PRESENTATION

CHRONIC
DIARRHEA
PRESENTED BY:
DR RUBAMA.M.YOUSUF
(HOUSEOFFICER) PEADS UN
CHRONIC DIARRHEA

It is defined as stool volume of more than 10g/kg/day in toddlers/infants

and greater than 200g/day in older children that lasts for 4 weeks or
more.
• PATHOPHYSIOLOGY
• Mechanism of diarrhea is generally divided into secretory
and osmotic.
• 1.SECRETORY DIARRHEA
• Usually associated with large volume of watery stools and
persists even when oral feeding is withdrawn.
• MECHANISM
• Active electrolytes and water fluxes towards intestinal lumen resulting
from either the inhibition of neutral NACL absorption in villous
enterocytes or an increase in electrogenic chloride secretion in
secretory crypts cells as a result of opening of the cystic fibrosis
transmembrane regulator (CFTR) chloride channel or both results in
more secretion from crypts than absorption in villous that persists
during fasting. Electrogenic secretion is induced by an increase of
intracellular concentration of cyclic AMP and cyclic GMP or calcium in
response to microbial enterotoxins or to endogenous endocrine or
nonendocrine molecules including inflammatory cytokines.
• 2.OSMOTIC DIARRHEA
• It depends on oral feeding and stool volume are usually not as massive as in secretory diarrhea.
• MECHANISM
• Non absorbed nutrients in the intesrinal lumen as a result of one or more of the following mechanism.
• Intestinal damage (e.g enteric infection)
• Reduced absorptive surface area ( e.g celiac disease)
• Defective digestive enzymes or nutrient carrier (e.g lactase deficiency)
• Decrease intestinal transmit time (functional diarrhea)
• Nutrient overload exceeding the digestive capacity ( over feeding, sorbitol in fruit juice)What ever the
mechanism, osmotic force generated by non absorbed solutes drives water into intestinal lumen.
ETIOLOGY
• 1. INFECTION
• Enteric infection are by far the most frequent cause of persistent or
chronic diarrhea both in developing and industrial countries. Co-
morbids condition such as HIV/AIDS, MALARIA, TB result in malnutrition
that impairs the child immune response prolonging diarrhea or
acquiring another enteric infection.
• * Chronic diarrhea in travellers depends on country origin common pathogens include giardia, ecoli,
shigella, campylobacter, salmonella, enteric virus.
• Less common includes amebiasis, strongyloides, tropical spruce.
• Opportunistic microorganism induce diarrhea exclusively more severe and for more prolonged periods
in specific population such as immunocompromised children (e.g- clostridium difficile or
cytomegalovirus in oncologic patients as well as in patients with inflammatory bowel disease.
Crptosporidium in AIDs patients.
• Post enteritis diarrhea syndrome is a condition in which small intestinal mucosal damage persists after
acute gastroenteritis.
• Sensitization to food antigen, secondary dissacharidase deficiency, persistent infection, reinfection with
an enteric pathogen or side effects of medication maybe responsible for causing post enteritis diarrhea.
• 2. INFLAMMATORY/IMMUNOLOGIC
• CELIAC DISEASE : Permanent gluten intolerance. Major protein of gluten reacts with immune
system to cause villous atrophy and decrease absorptive surface .
• FOOD ALLERGY: Abnormal food response to food protein cause proctitis/ colitis or an
enteropathy.
• INFLAMMATORY BOWEL DISEASE: Including crohn and ulcerative colitis cause chronic diarrhea
that is often associated with abdominal pain, elevated inflammatory markers and increase
concentration of fecal calprotectin or lactoferrin.
• AUTOIMMUNE ENTEROPATHY:Associated with production of antienterocyte and antigoblet cell
antibodies direct against component of enterocyte brush border or cytoplasm and by a cell
mediated autoimmune response with mucosal T-cell activation.
• 3. PANCREATIC DEFICIENCY
• CYSTIC FIBROSIS: Exocrine pancreatic insufficiency results in steatorrhea and protein
malabsorption.
• SHWACHMAN-DIAMOND SYNDROME: Exocrine pancreatic hypoplasia associated with
neutropenia, bone changes, intestinal protein losing enteropathy( characterized by low
serum protein level and elevated fecal alpha 1 antitrypsin)
• LIVER AND BILE ACID DIORDER: Liver disorder and cholestasis lead to reduction in bile
salts resulting in fat malabsorption causing chronic diarrhea in form of steatorrhea.Bile
acid loss associated with disease affecting terminal ileum such as crohn's disease
• 4.CARBOHYDRATE MALABSORPTION
• LACTOSE INTOLERANCE: secondary to lactase deficiency caused by intestinal
mucosal damage( usually as part of post enteritis syndrome which is a self
limited process)
• FRUCTOSE INTOLERANCE: Individual often develop bloating, abdominal pain,
diarrhea, flatulence associated with mutation in ASDOB gene that encoded for
the aldolase B enzyme that is found primarily in liver and involved in metabolism
of fructose. Hereditary fructose intolerance may have nausea, abdominal pain,
bloating, vomiting, diarrhea, hypoglycemia.continous ingestion of fructose
results in hepatomegaly and eventually cirrhosis.
• 5. MOTILITY DISORDER
• It include abnormal development and function of enteric nervous
