CHRONIC DIARRHOEA

And management

Dr jyoti prajapati Dr. s. s. yadav

CHRONIC DIARRHOEA Despite considerable advances in the

understanding and management of diarrheal disorders in childhood, they are still responsible for a major burden of childhood deaths globally, with an estimated2.5 million deaths.

More recent reviews of studies published in the past 10 years indicate that, while global mortality may have reduced, the incidence remained unchanged at about 3.2 episodes/child year.

These findings indicate the continuing need to focus on prevention and management of childhood diarrhea in developing countries.

Most diarrheal disorders resolve within the first week of the illness.

1 to 3% of acute diarrhoeas become chronic, With a high mortality and morbidity. Persistent diarrhea has been defined as an

episode that begins acutely but lasts for 14 days or longer.

Classification of chronic Diarrhoea (CD) Type I—chronic diarrhoea in a previously normal

child-90% Type Il—chronic diarrhoea in a child with

inherent defect-10%

type 1 (persistent or protracted)starts as acute diarrhoea, but instead of subsiding in the usual time,

the child goes on purging for a period of more than 2 weeks.

The various risk factors for this are: Protein-energy malnutrition Younger age < 18 months Lack of breast-feeding Bottle-feeding Cow's milk.,Soy protein Inappropriate use of antibiotics Improper therapy of ADD. Use of antimotility drugs like loperamide. Starvation during ADD. Vitamin A deficiency. Zinc deficiency. Poor hygiene leading to reinfection. Certain extra intestinal infections, e.g., septi cacmia, UTI

TYPE II CHRONIC DIARRHOEA1. Inflammatory causes Tuberculosis. Eosinophilic gastroenteritis. Crohn's disease. Behcel's syndrome. Necrotising enterocolitis. Allergic colitis. Henoch-Schonlein vasculitis.2. Malabcription states Pancreatic diseases Cystic fibrosis. Diamond-Shwachman syndrome. Chronic pancreatitis. Hereditary pancreatitis. Congenital lipase deficiency. Congenital trypsin deficiency.

Liver diseases Cholestatic jaundice. Primary bile acid malabsorption.Intestinal diseases Tropical sprue Coeliac disease Whipple's diseae Intestinal lymphangiectasia Anderson's disease (chylornicron reten tion disease) Bassen-Kornzweig syndrome (abetal ipoproteinaemia Enterokinasc deficiency Vitamin B12 malabsorption Juvenile pernicious anaemia. Transcobalamin II deficiency. Lactase deficiency-congenital/ac quired. Sucrase-isomaltase deficiency. Glucose-galactose malabsorption.

Metabolic disorders Darrow's syndrome (congenital chloride

diarrhoea). Abetalipoproteinaemia. Acrodermatitis enteropathica.Endocrine causes Hypoparathyroidism, Hyperthyroidism. Diabetes mellitus. Adrenal insufficiency. Congenital alterations in electrolyte transport Congenital chloride diarrhoea

Immune defects Agammaglobulinaemia. Isolated IgA deficiency. Defective CMI. Combined immunodeficiency.

Neoplasms lmmunoproliferative small intestinal dis ease (IPSID or

Mediterranean lym phoma). Western lymphoma. Ganglioneuroma. Vernor-Morrison syndrome (pancreatic cholera or

VIPoma). Zollinger-Ellison syndrome.

Motility disorders Toddler´s diarrhoea Hyperthyroidism Idiopathic bowel pseudo-obstruction Irritable bowel syndromeAnatomical or surgical disorder Necrotizing enterocolitis Short bowel syndrome Blind loop syndrome Hirschprung’s disease Intestinal lymphangiectasia

COMMON CAUSES OF CHRONIC DIARRHEA

INFANCY    Postgastroenteritis malabsorption syndrome  (persistent)   Cow's milk/soy protein intolerance   Secondary disaccharidase deficiencies    Cystic fibrosis CHILDHOOD Chronic nonspecific diarrhea     Secondary disaccharidase deficiencies    Giardiasis    Postgastroenteritis malabsorption syndrome    Celiac disease    Cystic fibrosis ADOLESCENCE    Irritable bowel syndrome    Inflammatory bowel disease     Giardiasis     Lactose intolerance

PATHOPHYSIOLOGY

osmotic diarrhea secretory diarrhea, mutations in apical membrane

transport proteins, reduction in anatomic surface area alteration in intestinal motility, and inhibition of transport of electrolytes

by inflammatory mediators

OSMOTIC DIARRHEA.

presence of nonabsorbable solutes colonic bacteria ferment the nonabsorbed

sugar to short-chain organic acids osmotic load water secreted

CAUSES

MALABSORPTION OF WATER-SOLUBLE NUTRIENTS -Glucose-galactose malabsorption  Congenital , Acquired Disaccharidase deficiencies.

