Causes of steatorrhoea include abnormalities of the small intestine and insufficiency of the exocrine pancreas. Calcification of the pancreas in chronic pancreatitis can be seen in 50% of cases (X-ray of the abdomen). Concomitant diabetes mellitus should be searched for. Non-infectious causes of intestinal abnormalities such as coeliac disease (hypersensitivity to gluten) and intestinal lymphoma are rare. Coeliac disease is associated with antibodies against gliadin (a component of gluten) and autoantibodies against tissue transglutaminase (anti-endomysium antibodies). People with this disorder are often HLA-DQ2-positive.
Some infections may result in malabsorption:
Giardia lamblia: microscopy of the faeces. These are often asymptomatic infections, so their importance should not be overestimated. Giardia can also give rise to secondary lactose-malabsorption: dairy products can no longer be tolerated.
Capillaria philippinensis: occurs mainly in the Far East but is rare. Infection is caused by eating raw fresh water fish. Like Strongyloides, this worm also leads to endogenous reinfection. It can therefore reproduce in the body, unlike most other worms. The eggs and larvae can be found in the stools (repeated analyses are necessary). Treatment is with mebendazole (Vermox®). It is a potentially fatal infection.
Strongyloides stercoralis: Serious infections cause diarrhoea, eosinophilia, pruritus and larva currens. The stools contain seldom eggs but larvae are present.
Cryptosporidia can cause malabsorption. The possibility of AIDS must be excluded. The parasite can be demonstrated using Ziehl stain.
Cyclospora can be compared with "large cryptosporidia" with variable acid-fastness on Ziehl stain. Treatment with cotrimoxazole is effective.
Tropical sprue is a disease of unknown origin, common in Asia but less so in Africa. The disease responds to treatment with tetracyclines and folic acid.
How long has the patient been suffering from diarrhoea? Is it acute (<14d)>14d)?
Is there blood or pus in the faeces (microscopy if necessary), or is it watery diarrhoea ?
Is there fever?
Additional questions are:
Is there tenesmus? Suggests that the rectum has been affected by inflammation or ulceration.
Is there abdominal pain? Not with cholera.
Is the patient vomiting? Makes dehydration worse and makes therapy more difficult.
Are there a number of people in the area with the same symptoms? An epidemic?
The assessment of dehydration is most important. Dehydration is due to an insufficient intake of liquids (drinking, IV fluid) and/or excessive loss of fluid (vomiting, diarrhoea, polyuria, sweating). If loss of gastro-intestinal fluid is the cause, the patient will urinate less (oliguria) in order to minimise the loss.
If a child has lost <>
If 5-10% of body weight is lost the eyes are sunken, the fontanelle is hollow, the skin is no longer elastic, the lips and mouth are dry and sometimes cracked. The child is miserable, restless and cries. There are no tears. Breathing becomes more rapid (acidosis). This must be distinguished from an accompanying pulmonary infection. Urine production decreases. The fluid deficit is 50-100 ml/kg.
With a fluid loss of >10% the child is still and cold. The pulse is rapid and difficult to feel (circulatory collapse). Skin folds do not disappear, the mucous membranes are very dry, the abdomen is hollow, the eyes are deeply set and the fontanelle is deeply sunken. Usually there is no more urine. The fluid deficit is >100 ml/kg.
Two things must always be considered:(1) the degree of dehydration, (2) is drug treatment necessary? The most important thing with acute diarrhoea is to deal with dehydration and in the second place to correct protein and calorie deficiency. Aetiological treatment will only be possible in a minority of cases, but should not be disregarded.
Children are very sensitive to dehydration. Fluid loss can occur very quickly with vomiting and diarrhoea: 500 ml of fluid in a child weighing 5 kg means a loss of 10% of body weight and implies a high risk of death.
IV rehydration is not always possible nor even desirable. An important development has been the discovery that many cases of dehydration of whatever origin can be counteracted by oral rehydration. This is possible because despite the diarrhoea, the mechanisms for absorbing water, sodium and glucose in the intestine are maintained. The minimum ingredients for this oral rehydration solution (ORS) are clean water, glucose and salt. While this can indeed bring about rehydration or prevent dehydration, a disadvantage is that the diarrhoea itself continues. The volume of stools is not reduced. Alternatives to glucose are ordinary sugar (sucrose; this is a glucose-fructose disaccharide) or rice powder. Rice powder is better because it reduces the volume of stools. In ideal circumstances potassium (against hypokalaemia) and bicarbonate or sodium citrate (against acidosis) can be added. Citrate is easier to store than bicarbonate. In the future there may perhaps be better formulae which also contain neutral amino-acids (glycine and alanine) and perhaps dipeptides.
The WHO has developed a standard formula. Each litre of water should contain:
| KCl | 1.5 gram |
| NaHCO3 | 2.5 gram or 2.9 gram sodium citrate |
| NaCl | 3.5 gram |
| Glucose | 20 gram or 50 gram of rice powder |
Under field conditions the following guidelines can be used :
1 teaspoon of salt + 6 teaspoons of sugar + 1 litre of boiled water.
