Persistent diarrhoea and chronic diarrhoea in children.7thsem 2017

Persistent diarrhoea and chronic diarrhoea in children

1. Persistent Diarrhoea and Chronic Diarrhoea Dr. Manoj Kumar Singh Assistant Professor, PMCH, PATNA

2. Definitions Persistent diarrhoea - Diarrhea with passage of 3 or more loose stools of presumed infectious etiology starting acutely and lasting for more than 14 days. Chronic diarrhea ; non infectious etiology, includes conditions causing malabsorption. Protracted diarrhea – Persistent diarrhea with weight loss and malnutrition

3. What is not persistent diarrhoea? If the period of normal stools is longer than two days , any subsequent diarrhoea should be considered to be a new episode. Chronic diarrhoea, which does not start with an acute infectious episode, may be due to a variety of metabolic or structural conditions or to parasitic infections. Protracted diarrhoea of infancy. Frequent passing of formed stools.

4. Epidemiology 10% of total diarrhea. 35 % of diarrheal deaths. For every 100 children, 7 suffers. PD in Malnutrition – 20 %. 60% < 6 months. 90 % < 1 year .

5. What causes persistent diarrhoea? The main feature is damage to the small and/or large intestine . Persistent colonisation by a microbe: Shigella Salmonella Campylobacter E. coli Klebsiella Giardia lamblia Cryptosporidium Entamoeba histolytica

6. What causes persistent diarrhoea? Dietary allergies: Certain dietary proteins Strong immune reaction in susceptible individuals Release of chemical from immune cells Damage to intestinal linings

7. What causes persistent diarrhoea? Carbohydrate intolerance: Malnutrition / Enteric infection / Lactase deficient population Decline in lactase concentration Lactose (main sugar in milk) not digested into glucose & galactose Lactose enters large intestine Osmotic effect Watery diarrhoea & abdominal distension

8. Associated infections of the urinary tract or another focus of infection (more commonly malnourished children ) contribute to failure to thrive and mortality. Prolongation of an acute diarrhea may rarely be a manifestation of cow milk protein allergy. The increased gut permeability in diarrhea predisposes to sensitization to oral food antigens. The use of antibiotics in acute diarrhea suppresses normal gut flora. This may result in bacterial overgrowth with pathogenic bacteria and/or overgrowth of fungi, resulting in persistent diarrhea and malabsorption. Cryptosporidium infection is frequently implicated in persistent diarrhea, even in immune competent children.

9. What increases risk of PD? Age: PD most frequently occurs during the first year of life. Nutritional status: Malnutrition is strongly associated with PD. Researchers have found a small increased risk of diarrhoea incidence in malnourished children, but a large increased risk of prolongation of the episode.

10. What increases risk of PD? Previous diarrhoea: Damage caused to the gut by the previous episode. Change in the child's defenses against infection. Feeding practice: Lack of breast feeding is associated with PD. Animal milk Formula feed. Bottle feeding.

11. What increases risk of PD? Decreased host immunity: Measles Moderate or severe PEM Specific gut infections : Shigella Enteropathogenic E. coli Cryptosporidium

12. What increases risk of PD? Delayed repair of intestinal damage : PEM Folate deficiency zinc deficiency Other factors: Research is continuing on the relation of several other factors to persistent diarrhoea. Vitamin A Iron Other micronutrients Behaviours related to water source and use Food preparation and consumption Hygiene

13. Mechanism of persistent diarrhoea PERSISTENT MUCOSAL INJURY Protein macromolecules absorbed Brush border enzymes reduced Decreased active transport of nutrients Sensitization by food proteins Carbohydrate malabsorption Decreased enteric hormones

14. Major consequences of PD Growth faltering. Worsening of malnutrition. Serious non-intestinal infection. Death during subsequent diarrheal or non-diarrheal illness. Dehydration may also occur.

15. Majority of patients with persistent diarrhea pass several loose stools daily but remain well hydrated. Dehydration develops only in some patients due to high stool output or when oral intake is reduced due to associated systemic infections . The major consequences of persistent diarrhea are growth faltering, worsening malnutrition and death due to diarrheal or nondiarrheal illness. The presence of secondary lactose intolerance should be considered when the stools are explosive (i.e. mixed with gas and passed with noise ) and in presence of perianal excoriation. The stool pH is low and stool test for reducing substances is positive. Unabsorbed dietary lactose once delivered to colon is converted to hydrogen and lactic acid by colonic bacteria. Lactic acid results in decreased stool pH, explosive stools are due to hydrogen and unabsorbed lactose gives positive reducing substances, if tested.