system such as Hirschsprung disease and chronic intestinal
pseudoobstruction associated with either constipation or diarrhea or
both.
• 6. SHORT BOWEL SYNDROME
• Many intestinal abnormalities such as stenosis, segmental atresia, gastroschisis and
malrotation may required surgical resection but the most frequent cause of short bowel
is necrotizing enterocolitis. The residual intestine maybe insufficient to carry on its
digestive absorption function, results in severe chronic diarrhea, malnutrition and
failure to thrive requiring long term treatment with parenteral nutrition.
• 8. NON SPECIFIC DIARRHEA
• It includes functional and toddlers diarrheain children younger than 4 years and irritable
bowel syndrome in 5 years of age or older.
• Toddlers diarrhea defined as daily painless recurrent passage of 4 or more large unformed
stools for 4 or more week with onset in infancy or pre-school year. Night defecation is
usually absent.
• Diarrhea may also be result of excessive intake of fluid and inabsorptable carbohydrate. If
childs fluid intake were more than 150ml/kg/24 hr fluid intake should be decrease and not
to exceed 90ml/kg/24 hr inorder to decrease stool frequency and volume.
• EVALUATION OF PATIENTS
• Medical approach should be based on diagnostic algorithms that begin with assesment for infectious
causes and then consider age of child, growth, clinical and epidemiologic factors.
• Early onset in neonatal period is rare and may suggest congenital or severe condition however
infection and food allergy are more frequent in this age group together with GI malformation.
• Later infancy and upto 2 years of age infectious and allergy are the most common.
• Inflammatory disease are more frequent in older children and aldolescents.
• Celiac disease and functional nonspecific diarrhea should always be considered independently of
age because of their relatively high frequency at all ages.
• Family and personal HX provide useful indication suggesting congenital, allergic or inflammatory
etiology.
• .Acute onset diarrhea that runs a protracted course suggest post enteritis diarrhea, secondary lactase
deficiency, small intestinal overgrowth or the onset of chronic nonspecific diarrhea.
• Diarrhea associated with specific food indicate nutrient basis such as intolerance.
• Weight is generally impaired before height but with time linear growth also become affected and both
parameter equally abnormal in long term.
• Assesment of nutritional status include dietary Hx and physical examination.
• Caloric intake should be determined.Biochemical markers include albumin, prealbumin, retinol binding
protein, serum iron, transferrin may assist in grading malnutrition..Evaluation of micronutrient
concentration should always be considered.
• Zinc, Mg, Vit A and folate deficiency are associated with chronic diarrhea and should be provided if
needed.
• .Sign of general inflammation such as fever, mucoid or bloody stool, abdominal pain may
suggest inflammatory bowel disease.
• Presence of eczema or asthma associated with an allergic disorder.
• Specific extraintestinal manifestation( arthritis, diabetes, thrombocytopenia) suggest
autoimmune disease.
• Abnormalities in the digestive absorptive function test suggest small
bowel involvement where as, intestinal inflammation demonstrated by
increased fecal calprotectin or lactoferrin supports colitis.
• Stool osmolar gap (stool ionic gap) calculated as 290mosm/kg
minus(2*stool Na+ stool K). If gap is above 100 mosm /kg indicate
osmotic diarrhea and if gap is below 50mosm/kg it indicate secretory
diarrhea.
• Cl conc. in stool to rule out CCD characterized by low osmolar gap d/t
high fecal loss (more than 90mmol/l).
• Abdominal U/S may help in detecting liver and pancreatic abnormalities or an increase
in distal ileal wall thickness suggest Inflammatory bowel disease.
• Plain abdominal xray useful in detection of abdominal distention suggestive of
intestinal obstruction, increase retention of colonic feaces.
• Structural abnormalities investigated through barium meal and small bowel follow
through.
• Endoscopy explore entire intestinal tract.
 TREATMENT

• It includes general supportive measures, nutritional rehabilitation, elimination diet, and medication.
• Lactose free diet should be started in all children with chronic diarrhea recommended by WHO.
• When oral nutrition is not feasible or fail enteral or perenteral nutrition should be considered.
• Micronutrients and vitamin supplements are part of nutritional rehabilitation, zinc is imp in both
prevention and therapy of chronic diarrhea since it promotes ion absorption, restores epithelial
proliferation and stimulates immune response.
• Functional diarrhea in children may benefit from a diet based on 4F principles ( reduce fructosr and
fluids, increase fat and fiber).
• pharmacological therapy includes based on the etiology anti infectious drugs, immune suppression
and drugs that may inhibit fluid loss and promote cell growth.
• Secretion of ion may be reduced by antisecretory.
IF BACTERIAL AGENT IS DETECTED SPECIFIC
ANTIBODIES SHOULD BE PRESCRIBED.