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Bacterial Clostridium difficile

Viral Nosocomial pathogens
Parasitic
In immunocompromised Hosts 2
 Increase in daily stool weight above
200gm
 Increase in frequency, fluidity or
amountS
 Acute lasts less than 7 - 14 days
 Chronic lasts more than 2 - 3 weeks

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 Approaches to the classification of
diarrhoea
 Mechanistic
Osmotic - eg carbohydrate/ fat malabsorption
 Secretory- mucosal disease, defects of ion
absorption, stimulant laxatives
Gut hormone
 Deranged motility - post vagotomy, IBS
carcinoid

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Causes of diarrhoea
Colonic
Colonic neoplasia Endocrine
Ulcerative and Crohn's colitis Hyperthyroidism
Microscopic colitis Diabetes
Small bowel Hypoparathyroidism
Coeliac disease Addison's disease
Crohn's disease Hormone secreting tumours (VIPoma,
Other small bowel enteropathies, gastrinoma, carcinoid)
(e.g. Whipples disease, tropical sprue, amyloid,
intestinal lymphangiectasia )
Bile Acid malabsorption
Disaccharidase/molecul glukose deficiency
Small bowel bacterial overgrowth
Mesenteric ischaemia
Radiation enteritis Other
Lymphoma Factitious/arteficial diarrhoea
Giardiasis Surgical' causes (e.g. small bowel
Pancreatic resections)
Chronic pancreatitis Autonomic neuropathy
Pancreatic carcinoma Drugs
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Cystic fibrosis Alcohol
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Chronic diarrhoea

Colonic Small bowel Pancreatic

Frequency
Age
Malignancy
Diarrhea

 Increase in frequency, size or

loosening/longgar of bowel movements.

 Differentiate from fecal incontinence or

functional bowel disease- normal stool
weight

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Pathophysiology
 Increased active anion secretion Na, CL, K,
HCO3 & H20:
 Decreased absorption of water and
electrolytes

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PATOGENESIS,PATOFISIOLOGI

 1.Pengurangan/penghambatan ion Na, CL,

K, HCO3 & H20:
 Kebanyakan hormon,toxin,merangsang
sekresi aktif dan menghambat penyrapan
ion-ion.
 Penderita kadang terbangun pagi,ok
meningkatnya pergerakan usus halus,usus
besar ok meningkatnya sekresi aktif cairan
kedalam usus,ok infeksi,peradangan.
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PATOGENESIS,PATOFISIOLOGI

 2.Terdapatnya zat yg sukar diadsorbsi atau

cairan dg tek.osmotik yg tinggi pdd usus.
 Larutan yg sulit diserap,mis.laksansia
 Penyimpangan pencernaan makanan(Mal
digestion)
 Kegagalan pengangkutan makanan non
elktrolit yg mempunyai tekanan osmotik
tinggi,mis.glukose

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PATOGENESIS,PATOFISIOLOGI
 3.Perubahan pergerakan dinding usus
 Penurunan pergerakan dd usus/peristaltik
,bertambah bakteri.
 Meningkatnya pergerakan usus menyebakan
berkurangnya wkt kontak makan dan
permukaan usus halus,mkn cepat msk ke
kolon
 Pengosongan kolon secara prematur,ok
proses peradangan kolon
/IBS,mempersingkat wkt kontak,ke
encerannya bertambah,mis Ca colon,DM. 11
Types

 Transmissible/penularan agents
 Noninfectious - abnormal mucosa
 Inflammatory Bowel disease
 Celiac disease, microscopic colitis, eosinophilic and
allergic gastroenteritis, radiation enteritis
 Noninfectious - normal mucosa
 Osmotic diarrhea
 Mal-absorption
 Rapid intestinal transit- IBS

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Infectious diarrhea

 Mostly feco-oral route

 Bacterial
 Viral
 Parasitic

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Bacterial

 Watery
 Enterotoxigenic-
 Vibrio cholera
 Enterotoxigenic E.coli
 Food borne toxins-
 Bacillus cereus
 Clostridium perfringens
 Mycobacterium avium-intracellular complex

wateryencerhgy

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Bacterial

 Bloody
 Invasive
 Campylobacter jejuni
 Destructive
 Shigella
 Enteropathogenic E.coli
 Clostridium difficile

bloodybrdarahdfy

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 Rotavirus
 Children less than 2 years
 Most common cause of diarrhea in children all over
the world
 Norwalk
 Older children and adults
These viruses injure the small intestinal mucosa
 Watery diarrhea
 CMV
 Immunocompromised

