Abdominal distension

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20 Abdominal distension

Michael Cox

Case

A 32-year-old woman presents with a 6-day history of progressive abdominal distension and nausea. She had recently been an inpatient with an episode of acute pancreatitis. The aetiology of the pancreatitis was familial pancreatitis, with her grandmother, father and one brother having episodes of recurrent pancreatitis. She looked well, was afebrile and was not jaundiced or pale. Abdominal examination revealed a moderately distended abdomen that was tense but not tender. The bowel sounds were normal. There was evidence of shifting dullness and a fluid thrill. A provisional diagnosis of ascites was made.

Laboratory blood tests were all normal in particular the amylase, lipase, liver function tests and albumin. A CT scan confirmed marked ascites. The pancreas was slightly enlarged but well perfused with a slightly prominent pancreatic duct. There were no loculated fluid collections or evidence of pseudocyst formation. A diagnostic aspiration of the fluid revealed it was straw-coloured. Analysis confirmed it was an exudate with no cells and an amylase of over 100 000 I/U (serum ascites–albumin gradient < 11 g/L). This confirmed the clinical suspicion of pancreatic ascites.

The following day an ERCP was performed. The pancreatic duct was dilated at 4 mm with no obvious stricture. There was a leak of contrast from the region of the distal body into the peritoneal cavity. An endoscopic pancreatic stent was inserted with good drainage noted. Over the next 3 days the abdominal distension resolved and she was discharged home. Three weeks later a follow-up CT scan confirmed complete resolution of the ascites and a relatively normal pancreas with the stent in situ. She remained well and the stent was removed after 6 months. Unfortunately, she had further episodes of recurrent acute pancreatitis over the next 4 years and is likely to develop chronic pancreatitis.

Preliminary Examination of the Abdomen

The traditionally taught five causes of generalised abdominal distension (the ‘five Fs’) are: flatus, fluid, faeces, fetus and fat. To this list should be added a sixth: massive organomegaly or ‘filthy big tumour’.

For the patient presenting with generalised abdominal distension, a preliminary abdominal examination is worthwhile before a detailed history is taken to determine which of the ‘six Fs’ is the most likely cause. The reason for this departure from the usual sequence of history followed by examination is that history taking can be greatly simplified if the clinician has some prior idea of the underlying problem.

1. Flatus

The cause of flatus is gaseous distension of the bowel often secondary to a bowel obstruction or paralytic ileus. There is generalised hyper-resonance to percussion. Any fluid contained within the distended bowel associated with a bowel obstruction or ileus is clinically undetectable. It lies posteriorly with the patient lying supine and is not percussible. It is contained within bowel loops and cannot shift. Auscultation of the abdomen may reveal hyperactive bowel sounds with mechanical obstruction and absent or just a few ‘tinkly’ bowel sounds with paralytic ileus.

2. Fluid or ascites

Intraperitoneal fluid collection is associated with dullness to percussion in the flanks with the patient lying supine. The dullness is described as shifting dullness because the upper limit of the dullness moves in relation to the abdominal wall as the patient is rolled onto the side. Massive ascites is also associated with a fluid thrill felt in one flank after tapping in the other. The distension is less globally distributed with ascites than with gaseous distension of the abdomen, with the effect that the flanks tend to sag.

3. Faeces

Stool can accumulate in the colon to produce abdominal distension. This can cause gaseous distension of more proximal bowel. The degree of distension tends to be less than can occur with ascites or bowel obstruction. The faeces can be recognised as firm to hard lumps that are indentable when prodded with the tip of the examining finger (Ch 11). The segments of colon overlying the brim of the pelvis on the left and right sides may be more prominent to the examining hand.

4. Fetus

Pregnancy and the associated enlarged uterus produce a globular firm mass, which arises out of the pelvis so that the examining hand cannot palpate an inferior border. In early pregnancy, the swelling is confined to the lower abdomen. The mass may reach as high as the epigastrium in late pregnancy. Further, bony fetal parts, such as the head and back, may be identifiable to palpation and fetal heart sounds may be heard on auscultation.

5. Fat

Within the abdomen, fat commonly produces abdominal distension. It is known colloquially as ‘pot belly’ or ‘beer gut’. It does not have characteristic features on clinical examination except that other parts of the body are usually also obviously fat. Obesity is so prevalent that a previously obese patient may present with further distension due to one of the other ‘five Fs’. Evaluation by physical examination is always more difficult under these circumstances.