Always weigh the child and assess its general condition.
Assess whether the weight loss is <5%,>10%.
Is it dysentery or not? If yes, is it amoebic or bacillary?
With mild to moderate dehydration use ORS. The volume that should be given is 1-2 times the fluid deficit. ORS is best given by the mother and should be given over a 4 to 6 hour period. It is best if it is given with a small cup and spoon. With very small children a syringe can be used to drip the fluid into the mouth. If the child vomits a few times the treatment should be continued nevertheless. Administration using a nasogastric drip infusion is rarely necessary. The success of the treatment should be monitored by assessing the general condition of the child and its weight.
With severe dehydration (>10%) or if the treatment with ORS is not successful, IV rehydration should be used. If it is not possible to inject into a vein and a venous cut-down is not feasible and the situation is desperate, the intraosseous route can be used: the fluid enters the bone marrow of the tibia and is taken up in this way. The infusion can be rapid at first (70 to 100 ml/kg over 3 hours). If the pulse can be felt clearly again and the child has generally improved, the treatment can then be switched to oral therapy.
Newborn children with a low birth weight are very sensitive to hypernatremia. Rehydration is achieved best with 2/3 ORS and 1/3 extra salt-free water.
Food must continue to be given while the patient has diarrhoea. It used to be thought that a period of fasting (24 to 48 hours) was good for the child, but this is counterproductive. Breastfeeding should not be stopped. A balanced diet, best low in residue and semi-solid is indicated. A good diet is also important after the diarrhoea. During episodes of diarrhoea, patients are catabolic (they break down their own muscle proteins for energy).
Most diarrhoea is transmitted by the faeco-oral route. The prevention of these infections will therefore depend on improved general hygiene, which is determined by the general level of poverty (standard of living). A few general tips and precautionary measures are recommended:
Food should be completely cooked/boiled.
Drinking water should be protected. This can be achieved in a village context (sand filters, protection of water-wells, etc). Water can be boiled and filtered, but boiling requires a lot of fuel, which is usually expensive.
Wash hands with soap.
Sanitary provisions: toilet and drinking water should be kept separate. Inexpensive, simple, build-it-your self, ventilated, odour-free, fly-free latrines that do not require any water can be made (the Blair latrine for example).
A rotavirus vaccine (Rotashield) was withdrawn from the market in 1999.
Food: avoid raw vegetables, fruit you cannot peel yourself, unpasteurised dairy products, fish, shellfish and meat that is raw or not cooked through. (Cook it, peel it or leave it). Avoid food from street stalls. Food should be protected against flies.
Drink: drink tea, coffee or bottled water, preferably sparkling (less risk of having been tampered with). Beer can quench the thirst, but large quantities of alcoholic drinks are not recommended. Avoid bottles sealed with reused crown caps. Ice cubes are not to be trusted. Drinking water can be filtered. This can be done in a number of ways (large porcelain filters such as Berkefeld, active charcoal filters, portable Katadyne filters). Afterwards the water can be boiled or purified chemically with silver salts such as Micropur®, Drinkwell® (not active against viruses), Chloramine (250 mg per 10-50 litres), sodium hypochlorite (Javel, Drinkwell chlorine®, Hadex®). An unpleasant taste of chlorine can be removed by adding the non-toxic sodium thiosulphate (Drinkwell-antichlorine® drops) work in for an hour. Lugol or 2% tincture of iodine (eight drops per litre) can also be used and is more active against amoebic cysts. Long-term use (more than 3 months) is not recommended. Thyroid disorders and pregnancy are contra-indications.
Chemoprophylaxis: This is normally not advised routinely, but does provide partial protection (e.g. ofloxacin). Only to be considered for short journeys where absolutely nothing should go wrong.
Several species of flies live in close proximity to people and often eat organic waste and faeces as well as food intended for people. They lay eggs -often hundreds- on their food. When an adult fly feeds on infected material (on faeces for example), pathogens are taken in through the mouth and into the intestine. Pathogens can stick to the pads of the feet and on hairs of the legs and body. Later the insect can land on unprotected food. When walking over the food, the micro-organisms are deposited. Like all Diptera, flies eat liquid food. The fly vomits a little fluid to make the food liquid. This vomit can contain microbes from a previous meal. At the same time the fly defaecates the leftovers from a previous (infected) meal. Many pathogens causing enteritis can be transmitted in this way. Flies can also transmit trachoma, an infectious disease of the eye (Chlamydia trachomatis), which can cause blindness.
Tropical sprue is an acquired disease of unknown origin. An infectious origin appears probable and the term "post-infectious malabsorption" is also used. Possibly there is an initial insult at the level of the jejunal-ileal enterocytes, followed by bacterial overgrowth with enterotoxic strains. The disease is characterised by abnormalities of the mucosa in the small intestine with chronic malabsorption, multiple nutritional deficiencies and anaemia. The malabsorption is generalised and affects absorption of proteins, fat, carbohydrates, minerals and vitamins.