EXCESSIVE INTAKE OF CARBONATED FLUID EXCESSIVE INTAKE OF NONABSORBABLE

SOLUTES -Sorbitol Lactulose Magnesium hydroxide

stops with fasting, has a low pH, positive for reducing substances

SECRETORY DIARRHEA.

activation cAMP, cGMP, and intracellular calcium,

active chloride secretion (crypt cells)+

inhibit the neutral coupled sodium chloride absorption

alter the paracellular ion flux( toxin-

mediated injury to the tight junctions) secretory diarrhea

CAUSES OF SECRETORY DIARRHEAACTIVATION OF CYCLIC AMP Bacterial toxins: enterotoxins of cholera,

Escherichia coli (heat-labile), Shigella, Salmonella, Campylobacter jejuni, Pseudomonas aeruginosa   

Hormones: vasoactive intestinal peptide, gastrin, secretin   

Anion surfactants: bile acids, ricinoleic acid

ACTIVATION OF CYCLIC GMP Bacterial toxins: E. coli (heat-stable) enterotoxin,

Yersinia enterocolitica toxin

CALCIUM-DEPENDENT   Bacterial toxins: Clostridium difficileenterotoxin    Neurotransmitters:acetylcholine, serotonin    Paracrine agents: bradykinin

 DIFFERENTIAL DIAGNOSIS OF OSMOTIC VS SECRETORY DIARRHEA

  OSMOTIC DIARRHEASECRETORY DIARRHEA

Volume of stool <200 mL/24 hr >200 mL/24 hr

Response to fasting Diarrhea stops Diarrhea continues

Stool Na+ <70 mEq/L >70 mEq/L

Reducing substances[*] Positive Negative

Stool pH <5 >6

CHRONIC NONSPECIFIC DIARRHEA (TODDLER'S DIARRHEA) well-appearing toddlers (1 and 3 yr ) morning brown and watery, undigested food

particles. MANAGEMENT- fluid intake should be reduced

to no more than 90 mL/kg/24 hr. -Dietory history-0ffending food should be decreased( apple,

pear, and prune juices)

PATHOGENESIS OF PERSISTENT DIARRHOEA

final common pathway to persistent diarrhoea is `prolonged small intestinal mucosal injury' or PSIMI.

PSIMI is caused, intensified and perpetuated by the following factors:

Malnutrition Ineffective villous repair. Persistent infection with one or more enteric pathogens. Malabsorption of nutrients, especially carbo hydrates and

fats. Increased absorption of foreign proteins. Deficient enteric hormones.All these factors contribute to the vicious cycle of mucosal

injury and malabsorption, leading to PD.

ROLE OF MALNUTRITION IN PSIMI

Normally, in the epithelium of the small bowel, absorptive cells are continuously lost from the villous tip and replaced by newer cells produced by the crypts of Lieberkuhn, once in 4-5 days.

In a child with malnutrition, the production of the absorptive cells of the villi is decreased, as it requires energy and nutrients.

These cells are responsible for the synthesis of disacchari dase enzymes like lactase and hence their concentration in the gut decreases. This leads to osmotic diarrhoea.

The absorption of nutrients, which also re quires energy, is decreased in malnutrition,

Malnutrition can depress the immune functions, leading to infections of the gut

gastrin and cholecystokinin are proteins in nature, their secretion is decreased in malnutrition.

gastric HCI and pancreatic enzymes are also decreased leading to maldigestion and diarrhoea.

MALNUTRION

ROLE OF BACTERIAL OVERGROWTH IN PSIMI

Bacterial contamination of the small gut causes PSIMI by the following mechanisms:

release toxins directly invade and damage the small bowel

mucosa > malabsorption deconjugate bile acids, --releasing free bile acids

in the small gut.

ROLE OF DECREASED ENTERIC HORMONES IN PSIMI

Gastrin - decreased ,HCI, pepsin secretion is decreased,-increased colonisation of the small bowel with bacteria-protein macromolecules are able to reach intact small

bowel-increased absorption by the damaged smalI bowel

mucosa These proteins are highly antigenic thus resulting in

the formation of circulating immune complexes. These are deposited in the damaged mucosa as well as the normal mucosa, perpetuating PSIMI.

