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Diarrhea Department of Pediatrics Soochow University Affiliated Children’s Hospital.

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Presentation on theme: "Diarrhea Department of Pediatrics Soochow University Affiliated Children’s Hospital."— Presentation transcript:

1 Diarrhea Department of Pediatrics Soochow University Affiliated Children’s Hospital

2 Aim and Claim Understanding the incidence and aetiology of gastroenteritis Familiar with clinical featurs and diagnosis of gastroenteritis Get hold of the management of dehydration

3 Definition In epidemiological studies, Diarrhea is defined as:  Passage of three or more loose or watery stools in a 24-hour period,  a loose stool being one that would take the shape of a container.

4 Definition In Pediatrics, Diarrhea is defined as an increase in the : Fluidity Volume Number relative to the usual habits of each individual. of stools

5 Importance of Diarrhea In under five children Diarrhea is a leading cause of: –Mortality( 死亡率 ) –Morbidity (发病率) –Malnutrition (营养不良)

6 High Childhood Mortality 3.2 million deaths/ year in <5y Children

7 High Childhood Morbidity 1.3 billion episodes / year in <5y children

8 Diarrhea Malnutrition Major Contributor to Malnutrition

9 If: Diarrhea + Malnutrition In Malnourished Children the RISK of DEATH form Diarrhea is: 4 fold that of well nourished children

10 Types of Diarrhea Acute watery diarrhea Dysentery (Bloody diar.) Persistent diarrhea

11 Morphology of Intestinal Mucosa The small intestinal mucosa comprises 2 main structures:  Villi (刷状缘) : Covered mainly (90%) by tall columnar absorptive cells (enterocytes) having a microvillar brush border, and Goblet cells  Crypts of Lieberkuhn (隐窝) : Covered mainly by short columnar secretory cells without brush border

12 Enterocyte Brush border (microvilli) Tight junction between cells Goblet cell Mucus layer “Niche”for bacteria Small Intestinal Mucosa

13 Defense barriers of the enterocytes: 1-Physical barrier: mucus2-Bacteriological (flora) 3- Immunological : Secretory IgA

14 Defense Barriers of Enterocytes 1.Physical Barrier: –The mucus secreted by goblet cells opposes penetration of pathogens –Tight junctions between enterocytes 2.Bacteriological Barrier: –Saprophytic Flora occupy enterocytic “ niches ” thus preventing their occupation by foreign pathogens 3. Immunological Barrier: –Secretory IgA included in the mucus neutralizes the action of bacteria and Viruses

15 Etiology of Acute Diarrhea

16  Viruses: Rotavirus (轮状病毒), Enteric Adenovirus (腺病毒), Calicivirus( 杯状病毒 ), Astrovirus (星状病毒) (70 – 80% of infectious diarrhea cases)  Bacteria: Salmonella (沙门氏菌), Shigella (志贺氏菌), Campylobacter jejuni (空肠弯曲菌) Yersinia Enterocolitica (耶尔 森氏菌) Escherichia coli (ETEC,EAEC, EIEC,EHEC,EPEC) Clostridium difficile (艰难梭菌) (10 – 20% of cases)  Parasites: Entamoeba histolytica (阿米巴滋养体), Giardia Lamblia (梨形鞭毛虫), Cryptosporidium (隐孢子虫) (10% of cases)

17 Etiology: Fecal-Oral Transmission Water Food Infected AnimalInfected Person Susceptible person

18 Etiology of Acute Diarrhea The most important causes of acute diarrhea in developing countries are: Rotavirus Enterotoxigenic Escherichia coli Shigella Campylobacter jejuni Cryptosporidium

19 Rotavirus

20 Pathogenesis of Rotavirus Diarrhea Rotavirus invades the absorptive enterocytes of villi but spares crypt cells. The viruses replicates and infected enterocytes are destroyed

21 Pathogenesis of Rotavirus Diarrhea Infected absorptive ente- rocytes are killed causing patchy epithelial cell destruc- tion and villous shortening 2- Destroyed absorptive cells are rapidly replaced by cells that migrate from the crypts. Villi become covered with immature non-absorptive secretory cells having: -no brush border - no brush border enzymes 1

22 Rotavirus No brush border Osmotic diarrhea

23 Enterotoxigenic Organisms Vibrio Cholerae Enterotoxi- genic E.Coli

24 Pathogenesis of Enterotoxigenic Diar. 1-Enterotoxigenic Bacteria secrete an Enterotoxin 2-Toxin stimulates the production of C-AMP (cyclic adenosine mono-phosphate) 3-Increased C-AMP leads to:  Inhibition of absorption of Na + & Cl - from the cells of villi  Stimulation of secretion of Cl - from crypt cells

25 Enterotoxigenic E. coli Secretory diarrhea

26 Pathogenesis of Secretory Diarrhea NET SECRETION X

27 Entero-Invasive Organisms Shigella

28 Pathogenesis of Invasive Diarrhea Invasive organisms like Shigella, Campylobacter jejuni, enteroinvasive E.coli, etc.:  Invade and destroy the mucosal epithelial cells in colon and distal part of ileum (回肠).  Formation of micro-abscesses and superficial ulcers; hence the presence of: Red and white blood cells in stools Visible blood in the stools.  These organisms produce also toxins that lead to: Tissue damage Increased mucosal secretion of water and electrolytes

29 Entero-Invasive Organisms Destruction Enterotoxin

30 Clinical Features  Viral infection may cause a prodromal illness followed by vomiting and diarrhea.  The vomiting may precede diarrhea and is not usually bile or bloodstained.  Abdominal pain and blood or mucus in the stools suggests an invasive bacterial pathogen.  The severity of diarrhea may be underestimated if it pools in the large bowel watery stool is mistaken for urine in the nappy.

