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Persistent Diarrhoea

B. Bhaskar Raju

Definitions

Persistent diarrhoea is presently defined by the WHO as persistence of actue diarrhoea/dysentery beyond 15 days.

The term acute diarrhoea is reserved for acute onset of diarrhoea, usually infective, in a previously normal child. Hence it follows, that the term persistent diarrhoea should be used only for childern who are essentially normal having diarrhoea beyond 2 weeks due to either persistence of the infection or post infective sequelae like disaccharide intolerance.

The term chronic diarrhoea is reserved for diarrhoea lasting more then 15 days in children who have some basic defect either in the GI tract, immune system or other organs. Therefore , chronic diarrhoea need not be infective, are often only controllable, unlike persistent diarrhoea which are potentially curable. Diarrhoea due to inflammatory bowel diseases, immuno deficiency, pan malabsorptions etc would be classified as chronic diarrhoea.

The adjective protracted is often used to describe both persistent and chronic diarrhoea, when diarrhoea results in significant weight loss. This expression is useful since it differentiates the more benign persistent diarrhoea due to simple disaccharide intolerance from diarroeas complicated by coexisting severe sepsis and structural villous damage.

Simple Persistent Diarrhoea

Recoginsed by:-

  • Reasonably healthy looking child
  • No dehydration
  • No toxemia
  • Preserved appetite
  • No weight loss
  • Perianal excoriation

Majority of these are simple disaccharide intolerances which respond dramatically to dietary modification designed to avoid sugars. A few may be mild giardiasis or similar infestations which a routine stool exam should be able to pick up. These cases do not require any hospitalisation, antibiotic therapy or ORS.

Persistent Protracted Diarrhoea

This is a much more complicated problem characterised by:-

  • Persistant diarrhoea not responding to dietary modification.
  • Significant gut and extra gut sepsis
  • Progressive loss of weight to marasmic or kwashiorkar states
  • Variable villi damage
  • Usually requires hospitalisation, investigations and aggressive therapy.

Aetiology / Pathogensis

While several factors come into play in the causation of persistent protracted diarrhoea (PPD), the final pathogenesis swirls around one single factor or its ramifications i.e., structural damage to the villi and consequent malabsorption produced by them.

Major factors

  • Malnutrition (of both macro and micro nutrients) and its consequences.
  • Infections (specific and non-specific)

Minor factors

  • Macro molecular absorption and food allergies
  • Inappropriate antibiotic usage
  • Non-compatible diets
  • Infestations (giardia, strongyloides)
  • Hypermotility, increased gastrocolic reflex
  • Deconjugated bile acids
  • Non-specific toxins
  1. Nutrition

    Loss of electrolytes, water and other nutrients through persistent diarrhoea coupled with iatrogenic reduction in oral intake results in acute malnutrition which has devastating effect on:

    • gut and systemic immunity
    • digestive and absorptive capacity
    • cell turnover especially in the GI tract
    • all of which help in perpetuating both infection and the diarrhoea.
  2. Infection (Gut)

    Specific:

    Many infections do not clear out of the gut in the expected 5-7 days thanks either to the baby's inadequate immune response or the aggressive virulence of the organism itself which makes it prone to persistence. In the latter category are included.:-

    • Rotavirus
    • Shigella spp
    • Salmonella spp
    • Yersinia enterocolitica
    • Campylobacter jejuni.
    • Clostridium difficile
    • Entamoeba histolytica
    • HIV / fungi

    Non-specific infections (gut):

    Contaminated bowel syndrome (CBS) :- The ascent of colonic bacteria into normally sterile small intestine, which occurs due to break down of local gut defences in severe malnutrition results in

    • copious secretory watery diarrhoea
    • osmotic diarrhoea due to damage to absorbtive surface
    • Hypermotility due to bacterial deconjugation of bile acids

    CBS can be clinically reconginsed by

    • emaciated child
    • persistent dehydration
    • persistent hypo electrolytemia
    • profuse watery diarrhoea not responding to diet withdrawl.
    • Significant tympanic abdominal distension

    Extra-Gut sepsis

    In our series in ICH & HC, Chennai nearly 40% of PPD had evidence of extra gut sepsis needing specific treament. The commonest were UTI, pneumonitis, CSOM besides ubiquitous skin infections. While these may not contribute directly to the diarrhoea their resolution is a must for complete recovery.

    Among the minor factors the one that is being increasingly recognized as an important cause of villous injury is macromolecular absorption, hypersensitive reaction and consequent inflammatory damage. Major culprits are cow's milk and soya bean milk proteins, both of which are widely used in diarrhoea . Except chicken and rice proteins virtually all others are potential allergens and it will be wise to avoid their usage in protracted diarrhoea.

    Assesment and evaluation of PPD child

    Knowing the multifactorial nature of the etiology, any evaluation should have an organised approach to identify each of the many factors that may play a role in an individual child. Besides assessment of altered homeostasis (hypoelectrolytemia, hypoglycemia, raised BUN etc) investigations should include.