CCK-PZ Decreased> maldigestion, malabsorption and

steatorrhoea.Gastric inhibitory polypeptide decreased in small bowel damage. essential for the release of insulin and for glucose

utilization energy supply to the gut mucosa is decreased and

hence the cell turnover and production of enzymes are decreased.

ROLE OF BILE ACIDS IN PSIMIabnormal bacterial flora of the small bowel

deconjugates BA. The unconjugated bile acids cause diarrhoea by two mechanisms:

directly damage the small bowel mucosa, causing malabsorption and osmotic diarrhoea.

secretory diarrhoea. fat malabsorption and steatorrhoea

INCREASED ABSORPTION OF FOREIGN PROTEINS in PD, the small bowel mucosa is damaged and

hence large protein molecules are absorbed intact into the blood‑stream.

This leads to the formation of circulating immune complexes that aggravate PSIMI.

Classic examples of this phenomenon are cow's milk protein intolerance and soya protein intolerance.

ROLE OF PINE REGULATORY SYSTEM IN THE BOWEL

In a child with PD, there are mechanisms other than osmotic and secretory, as pure osmotic and pure secretory diarrhoea are uncommon. These include:

Paracrine-bradykinin, histamine Immune-Cytokines Neural serotonin, acetylcholine Endocrine-gastrin, vasoactive intestinal peptide This regulatory system is referred to as the "PINE"

system. It produces coordinated changes in mucosal and

muscular functions, which permit adaptive responses to changing conditions.

Acting simultaneously, these mechanisms regulate mucosal permeability, intestinal trans port, and the motility and metabolism of the gut.

Acute diarrhoea may be an appropriate response to acute infections.

A maladaptive response may be responsible for chronic diarrhoea.

EVALUATION OF A CHILD WITH CHRONIC DIARRHOEA

Stool history- -site of pathology, i.e., - -whether it is a SBD or LBD, and - -the nature of the disease process. SBD, -profuse watery, usually offensive stools,

without blood. LBD -small quantity,frequently with blood and

mucus. Odourless blood tinged stools - shigellosis frequent mucoid stools in a healthy child without

blood -IBS Nocturnal diarrhoea favours organic disease over

IBS.

persistent profuse watery diarrhoea soon after birth, ==congenital microvillusatrophy & Darrow's syndrome (congenital chloride diarrhoea).

Such picture in a 6-month-old baby- autoimmune enteropathy,

Infant having chronic diarrhoea, with a history of delayed passage of meconiurn and if constipation preceded diarrhoea,-Hirschsprung's disease

A strong family history and Down syndrome are additional points for HD.

Dietetic history record a detailed history of feeding, prior to the

onset of the disease and during the disease. It may provide vital clues to the aetiology, e.g.,

cow's milk protein in tolerance, lactose intolerance, gluten enter opathy. Soy protien intolerance, egg protien enteropathy.

Overfeeding, concentrated formula feeds> osmotic diarrhoea..

Chewing gums and chocolates plenty of undiluted fruit juices (e.g., pineapple

juice has an osmolali ty of 900 mOsm/L and apple juice 650 mOsm/L

Patients with gluten enteropathy, usually become symptomatic several months after the introduction of the offending food, but occasionally it may take even years.

In cystic fibrosis, the appetite is voracious, unlike coeliac disease, where it is poor.

TREATMENT HISTORY If achild on antibiotics develops diarrhoca, -

pseudomembranous colitis. drugs - neomycin, colchicine, cholestyrarnine,

digitalis, and propranolol. Laxatives abuse(Factitious diarrhoea by proxy) A family history- IBD, IBS

DIAGNOSIS

A complete clinical history is mandatory. Some clinical signs

and symptoms are relevant for a diagnostic approach Age of onset Nutritional assessment Associated symptoms: fever, vomiting, abdominal

pain, anorexia. Stool characteristics: blood, mucous, nondigested

substances, steatorrhoea. Physical examination: FTT, abdominal distension,

visceromegaly, tenderness, presence of abdominal masses.

Other organs affected, e.g. skin, respiratory system.

degree of dehydration and malnutrition should be assessed.

General examination in a child with CD may give vital clues to the diagnosis.

Hyperpigmentation- Addison's disease, coeliac disease or Whipple's disease.

Generalized lymphadenopathy- lymphoma, AIDS or Whipple's disease.

