1. CHRONIC DIARRHEA

2. DEFlNlTlON
. diarrhea, defined as increased total daily stool output, is usually associated with increased stool water content For infants and children this would result in stool output >10 glkgl24 hr, or more than the adult limit of 200g/24hr. When diarrhea lasts >2wk, it is considered chronic. Diarrhea in children accounts for ~5,000,000 deaths per year in the developing world.

3. PATHOPHYSIOLOGTY
the pathophysiologic mechanisms of diarrhea include osmotic diarrhea, secretary diarrhea, mutations in apical membrane transport proteins, a reduction in anatomic surface area, alteration in intestinal motility, and inhibition of transport of electrolytes by inflammatory mediators.

4. Common causes of chronic diarrhea
►INFANCY
Postgastroenteritis malabsorption syndrome
Cows milk/soy protein intolerance
Secondary disaccharidase deficiencies
Cystic fibrosis
►CHILDHOOD
Chronic nonspecific diarrhea
Giardiasis
Celiac disease
►ADOLESCENCE
Irritable bowel syndrome
Inflammatory bowel disease
Lactose intolerance

5. Osmotic Diarrhea
. Osmotic diarrhea is caused by the presence of nonabsorbable solutes in the gastrointestinal tract. The classic example of osmotic diarrhea is lactose intolerance due to lactose enzyme deficiency in which lactose is not absorbed in the small intestine and reaches the colon intact. The colonic bacteria ferment the nonabsorbed lactose to short-chain organic acids, generating an osmotic load and

6. causing water to be secreted into the lumen
causing water to be secreted into the lumen. Osmotic diarrhea stops with fasting, has a low pH, and is positive for reducing substances. The sum of sodium plus potassium multiplied by two in the stools will be less than the measured stool osmolarity, a finding suggesting the presence of other osmols in the stool.

7. Causes of Osmotic Diarrhea
►MALABSORPTION OF WATER-SOLUBLE NUTRIENTS
Glucose-galactose malabsorption
Congenital
Acquired
Disaccharidase deficiencies(lactase and sucrase-isomaltase)
►EXCESSIVE INTAKE OF CARBONATED FLUIDS
►EXCESSIVE INTAKE OF NONABSORBABLE SOLUTES
Sorbitol
Lactulose
Magnesium hydroxide

8. Secretory diarrhea.
The mechanisms for secretory diarrhea include activation of the intracellular mediators such as cAMP, cGMP, and intracellular calcium, which stimulate active chloride secretion from the crypt cells and inhibit the neutral coupled sodium chloride absorption. The classic example of secretory diarrhea is that induced by cholera and

9. Escherichia coli enterotoxins that bind to a specific enterocyte surface receptor. .Other causes of secretory diarrhea include vasoactive peptides which activate G protein-coupled receptors resulting in an increase in intracellular mediators causing secrerory diarrhea.

10. Causes of secretory diarrhea
►ACTIVATION OF CYCLIC ADENOSINE MONOPHOSPHATE
Bacterial toxins :enterotoxins of cholera, E.coli(heat-labile), Shigella, salmonella, campylobacter jejuni, Pseudomonas aerogenosa
Hormones: vasoactive intestinal peptide, gastrin, secretin
Anion surfactants: bile acids.
►ACTIVATION OF CYCLIC GUANOSINE MONOPHOSPHATE
Bacterial toxins: E.coli(heat-stable), Yersinia enterocolitica toxin
►CALCIUM-DEPENDENT
Bacterial toxins: Clostridium difficile enterotoxin
Neurotransmitters: acetylcholine, serotonin
Paracrine agents: bradykinin

11. Differential Diagnosis of Osmotic Vs Secretory Diarrhea
OSMOTIC DIARRHEA SECRTORY DIARRHEA
Stool volume <200ml/24hr >200ml/24hr
Response to fasting diarrhea stops diarrhea continues
Stool Na <70mEq/L mEq/L
Reducing substances positive negative
Stool pH < >6
Stool leucocytes no WBCs WBCs present

12. Evaluation of patient with chronic diarrhea
Phase I
►Clinical history including specific amounts of fluids ingested per day
►Physical examination including nutritional assessment
►Stool examination(pH, reducing substances, smear for white blood count, fat, ova, and parasites)
►Stool culture
►Stool for Clostridium difficile toxin
►Blood studies(complete blood count, ESR, BUN, and creatinine)

13. Phase II
►Sweat chloride
►72 hr stool collection for fat determination
►Stool electrolytes, osmolality
►Stool for phenolphthalein, magnesium sulfate, phosphate
►Breath hydrogen tests

14. Phase III
►Endoscopic studies
►Small bowel biopsy
►Sigmoidoscopy or colonoscopy with biopsies
►Barium studies
Phase IV
►Hormonal studies: vasoactive intestinal polypeptide, gastrin, secretin, 5-hydroxyindoleacetic assays.

15. Stool without fat content
Management
Stool with fat content
Stool without fat content

16. Malnutrition

17. Malnutrition
Malnutrition results from imbalance between the body's needs and the intake of nutrients. It can lead to syndromes of deficiency, dependency, toxicity, or obesity.
It is caused by:
-underconsumption
-overconsumption

18. Protein Energy malnutrition (anthropometric measurements)
Underweight
Measurements that fall below 2 standard deviations under the normal weight for age.
Stunting
Measurements that fall below 2 standard deviations below height for age.
Wasting
Measurements that fall below 2 standard deviations below weight for height.