    • objective assessment of malnutrition (e.g serum albumin, serum RBP etc)
    • evaluation of gut and extra gut sepsis (e.g. stool c/s, n/d aspirate c/s, blood culture X-ray chest, Mx etc)
    • assessment of malabsorbtion (e.g. stool RS. Stool chromatography)
    • Identification of site of gut infection
      : small bowel : large bowel (with stool Na, microscopy)

    The above plan will give us a quick report on the several problems that needs to be faced while organising the management of the diarrhoea. Children will also require individualised plan for identification of extra gut sepsis.

    Management Of PPD

    It is traditional to view management of PPD in 3 phases.
    Phase 1(0-24hrs) emergency management

    This includes correction of dehydration, dyselectrolytemia, hypoglycemia, pre-renal azotemia, avitaminosis A, hypo thermia etc.
    Phase II (1-7 days) - control of diarrhoea.
    Having analysed the causes of diarrhoea in an individual child one has to plan an aggressive and simultaneous attack on all the major factors - malnutrition, infection and malabsorbtion. Combating any of them in isolation while neglecting to tackle the others simultaneously will not give dividends and is the commonest cause for failure of therapy of PPD.

    Infections (specific):

    While rotavirus does not require any antibiotic cover, all other infections mentioned earlier will need specific antibiotic cover. Children are ideally started on a broad spectrum coverage (cefotaxime, amikacin) pending specific sensitivity information. The antibiotics we have found useful in salmonella, shigella are III generation cephalosporins and fluoro quinoloes. Campylobacter responds to macrolide while Yersinal infections may be amenable to cotrimaxazole. In general, culture studies, cost and prior experience in the institution should guide the choice of antibiotic cover in PPD.

    CBS if suspected will need anaerobic cover in the form of IV metronidazole, clindamycin or III generation cephalosporins like cefaperazone. In addition, local therapy (to combat the deliterious effects of the organism and toxin in the small bowel) in the form of cholestryramine, high dose locally acting non-absorbable antibiotic (orally administered aminoglycosides) may also be used. Extra gut sepsis if identified will need to be tackled simultaneously.

    Malnutrition/Malasorbtion:

    Malnutrition which is florid in PPD needs aggressive attention. TPN which would be the obvious and ideal choice is percluded in most cases due to exorbitant cost, high rate of complications and the lack of expensive infrastructure in most centres. A cheaper, equally effective alternative would be to split the nutritive provisions into part oral (60%) and part para-enteral (40%). A fluid (PPN) containing hypertonic glucose and amino acids, proteins in the form of plasma/albumin coupled with a cereal and pulse based oral porridge (without glucose/fat) would usually do the trick.

    Example of PPN solution:-

    • pediatric maintenance solution 250 ml
    • 25% dextrose 75ml
    • amino acid solution 150 ml
    • Sodabicarb 18 ml
    • KCL 5 ml
    • Multivitamin infusion 2 ml
      Total = 500ml

    About 100ml/kg/dayof the above solution can be used.

    Diet In Persistent Diarrhoea

    Formulating a diet is fairly simple if the following rules are observed:-

    1. Choose a good source of carbohydrate, protein and fat.
    2. Avoid proprietary foods
    3. Avoid allergenic proteins like soya bean, casein
    4. Introductory diet should be essentially cereal pulse combination without fat and glucose, both of which can be added as the diarrhoea improves.
    5. Start with continuous NG tube drip feeds to be followed later by bolus feeds.
    6. Be prepared to accept certain exacerbation of the diarrhoea on initiation of oral diet which is inevitable.
    7. Never starve a child beyond 24 hours as this will only initiate physiological regression of the villi. Rice, is by far the best and the most hypoallergenic, culturally accepted source of carbohydrate available and is much superior to other cereals, potatoes, arrowroot etc. as source of CHO. The 7 % protein content also helps.

    The protein source can be chosen from bengal gram, any of the traditional dhals, comminuted chicken, ground nuts etc. Coconut oil is the ideal starting fat source, thanks to its high MCT content. While other oils, ghee and butter can be added as absorption improves.

    Multivitamins, micro nutrients like iron, zinc etc. should always be apart of nutritional therapy of PPD.

    Phase III (Rehabilitation)

    With the above concentrated attack on the twin problems of malnutrition and infection the child should exhibit an improvement in the stool consistency within a weeks time.

    The third phase is to:

    1. Aid rapid weight gain
    2. Educate the parents to prevent recurrences.
    3. Slowly wean the child back to normal diet for that age and culture.

    A heavy dependence on home available protein and energy rich traditional diets is the best way to assure adequate nutrition for the baby after release from medical supervision. While most cases do tolerate mother's milk in PPD, in some at least it may be necessary to temporarily discontinue it. These mothers must be encouraged to go back to breast feeding the baby during rehabilitation phase. When good non-milk protein and energy sources are available and accepted by the baby, it will be advisable to keep them off cow's milk for 4-6 weeks.

    With the above rational approach to management of PPD, we have managed to dramatically improve the survival rate in what was considered a bleak disease hardly a decade ago. The enthusiasm thus generated however has to be tempered by the sobering fact that more than 10% of our PPD are HIV positive and their number is increasing year by year.