Tropical sprue occurs chiefly in the Caribbean, India, Nepal and Southeast Asia, in both the indigenous populations and immigrants. Cases have been reported from Mauritius, Fiji, southern Italy, Guyana and Central America. In Africa the disease is apparently very rare, although cases have been reported from Zimbabwe.
Tropical sprue can have an insidious onset or can start acutely. The symptoms are those of chronic malabsorption. Generally it presents as a clinical triad of painful tongue, loss of weight and persistent abdominal discomfort with diarrhoea. Patients are noticeably tired, both physically and mentally. Amenorrhoea is very common. There is loss of weight with muscle atrophy. Hypoalbuminaemia leads to oedema.
Due to malabsorption of carbohydrates there is increased gas production in the intestines, with borborygma, a bloated feeling in the abdomen and intestinal cramps. The D-xylose absorption test is abnormal in more than 90% of cases. Fat malabsorption leads to steatorrhoea with more than 10 g of fat in the faeces. This occurs in 95% of patients. The stools are pale, very odorous and quite voluminous, up to 5 times the normal amount. Dehydration, hyponatraemia and hypokalaemia are very common.
Calcium deficiency may lead to tetany with positive Trousseau’s sign [in latent tetany, the occurrence of carpopedal spasms accompanied by paresthesia elicided when the upper arm is compressed (diminished blood supply), such as by a tourniquet or a blood pressure cuff. It occurs when the concentration of ionised free calcium is below a certain treshold; this concentration is pH-dependent].
Hypokalaemia leads to reduced tendon reflexes and abnormalities on the electrocardiogram. There is usually a deficiency of vitamin B12, folic acid and sometimes also iron. Anaemia occurs and is typically macrocytic with megaloblastic bone marrow.
In long-term cobalamine deficiency there may be peripheral neuritis and involvement of the spinal cord, chiefly of the dorsal columns (proprioception). The tongue is red and painful. As well as glossitis there may be stomatitis with superficial erosions.
Deficiencies in fat-soluble vitamins (A, D, E, K) lead to prolongation of the coagulation time and osteomalacia.
Vitamin A deficiency is characterised by a dry, rough skin with follicular hyperplasia and Bitot’s spots on the conjunctivae. In severe deficiency night-blindness and xerophthalmia may occur.
Tropical sprue should be suspected in anyone with megaloblastic anaemia and malabsorption who has lived in an endemic region. Biopsy of the jejunum shows typical abnormalities. Intestinal villi become shorter and broader. In the intestinal wall there is an inflammatory infiltrate, chiefly consisting of lymphocytes, plasma cells and a few eosinophils. The enterocytes exhibit large vacuoles. Radiography of the small intestine shows non-specific changes. There is flocculation of the contrast material and segmentation of the barium column, distension of the lumen and thickening of the mucosa. The mucosal folds in the small intestine are irregular and thickened, which gives the impression of a stack of coins. In advanced cases, no mucosal folds at all can be seen. There is no deconjugation of bile salts, unlike, for example, in the blind-loop syndrome. A flat mucosa is very unusual and should lead to suspicion of a different disease (e.g. gluten enteropathy).
The differential diagnosis is that of chronic malabsorption. In includes persistent giardiasis, isosporiasis, strongyloidosis, intestinal capillariasis, gluten enteropathy (coeliac disease), chronic pancreatitis, intestinal tuberculosis, intestinal amyloidosis, Whipple’s disease, the blind-loop syndrome, bacterial overgrowth, diverticula and jejunocolic fistulae. Crohn’s disease is rare in developing regions.
Treatment is based on tetracyclines 250 mg QDS or vibramycin 100 mg daily for three weeks to several months. Folic acid supplements (5 to 10 mg daily) and multivitamins and if necessary iron should be added to the treatment. Response to treatment is generally swift with an initial improvement within three days. Further recovery takes place in the course of the following three months.
A problem that occurs during or after a trip does not necessarily need to have a causal connection with that trip. It should be determined whether it is an acute or a chronic problem, if the spleen is enlarged and whether or not there is fever. Try to make a distinction between a (infectious) disease which results in leukopaenia and leukopaenia which results in infection.
Infectious diseases that are frequently accompanied by leukopenia include:
typhoid fever (Salmonella typhi)
typhus or spotted fever (rickettsiosis)
arboviroses
brucellosis
visceral leishmaniasis
miliary tuberculosis
Malaria is a common illness, but only occasionally causes leukopenia. Leukopenia in kala azar and malaria are associated with hypersplenism, which can give rise to leukopenia, thrombocytopenia, anaemia or pancytopenia. Leukopenia will in rare cases also be encountered in AIDS and tuberculosis.
Other differential diagnosis:
Bone marrow suppression (e.g. due to medication, agranulocytosis with thyreostatics, chloramphenicol, or amodiaquine) or bone marrow infiltration can likewise cause leukopenia.
Certain autoimmune diseases, e.g. Felty syndrome, may likewise be accompanied by leukopenia.
Felty syndrome is characterised by the triad of seropositive rheumatoid arthritis, splenomegaly and granulocytopenia.