19. Undernutrition Undernutrition can result from: inadequate intake;
malabsorption;
abnormal systemic loss of nutrients due to diarrhea, hemorrhage, renal failure, or excessive sweating; infection; or addiction to drugs.

20. Secondary malnutrition
Secondary malnutrition occurs when a person has a condition or illness that prevents proper digestion or absorption of food.

21. Common causes of 2º malnutrition
Diarrhea
Respiratory illness
Measles
Loss of appetite (anorexia).
Alteration of normal metabolism.
Prevention of nutrient absorption.
Diversion of nutrients to the parasitic agents themselves.

22. Protein-Calorie Malnutrition (PCM) or Protein-Energy Malnutrition(PEM)
PCM is classified according to degree of severity:
Normal: %
1st degree: mild form characterized by growth failure in children and wasting in adults. Weight as a percentage of expected weight: 85-90%
2nd degree: moderate form with additional biochemical changes, weight as a percentage of expected weight: 75-85%
3rd degree: severe PCM with the development of additional clinical signs, weight as a percentage of expected weight: < 75%

23. Kwashiorkor
Kwashiorkor is a form of malnutrition caused by inadequate protein intake.
It is a protein deficiency disorder of children.
From the language of Ghana, means “the evil spirit which infects the first child when the second is born.”

24. Kwashiorkor (cont’d)
Prevalent in overpopulated parts of the world where diet = mainly starchy vegetables, (cassava & plantains – almost completely devoid of protein)
Most common in areas of famine, limited food supply, low levels of education.
Early symptoms: fatigue, irritability, and lethargy.

25. Kwashiorkor

26. Kwashiorkor (cont’d)
As protein deprivation continues, growth failure, loss of muscle mass, generalized swelling (edema), and decreased immunity occur.
Swollen and severely bloated abdomen d/t edema from decreased albumin in the blood, skin changes resulting in a loss of color or a reddish discoloration of hair.

27. Kwashiorkor (cont’d)
Skin conditions (such as dermatitis, changes in pigmentation, thinning of hair, and vitiligo) are seen frequently.
Shock and coma precede death.

28. Marasmus Chronic under consumption of calories and protein.
Occurs most often in children from 6 to 18 months of age.
Protein deficiency occurs, as available protein must be used to supply energy, not to build body protein.
Many of the symptoms of the child with kwashiorkor, but they look different.

29. Marasmus Hearts weak, muscles wasted.
Little or no fat to insulate against cold, and body temp may be below normal.
Low resistance to infection; often associated with gastrointestinal infection.
Impairs brain development.
Occurs in adults in countries where calorie deficiency prevalent

30. Marasmus

31. Marasmus (Causes)
Nutrition: in many low-income countries, food variety is limited, results in mineral & vitamin insufficiencies
Infections: often trigger, aggravate, or combine w/marasmus
Socioeconomic factors: Frequently appears during weaning, especially if poor weaning foods

32. Marasmus (Causes)
Other socioeconomic factors: famines associated w/climactic disasters/political events/war
Sociofamilial environment important: children of young, inexperienced mothers; twins, and female infants at risk
According to WHO, 49% of 10.4 million deaths per year occurring in children younger than 5 years in developing countries associated with PEM.

34. Management

35. Assessment of severe malnourished child
Dehydration
Infection
Intake of food & drinks & degree of anorexia
Blood glucose
Hemoglobin or hematocrit
Urine examination
Stool examination for giardia
CXR & PPD if TB is suspected.

36. General principle of treatment
Acute or stabilisation phase Rehabilitation phase
Week week 2-6
Day Day 3-7
Look for & treat
Hypoglycemia
Hypothermia
Dehydration
Infection
Specific treatment for all children
Electrolytes
Micronutrients
Sensory stimulation
Initial feeding
Feeding to achieve catch-up growth

37. Stabilization or Acute Phase
Correction of shock & dehydration
i.v if shocked
ORS (low osmolarity with extra potassium)
Life threatening complications:
Hypoglycemia (<54 mg/dl)
Hypothermia (<350 c). Keep the child well clothed, with the head covered, in a warm enviourment
Two hourly feeding (day & night)
Treatment of infections
Electrolytes imbalance: K+, mg++

38. Stabilization or Acute Phase
Micronutrient deficiencies
Vit A & Zinc (impair immune function & have direct effect on the structure & function of the mucosa.
Iron
Folic acid
Copper (neutropenia, bone abnormalities, microcytic anemia)
Selenium ) impaired cardiac function)
Dietary treatment
Feeding should be started as soon as possible
Diet should have low osmolarity and low lactose
The child should be fed every two hours-or every three hours

39. Rehabilitation phase
The return of appetite heralds the rehabilitation phase and usually occurs a week after treatment is started.
The goal is to achieve weight gain >10g/kg/day until the patient is fully recovered.
Increase in energy & protein intake should be gradual to avoid cardiac failure.
A child is considered to have recovered on reaching a weight foe height that is 90% of the Median.

40. It’s a vicious cycle: poor health leads to poor nutrition & poor nutrition leads to poor health.

41. THANK YOU