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Ascites refers to the presence of an abnormal amount of fluid in the abdomen. It is the main complication of portal hypertension. In 60% of patients, it develops within 10 years. Ascites has a mortality of 50% after 8 years.

Ascites is caused by a decrease in osmotic pressure, which is caused by hypoalbuminemia and an increase in hydrostatic pressure, which is caused by portal hypertension. This causes a transition of fluid from the splanchnic venous system, the endothelium only allows water to pass through and the ascitic fluid is poor in protein. In post-sinusoidal portal hypertension, there is also a loss of proteins through the sinusoids, which have fenestrations. This gives rise to protein-rich ascitic fluid.

Portal hypertension is characterized by a relative underfilling (by peripheral vasodilation) and by the loss of fluid and proteins in the peritoneum. This results in a further systemic underfilling. This gives rise to reflex fluid retention in the kidneys. This fluid retention activates the renin-angiotensin-aldosterone system, resulting in sodium retention. Therefore, treatment with an aldosterone antagonist, such as spironolactone, is a responsible therapy for ascites.

During the clinical examination, the central venous pressure must always be measured to rule out right heart decompensation. This condition also causes malleolar edema. On inspection, the abdomen swells, the flank sags, there is diastasis of the recti muscle, skin striae develop and the umbilicus stretches sideways ('smiling umbilicus'). Skin edema and malleolar edema can also develop due to hypoalbuminia. Percussion and palpation reveal a shifting dullness in the flanks ('shifting dullness') and the iceberg sign ('signe de glaçon'). Pronounced ascites can be associated with an umbilical hernia. The diagnosis is confirmed by means of an ultrasound. This is particularly useful in people with obesity.

In patients with ascites who are admitted to the emergency department, a paracentesis should always be performed. This paracentesis should be performed in the left iliac fossa, because there is the least chance of puncturing the small intestine. The following determinations should be made on the ascites fluid:

- albumin: to establish the diagnosis;

- leukocytosis and cultures (on hemoculture bottles): to rule out spontaneous bacterial peritonitis.

The best parameter to detect the cause of ascites is the serum albumin minus the ascites-albumin difference (SAAG). If this has a value of higher than 11g/l, there is a high probability that the ascites is caused by portal hypertension due to classical cirrhosis. Cardiac ascites is characterized by the presence of many proteins.

Differential diagnosis of ascites:

- portal hypertension (80%);

- ovarian neoformations and/or peritoneal metastasis;

- peritoneal irritation including pancreatitis;

- cardiac causes (including constrictive pericarditis and cardiac decompensation, which is accompanied by increased central venous pressure);

- nephrotic syndrome, which is accompanied by diffuse edema and albuminuria.

The ascitic fluid should not be treated too aggressively ('go low, go slow'). A weight loss of half a kilogram per day is ideally aimed at, to prevent further hypovolaemia and secondary pre-renal renal insufficiency.

Phase 1 of the treatment consists of a low-salt, high-protein diet and the administration of diuretics: currently spironolactone and furosemide, with regular monitoring of electrolytes and creatinine. Attention should be paid to the side effects of the diuretics: hyponatremia (dilution), which occurs in 30% of hospitalised patients, hyperkalaemia due to spironolactone, gynaecomastia due to spironolactone and calf cramps.

Measures to be taken in case of hyponatremia: rapid normalization indicates brain damage (hypernatremia can be provoked by lactulose enemas). Initially, diuretics are stopped. Underfilling is treated with human albumin and, if necessary, terlipressin (starting with 0.5 mg intravenously in a bolus, 4 to 6 hours), to treat systemic hypotension.

In phase 2 of the treatment, in case of insufficient effect of the diuretics, paracentesis can be performed regularly. However, if >= 5 liters of ascitic fluid are drained, this must always be accompanied by administration of albumin (8 grams per liter of ascitic fluid removed), to prevent the hepatorenal syndrome. As many as 5 to 10% of patients do not respond to this treatment.

Finally, in phase 3, in patients with therapy-resistant ascites, TIPS should be considered in patients without contraindications. Then, the need for paracentesis disappears in 85% of patients, but 30% develop hepatic encephalopathy.

In patients with a MELD score higher than 19, there is a high risk of liver failure, due to increased hypoperfusion of the liver and hepatic encephalopathy due to increased shunting. This procedure is therefore contraindicated in patients with poor liver function and/or pre-existing hepatic encephalopathy. If this does occur, a reduction stent can be placed in the TIPS stent.

Presents as a patient with ascites and general deterioration. On clinical examination, peritoneal irritation is not very pronounced and the diagnosis is made by means of a puncture of the ascitic fluid. This ascitic fluid is cloudy, rich in cells and contains leukocytes: > 500/mm2, of which > 250/mm2 granulocytes. Culture of the ascitic fluid yields, among other things, E.coli. If various pathogenic bacteria are present in the ascitic fluid, this may indicate secondary bacterial peritonitis (including a perforated appendix).

If cytosis is present in the ascitic fluid, antibiotics must be started immediately, for example a third-generation cephalosporin or quinolone. Afterwards, secondary prevention with peroral antibiotics (type quinolone) is necessary until the ascites disappears.

Presents as a patient with ascites with increased creatinine. This is an increase in serum creatinine in a patient with ascites. Because patients with cirrhosis have little muscle mass, a small increase in creatinemia is already significant, namely an increase in creatinine in 24 hours greater than or equal to 0.3 mg/dl or an increase greater than or equal to 50% of the basal value. This is a functional renal impairment due to the reduction in the effective arterial blood volume with reflex vasoconstriction in the cortex of the kidney. The fact that the hepatorenal syndrome disappears after liver transplantation is evidence of this.

