Disorders of ECF Volume: Cirrhosis of the Liver

Fig. 8.1

Mechanisms of renal Na⁺ and water retention and edema formation in cirrhosis. EABV effective arterial blood volume, ADH antidiuretic hormone, ANP atrial natriuretic peptide, AII angiotensin II

Clinical Evaluation

A brief discussion of clinical evaluation of cirrhosis is presented here. The most common presentation of patients with cirrhosis (acute or chronic) is dyspnea, abdominal discomfort due to ascites, and lower leg edema. Taking history of prescribed medications, dietary salt intake, over-the-counter medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), dizziness, and recent alcohol use is an integral part of clinical evaluation.

Physical examination starts with measuring blood pressure and pulse rate, and orthostatic changes, if indicated. Neck, lung, heart, and abdominal examination for jugular venous distention (JVD), crackles and pleural effusion, marked S₃ and P₂, murmurs, and ascites should be performed. Examination of lower extremities for pulses, edema, and skin discoloration is extremely important. Mental status, such as depression, confusion, forgetfulness, and difficulty in concentration, needs to be evaluated for encephalopathy.

Pertinent laboratory tests include complete blood count (CBC), Na⁺, K⁺, Cl−, HCO₃ −, blood urea nitrogen (BUN), creatinine, and glucose. Other tests include Ca²⁺, Mg^2 +, phosphate, and albumin. Liver function tests and lipid panel are needed as indicated.

Pertinent electrolyte abnormalities in patients with cirrhosis are hyponatremia and hyper- or hypokalemia due to diuretics. BUN and creatinine levels will explain the status of the kidney function. Liver function tests are abnormal in many patients with cirrhosis. Anemia (< 10 g/dL) is also common in many patients.

Treatment of Edema

Restrict dietary Na⁺ to 88 mEq (2 g Na⁺ diet). Less than 60 mEq Na⁺ diet may be unpalatable. Patients gain weight on unrestricted salt diet. Remember that retention of 135–140 mEq of Na⁺ will increase the ECF volume by 1 L or increase the weight by 1 kg.

Water restriction may not be necessary until serum Na⁺ falls < 135 mEq/L.

Measure urine [Na⁺] during routine outpatient visit to document compliance to diet. Determination of weight at home and office is extremely helpful. Ideal weight loss in patients without edema is approximately 0.5 kg/day.

If salt and water restriction fail, start spironolactone at 100 mg/day, and stepwise increase the dose every 7 days to a maximum of 400 mg/day. If no response is seen in edema or hyperkalemia is absent, start furosemide 20–40 mg/day. Evaluate weight, edema, and volume status in 7 days and then every 2 weeks. Titrate furosemide dose to 160 mg/day.

Bed rest is sometimes helpful. Na⁺ is retained by the kidneys during daytime when the patient is walking, and it is excreted during recumbency. Note that there are no clinical trials to show that bed rest improves edema or promotes the efficacy of medical therapy .

Formation of Ascites

From Fig. 8.1, it is clear that Na⁺ and water are retained even in early stages of cirrhosis because of activation of renin–angiotensin II (AII)–aldosterone, sympathetic nervous system, and nonosmotic release of ADH. However, edema and ascites may not be evident in some patients because of their strict dietary regimen. If the above management of edema fails, patients start developing ascites, which is the most common complication of cirrhosis . About 60 % of patients with compensated cirrhosis develop ascites within 10 years during their course of disease. Patients with portal hypertension only develop ascites .

The traditional “underfill” theory suggests that ascites formation begins when a critical imbalance of Starling forces (increase in portal hydrostatic pressure and decrease in colloid oncotic pressure) develops in the hepatic sinusoids and splanchnic circulation with resultant transudation of fluid into the peritoneal cavity. As ascites increases, there is a decrease in EABV, which stimulates Na⁺ retaining mechanisms, resulting in edema. Thus, formation of ascites occurs prior to Na⁺ retention. A second theory called “overflow” theory was proposed on the basis of experimental evidence. According to this theory, Na⁺ retention by the kidney precedes the development of ascites, causing an increase in plasma volume, which then overflows into the peritoneal cavity to form ascites. These two theories do not adequately explain the formation of ascites. A third theory called peripheral vasodilation theory was proposed, which states that the decreased EABV, secondary to splanchnic arterial vasodilation, triggers Na⁺ retaining mechanisms and ADH to form edema (Fig. 8.1) .

Treatment of Ascites

The European Association for the Study of the Liver guidelines classifies ascites into three grades based on the amount of fluid accumulation in the peritoneal cavity. This grading system avoids unnecessary therapeutic measures. Table 8.1 shows the grading system and suggested treatment for ascites.

Table 8.1

Grading of ascites and suggested treatment

Grade	Definition	Suggested treatment
Grade 1 ascites	Small volume (mild) detectable by ultrasound	No treatment. How frequently patients progress to grade 2 ascites is unknown
Grade 2 ascites	Moderate amount of fluid with distension of abdomen	Salt restriction and diuretics
Grade 3 ascites	Large amount of fluid with marked distension of abdomen	Large-volume paracentesis, with salt restriction and diuretics

Salt Restriction

Na⁺ diet (88 mEq/day) or 5 g salt (1 teaspoon) diet (85 mEq).

No restriction of water unless patient has hyponatremia.

Diuretics

Spironolactone and furosemide. Patients with first episode of moderate ascites should receive spironolactone 100 mg/day with increasing dose every 7 days to a maximum of 400 mg/day. Monitor serum K⁺. If no response to spironolactone or hyperkalemia is evident, start furosemide at 40 mg/day to a maximum of 160 mg/day. Maintain combination therapy ratio at 100 (spironolactone):40 (furosemide) mg. With this combination, serum [K⁺] is usually maintained at normal levels.

Patients with recurrent tense ascites should be started simultaneously with both spironolactone and furosemide, as suggested above. Weight loss during diuretic therapy should be approximately 0.5 kg/day for nonedematous patients and approximately 1 kg/day for edematous patients. The combination therapy reduces hospital length of stay for hospitalized patients .

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