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 Protozoa
 Giardia lamblia
 Entamoeba histolytica
 Cryptosporidium
 Helminths
 Ascaris lumbricoides
 Ancylostoma
 Strongyloides stercoralis
 Trichinella spiralis
 Capillaria philippensis

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 Clostridium difficile
 Nosocomial pathogens in healthcare and long
term care facility
 Poor handwashing
 Clindamycin, cephalosporins, ampicillin

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 Besides the common pathogens,
 Giardia
 Legionella
 Candida albicans
 Cryptosporidium species
 Mycobacterium avium-intralcellulare
 CMV

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 Tropical sprue
 In those who live or travel to the tropics
 Overgrowth of predominantly coliform bacteria
in the small intestine
 Whipple’s Disease
 Infection by Tropheryma whippelii
 HLA B27

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History

 Is it truly diarrhea?
 Duration-
 acute <3 weeks
 Chronic >4 weeks
 Texture/susunan
 Frequency
 Blood?

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History

 Fever
 Vomiting
 Abdominal pain
 Fainting/mau pingsan or dizzyness/puyeng
 Travel
 Drug use
 Diet
 Weight loss

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Physical

 Vital signs
 Hyperventilation- acidosis
 Volume status
 Dry Skin
 Dry mucous membranes
 Resting tachycardia
 Hypotension
 Sunken eyeballs/cekung
 Scaphoid abdomen/mencembung

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Physical

 Abdominal and rectal exam.

 Distension
 Bowel sounds
 Tenderness
 Masses
 Stool swab- culture

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Physical

 Chronic diarrhea
 Malnutrition
 Weight loss
 Muscle wasting
 Tetany
 Oral and skin lesions
 Peripheral neuropathy
 Ataxia
 Edema

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 <45  >45
 Female sex  Family history
 Other ‘functional’ Sx

Irritable bowel Colonic pathology

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 Flexible sigmoidoscopy
Fine et al 2000
800 patients studied
Microscopic colitis
10% >Crohn’s >UC 99.7% of pathology
accessible /dpt diperoleh with FS/feces

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 Neoplasia
37% asymptomatic
individuals have adenomas
8% adenomas>1cm
(Lieberman 2000)
Prevalence in symptomatic?

 Higher prevalence of proximal

non-neoplastic pathology
e.g microscopic
colitis, IBD 7-31%

 Colonoscopy or barium enema

and flexi sigmoidoscopy

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 Type Duration

Acute < 2 weeks

Persistent 2-4 weeks

Chronic > 4 weeks

 Warrants evaluation to exclude
serious underlying pathology

 Mostof the causes: NON-

infectious

 Classification
by
pathophysiological mechanism
 rational approach to
management
 Laboratory tools are extensive 
costly and invasive  rationally
directed by a careful History and PE.

 When this strategy is unrevealing,

simple triage tests (Hx, PE, routine
blood studies) are often warranted.
 Characterize the mechanism of diarrhea
 Identify diagnostically helpful assoc.
 Assess px’s fluid/electrolyte & nutritional
status
 2/3of cases, the causes remain
unclear after the initial encounter 
further testing is required:
 Quantitative stool collection and analyses
 important objective data and establish a
diagnosis/characterize the type of diarrhea
as a triage for focused additional studies

 Stool ( >200g/d )  electrolyte

concentration, pH, occult blood testing,
leukocyte inspection/protein assay, fat
quantitation, and laxative screens.
 When a specific diagnosis is suggested on the
initial encounter, therapeutic trial is often
appropriate, definitive, and highly cost effective.
Examples:

 Chronic watery diarrhea  ceases with fasting in an

otherwise healthy young adult  may justify a trial of
lactose-restricted diet

 Bloating w/ diarrhea after a mountain backpacking

trip  trial of metronidazole (giardiasis)

 Anypatient with chronic diarrhea + hematochezia

 evaluated with stool microbiologic studies and
colonoscopy
 Secretory diarrheas
 Microbiologic studies should be done, including:
fecal bacterial cultures, inspection for ova and
parasites and Giardia antigen assay
 Suggested history & other findings screening
for peptide hormones (gastrin, VIP, calcitonin,
TH/TSH, urinary 5-HIAA, and histamine)
 Upper endoscopy, colonoscopy w/ biopsy and
small bowel barium x-rays  rule out
structural/occult inflammatory disease
 Osmotic diarrhea
 Tests for 2 most common causes:
 Lactose intolerance/malabsorption  lactose breath
testing or therapeutic trial w/ lactose exclusion & lactose
challenge
 Magnesium ingestion  fecal magnesium levels
 pH  low fecal pH suggests CHO malabsorption