16. ASSESSING CHILD WITH PERSISTENT DIARRHOEA

17. Physical examination Assessment of dehydration Condition Eyes Tears Mouth & tongue Thirst Well alert Normal Present Moist Drinks normally, not thirsty Restless, irritable Sunken Absent Dry Thirsty, drinks eagerly Lethargic/unconscious Very sunken & dry Absent Very dry Drinks poorly or is not able to drink Skin pinch Goes back quickly Goes back slowly Goes back very slowly Classify as: No signs of dehydration Some dehydration Severe dehydration Treat as: Plan A Plan B Plan C

18. Physical examination Pulse: As dehydration increases, the radial pulse and femoral pulse become more rapid. When there is hypovolaemic shock, it may disappear completely. The femoral pulse, however, remains palpable.   Breathing: The rate of breathing is increased in children with severe dehydration, due in part to their base-deficit acidosis. The absence of cough and chest indrawing helps to differentiate these children from children with pneumonia.

19. Physical examination Assessing dehydration in malnutrition: Skin turgor appears poor in children with marasmus owing to the absence of subcutaneous fat. Diminished skin turgor may be masked by edema in children with kwashiorkor . Eyes may also appear sunken. The salivary and lacrimal glands are atrophied in severe malnutrition, so the child usually has a dry mouth and absent tears. In both types of malnutrition the child's irritability or apathy make assessment of the mental state difficult.

20. Physical examination Source: The treatment of diarrhoea, A manual for physicians and other senior health workers, WHO. Diagnosis of moderate or severe malnutrition Assessment Weight-for-age Weight-for-height MAC Other Moderate malnutrition 60-75% 70-80% Yellow band 11.0 - 12.5 cm Severe malnutrition <60% <70% Red band Less than 11.0 cm Obvious marasmus or edema with muscle wasting

21. Lab investigations PD can be managed without elaborate lab tests with very high level of success. Stool microscopy: Pus cells >20/ hpf – invasive diarrhoea Trophozoites of E. histolytica & G. lamblia Acid fast staining (modified Z-N stain): Cyclospora , Isospora & Cryprosporidium .

22. Lab investigations Stool culture: Salmonella & Shigella Detecting lactose intolerence : Milk withdrawal and challenge. pH of stool <5.5 on two separate occasion on milk diet. Test for reducing sugars in the stool.

23. Lab investigations Associated infections: Hemogram Urine routine & culture X-ray chest Blood culture Others: ABG, serum electrolytes, renal function tests.

24. MANAGEMENT

25. Management The objective of treatment is to restore weight gain and normal intestinal function. Treatment of persistent diarrhoea consists of giving: Fluids to prevent or treat dehydration. Nutritional management is the cornerstone – Dietary management – Supplemental vitamins & minerals Give Nutritious diet that does not cause diarrhoea to worsen. Supplementary vitamins and minerals , including zinc for 10 - 14 days. Antimicrobial(s) to treat diagnosed infections .

26. Two-thirds of patients with persistent diarrhea can be treated on outpatient basis. Patients in need of hospital admission are those with --- A ge less than 4 months and not breastfed . Presence of dehydration . S evere malnutrition (weight for height <3 SD, mid-upper arm circumference <11.5 cm for children at 6-60 months of age, or bilateral pedal edema); or P resence or suspicion of systemic infection.

27. Prevent or treat dehydration ORS solution is effective for most children with persistent diarrhoea. In a few, however, glucose absorption is impaired and ORS solution is not as effective as usual. These children require IV rehydration until ORS solution can be taken without causing diarrhoea to worsen.

28. Identify & treat specific infections Routine treatment of persistent diarrhoea with antimicrobials is not effective and should not be given. Some children, however, have non-intestinal (or intestinal) infections that require specific antimicrobial therapy. The persistent diarrhoea of such children will not improve until these infections are diagnosed and treated correctly .

29. Non-intestinal infections Every child with persistent diarrhoea should be examined for non-intestinal infections, such as: Pneumonia Sepsis Urinary tract infection Otitis media. Treatment of these infections with antimicrobials should follow standard guidelines.