31 Stool Characteristics and Determining Their Source Stool Characteristics Small Bowel Large Bowel Appearance Watery Mucousy and/or bloody Volume Large Small Frequency Increased Increased Blood Possibly positive but Possibly grossly bloody never gross blood Ph Possibly 6.5 Reducing substances Possibly positive Negative WBCs 10/high power field Serum WBCs Normal Possible leukocytosis, bandemia

32 Stool Characteristics and Determining Their Source Stool Characteristics Small Bowel Large Bowel Organisms Viral Invasive bacteria Rotavirus E Coli Adenovirus Shigella species Calicivirus Salmonella species Astrovirus Campylobacter species Norwalk virus Yersinia species Aeromonas species Toxic bacteria Toxic bacteria E coli Clostridium difficile Clostridium perfringens Cholera species Vibrio species Parasites Parasites Giardia species Entamoeba organisms Cryptosporidium species

33 Clinical Findings of Dehydration mild moderate severe Lose of body 5(%) 6 ~ 9(%) >10(%) weights Thirst Absence of tears Sunken eyes Sunken fontanel Skin and mucous slightly dry dry parched membranes Urine output normal decreased decreased Mental status intact irritable lethargy coma,shock signs

34 Assessment Of Dehydration

35 Assessment of Dehydration  G eneral condition (sensorium): Lethargic / irritable / normal  E yes : Sunken / normal  M outh (offer a drink & watch the child): Drinking poorly / drinking eagerly / drinking normally  S kin turgor (skin pinch): Returns very slowly / returns slowly / returns immediately 4 Important Signs:

36 Assessment of Dehydration 2 or more signs in 1 column indicate that the child falls in that column

37 Severe dehydration will have two of these signs: –Sensorium(general condition): lethargic or unconscious –Sunken eyes –Drinking poorly or not at all –Very slow skin pinch (more than 2 seconds) Assessment of Dehydration

38 Some dehydration will have two of these signs: –Restlessness or irritability –Sunken eyes –Drinking eagerly –Slow skin pinch No dehydration –No signs or less than 2 signs

39 Assessment of Dehydration SeverityInfants (weight <10 kg)Children (weight >10 kg) Mild dehydration5% or 50 mL/kg3% or 30 mL/kg Moderate dehydration6%-9% or mL/kg 6% or 60 mL/kg Severe dehydration > 10% or > 100 mL/kg 9% or 90 mL/kg

40 Differential Diagnosis(1)  Young infants(aged 2-12weeks)—pyloric stenosis— vomiting  Older infant and toddlers(aged 1-2years)— intussusception—vomiting,abdominal pain and redcurrant jelly

41 Differential Diagnosis(2)  Appendicitis  Crohn Disease  Irritable Bowel Syndrome  Malabsorption Syndromes  Meckel Diverticulum  Protein Intolerance  Short Bowel Syndrome  Ulcerative Colitis

42 Objectives  Prevent dehydration, if there are no signs of dehydration;  Preat dehydration, when it is present;  Prevent nutritional damage, by feeding during and after diarrhoea; and  Reduce the duration and severity of diarrhoea, and the occurrence of future episodes, by giving supplemental zinc. Management

43 ORT  OR therapy(ORT) is the cornerstone of treatment, especially for small bowel infections that produce a large volume of watery stool output.  A 5-cc or 10-cc syringe without a needle is a very useful tool. The syringe can be used to quickly place small amounts of fluid in the mouth of a child who is uncooperative.

44 Diet  A strong body of evidence now suggests that resuming the prediarrhea diet is perfectly safe and must be encouraged,  In an incident of worsening of diarrhea proven to be secondary to a clinically important lactose malabsorption in infants positive for rotavirus, a very transient use of lactose-free formulas (5-6 d) can be considered.  Strong evidence in the literature demonstrates that the continued use of breast milk is actually beneficial in children with acute diarrhea.

45 Special Information  Anti-diarrheal agents and antiemetics are notrecommended for use in children with AGE.  Antimicrobial therapies are recommended only for selected children with AGE who present with special risks or evidence of a serious bacterial infection (SBI).  Probiotics (Lactobacillus GG) have been shown to reduce the duration of diarrhea and the duration of shedding of rotavirus. Lactobacillus GG may be considered as adjunctive therapy.

46 Summary  The causes of GE are viruses(70—80%),bacteria(10—20%)and parasites(10%)  Patients may present diarrhoea,vomiting,abdominal pain and fever  The stool may be watery,mucuous,bloody or pyic  Dehydration is classed as mild,moderate and severe.According to dehydration,you can estimate fluid deficit.  GE need to differentiate varieties of diarrhoea  Management of GE

47 Quiz  Physical parameters associated with degree of dehydration( Table: Clinical Findings of Dehydration )  How to estimate fluid deficit (Table: Assessment of Dehydration )

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