 Steatorrhea
 Endoscopy w/ small bowel biopsy(includes
aspiration for Giardia and quantitative cultures)
 Small-bowel radiograph
 (-) radiograph/ pancreatic exocrine disease 
Pancreatic exocrine insufficiency ruled out 
secretin-cholecystokinin stimulation test
 Chronicinflammatory-type of diarrheas
(presence of blood/leukocytes in the stool)
 Stool cultures
 Inspection for ova/parasites
 C. difficile toxin in assay
 Colonoscopy w/ biopsies
 Small-bowel contrast studies
 Capsule
endoscopy?
Established role in the investigation of
iron deficiency anaemia
? Suspected small bowel
malabsorption

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 Villous erosion Thickened infiltrated folds (Jejunum)

Apthous ulcerations (ileum) Linear ulcerations

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Jejunal Crohn's Disease
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 Stool culture
 Positive in only 40 to 60%
 Stool for ova and parasites
 Stool for Clostridium difficile toxin
 Stool Sudan test for fat
 Stool Electrolytes-differentiates secretory
diarrhea from osmotic diarrhea
 Stool pH-<7 indicates carbohydrate
malabsorption

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Management

 Fluid therapy
 Persons with moderate to severe diarrhea lose large
amounts of Na, CL, K, HCO3 & H20
 Pre renal azotemia, hypokalemia, metabolic acidosis
 ORS/Oral Resust Solution
 IV Fluids

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Physiologies

 In the normal state, approximately 10 L of

fluid enter the duodenum daily, of which all
but 1.5 L are absorbed by the small intestine.
The colon absorbs most of the remaining
fluid, with only 100 mL lost in the stool. From
a medical standpoint, diarrhea is defined as a
stool weight of more than 250 g/24 h
 Total body water

Extracellular fluid
 1/3 total body’s
fluid vol.
Intracellular Fluid
 ↑ Na+ and Cl –
 2/3 total body’s
fluid vol.
1. Intravascular
 ↑ K+, Mg++,
Fluid
phosphate
2. Interstitial Fluid
 Na-K-ATPase
pump
Jenis Patogen Pilihan pertama Alternatif
Enterotoxigenik (cholera like) diarrhea

Vibrio cholerae Doksisiklin, tetraciklin, kotrimoksazol, norfloksasin, siprofloksasin kloramfenikol, eritromisin,

E coli norfloksasin, siprofloksasin kotrimoksazol

C.difficile metronidazol vancomisin, bacitracin

Invasive (Dysentery Like ) diarrhea

ofloksasin, norfloksasin, si
shigella kotrimoksazol asam nalidiksat, azitro

Campylobacter erytromisin, azitromisin, klaritomisin siprofloksasin, norfloksasin

kotrimoksazol, ofloksasin, norfloksasin, siprofloksasin,

Salmonella seftriakson, sefotaksim azitromisin

Travvelers diarrhea

Profilaksis norfloksasin, siprofloksasin, kotrimoksazol

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Terapi norfloksasin, siprofloksasin, kotrimoksazol, azitromisin
 Must contain Potassium and a base
 Ringer’s lactate

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Electrolyte solution

Isotonic solution Hypotonic solution

Plasma

290 308 273 278 290

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Normal Ringer D5 KAEN 3B

saline asetat/ laktat Aminofluid
 Antibiotics
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 Invasive bacterial Enteritis- esp.Shigellae

 Quinilone orally twice daily for 3 days
 Cholera
 Traveler's diarrhea
 Prophylactic- not recommended
 A single dose of oral Quinilone at onset
 Clostridium difficile
 Metronidazole
 Oral Vancomycin
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 Informasi pada pasien
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 Informasikan tanda dehidrasi

 Diet :

ASI pada bayi

Sari buah segar dan pisang
Hindari makanan berserat
Hindari minuman bergula
 Kontinuitas terapi

 Penggunaan obat, Efek samping dan penanganan

 Terapi suportif
 Conclusions
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 Baseline investigations (primary care)

 lower GI endoscopy with biopsy
 Consider factitious diarrhoea
 Small bowel malabsorption -
Distal duodenal biopsies -
small bowel imaging
 Pancreatic insufficiency
- faecal elastase, Pancreolauryl test, pancreatic imaging
 Other – SB bacterial overgrowth, BAM etc

In 1/3 patients no diagnosis made:

‘chronic idiopathic diarrhoea’

THE END
Good nutrition and hygiene can
prevent most diarrhea.

Thank You!

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