6. Filthy big tumour (massive organomegaly)

Features of massive organomegaly are covered in Chapter 19.

History and Further Examination

A classification of the causes of abdominal distension is presented in Table 20.1 and relevant symptoms are listed in Table 20.2. The duration of abdominal distension and its association with abdominal pain are key questions. Thus, abdominal pain should not usually be expected to be a feature, except with abdominal distension due to gas in bowel obstruction; with the other causes, there may be milder discomfort due to stretching of the parietal peritoneum or the capsule of an organ. Localised pain can occur with organ swelling. Similarly, the speed of development for most causes is slow, except with abdominal distension from gas, in which case it can be fast. Tense swelling of the abdomen due to fluid or a large tumour can cause increased intraabdominal pressure leading to heartburn, nausea, vomiting or dyspnoea (from elevation of the diaphragm). The specific clinical features for each cause are described below.

Table 20.1 Classification of causes of abdominal distension: the ‘six Fs’

Cause Example Distension
1. Flatus (gaseous distension)    
Bowel obstructed    
Open   Generalised
Closed Sigmoid volvulus Localised
  Caecal volvulus Localised
Bowel not obstructed    
  Paralytic ileus Generalised
  Pseudo-obstruction Generalised
  Irritable bowel syndrome Generalised
  Acute gastric dilatation Localised
  Gas bloat Generalised
2. Fluid (ascites) See Table 20.3 for detail Generalised
3. Faeces   Localised
4. Fat   Generalised
5. Fetus   Localised
6. Filthy big tumour (organomegaly)    
Liver See Chapter 19 Localised
Spleen See Chapter 19 Localised
Ovary Ovarian cyst Localised
Uterus Fibroids Localised
Kidney Polycystic kidney Localised
Hydronephrosis – Localised
Bladder Obstructed bladder Localised
Mesentery Tumour Localised
Retroperitoneum Tumour Localised or generalised

Table 20.2 Possible symptoms with abdominal distension

Symptom Relevance/significance
Abdominal pain:

• abdominal tightness/vague generalised ache;
• colicky (periumbilical or lower abdominal).

Non-specific
Bowel obstruction
Nausea/vomiting Bowel obstruction Anorexia Non-specific, malignancy, cirrhosis Loss of weight Non-specific, malignancy, cirrhosis Bowel habit (recent and usual) Bowel obstruction, constipation Respiratory symptoms Secondary to elevation of the diaphragm Previous history of malignant disease As a possible cause of ascites Alcohol or drug abuse As a cause of liver disease and ascites Jaundice Associated with liver disease Easy bruising/spontaneous bleeding Associated with liver disease Missed menstrual cycle(s) Pregnancy

Clinical Features

Gaseous distension of the bowel (flatus)

Mechanical obstruction of the bowel (small or large)

The distension is usually acute in onset and develops over hours to days. The obstruction may be open or closed. Examples of open obstructions are a band adhesion occluding the lumen of the small bowel and a cicatrising carcinoma of the sigmoid colon. With these, the distension is generalised. Examples of closed obstructions are sigmoid and caecal volvulus. The time frame of development is similar. The abdominal distension with a sigmoid volvulus is directed from the pelvis towards the right hypochondrium, because the sigmoid mesocolon is attached to the left false pelvis. The abdominal distension with a caecal volvulus is directed from the pelvis towards the left hypochondrium, because of the attachment of the caecum to the right false pelvis.

The distension is associated with other features of bowel obstruction, namely colicky abdominal pain, vomiting and constipation. The diagnosis and management of bowel obstruction is discussed in Chapter 4.

Paralytic ileus

This is often preceded by an abdominal operation. Operations involving retroperitoneal structures (e.g. repair of an aortic aneurysm), operations during which there is considerable handling of the bowel and prolonged operations are more prone to paralytic ileus. Irritation of the retroperitoneum as occurs with severe pancreatitis or a spontaneous retroperitoneal haemorrhage can precipitate an ileus. An intraabdominal inflammatory process such as acute diverticulitis and biochemical disturbances such as hypokalaemia, hypomagnesaemia and chronic kidney disease can also precipitate an ileus. In contradistinction to a mechanical bowel obstruction, there is no colicky pain with paralytic ileus, just the discomfort associated with distending the parietal peritoneum. The condition settles spontaneously with correction or resolution of precipitating factors. Gastric decompression and fluid replacement (and sometimes intravenous hyperalimentation) are required while resolution occurs.