30. Non-intestinal infections Associated systemic infection: Combination of parenteral ampicillin & aminoglycosides is usually appropriate. Severe malnutrition: Treat as for systemic infection, even if uncertain about presence of systemic infection.

31. Intestinal infections Shigella: PD with blood in the stool should be treated with an oral antimicrobial effective. Amoebiasis : M/E of fresh faeces reveals trophozoites of E. histolytica containing red blood cells, or Two different antimicrobials usually effective for Shigella in the area have been given without clinical improvement. Giardiasis: Cysts or trophozoites of G. duodenalis are seen in the faeces.

32. Nutritional management This is essential treatment for all children with persistent diarrhoea. Outpatients should be given a diet appropriate for their age, but with a limited content of lactose. Children treated in hospital require special diets until their diarrhoea lessens and they are gaining weight. In either situation, the goal is a daily intake of at least 110 calories/kg .

33. Feeding of outpatients Continue breastfeeding. If yoghurt is available, give it in place of any animal milk; yoghurt contains less lactose and is better tolerated. Limit animal milk to 50 ml/kg/day. Mix the milk with the child's cereal. Do not dilute the milk. Give other foods that are appropriate for the child's age as khichri , rice, dal, vegetables, egg, meat, fish etc. Infants older than 6 months whose only food has been animal milk should begin to take solid foods. Give frequent small meals, at least six times a day .

34. Feeding in hospital < 6 months • Encourage exclusive breast feeding. • Re-establish breast feeding. • Replace animal milks with curds or lactose free formula. • Cooked rice may be mixed if necessary.

35. Feeding in hospital The first diet (Diet A) : reduced lactose Start as soon as the child can eat and should be given six times a day. Many children will eat poorly, however, until any serious infection is treated for 24-48 hours. Such children may require nasogastric feeding initially. The diet should contain at least 70 Kcal/100g .

36. Feeding in hospital Milk or yoghurt as a source of animal protein, but no more than 3.7 g lactose/kg body weight/day , and provide at least 10% of calories as protein. A mixture of cow's milk, cooked cereal, vegetable oil and cane sugar is satisfactory. Diets can also be prepared from local ingredients following the above guidelines.

37. Feeding in hospital The following example provides 83 Kcal/100g, 3.7g lactose/kg body weight/day and 11% of calories as protein: Full - fat dried milk 11 gm (or whole liquid milk 85 ml) Rice 15 gm uncooked rice Vegetable oil 3.5 gm Cane sugar 3.0 gm Water to make 200 ml 130 ml/kg provides 110 kcal/kg

38. Feeding in hospital The second diet (Diet B) : lactose-free with reduced starch About 65% of children will improve on the first diet . The remainder have impaired digestion of starch and disaccharides other than lactose. These children, if free of systemic infection, are advised diet B which is free of milk (lactose) and provides carbohydrates as a mixture of cereals and glucose. Milk protein is replaced by chicken, egg or protein hydrolysate . The starch content is reduced and partially substituted by glucose. Substituting only part of the cereal with glucose increases the digestibility but at the same time does not cause a very high osmolarity. The following example provides 75 Kcal/100g :

39. Feeding in hospital Whole egg 64 gm Rice 3 gm Vegetable oil 4 gm Glucose 3 gm Water to make 200 ml 145 ml/kg provides 110 kcal/kg If finely ground, cooked chicken meat (12 g) is used in place of whole egg, the diet provides 70 Kcal per 100 g.

40. Feeding in hospital The third diet (Diet C) : monosaccharide based diet Overall, 80-85 % of patients with severe persistent diarrhea will recover with sustained weight gain on the initial diet A or the second diet B . A small percentage may not tolerate a moderate intake of the cereal in diet B. These children are given diet C which contains only glucose and a protein source as egg white or chicken or commercially available protein hydrolysates . Energy density is increased by adding oil to the diet. Chicken, (or) Egg 15 gm ½ egg white Glucose 7 gm Oil 7gm water 150 ml 67 Kcal/100 gm

41. Supplement vitamins and minerals Supplemental multivitamins and minerals, at about twice the RDA, should be given daily to all children for at least 2-4 weeks. Iron supplements should be introduced only after the diarrhea has ceased . Vitamin A (as a single dose) and zinc are supplemented as both of them enhance the recovery from persistent diarrhea. A single oral dose of vitamin A should be given routinely, at 2,00,000 IU for children>12 months or 100,000 IU for children 6-12 months . One should administer 10-20 mg per day of elemental zinc for at least 2 weeks to children between 6 months and 3 yr of age.

