and Ian A. D. Bouchier2
(1)
Bishop Auckland, UK
(2)
Edinburgh, Midlothian, UK
Major causes of persistent steatorrhoea are coeliac disease, chronic pancreatic disease including cystic fibrosis, pancreatic carcinoma and gastric surgery. There are many other causes, and acute self-limiting steatorrhoea is a common feature of infective diarrhoea.
7.1 Faecal Fat Excretion
This is not popular with routine laboratories, and not very widely available.
Fat is present in the faeces in three forms: as neutral fat (triglycerides, ‘unsplit’ fat); free fatty acids (‘split’ fat); and sodium, potassium and calcium salts of the fatty acids (soaps). The origin of the faecal fat is not fully understood. It is in part exogenous, being derived from unabsorbed dietary fat, but also partly endogenous from the bile, desquamated cells and the breakdown of bacteria.
7.1.1 Method
It is important that the patient is eating a normal diet: patients with steatorrhoea often control diarrhoea by reducing fat intake. Patients should be told that satisfactory results depend on diet, and it is worth arranging a consultation with the dietitian to ensure an adequate intake.
The faeces excreted over a period of 3 or 5 consecutive days are collected and sent to the laboratory. The samples should be in clearly labelled and dated containers. If the patient is constipated a longer period of collection may be undertaken and this must be made clear to the laboratory. Periods of collection shorter than 3 days are unsatisfactory and inaccurate, as the amount of fat contained in a single stool specimen can vary widely.
The faeces should be uncontaminated by barium and the patient must not be taking castor oil. Liquid paraffin does not affect the neutral fat level when the van de Kamer method is used.
The collection of stools should present no problems in hospital, where stools passed into bedpans can be transferred to labelled tins. The out-patient collection of stools is much more difficult and uncertain. The following technique has been suggested for out-patients. A polythene sheet is cut into the shape of a widemouthed cone 24 inches in diameter. This can be held conveniently in place between the seat and the basin of the lavatory, and after defecation the sheet and faeces are transferred to a container. One can is used for each day and at the end of the day the lid is sealed with adhesive tape. It is desirable but not essential that the cans are stored in a refrigerator until analysis.
In the laboratory the stool is mixed with water, homogenized, and the collection pooled. After thorough mixing, a 10 ml aliquot is analysed by hydrolysis, extraction and titration of the fatty acids. The result may be expressed as fatty acids but is usually expressed as amount of neutral fat excreted per day.
7.1.2 Interpretation
The normal maximum daily output of fat is 18 mmol or about 7 g in adults, but the upper limits vary in different laboratories. A patient who excretes more than the normal daily amount of fat in the stool is said to have steatorrhoea. There is very little difference in the amount of fat excreted in the stool when normal subjects take diets containing 50–250 g fat/day but in patients with malabsorption the stool fat content is more closely related to the dietary fat intake. The ordinary mixed diet in the UK contains 70–90 g fat/day.
The method gives poor recovery of short- and medium-chain fatty-acid triglycerides. This is normally not a problem as the average diet contains almost exclusively long-chain triglycerides, but some artificial diets contain fat as medium-chain triglycerides which do not require digestion prior to absorption. Markers such as cuprous thiocyanate, carmine or radio-opaque pellets have been used to ensure complete collections. In theory this is an attractive method, but it is handicapped by the fact that luminal contents are not homogeneous and that solids, oils and aqueous solutes travel at different rates.
7.1.3 Indications
The faecal fat output was a widely used index of the state of digestion and absorption in the small intestine. Steatorrhoea is a feature of a number of diseases involving the small intestine, the pancreas and the hepatobiliary system, and is also seen in many patients who have undergone partial gastrectomy or vagotomy and drainage procedure. The terms steatorrhoea and malabsorption are frequently used interchangeably. Steatorrhoea implies only an excess of fat in the stool, but the presence of steatorrhoea is usually one of cardinal features of malabsorption in which fluid, electrolytes, vitamins, carbohydrates and proteins may be poorly absorbed.
7.2 Macroscopic Appearance
The macroscopic appearance of a stool containing excess fat is sometimes characteristic: bulky, yellow or grey, soft and sticky with a rancid odour. The stool may be liquid, frothy and have floating oil droplets. On the other hand the stool may appear perfectly normal or even rather small and hard. Stools float in water because of increased gas content, which does not correlate with fat content.
7.3 Stool Weight
The stool weight in Britain ranges normally up to a limit of 250 g/day. Steatorrhoea is unlikely but not impossible if the stool weight is less than 80 g/day. A clinically useful guide to the severity of steatorrhoea is obtained by weighing the stool daily, even though the correlation between the stool fat content and the stool weight is not close. By following progress in this way it is possible to avoid overburdening the laboratory.
7.4 Prothrombin Time (PR, INR)
This reflects vitamin K absorption as well as liver synthesis. If the prothrombin time is more than 3 s longer than control and reverts to normal after treatment for 3 days with vitamin K 10 mg 1 M or IV daily, then vitamin K malabsorption is established. This may accompany any cause of steatorrhoea. An INR of 1.3 or more gives equivalent information.
7.5 Serum Vitamin D
In addition to dietary sources of vitamin D, there is an appreciable synthesis in the skin under the influence of daylight. Low values may be found in inadequate vitamin D intake and in individuals (especially with pigmented skins) who are not exposed to sufficient daylight. Values are markedly seasonal with higher values in summer.