Pseudo-obstruction

The time course of pseudo-obstruction is more protracted than with mechanical obstruction; the degree of distension may fluctuate considerably. Pseudo-obstruction is discussed in Chapter 7.

Irritable bowel syndrome

This may be associated with chronic fluctuating abdominal distension of moderate degree. This condition is considered in detail in Chapter 7.

Acute gastric dilatation

This is most commonly seen soon after abdominal surgery or major trauma (not necessarily abdominal trauma). Diabetes mellitus is another cause. The key manifestation is copious vomiting of ‘coffee grounds’, a mixture of gastric secretions and old blood. Hypokalaemic alkalosis may result from the persistent vomiting. The condition is managed by decompression with a nasogastric tube and fluid replacement.

Gas bloat

This particular chronic problem can occur as a complication of antireflux surgery for gastro-oesophageal reflux (Ch 1). It results from air swallowing in a patient who has a diminished ability to belch because of their surgery. The degree of distension of stomach and bowel can vary considerably. It is generally worse postprandially. There is usually some degree of discomfort. This may vary from a vague feeling of fullness to a more localised epigastric discomfort to central abdominal colicky pain. It may be relieved to a degree by passage of flatus.

Ascites (fluid)

This usually develops gradually and continuously, with the onset over weeks to months, and is relatively painless. When the ascites is gross, there may be a vague discomfort caused by stretching of the abdominal wall and the parietal peritoneum. When ascites is painful, infected ascites, hepatoma or pancreatitis should be considered. There may be respiratory symptoms due to respiratory embarrassment with gross ascites or development of a pleural effusion (usually on the right due to a leak of fluid through the diaphragmatic lymphatics).

The main causes of ascites and their prevalence are listed in Table 20.3. These are:

• cirrhosis: 80% of patients with ascites have cirrhosis. The causes of cirrhosis are discussed in Chapter 24. Risk factors to enquire about include alcohol abuse, intravenous drug use, tattoos, blood transfusion and living in developing countries where the prevalence of hepatitis B and hepatitis C is high. These patients may have splenomegaly due to portal hypertension as well as other stigmata of chronic liver disease including spider naevi, palmar erythema, proximal muscle wasting, jaundice, fetor, flap, testicular atrophy and gynaecomastia;
• malignancy: 10% of patients have ascites secondary to malignancy. The three malignancies most commonly associated with ascites are gastric, colonic and ovarian carcinomas. Most of these patients have a past history of malignancy. In some, abdominal distension is the presenting feature. There may be hepatomegaly or lymphadenopathy or other evidence of tumour spread;
• cardiac ascites: cardiac ascites is secondary to severe right-sided heart failure, most commonly due to constrictive pericarditis. Other signs include an elevated jugular venous pressure, pulsatile tender hepatomegaly and peripheral oedema;
• hypoproteinaemia: ascites due to hypoproteinaemia (e.g. from starvation, or excessive loss from protein-losing enteropathy or nephrotic syndrome) is minor in degree and associated with peripheral oedema;
• pancreatic ascites: this is only seen after severe acute pancreatitis or a blunt transacting injury to the pancreas. It is due to a persistent leak of pancreatic fluid from the pancreatic duct into the peritoneal cavity. The leak may be due to a side hole in the pancreatic duct or due to complete dissociation of the proximal and distal duct;
• chylous ascites: this results from surgical trauma to cisterna chyli or rarely due to obstruction by lymphatic spread of tumour.

Table 20.3 Causes of ascites

Cause Prevalence (%)
Cirrhosis 80
Malignancy 10
Heart failure 5
Tuberculosis 1
Other: hypoproteinaemia caused by starvation (kwashiorkor and malignancy) or excessive loss (protein-losing enteropathy, nephrotic syndrome); pancreatic ascites; chylous ascites 4

Faecal impaction of the colon (faeces)

This is a chronic problem caused by chronic constipation, and is most commonly seen in elderly people. The various causes of constipation are considered in detail in Chapter 11. Abdominal distension is an uncommon feature of the most severe end of the spectrum. A history of infrequent, usually hard bowel actions is expected. A history of laxative abuse is also very common. Lower abdominal colicky pain may be associated. When such pain occurs it should be relieved by the passage of flatus or a large evacuation of the bowel.

Pregnancy (fetus)

This is associated with a menstrual-free period in women.

