bowel obstruction, which can lead to intestinal perforation,
peritonitis, septicemia, secondary infection, and septic shock.
In most cases, gallbladder and bile duct diseases occur in people who are older than 40 years;
they are more prevalent in women and Native Americans.
Complications
Each of these disorders produces a set of complications.
Cholelithiasis may lead to any of the disorders associated with gallstone formation:
cholangitis, cholecystitis, choledocholithiasis, and gallstone ileus.
Cholecystitis can progress to gallbladder complications, such as empyema, hydrops or
mucocele, and gangrene. Gangrene may lead to perforation, resulting in peritonitis, fistula
formation, pancreatitis, limy bile syndrome, and porcelain gallbladder. Other complications
include chronic cholecystitis and cholangitis.
Cholecholithiasis may lead to cholangitis, obstructive jaundice, pancreatitis, and secondary
biliary cirrhosis.
Cholangitis may progress to septic shock and death, especially in the suppurative form.
Gallstone ileus may cause bowel obstruction, which can lead to intestinal perforation,
peritonitis, septicemia, secondary infection, and septic shock.
Signs and Symptoms
Although gallbladder disease may produce no symptoms, acute cholelithiasis, acute cholecystitis,
and choledocholithiasis produce the symptoms of a classic gallbladder attack. Attacks usually
follow meals rich in fats or may occur at night, suddenly awakening the patient. They begin with
acute abdominal pain in the right upper quadrant that may radiate to the back, between the
shoulders, or to the front of the chest; the pain may be so severe that the patient seeks emergency
department care. Other features may include recurring fat intolerance, biliary colic, belching,
flatulence, indigestion, diaphoresis, nausea, vomiting, chills, low-grade fever, jaundice (if a stone
obstructs the common bile duct), and clay-colored stools (with choledocholithiasis).
Clinical features of cholangitis include a rise in neutrophils, jaundice, right upper quadrant
abdominal pain, high fever, and chills; biliary cirrhosis may produce jaundice, related itching,
weakness, fatigue, slight weight loss, and abdominal pain. Gallstone ileus produces signs and
symptoms of small-bowel obstruction—nausea, vomiting, abdominal distention, and absent
bowel sounds if the bowel is completely obstructed. Its most telling symptom is intermittent
recurrence of colicky pain over several days.
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Diagnosis
Ultrasonography detects gallstones. Other tests may include the following:
Abdominal CT scan may detect stones in the gallbladder.
Percutaneous transhepatic cholangiography, done under fluoroscopic control, distinguishes
between gallbladder or bile duct disease and cancer of the pancreatic head in patients with
jaundice.
ERCP visualizes the biliary tree after insertion of an endoscope down the esophagus into the
duodenum, cannulation of the common bile and pancreatic ducts, and injection of contrast
medium.
HIDA scan detects obstruction of the cystic duct.
Magnetic resonance cholangiopancreatography can detect gallstones, choledocholithiasis,
masses, biliary strictures, and dilation.
Elevated total bilirubin, urine bilirubin, and alkaline phosphatase levels support the diagnosis.
The WBC count is slightly elevated during a cholecystitis attack. Differential diagnosis is
essential because gallbladder disease can mimic other diseases (myocardial infarction, angina,
pancreatitis, pancreatic head cancer, pneumonia, peptic ulcer, hiatal hernia, esophagitis, and
gastritis). Serum amylase levels distinguish gallbladder disease from pancreatitis. With suspected
heart disease, serial cardiac enzyme tests and electrocardiography should precede gallbladder and
upper GI diagnostic tests.
Treatment
Surgery, usually elective, is the treatment of choice for gallbladder and bile duct diseases.
Laparoscopic cholecystectomy and cholecystectomy with operative cholangiography are the
most frequently performed surgeries. Open cholecystectomy is reserved from complicated cases.
Other treatments include a low-fat diet to prevent attacks and vitamin K for itching, jaundice, and
bleeding tendencies due to vitamin K deficiency. Treatment during an acute attack may include
insertion of a nasogastric tube and an I.V. line and, possibly, antibiotic administration.
ERCP with sphincterotomy is the treatment of choice for choledocholithiasis with obstruction
or cholangitis due to obstruction.
Ursodeoxycholic acid, which dissolves radiolucent stones, provides an alternative for patients
who are poor surgical risks or who refuse surgery.
Special Considerations
Patient care for gallbladder and bile duct diseases focuses on supportive care and close
postoperative observation.
Before surgery, teach the patient to deep-breathe, cough, expectorate, and perform leg
exercises that are necessary after surgery. Also teach splinting, repositioning, and ambulation
techniques. Explain the procedures that will be performed before, during, and after surgery to
help ease the patient’s anxiety and to help ensure cooperation.
After surgery, monitor the patient’s vital signs for signs of bleeding, infection, or atelectasis.
Evaluate the incision site for bleeding. Serosanguineous drainage is common during the first
24 to 48 hours if the patient has a wound drain. If, after a choledochostomy, a T-tube drain is
placed in the duct and attached to a drainage bag, make sure that the drainage tube has no
kinks. Also check that the connecting tubing from the T-tube is well secured to the patient to
prevent dislodgment.
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