The normal adult range of values is 25–75 nmol/l in summer and 15–60 nmol/l in winter. Laboratories can separate 25-0H-ergocalciferol (dietary origin), low in malabsorption, from 25-0H-cholecalciferal (endogenous synthesis).
7.6 Vitamin A Absorption
The fasting patient is given 7500 iu vitamin A/kg (maximum 350,000 iu) in 7 ml peanut oil and with a standard light breakfast.
Blood is taken before and 4, 5 and 6 h after the vitamin dose. Normal diet is allowed after the 4-h sample. All blood samples are protected from the light by taking them into tubes covered with silver paper, and storing in the dark until analysis. The serum vitamin A level may be conveniently measured by fluorimetry.
The normal fasting serum vitamin A is 0.8–5.4 micromol/l, and the maximum increase after administration of vitamin A is 6–61.7 micromol/l. In malabsorption many of the fasting values fall in the normal range but the maximum increase is <6 micromol/l. This test is unreliable in pancreatic disease, though average values are reduced.
7.7 Oxalate Loading Test
Patients with steatorrhoea absorb excess dietary oxalate. Measurement of urinary oxalate after an oral oxalate load can be used as a screening test for steatorrhoea. Patients are given a standard diet containing 50 g fat, 1 g calcium and 30 mg oxalate for a week. On the last 3 days of this diet they are given sodium oxalate 300 mg twice daily with meals, and on the last day a 24-h urine collection is made. Patients with steatorrhoea excrete more than 0.44 mmol oxalate/24 h. Hyperoxaluria may also occur in patients with bile acid malabsorption. The test cannot be used in patients with substantially diseased or resected large intestine, as the colon is the main site of oxalate absorption.
7.8 Breath Tests
Anaerobic bacteria are found in great numbers in the large bowel (1015/ml) and lesser numbers in the normal small bowel (102–105/ml). They produce hydrogen and methane from dietary substrates, especially sugars, which can be measured in breath. These gases are absent in fasting subjects.
7.8.1 Procedure
Patients are studied after a 12 h fast( water only), and should not have taken antibiotics or had bowel preparation in the previous month. They should avoid laxatives for 3 days.
Breath hydrogen and methane are measured simultaneously in an analyser such as GastroCH4ECK.
Lactulose 10 g (3 × 5 ml teaspoons) is given by mouth. This is a non-absorbed hexose-pentose compound. Basal breath samples are taken, and then at 15 min intervals for 120 min. If a rise in H2 plus CH4 >20 ppm occurs the test is positive and may be terminated.
7.8.2 Results
A rise at 30 min >20 ppm indicates small bowel bacterial overgrowth.
A rise at 60–90 min shows normal orocaecal transit: a rise <60 min shows rapid transit, and one >100 min shows delayed transit.
Glucose 50 g in 250 ml water can be used as substrate in patients without fructosaemia or hypoglycaemia to detect colonisation, when the reference is 10 ppm above baseline. Though the sensitivity of the two substrates is compable at 62–68%, glucose is much more specific, 83 vs 44%.
A rise at 60 min shows jejunal colonisation and at 90 min ileal colonisation.
Lactose 50 g in 250 ml warm water can be used as a substrate in tests for lactase deficiency.
Breath samples are taken at baseline and 15, 30, 45, 60, 90 and 120 min (plus 150 and 180 min if necessary).
A rise >20 ppm in hydrogen or 12 ppm in methane indicates lactose intolerance.
A rise >10 ppm at 30 min can mean small bowel overgrowth or lactose intolerance.
7.9 Bile Acid Malabsorption
Some uncommon forms of diarrhoea are caused by excessive loss of bile acids into the colon from the small intestine. This can be measured by giving 75selenium-labelled tauro-homocholic acid, (SeHCAT) by mouth, and measuring retention in the body. Normal conservation of bile acids in the enterohepatic circulation means that 80% of activity is retained in the body at 24 h, 50% at 72 h, and 15% or more at 7 days. A convenient test is to count the patient’s whole body with a gamma camera at 1 week to separate pathologically low retention from normal.
Although theoretically attractive, this test confers no definite advantage over a therapeutic trial of bile-acid binding resin such as colestyramine or colestipol.
7.10 Monosaccharides
7.10.1 Xylose Excretion
Xylose is a pentose sugar which is absorbed in the jejunum and excreted unchanged in the urine. The original xylose absorption test depended markedly on renal function and age. Results may be spuriously low in patients with ascites. A range of doses has been administered (5, 15 and 25 g) and xylose has been measured in both urine and blood. Results are often so difficult to interpret that many gastroenterologists have abandoned the test altogether.
If it is to be used in diagnosis then the method described by Haeney is the most attractive.
7.10.1.1 Method
The patient is fasted overnight, apart from fluids which are encouraged. Height and weight are measured and surface area is derived from Geigy Scientific Tables. After a baseline blood sample has been taken to estimate non-xylose reducing component, D-xylose 5 g in 250 ml water is drunk quickly. Venous blood is sampled 1 h later.
7.10.1.2 Interpretation
The result is corrected for surface area by the formula:
corrected blood value = measured value × actual surface area (m2) divided by standard mean surface area (1.73 m2)
The normal corrected value is 0.65–1.33 mmol/l, and patients with malabsorption have values below this.
7.10.1.3 Indications
- 1.
A screening test for steatorrhoea caused by small bowel disease.
- 2.
To measure jejunal absorptive capacity in monitoring disease progress.Related posts:
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