Abdominal distension due to obesity (fat)

This is painless and longstanding. The deposition of fat is in the mesentery of the bowel and the omentum to a greater degree, and in the anterior abdominal wall to a lesser degree in men. In women there is a greater proportion of fat deposited in the abdominal wall, as compared to the mesentery of the bowel and omentum.

Organomegaly

The presenting history of patients with organomegaly resulting in abdominal distension is covered in Chapter 19.

Investigations

The appropriate investigations to evaluate abdominal distension are detailed below.

Plain radiology of the abdomen

This may demonstrate a small or large bowel obstruction and paralytic ileus (Figs 20.1 and 20.2) as well as faecal loading. The fluid of ascites may give a ‘ground glass’ appearance, a non-specific vague increased whiteness to the abdominal cavity.

image

Figure 20.1 Plain abdominal x-ray film showing small bowel obstruction. There is dilatation of the small bowel. It is recognised as small bowel from its central position and its transverse mucosal bands—the valvulae conniventes (black arrow). Air-fluid levels are seen on the erect view. The supine view gives a better view of the distribution of the dilated loops. From the number and position of the displayed dilated loops, the obstruction would be at the level of the mid-small bowel. The round radio-opaque shadow in the left hypochondrium is a tablet (open arrow).

From Talley NJ, O’Connor S. Clinical examination. 6th edn. Sydney: Elsevier Australia; 2010.

image

Figure 20.2 Plain abdominal X-ray film showing generalised ileus. The large bowel is filled with gas and is dilated except in the descending colon. Dilated small bowel is also seen in the right hypochondrium (arrow). As gas is seen around to the rectum (arrow), mechanical obstruction is excluded.

From Talley NJ, O’Connor S. Clinical examination. 6th edn. Sydney: Elsevier Australia; 2010.

Ultrasound or CT of the abdomen

This will confirm the presence of ascites (Fig 20.3) and define organomegaly.

image

Figure 20.3 Abdominal CT showing ascites.

Blood tests

Liver function tests may indicate underlying chronic liver disease (Ch 24). A pregnancy test will confirm the presence of pregnancy.

There is no specific relevant test for obesity. Measure the weight and height to calculate the body mass index (BMI = weight [kg] divided by height squared [m2]). A BMI of 30 or over indicates frank obesity; a BMI of 40 or over indicates severe obesity (Ch 26). The diagnosis can usually be made on clinical grounds.

Of the various causes of abdominal distension, only ascites will be discussed in further detail in this chapter. Bowel obstruction is discussed in Chapter 4. Constipation is discussed in Chapter 11. Pregnancy is beyond the scope of this text.

Diagnosis of Ascites

There are two clinical steps to determining the cause of ascites. First, the clinical history and examination need to be focused on elucidating which pathological process underlies the accumulation of ascites. Secondly, a sample of the ascites needs to be examined. The sample is aspirated and its appearance noted before it is sent to the laboratory for biochemical, cytological and microbiological analysis. Blood needs to be sent at the same time for estimation of the serum albumin level.

The features of ascitic fluid are summarised in Table 20.4.

Table 20.4 Characteristics of paracentesis fluid

image

Appearance

Blood staining suggests malignancy or a traumatic ascitic tap, either current or past; turbidity or white fluid suggests infected or chylous ascites.

Serum-ascites albumin gradient

Calculate this by subtracting the ascitic fluid albumin from the serum albumin value; the serum-ascites albumin gradient (SAAG) correlates with portal pressure. If the SAAG is 11 g/L or more, then portal hypertension is the likely diagnosis (97% accurate). Peritoneal carcinomatosis, tuberculosis and pancreatic ascites have a gradient under 11 g/L (Table 20.5).

Table 20.5 Classification of ascites by serum-ascites albumin gradient (SAAG)

SAAG: high (≥ 11 g/L) SAAG: low (< 11 g/L)
Cirrhosis
Alcoholic hepatitis
Cardiac ascites
Massive liver metastases
Fulminant hepatic failure
Cirrhosis plus another cause

Peritoneal carcinomatosis
Tuberculous peritonitis
Pancreatic ascites
Bile leak

Other biochemistry

If pancreatic ascites is suspected, the ascitic amylase level needs to be assessed; it is very high in pancreatic ascites. A low pH (under 7.35) suggests spontaneous bacterial peritonitis or systemic acidosis. The lactate level is elevated in spontaneous bacterial peritonitis. If chylous ascites is suspected, the diagnosis can be confirmed by staining the specimen for fat.