42. Additional supplements for severely malnourished infants and children Magnesium and potassium supplementation is provided to these children. Magnesium is given by intramuscular route at 0.2 ml/kg/dose of 50% magnesium sulphate twice a day for 2-3 days. Potassium is supplemented at 5-6 mEq /kg/day orally or as part of intravenous infusion during the initial stabilization period.

43. MONITORING THE RESPONSE TO TREATMENT

44. Children treated in hospital The following should be measured and recorded in a standard manner, at least daily: Body weight Temperature Food taken, and Number of diarrhoea stools. Successful treatment is characterized by: Adequate food intake Weight gain Fewer diarrheal stools Lack of fever.

45. Indications for change from the initial diet (diet A) to the next diet (diet B or diet C The diet should be changed to the next level if the child shows M arked increase in stool frequency (usually more than 10 watery stools/day ) at any time after at least 48 hr of initiating the diet ; F eatures of dehydration any time after initiating treatment ; or F ailure to gain weight gain by day 7 in the absence of initial or hospital acquired systemic infection . Unless signs of treatment failure occur earlier, each diet should be given for a minimum period of 7 days.

46. Dietary failure An increase in stool frequency (usually more than 10 watery stools/day) any time after at least 48 hr of initiating diet. Return of signs of dehydration any time after initiating treatment. Failure to establish daily weight gain within 7 days.

47. Dietary failure Give first diet for 7 days. If signs of dietary failure occur stop first diet and give the second diet also for seven days. If responding satisfactorily to either diet give additional fresh fruit and well cooked vegetables. After 7 days treatment with the effective diet, they should resume an appropriate diet for age, including milk, that provides at least 110 Kcal/kg/day.

48. Resumption of regular diet after discharge Children discharged on totally milk free diet should be given small quantities of milk as part of a mixed diet after 10 days . If they tolerate this and have no signs of lactose intolerance (abdominal pain, abdominal distension and excessive flatulence ) then milk can be gradually increased over the next few days. Age appropriate normal diet can then be resumed over the next few week.

49. Monitoring Response to Treatment Successful treatment is characterized by A dequate food intake, Reduced frequency of diarrheal stools (<2 liquid stools/day for 2 consecutive days) and W eight gain. Most children will lose weight in the initial 1-2 days and then s how steady weight gain as associated infections are treated and diarrhea subsides. All children should be followed regularly even after discharge to ensure continued weight gain and compliance with feeding advice .

50. Prevention Exclusive breast feeding. Proper complementary feeding. Improved feeding practices. Prevention and management of malnutrition. Use of safe water. Hand washing. Food safety. Use of latrines and safe disposal of stools. Immunization.

51. CHRONIC DIARRHEA

52. A stool output that exceeds 10 mL/kg/day is considered diarrhea . Diarrhea which lasts for more than 4 week, is usually non infectious and associated with malabsorption is labeled as chronic diarrhea.

53. Approach To Chronic Diarrhea History is the most important step, it usually makes the DD narrow and gives clues to the cause of chronic diarrhoea. Sex :- IBD in paediatrics is common in MALE. STOOL HISTORY -- Frequent mucoid stools in a healthy child without blood – IBS. Nocturnal diarrhoea is usually associated with organic disease rather than IBS . Infant having chronic diarrhoea, with a history of delayed passage of meconium and if constipation preceded diarrhoea- Hirschsprung's disease. Associated symptoms -- No symptoms, well child- toddlers diarrhoea. Abdominal distension and weakness- Coeliac disease. Severe abdominal pain, Bloody diarrhoea and oral ulcers - IBD. Vomiting and rash- Eosinophilic enteritis. Infant with severe napkin dermatitis resistant to most treatment – Acrodermatitis enteropathica .

