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SECONDARY TO
KIDNEY DISEASE
DEFINITION:
Ascites is an accumulation of serous fluid in the peritoneal cavity.
Causes include cirrhosis of the liver, tumour, tuberculous peritonitis, and interference in venous
circulation, cardiac or renal failure. MALIGNANT A.., A condition sometimes occurring in the
end stage of cancer with metastasis to the peritoneum; treatment may consist of peritoneovenous
shunt.-SYN. Hydroperitoneum, abdominal dropsy.
Ascites is the accumulation of fluid in the peritoneal cavity, causing abdominal swelling. Causes
include infection (such as tuberculosis), heart failure, portal hypertension, cirrhosis, and various
cancers (particularly of the ovary and liver). Obstruction to the drainage of lymph from the
abdomen results in chylous ascites. (Chyle)
Chyle is an alkaline milky liquid found within the lacteal after a period of absorption. It consists
of lymph with a suspension of minute droplets of digested fats, which have been absorbed from
the small intestine. It is transported in the lymphatic system to the thoracic duct.
PATHOPHYSIOLOGY:
The mechanism responsible for the development of ascites is 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 suspected causative factor. The failure of the liver to metabolize
aldosterone increases sodium and water retention by the kidney. 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. The process becomes self-perpetuating as loss of fluid into the
peritoneal space causes further sodium and water retention by the kidney in an effort to maintain
the vascular fluid volume.
As a result of liver damage, large amount of albumin rich fluid, 15L or more, may accumulate in
the peritoneal cavity as ascites. With the movement of albumin from the serum to the peritoneal
cavity, the osmotic pressure of the serum decreases. This, combined with increased portal
pressure, results in movement of fluid into the peritoneal cavity.
CLINICAL MANIFESTATION:
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.
UMBILICAL HERNIAS
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 2-3 months for the patients taste buds to adjust to unsalted foods. In the meantime, the
taste of unsalted foods can be improved by using salt substitutes such as lemons juice, oregano,
and thyme. 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. The patient should make liberal use
of powdered, low-sodium milk and milk products. If fluid accumulation is not controlled with
this regimen, daily sodium allowance may be reduced further to 500 mg, and diuretics may be
administered.
Dietary control of ascites via strict sodium restriction is difficult to achieve at home. The
likelihood that the patient will follow even a 2-g sodium diet increases if the patient and the
person preparing the meals understand the rationale for the diet and receive periodic guidance
about selecting and preparing appropriate foods. Approximately 10% of patient with ascites
respond to these measures alone. Nonresponders and those who finds sodium restriction difficult
require diuretic therapy.
DIURETICS:
Use of diuretics along sodium restriction is successful in 90% of patients with ascites.
Spironolactone (Aldactone), an aldosterone-blocking agent, is the most often the first-line
therapy in patient with ascites from cirrhosis. When used with other diuretics, spironolactone
helps prevent potassium loss. Oral diuretics such as furosemide (Lasix) may be added but should
be used cautiously, because long-term use may induce severe sodium depletion (hyponatremia).
Ammonium chloride and acetazolamide (Diamox) are contraindicated because of the possibility
of precipitating hepatic coma. Daily weight loss should not exceed 1 to 2 kg (2.2 to 4.4 lbs) in
patients with ascites and peripheral edema or 0.5 to 0.75 kg (1.1 to 1.65 lbs) in patients without
edema. Fluid restriction is not attempted unless the serum sodium concentration is very low.
Possible complications of diuretic therapy include fluid and electrolyte disturbances (including
hypovolemia, hypokalemia, and hyponatremia and hypochloremic alkalosis) and
encephalopathy. 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.
BED REST:
In patients with ascites, an upright posture is associated with activation of the renin- angiotensinaldosterone 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 useful therapy, especially to the patients whose condition is refractory to diuretics.
PARACENTESIS:
Paracentesis is the removal of fluid (ascites) from the peritoneal cavity through a puncture or
small surgical incision through abdominal wall under sterile conditions. Ultrasound guidance
may be indicated in some patients who are at high risk for bleeding because of an abnormal
coagulation profile and in those who have had previous abdominal surgery and may have
adhesion. Paracentesis once considered a routine form of treatment for ascites. However, it is
now performed primarily for diagnostic examination of a ascetic fluid, for treatment of massive
ascites that is resistant to nutritional and diuretic therapy and that is causing severe problems to
the patients, and as prelude to diagnostic imaging studies, peritoneal dialysis, or surgery. A
sample of ascetic fluid may be send to the laboratory for cell count, albumin and total protein
levels, culture, and other tests.
Large-volume (5-6 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. Refractive,
massive ascites is unresponsive to multiple diuretics and sodium restriction for 2 weeks or more
and can result in 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 hyponatremia and renal
dysfunction associated with decreased effective arterial volume. The beneficial effects of
albumin administration on hemodynamic-stability and renal functional status may be related to
an improvement in cardiac function as well as a decrease in the degree of arterial vasodilation.
Although the patient with cirrhosis has greatly increased extracellular blood volume, the kidney
incorrectly senses that the effective volume has decreased. The renin-amgiotensin- aldosterone
axis is stimulated, and sodium is reabsorbed. In addition, antidiuretic hormone (ADH) secretion
increases, which leads to increased retention of free water and sometimes to the development of
dilutional hyponatremia. Therapeutic paracentesis provides only temporary removal of fluids;
ascites rapidly recurs, necessitating repeated fluid removal.
PARACENTESIS
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.
CONTINUING CARE:
A referral for home care may be warranted, especially if the patient lives alone or cannot provide
self care. The home visits enable the nurse to assess the changes in the patients condition and
weight, abdominal girth, skin and cognitive and emotional status. The home care nurse assesses
the home environment and the availability of resources needed to adhere to the treatment plan
(e.g. a scale to obtain daily weights, facilities to prepare and stores appropriate foods, resources
to purchase needed medications). It is important to assess the patients adherence to the treatment
plan and the ability to buy, prepare, and eat appropriate foods. The nurse reinforces previous
teaching and emphasizes the need for regular follow-up and the importance of keeping scheduled
health care appointments.