In a child born of consanguinous parents with malabsorption and chronic lung disease, cystic fibrosis should be ruled out

recurrent fever- tuberculosis, lynphoma, and IBD

marked loss of weight- malabsorption, lymphomas, IBD, TB

flushing,- malignant carcinoid syndrome and Vernor-Morrison syndrome (pancreatic cholera)

ageusia -zinc deficiency periorifcial and acral vesicular and scaly

lesions, acrodermatitis emeropathica

perianal fistula - Crohn's disease. Clubbing - malabsorption syndromes, IBD. chronic liver disease- IBD Hepatomegaly -lymphomas, metastatic

carcinoid, IBD and Whipple's disease. Ascites - TB and lymphoma.

INVESTIGATIONA meticulous history and a thorough physical

examination, supplemented by a few simple in

vestigations are usually sufficient in the majority of cases. A few cases may require more sophisticated tests.

STOOL EXAMINATIONMicroscopy Polymorphs and RBCs - bacterial colitis,

whipworm colitis, amoebic colitis and in IBD. Eosinophils are seen in milk or soya protein

intolerance.

Stool pH and Reducing Substance

A stool pH < 5.5 (on cow's milk) or < 5 (on breast milk) is suggestive of carbohydrate malabsorption and proximal small bowel damage.

Stool pH gives a clue to the amount of organic acids in stool while the increased amounts of reducing substances indicate the presence of unabsorbed sugars.

If in a neonate, the stool pH is low and reducing substance is present, a diagnosis of primary lactase deficiency or glucose-galactose malabsorption is probable.

If a similar picture is found shortly after the introduction of cereals or sucrose, sucrase-isomaltase deficiency should be suspected.

Demonstration of Reducing Sugars in Stool Benedict's test - 1 ml of distilled water is added

to 0.5 ml liquid stool and shaken well. 8 drops of this are added to 5 ml of preboiled Benedict's solution and boiled for I minute.The solution is cooled and the precipitate is examined for colour change.

To detect non reducing sugars like sucrose and trehalose, I nil of N/10 HCl (instead of distilled water) is added to 0.5 ml of liquid stool and boiled for 1 minute. (hydrolysation test)

Stool Culture Stool culture is positive only in 20% of patients

with acute diarrhoea and it is even lower in PD.

Alkalinisation of Stool If, in a child with unexplained chronic diarrhoea,

alkalinisation of the stool produces a pink colour, the possibility is phenolphthalein ingestion and the most probable diagnosis is Laxative abuse (Factitious diarrhoea by proxy).

Occult Blood In acute diarrhoea- bacterial or para sitic colitis chronic diarrhoea- IBD like ulcerative colitis and

Crohn's colitis and IPSID(Immunoproliferative small intestinal desease).

CBC Haemoglobin bacterial infections like septicaemia, urinary tract

infection etc. ESR - very high in septicaemia and lymphoma of

the bowel.

Peripheral Blood Picture iron deficiency anaemia or dimorphic anaemia. abetalipoproteinaemia (acanthocytes)Biochemical Investigations Serum electrolytes, blood urea, sugar and plasma proteins.Blood and Urine Culture Systemic infections are important causes of CD in

infancy. Cultures from various sites, before starting antibiotics, are extremely useful in detecting these infections.

D-xylose Test This helps to find out whether there is damage to

the small bowel mucosa. 5 g of D-xylose is given orally and the urine con tent

estimated for the next 5 hours. if it is less than I g, there is a defect in the absorption from small bowel and the further tests to be done are:

Barium meal follow through: This will detect ulcers and strictures of small bowel.

Small bowel biopsy: tropicalsprue, coeliac disease, tuberculosis,lymphoma,abetalipoproteinaetnia, Whipple's disease, amyloidosis, lymphang icetasia

If the D-xylose test is normal, the site of pathology could be pancreas. pancretic func tion tests and USG will be useful.

Proctosigmoidoscopy- To differentiate SBD from LBD(colitis). To visualize pseudomernbrane/polyps/ulcers/tumours. Direct swabs for microscopy and culture. Rectal biopsy.Rectal Biopsy Helps in the Diagnosis Of Ulcerative colitis. Crohn's disease. Schistosonniiasis. Trichuriasis. Amyloidosis. Whipple's disease.