54. NON GI SYMPTOMS – • Recurrent respiratory tract infections- CF. • Weakness, fatigue and weight loss- IBD, Addison and HIV. • Headache and mood changes - IBS. • Eczema- cow’s milk allergy and Eosinophilic enteritis. • Generalized lymphadenopathy- HIV. • Recurrent fever and weight loss-TB. Family history Same illness or respiratory problems - CF. IBD and IBS. Dietetic history : Provide vital clues to the aetiology, e.g., cow's milk protein intolerance, lactose intolerance , gluten enteropathy. Soy protein intolerance, egg protein enteropathy. Overfeeding, concentrated formula feeds> osmotic diarrhoea .

55. EXAMINATION Weight loss is seen in many disorders like CF, Coeliac disease, IBD. weight and height are usually normal in toddlers diarrhoea . • Pallor - CF, Coeliac disease. • Fever - Infection, TB, CF and HIV. • Clubbing - CF • Hyperpigmentation- Addison’s disease, Coeliac disease • Generalized lymphadenopathy- Lymphoma, HIV. • Periorificial and acral vesicular and scaly lesions- Acrodermatitis enteropathica . • Stomatitis and Perianal fistula- Crohn’s disease. • Hepatomegaly -lymphomas, metastatic carcinoid, IBD and Whipple’s disease . • Ascites - TB and lymphoma.

56. Approach To Chronic Diarrhea Age <6 mo Age >6 mo to 5 yr Age >5 yr Cow milk protein allergy Lymphangiectasia Urinary tract infection Short bowel syndrome Immunodeficiency states Cystic fibrosis Anatomical defects Intractable diarrheas of infancy Microvillous inclusion disease Tufting enteropathy Autoimmune enteropathy Glucose galactose malabsorption Congenital sodium/chloride diarrhea Cow milk protein allergy Celiac disease Giardiasis Toddler diarrhea Lymphangiectasia Short bowel syndrome** Tuberculosis Inflammatory bowel disease Immunodeficiency Bacterial overgrowth Pancreatic insufficiency Celiac disease Giardiasis Gastrointestinal tuberculosis Inflammatory bowel disease Immunodeficiency Bacterial overgrowth Lymphangiectasia Tropical sprue Immunoproliferative small intestinal disease Pancreatic insufficiency Age of onset -- Causes of chronic diarrhea according to age of onset, in order of importance.

57. In infants < 6months, Cow milk protein allergy and I ntestinal lymphangiectasia should be considered first . In young children, Celiac disease is the most common cause of chronic diarrhea in North India. Cow milk protein allergy usually resolves by 3-5 yr ; hence, this diagnosis should not be considered in children with onset of diarrhea beyond 5 yr.

58. Small or large bowel type of diarrhea -- differentiating point is as follow --

59. Of Osmotic Diarrhea

60. Toddlers diarrhea Toddler diarrhea is a diagnosis of exclusion after common causes have been ruled out . The onset of diarrhea is between 6 months and 3 yr of age . The child passes 3-6 loose stools, mostly during waking hour. Diarrhea worsens with low residue, low fat or high carbohydrate diet. The child is well thriving , good nutritional state there is no anemia or vitamin deficiencies and the diarrhea resolves spontaneously by about 4 yr of age. Treatment includes normalization of feeding patterns according to the “four Fs ”: Fat, Fibre, Fluid, and Fruit juices Treatment is with dietary modification ; a high (>40%) fat , low carbohydrate diet (especially with decreased intake of juices) and increase in dietary fiber is recommended

61. Celiac Disease This is an enteropathy caused by permanent sensitivity to gluten in genetically susceptible subjects. It is the most common cause of chronic diarrhea in children over 2 yr of age in North India. High-risk groups include subjects with Type 1 diabetes mellitus, Down syndrome, selective IgA deficiency, autoimmune thyroid disease, Turner syndrome , Williams syndrome, autoimmune liver disease and first-degree relatives of celiac disease patients. These subjects are at an increased risk of developing celiac disease and thus should be screened.

62. Presentation The classical presentation is with small bowel diarrhea, growth failure and anemia . A temporal association of diarrhea and introduction of wheat products at weaning may be present. Onset of diarrhea before introduction of wheat products in diet negates a diagnosis of celiac disease. It may also present without chronic diarrhea as refractory iron deficiency or dimorphic anemia not responding to oral supplements , short stature, delayed puberty , rickets and osteopenia. Examination reveals failure to thrive, loss of subcutaneous fat, clubbing, anemia , rickets and signs of other vitamin deficiencies sometimes epilepsy.

