Assessment and Management of

Patients With Hepatic Disorders

Dr. Lubna Dwerij
Introduction
 Liver function is complex, and liver dysfunction affects all
body systems.
 For this reason, the nurse must understand how the liver
functions and must have expert clinical assessment and
management skills to care for patients undergoing complex
diagnostic and treatment procedures.
 Liver disorders are common and may result from a virus,
exposure to toxic substances such as alcohol, or tumors.
 The liver is a large, highly vascular organ located behind the
ribs in the upper right portion of the abdominal cavity.
 It weighs between 1200 and 1500 g and is divided into four
lobes.
Anatomic and Physiologic Overview
 The liver, the largest gland of the body, can be considered
a chemical factory that manufactures, stores, alters, and
excretes a large number of substances involved in
metabolism.
 The location of the liver is essential in this function
because it receives nutrient-rich blood directly from the
gastrointestinal (GI) tract and then either stores or
transforms these nutrients into chemicals that are used
elsewhere in the body for metabolic needs.
Anatomic and Physiologic Overview
 The liver is especially important in the regulation of
glucose and protein metabolism.
 The liver manufactures and secretes bile, which has a
major role in the digestion and absorption of fats in the GI
tract.
 The liver removes waste products from the bloodstream
and secretes them into the bile.
 The bile produced by the liver is stored temporarily in the
gallbladder until it is needed for digestion, at which time
the gallbladder empties and bile enters the intestine
Functions of the Liver
 Glucose Metabolism
 Ammonia Conversion: The liver converts ammonia, a
potential toxin, into urea, a compound that is excreted in
the urine
 Protein Metabolism
 Fat Metabolism
 Vitamin and Iron Storage
 Bile Formation
 Bilirubin Excretion
 Drug Metabolism
MANIFESTATIONS OF HEPATIC DYSFUNCTION
 Hepatic dysfunction results from damage to the liver’s
parenchymal cells, directly from primary liver diseases, or
indirectly from either obstruction of bile flow or
derangements of hepatic circulation.
 Liver dysfunction may be acute or chronic; the latter is far
more common.
 The rate of chronic liver disease for men is twice that for
women, and chronic liver disease is more common in Asian
and African countries than it is in Europe and the United
States.
MANIFESTATIONS OF HEPATIC DYSFUNCTION
 Disease processes that lead to hepatocellular dysfunction
may be caused by infectious agents such as bacteria and
viruses and by anoxia, metabolic disorders, toxins and
medications, nutritional deficiencies, and hypersensitivity
states.
 The most common cause of parenchymal damage is
malnutrition, especially that related to alcoholism.
 Among the most common and significant manifestations of
liver disease are jaundice, portal hypertension, ascites
and varices, nutritional deficiencies (resulting from the
inability of damaged liver cells to metabolize certain
vitamins), and hepatic encephalopathy or coma.
MANIFESTATIONS OF HEPATIC
DYSFUNCTION
The consequences of liver disease are numerous and
varied. Their ultimate effects are often incapacitating or
life-threatening, and their presence is ominous. Treatment
often is difficult.
Portal Hypertension
 Portal hypertension is the increased pressure throughout
the portal venous system that results from obstruction of
blood flow through the damaged liver.
 Commonly associated with hepatic cirrhosis, it can also
occur with non-cirrhotic liver disease.
 Although splenomegaly (enlarged spleen) with possible
hypersplenism is a common manifestation of portal
hypertension, the two major consequences of portal
hypertension are
 Ascites and varices.
Ascites
 The mechanisms responsible for the development of
ascites are not completely understood.
 Portal hypertension and the resulting increase in capillary
pressure and obstruction of venous blood flow through the
damaged liver are contributing factors.
 The vasodilation that occurs in the splanchnic circulation
is also a suspected causative factor.
 The failure of the liver to metabolize aldosterone
increases sodium and water retention by the kidney.
Ascites
 Sodium and water retention, increased intravascular fluid
volume, increased lymphatic flow, and decreased
synthesis of albumin by the damaged liver all contribute
to the movement of fluid from the vascular system into
the peritoneal space.
 As a result of liver damage, large amounts of albumin rich
fluid, 15 L or more, may accumulate in the peritoneal
cavity as ascites.
 Ascites may also occur with disorders such as cancer,
kidney disease, and heart failure.)
Clinical Manifestations
 Increased abdominal girth and rapid weight gain are
common presenting symptoms of ascites.
 The patient may be short of breath and uncomfortable
from the enlarged abdomen, and striae and distended
veins may be visible over the abdominal wall.
 Umbilical hernias also occur frequently in those patients
with cirrhosis. Fluid and electrolyte imbalances are
common.
Assessment and Diagnostic Findings
 The presence and extent of ascites are assessed by
percussion of the abdomen.
 When fluid has accumulated in the peritoneal cavity, the
flanks bulge when the patient assumes a supine position.
 The presence of fluid can be confirmed either by
percussing for shifting dullness or by detecting a fluid
wave.
 Assessing for abdominal fluid wave.
 The examiner places the hands along the sides
of the patient’s flanks, then strikes one flank
sharply, detecting any fluid wave with the other
hand.
 An assistant’s hand is placed (ulnar side down)
along the patient’s midline to prevent the fluid
wave from being transmitted through the tissues
of the abdominal wall.
Medical Management
 Dietary Modification
 The goal of treatment for the patient with ascites is a
negative sodium balance to reduce fluid retention.
 Table salt, salty foods, salted butter and margarine, and
all ordinary canned and frozen foods that are not
specifically prepared for low-sodium (2-g sodium) diets
should be avoided.
 It may take 2 to 3 months for the patient’s taste buds to
adjust to unsalted foods.
 In the meantime, the taste of unsalted foods can be
improved by using salt substitutes such as lemon juice,
oregano, and thyme.
Medical Management
 Commercial salt substitutes need to be approved by the
physician, because those that contain ammonia could
precipitate hepatic coma.
 Most salt substitutes contain potassium and should be
avoided if the patient has impaired renal function.
 If fluid accumulation is not controlled with this regimen,
the daily sodium allowance may be reduced further to 500
mg, and diuretics may be administered.
Medical Management
 Diuretics
 Use of diuretics along with sodium restriction is successful
in 90% of patients with ascites.
 Spironolactone (Aldactone), an aldosterone-blocking
agent, is most often the first-line therapy in patients with
ascites from cirrhosis.
 When used with other diuretics, spironolactone helps
prevent potassium loss.
Medical MaAnagement
 Diuretics
 Oral diuretics such as furosemide (Lasix) may be added but
should be used cautiously, because long-term use may induce
severe sodium depletion (hyponatremia).
 Daily weight loss should not exceed 1 to 2 kg (2.2 to 4.4 lb) in
patients with ascites and peripheral edema or 0.5 to 0.75 kg
(1.1 to 1.65 lb) in patients without edema.
 Possible complications of diuretic therapy include
 Fluid and electrolyte disturbances (including hypovolemia,
hypokalemia, hyponatremia, and hypochloremic alkalosis)
 Encephalopathy.
Medical Management
 Diuretics
 Encephalopathy may be precipitated by dehydration and
hypovolemia. In addition, when potassium stores are
depleted, the amount of ammonia in the systemic
circulation increases, which may cause impaired cerebral
functioning and encephalopathy.
Medical Management
 Bed Rest
 In patients with ascites, an upright posture is associated
with activation of the renin–angiotensin–aldosterone
system and sympathetic nervous system.
 This causes reduced renal glomerular filtration and sodium
excretion and a decreased response to loop diuretics.
 Therefore, bed rest may be a useful therapy, especially for
patients whose condition is refractory to diuretics.
Medical Management
 Paracentesis
 Paracentesis is the removal of fluid (ascites) from the
peritoneal cavity through a puncture or a small surgical
incision through the abdominal wall under sterile
conditions.
 Paracentesis was once considered a routine form of
treatment for ascites.
 However, it is now performed primarily for diagnostic
examination of ascitic fluid; for treatment of massive
ascites that is resistant to nutritional and diuretic therapy
and that is causing severe problems to the patient.
Medical Management
 A sample of the ascitic fluid may be sent to the laboratory
for cell count, albumin and total protein levels, culture,
and other tests.
 Large-volume (5 to 6 L) paracentesis has been shown to be
a safe method for treating patients with severe ascites.
 This technique, in combination with the IV infusion of salt-
poor albumin or other colloid, has become a standard
management strategy yielding an immediate effect.
Medical Management