Other causes of acute renal impairment must always be excluded, such as volume depletion due to diuretics, sepsis and renal insufficiency due to the use of nephrotoxic drugs. An important precipitating factor is spontaneous bacterial peritonitis.

Progressive increase over several weeks is also seen in patients with difficult to treat ascites due to decreased cardiac output (due to heart failure) that can no longer fully compensate for the hypovolemia.

These phenomena can also superimpose on an underlying renal disease and this is called acute on chronic renal failure, which will not improve renal function after a liver transplant.

Treatment consists mainly of prevention. If an increase in creatinine is found, all diuretics should be stopped and albumin should be administered at a dose of 1g/kg body weight albumin 20% for two days. If the patient does not respond to this, terlipressin should be started intravenously (bolus injections 0.5 mg every 4 to 6 hours). Untreated, this complication has a mortality of 100%.

Presents as a patient with ascites and dyspnea. Hepatic hydrothorax occurs after a period of difficult to treat ascites. This is a massive pleural effusion, mainly on the right. The right diaphragm has openings. The decreased intrathoracic pressure sucks the ascitic fluid from the abdomen. The treatment is to drastically control the portal hypertension, using TIPS if the MELD score is not too high. Ultimately, hepatic hydrothorax is an indication for liver transplantation.

Presents as drowsiness in a patient with indirect signs of cirrhosis. During the course of their disease, 30% of patients develop hepatic encephalopathy. This concerns psychological and neurological disorders in patients with liver disease. Hepatic encephalopathy occurs in patients with both acute liver failure and cirrhosis.

Clinical examination may reveal the following abnormalities:

- Foetor hepaticus;

- Flapping tremor;

- Parkinsonian extrapyramidal symptoms.

There are four stages:

- Stage 1: reversal of the day-night rhythm, with daytime sleepiness and constitutional apraxia (impaired writing and impaired digit connection test);

- Stage 2: disorientation in time and space, flapping tremor, hyperreflection and rigidity;

- Stage 3: stupor, hyporeflexia and foot clonus;

- stage 4: coma.

Clinically, three stages are distinguished:

- minimal HE (can only be determined by psychometric testing);

- 'covert' HE (grade &) (can be determined by means of the 'animal naming test', in which the patient has to name as many animals as possible in one minute);

- 'overt' HE (grade 2 to 4).

In a cirrhotic patient, hepatic encephalopathy occurs due to a combination of insufficient synthesis activity of the liver and pronounced shunting. The reduced synthesis capacity causes an increase in serum ammonia. There is an increase in Blood-Brain-Barrier permeability (mainly only permeable to water). This leads to swelling of the astrocytes and a mild form of cerebral edema.

Large portosystemic shunts (larger than 8 mm in diameter) can occur anywhere. The two most common are splenorenal shunts (between the vena lienalis and the vena renalis) and at the opening of the umbilical veins.

Hepatic encephalopathy can be provoked by an increase in ammonia supply due to gastrointestinal bleeding or constipation, by hypo- and hypernatremia (diarrhea due to lactulose), by acidosis (spironolactone overdose), by the use of conventional sleeping medication and sedatives, by infections and by TIPS. Over time, the additional breakdown of ammonia via the muscles and kidneys also fails.

There is no gold standard for making a diagnosis. Diagnosis is based on the clinic. A rise in serum venous ammonia may be helpful, but is not valuable in patients with known cirrhosis.

In patients with alcoholic cirrhosis who are found in a coma, a differential diagnosis with a subdural hematoma should always be made.

In patients without liver disease but with increased venous ammonia encephalopathy, the presence of a congenital urea cycle deficiency or congenital extrahepatic portosystemic shunts (Abernethy malformation) must be excluded.

Treatment consists mainly of finding and correcting the provoking factors. There is no place for low-protein diets. The first line of treatment is lactulose with the aim of obtaining at least two soft stools per day. This can be given orally, or in the case of stupor or coma, with the aid of enemas (dilute 150 ml lactulose with 350 ml water). Under the influence of the bacterial flora, lactulose is broken down into acids. These give rise to the formation of ammonium, which cannot diffuse into the blood. This results in acid dialysis with a decrease in ammonia. Another explanation is the laxative effect.

The current second-line therapy consists of rifaximin 550mg twice daily. It is a non-absorbable antibiotic. The exact mechanism of action is unknown, but the intestinal barrier function improves and there is an increased activity of the enzymes involved in liver detoxification.

In case of large spontaneous porto-systemic shunt and a preserved liver synthesis capacity: embolization of the spontaneous porto-systemic shunt. In case of TIPS: reduction stent.

Presents as cyanosis in a patient with advanced liver disease. This is a functional right-left shunt due to dilation of the vascular bed, due to the increased concentrations of nitric oxide in the blood. Clinically, the central cyanosis and tachypnea are noticeable. The patient may develop clubbing of the fingers.

Severe hepatopulmonary syndrome occurs when the PaO2 < 70 mm Hg. The diagnosis is made with echocardiography with contrast. In this case, the bubbles appear immediately in the left half of the heart, after three beats. The only good treatment is liver transplantation.

In every patient with dyspnea, this must be ruled out. Screening can be done using echocardiography. This examination usually overestimates the pulmonary pressures. The diagnosis is made using cardiac catheterization, to examine the right side of the heart. Failure to recognize this can lead to sudden death during a surgical procedure. The cause of death in these patients is sudden death.

The differential diagnosis must be made with pulmonary hypertension due to left heart failure and other forms of pulmonary arterial hypertension, such as systemic diseases and drug-induced forms. The patients are eligible for pulmonary arterial hypertension-lowering medication.

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