63. Diagnosis Serology – IgA antibody against tissue transglutaminase ( tTG ) is an ELISA based test, recommended for initial testing of celiac disease. It has a high sensitivity (92-100 %) and specificity (91-100%) in both children and adults. IgA anti endomysial antibody is an equally accurate test ( sensitivity 88-100 %; specificity 91-100 %) but is more difficult to perform. The diagnosis of celiac disease should not be based only on celiac serology as serology may be false positive, false negative and inter laboratory variations are also present. Upper GI endoscopy – It may be normal or show absence of folds or scalloped folds. Multiple ( 4-6 in number) endoscopic biopsies from the bulb and second/ third part of duodenum should be taken in all cases. Histology-- The characteristic histological changes in celiac disease are increased intraepithelial lymphocytes (> 30/100 enterocytes), increased crypt length, partial to total villous atrophy, decreased villous to crypt ratio and infiltration of plasma cells and lymphocytes in lamina propria .

64. Diagnosis of celiac disease (based on the modified criteria of the European Society of Pediatric Gastroenterology, Hepatology and Nutrition, ESPGHAN) requires the following : i . Clinical features compatible with diagnosis. ii . Positive intestinal biopsy as described above with or without serology . iii . Unequivocal response to gluten free diet (GFD) within 12 weeks of initiation of GFD. Treatment -- The treatment involves life-long GFD and correction of iron, folate and other vitamin/mineral deficiencies by supplementation. The patient should be assessed at 3 months for response to GFD. After initiation of GFD, all symptoms should subside and weight and height gain should be present . A small percentage of patients with celiac disease fail to respond to a gluten-free diet. In some patients who are refractory, corticosteroids may be helpful.

65. Cow Milk Protein Allergy Cow milk protein allergy (CMPA) affects 2 to 5% of all children in the West, with the highest prevalence during the first year of life. In India, CMPA accounts for -13% of all malabsorption cases in children <2 yr of age. A family history of atopy is common in children with CMPA. Nearly 50 % children out grow the allergy by 1 yr and - 95% by 5 yr of age . It is the most common food allergy in small children who are top fed but can also occur occasionally in breastfed babies due to passage of cow milk antigen in breast milk. There are two kinds of reactions to cow milk: ( i ) Immediate , i.e. IgE mediated: It occurs within minutes of milk intake and is characterized by vomiting, pallor, shock-like state, urticaria and swelling of lips. ( ii) Delayed , i.e . T cell mediated: It has an indolent course and presents mainly with GI symptoms.

66. Presentation The most common presentation is with diarrhea with blood and mucus . Depending upon the site and extent of involvement, the child may have small bowel, large bowel or mixed type diarrhea . In an Indian study 40% children presented with bloody diarrhea, 33% watery and 7% with a mixed type of diarrhea. Uncommonly reflux symptoms and hematemesis may be present indicating upper GI involvement. Respiratory symptoms (allergic rhinitis and asthma) and atopic manifestations (eczema , angioedema) may be seen . Iron deficiency anemia, hypoproteinemia and eosinophilia are commonly present.

67. Diagnosis In India non - IgE mediated CMPA is more common . In s igmoidoscopy aphthous ulcers and nodular lymphoid hyperplasia is seen and rectal biopsy shows plenty of eosinophils , give clue to the diagnosis in >95% cases irrespective of the clinical presentation and should be the first line of investigation in suspected cases. The gold standard for diagnosis of any food allergy is the elimination and challenge test. Typically the symptoms subside after milk withdrawal and recur within 48 hr of re-exposure to milk.

68. Treatment– All animal milk/milk products have to be removed from the diet. Soy or extensively hydrolysed formula, both of which are equally effective in terms of growth and nutrient intake can be used as alternatives. Soy is more palatable and cheap but it is not recommended in infants <6 months of age. Also 10-15% of CMPA have concomitant soy allergy, thus necessitating use of extensively hydrolysed formulae. A minority of children may not tolerate the extensively hydrolysed formulae and need elemental amino acid formulas. Parental education regarding diet and calcium supplementation is essential.

69. Intestinal Lymphangiectasia It is characterized by ectasia of the bowel lymphatic system, which on rupture causes leakage of lymph in the bowel. The disease is often associated with abnormal lymphatics in extremities. Signs and symptoms-- include peripheral edema which could be bilateral and pitting due to hypoalbuminemia or asymmetrical and nonpitting due to lymphedematous limb. Diarrhea , abdominal distension and abdominal pain are commonly present. Abdominal and/or thoracic chylous effusions may be associated .