Cells

Examination of the ascites for polymorphonuclear cells is important to diagnose spontaneous bacterial peritonitis. A cell count of 250 × 106 polymorphs/L (250 polymorphs/mm3) or more, or 500 × 106 white cells/L (500 cells/mm3) or more, is strongly suggestive of the diagnosis. The cause is usually a gram-negative organism sensitive to treatment with a third-generation cephalosporin (e.g. cefotaxime).

Cytology

If the SAAG is less than 11 g/L or malignancy is otherwise suspected, a cytological examination looking for malignant cells should be performed after the sample has been centrifuged. Establishment of the primary site is usually not possible using this specimen.

Culture

As spontaneous bacterial peritonitis is insidious in onset and may have few associated symptoms and signs, a sample of ascites is always cultured. It is advisable to insert the specimen into blood culture bottles after collection to maximise the chance of a positive result. At the same time, the ascites should be cultured for acid-fast bacilli to diagnose the occasional case of tuberculous peritonitis.

Management of Ascites

This depends on the underlying diagnosis, as follows.

Liver disease

The management of ascites in liver disease is covered in Chapters 24 and 25.

Malignant ascites

It is important to try to establish the site of the primary tumour because systemic hormonal or chemotherapy can result in regression of the intraperitoneal tumour and the ascites, especially if the primary site is colonic, gastric, breast or ovary. Clinical re-examination of breasts and abdomen may be helpful. The investigations used to establish the common sites of the primary tumour, namely colon, stomach, pancreas, ovary and breast, are shown in Table 20.6.

Table 20.6 Investigations for primary tumour in patients with malignant ascites

Site of primary Relevant investigations
Colon Colonoscopy and biopsy
Stomach Gastroscopy and biopsy
Pancreas
Ultrasound ± CT scan ± fine needle aspiration
EUS ± needle biopsy
CA-19-9

Ovary
Pelvic ultrasound ± CT scan
CEA, CA125

Breast
Mammography or fine needle aspiration cytology if palpable lump
Breast biopsy and oestrogen receptors

CEA = carcinoembryonic antigen; CT = computerised tomography; EUS = endoscopic ultrasound.

In the event that the primary site is colon, stomach or pancreas, local therapy may be required to palliate the discomfort of distension. The therapeutic options are limited and none is really satisfactory. They include (1) repeated major paracentesis, which is time-consuming and results in the development of hypoalbuminaemia and malnutrition; and (2) peritoneovenous shunting, which can block and can be complicated by coagulopathy. Frequently, the best option is analgesia and general support.

Cardiac ascites

The management is directed at treating the cardiac cause. This may involve pericardectomy if constrictive pericarditis is the underlying problem.

Pancreatic ascites

Pancreatic ascites may settle with conservative management. This includes ‘pancreatic rest’ with enteric nutrition via a nasojejunal feeding tube. If the ascites fails to resolve over 2 weeks, it is unlikely to resolve and therapeutic intervention is required. Endoscopic retrograde cholangiopancreatography should be performed to define the location of the disruption of the main pancreatic duct. If the duct is intact with a leak from a side hole, the leak may resolve with endoscopic pancreatic stenting. If there is complete disruption of the duct a distal pancreatectomy is required.

Key Points

• The aetiology of diffuse abdominal distension can be defined with the ‘5 Fs’ rule: flatus, fluid, faeces, foetus or fluid.
• For flatus and faeces, consider obstructive lesions in the small or large bowel or a motility disturbance.
• For fluid consider hepatic, inflammatory, malignant or pancreatic causes.
• Foetus is usually self-evident but must be considered.
• Fat or obesity is diagnosed after the other 4 ‘Fs’ have been excluded.

Further reading

Runyon B.A., Montano A.A., Akriviadis E.A., et al. The serum-ascites albumin gradient is superior to the exudate/transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117:215-220.

Saadeh S., Davis G.L. Management of ascites in patients with end-stage liver disease. Rev Gastroenterol Disord. 2004;4:175-185.

Smith E.M., Jayson G.C. The current and future management of malignant ascites. Clin Oncol. 2003;15:59-72.

Williams J.W.Jr., Simel D.L. The rational clinical examination. Does this patient have ascites? How to divine fluid in the abdomen. J Am Med Assoc. 1992;267:2645-2648.

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