 Refractive, massive ascites is unresponsive to multiple

diuretics and sodium restriction for 2 weeks or more and
can result in severe sequelae such as respiratory distress,
which requires rapid intervention.
 Albumin infusions help to correct decreases in effective
arterial blood volume that lead to sodium retention.
 Use of this colloid reduces the incidence of
postparacentesis circulatory dysfunction with renal
dysfunction, hyponatremia, and rapid reaccumulation of
ascites associated with decreased effective arterial
volume.
Medical Management
 Therapeutic paracentesis provides only temporary removal
of fluid; ascites rapidly recurs, necessitating repeated
fluid removal.
Nursing Management
 If a patient with ascites from liver dysfunction is
hospitalized, nursing measures include assessment and
documentation of intake and output, abdominal girth, and
daily weight to assess fluid status.
 The nurse monitors serum ammonia and electrolyte levels
to assess electrolyte balance, response to therapy, and
indicators of encephalopathy.
Nursing Management
 Teaching Patients Self-Care
 The patient treated for ascites is likely to be discharged with
some ascites still present.
 Before hospital discharge, the nurse teaches the patient and
family about the treatment plan, including
 The need to avoid all alcohol intake.
 Adhere to a low-sodium diet.
 Take medications as prescribed.
 Check with the physician before taking any new medications.
 Additional patient and family teaching addresses skin care and
the need to weigh the patient daily and to watch for and
report signs and symptoms of complications.
Reference
 Hinkle, J. L., & Cheever, K. H. (2014). Brunner & Suddarth's textbook of
medical-surgical nursing (Edition 13.). Wolters Kluwer Health/Lippincott
Williams & Wilkins.