Tests for Tuberculosis Mantoux test. BCG test, if the chili has PEM. X-ray chest. Barium meal follow-through for ulcers,

strictures, malabsorption pattern etc. Barium enema-if colonic lesion is suspected. Duodenal, jejunal or colonic biopsy-for tissue

diagnosis.It is important, to screen all patients with PD

for AIDS

MANAGEMENT OF PERSISTENT DIARRHOEAAbout 30% of patients with PD require hospitalization, if they have

1 or more of the following: Age: Less than 4 months and not breast feed. Severe PEM. Dehydration Presence of systemic infections.

Patients with PD and malnutrition are highly prone to systemic infections, including septicaemia. Infection should be ruled out if the child has any of the following signs or symptoms:

Fever. Hypothermia. Inability to drink. Abdominal distension. Lethargy or drowsiness. Cold skin. Dyspnoea.

MANAGEMENT

The management of PD consists of 3 phases: Resuscitation phase (24-48 hours). Control of diarrhoea (up to 7 days). Rehabilitation phase (up to 8 weeks).

RESUSCITATION PHASE

Correction of dehydration, shock, electrolyte disturbance, hypoglycaemia and renal failure.

IV line , vital signs monitored and blood group and cross-matching.

Appropriate antimicrobials first 24 hours the child is given iv fluids and nil

orally, except sips of ORS. This helps to differentiate osmotic diarrhoea

(when diarrhoea may decrease) from secretory diarrhoea (when diarrhoea persists).

This also provides some time for the crypt cells to replace the damaged villus cells.

CONTROL OF DIARRHOEAThe major factors responsible for PD bacterial contamination of the gut, systemic infections, food allergen (cow milk, soy protein, egg protein

etc. lactose intolerance, toxins, bile acids

In several studies it was shown that by using a combination of high-dose oral gentamicin, cholestyramine & metronidazole,(“bowel cocktail”) diarrhoea subsides rapidly in about 90% pt.

Gentamicin - bactericidal action, Cholestyrarnine- bind bile acids and bacterial

toxins and metronidazole - antianaerobic effect. supports the hypothesis that bacterial overgrowth is

major factor responsible, `bowel cocktail' has been studied in different

combinations in various studies and it was found that the response was equally good without cholestyramine.

Many infants with PD are very sick and have features of systemic infections like septicaemia and bronchopneumonia.

-combination of oral gentamicin (50 mg/kg of the parenteral preparation in 6 divided doses for 3-5 days) and parenteral cefotaxime (100 mg/kg) is extremely effective in sick infants

In a recent study co trimoxazole was found to be very useful in children with PD.

nitrazoxanide Albendazole Shigellosis – ciprofloxcacin Emebiasis -metronidazole

REHABILITATION PHASE

Aims To improve the general health and nutritional

status. To correct nutritional deficiencies. For catch-up growth. To educate the parents, especially to prevent

future relapse.These patients should be followed up regularly, as

they are predisposed to develop PD again.

DIETARY MANAGEMENT

GOALS Avoid all feeds till diarrhoea is at least partially

controlled-(2nd day of treatment). Small frequent feeds start with a high carbohydrate, low protein, and no fat

regime. As the patient improves, coconut oil may be added.

Always avoid those food substances, which may be responsible for PD e.g., milk and milk products in cow's milk allergy; gluten-containing food in coeliac disease.

Provide adequate micronutrients and vitamins. The diet should not be hyperosmolar and should not

produce adverse effects or worsen the diarrhoea.

Problems and Remedies Anorexia-try nasogastric feeding. Intolerance-change diet, postpone alimentation. Poor weight gain--add fat and pancreatic

enzymes. Trace element deficiency-oral zinc, Mg Hypothermia - wrap the baby well.

DIET IN PERSISTENT DIARRHOEA

The small bowel mucosa of a child with PD is extensively damaged due to

bacterial contamination, ineffective villous repair, Malnutrion etc. Hence, one should be very cautious in introducing

food.

There is a lot of controversy and confusion whether cow's milk can be given or not in PD.

It should be remembered that in a child with severe malnutrition and PD, PSIMI has already set in.

If such a child is given cow's milk, the following may occur:

There is deficiency of lactase as the enterocytes are damaged> osmotic diarrhoea

Cow's milk proteins maybe absorbed intact into the bloodstream through the damaged mucosa, thereby aggravating PSIMI.

Hence when the child is very sick, it is better to avoid cow's milk.

LOW LACTOSE DIET(PLAN A)

many children tolerate milk feeds in reduced amounts, and child is not very sick, he may be given a low lactose diet, containing 50 ml/kg/day of milk.