70. Investigation-- Presence of hypoalbuminemia , low immunoglobulins , hypocalcemia and lymphopenia is characteristic of lymphangiectasia . Barium meal follow-through shows thickening of jejunaI folds with nodular lucencies in mucosa. Duodenal biopsy reveals dilated lacteals in villi and lamina propria . Treatment-- consists of a low fat, high protein diet with MCT oil, calcium and fat soluble vitamin supplementation. Intravenous albumin is required for symptomatic management and total parenteral nutrition (TPN) is reserved for management of chylous effusions. Resection may be considered if the lesion is localized to a small segment of intestine.

71. Immunodeficiency Both congenital and acquired immunodeficiency can cause chronic diarrhea. It should be suspected if there is history of recurrent infections at multiple sites (chest/GI/skin) and wasting . The common immunodeficiency conditions presenting with diarrhea include IgA deficiency, severe combined immunodeficiency (SCID), common variable immunodeficiency (CVID) and chronic granulomatous disease (CGD). Diarrhea is either due to enteric infections like giardia, cryptosporidium, CMV, etc. or due to bacterial overgrowth . Treatment involves administration of antimicrobials for bacterial overgrowth and opportunistic infections and therapy for underlying cause ( IV immunoglobulins , y interferon or bone marrow transplantation).

72. Drug Induced Diarrhea Diarrhea can be a side effect of many pharmacologic agents . Altered GI motility , mucosal injury and/or change in intestinal microflora are the main etiologic factors. Antibiotics can cause loose watery stools by altered bacterial flora or bloody stools secondary to Clostridium difficile overgrowth and pseudomembranous colitis (PMC ). Stopping the offending agent is often enough. Metronidazole or oral vancomycin is the drug of choice for PMC.

73. Inflammatory Bowel Disease (IBD) IBD is a chronic inflammatory disease of the GI tract and is of two main types, Crohn disease and ulcerative colitis. Nearly 25% of all IBD presents in the pediatric age group. The average age of presentation in children is -10-11 yr. Genetics is a very important risk factor for IBD and up to 30 % patients may have a family member with IBD. Treatment-- The main drugs used for IBD are 5 aminosalicylates (5-ASA ), steroids and immunomodulators (6-mercaptopurine, azathioprine, methotrexate and monoclonal antibodies against tumor necrosis factor, i.e. infliximab). Surgery is indicated in ulcerative colitis patients with severe acute colitis refractory to medical disease. Uncontrolled hemorrhage , perforation, toxic megacolon , abscesses and obstruction are the other indications for surgery in patients with IBD.

74. Differentiation between Crohn disease and ulcerative colitis Crohn disease Ulcerative colitis Distribution Entire gastrointestinal tract Discontinuous lesions Colon only Continuous involvement Bloody diarrhea Less common Common Abdominal pain Common Less common Growth failure Common Less common Perianal disease Abscess; fistulae Absent Serology Anti sacchromyces cerevisae antibody (ASCA) positive Perinuclear anti neutrophilic cytoplasmic antibody (p-ANCA) positive Endoscopy Deep irregular serpigenous or aphthous ulcers with normal intervening mucosa (skip lesions) Granularity, loss of vascular patter, friability and diffuse ulceration Histopathology Transmural inflammation with noncaseating granuloma Mucosa! disease with cryptitis , crypt distortion, crypt abscess and goblet cell depletion

75. Abdominal Tuberculosis The gastrointestinal tract, peritoneum, lymph nodes and/ or solid viscera can be involved in abdominal tuberculosis. The peritoneal involvement is of two types: wet (or ascitic ) and dry (or plastic) type . On the other hand, the intestinal involvement may be ulcerative, hypertrophic or ulcerohypertrophic type . Clinical features-- may include chronic diarrhea , features of subacute intestinal obstruction (abdominal pain, distension, vomiting , obstipation), ascites, lump in abdomen ( ileocecal mass , loculated ascites, lymph nodes) and/or systemic manifestations (fever, malaise, anorexia and weight loss ). Antitubercular drugs are the mainstay of treatment. Surgery is indicated if there is bowel perforation, obstruction or massive hemorrhage .