Water should not be added, it can be mixed with cereals like rice, and sugar.

Yoghurt (curd) -contains lactase enzyme which digests lactose and so the lactose content of yogurt is only 70% of that of milk.

rice-lentil + yoghurt Yoghurt mixed + mashed potatoes + coconut oilFeeding should be started after the resuscitation phase. Initially 6--7 feeds /d (110 kcal/day. )Then 150 ml/kg/day, to achieve weight gain.Nasogastic tube feeding may be necessary, if the child has

severe anorexia.

Indicators of Treatment Failure Passage of >7 stools per day at the end of one

week. Weight loss or poor weight gain, in spite of an oral

intake of at least 100 ml/kg/day, over the previous 3 days.

If the child develops dehydration at anytime. Significant increase in diarrhoea with in 48 hr

LACTOSE FREE DIET(PLAN B)

if a child does not respond to low lactose diet: These patients may be given milk-free diet.

Rice-Bengal gram-fat mixtureA diet containing rice, Bengal gram, glucose and coconut oil Roasted Bengal gram powder: 25 g. Rice powder: 20 g. Glucose: 20 g. Coconut oil: 15 ml. Salt to taste. Water to make up to 400 ml.This gives:Protein: 7 g.Calories: 400.Approximate cost: 2/-

Advantages of rice, Bengal grain, fat gruel Cheap Easily available and acceptable. Well tolerated. Appreciable weight gain. High nutritional value.Rice-moong dal gruel 50 g of raw rice, 30 g moong dal, water, 30 g

sugar coconut oil. It provides 67 calories/l00 ml.

plan c or monosaccharide diet Chicken-glucose puree diet 100 g of boneless chicken ,40 g glucose and

coconut oil. ( 72 calories/1 00 ml)

Role of Lactose-free Milk

if. a patient has significant lactose intolerance (isolated) , they may be tried, otherwise not helpful.

S’d not be given in acute diarrhoea. cost is horrible taste is terrible. Not palatable aggravate diarrhoea by “soy protein intolerance”.

Vitamin and Mineral Supplementation vitamin A Folic acid, vitamin B12 and iron (have a tropic

action on the intestinal epithelium should be given.)

Zinc , mild zinc deficiency may aggravate the severity and duration of diarrhoea. It may be given in the dose of 50-100 mg/day..

Parenteral Nutrition The severely affected digestive tract of the child

may not tolerate even the most theoretically perfect diet, given in the most careful manner.

Indications for TPN Persistent diarrhoea with intolerance to oral

realimentation diets after 10 days. Severe forms of IBD and resistant colitis. Severe necrotising enteritis.Some of the Problems of' TPN Needs trained personnel and round the clock

monitoring and team work. Very high cost Sepsis Cholestasis which may lead to cirrhosis.

Partial Parenteral Nutrition if TPN is not feasible, a partial parenteral

nutrition (combined parenteral and oral) may be tried in selected patients.

The Composition of PPN Fluid is as Follows Paediatric maintenance solution: 250 ml (Isolyte

P) 25% dextrose: 150 nil Amino acid solution: 100 ml NaHCO3: 20 ml KCI: 5 ml MVI: 2 ml Dose 50-75 ml/kg'day; 54 ml provides 300 cals

INTRACTABLE DIARRHEA SYNDROME

permanent defect in the the structure or function of intestine , leading to progressive ,often irreversible intestinal failure, requiring parenteral nutrition for survival.

Structural enterocyte defect Immune based disorders Short gut Multiple food intolerance

recovery Failure

Persistent diarrhoea In a malnourished child

SUMMARY

Diarrhoea and malnutrion interaction is a vicious cycle and is a leading cause of morbidity and mortality.

Persistent diarrhea lasts for 14 days or longer.

final common pathway to persistent diarrhoea is `prolonged small intestinal mucosal injury' or PSIMI.

A meticulous history and a thorough physical examination, supplemented by a few simple in vestigations are usually sufficient in the majority of cases.

degree of dehydration and malnutrition should always be assessed.

Patients with PD and malnutrition are highly prone to systemic infections.

Avoid all feeds till diarrhoea is at least partially controlled

when the child is very sick, it is better to avoid cow's milk.

Always avoid those food substances, which may be responsible for PD.

Give as per plan A,B,C change when necessory.

Give TPN or PPN Lactose free milk is not much helpful, s’d

be avoided.

THANKS