Download Diarrhoea

IMS : Diarrhoea
By Semester 6 and Smester 7
Agenda of the day
• Overview of diarrhoea
-Ambiga and Hui Yan
• Acute Diarrhoea (Acute Gastroenteritis)
-Wen Jiun and Vanessa
Epidemiology of Diarrhoea
• Leading cause of illness and death among
children in developing countries.
• estimated 1.3 thousand million episodes
and 4 million deaths occur each year in
under-fives.
• Main cause of death from acute diarrhoea
is dehydration. Other important causes of
death are dysentery and undernutrition.
Definitions
Acute Diarrhoea
– sudden onset and lasts less than two weeks
– 90% are infectious in etiology
– 10% are caused by medications, toxin ingestions, and
ischemia
Chronic Diarrhoea
– Diarrhoea which lasts for more than 4 weeks
– Most of the causes are non-infectious
Persistent Diarrhoea
-Diarrhoea lasting between 2 to 4 weeks
Clinical Features
• Stools
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Loose
Blood stained
Offensive smell
Steatorrhea (floating, oily, difficult to flush)
Sudden onset of bowel frequency
Crampy abdominal pain
Urgency
Fever
Loss of appetite
Loss of weight
Classifications of Diarrhoea
• Duration( Acute, Chronic)
• Causes( infectious, post-infectious, drugs, endocrine,
factitious)
• Chronic DirrhoeaPathophysiologic mechanism
(osmotic, secretory, inflammatory, abnormal
motility)
• Acute Diarrhoea
Viral,Bacterial,
Protozoa (90%)
Medications
Laxatives or diuretic
abuse
Ingestion of
environmental
preformed toxin such
as seafood
Ischemic Colitis
Graft versus Host
• Chronic Diarrhoea
Irritable Bowel
Syndrome
Diverticular disease
Colorectal Cancer
Bowel Resection
Malabsorption
Inflammatory Bowel
Disease
Celiac Disease
Carcinoid tumour
Mechanism of Diarrhoea
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Osmotic Diarrhoea
Secretory Diarrhoea
Inflammatory Diarrhoea
Abnormal Motility Diarrhoea
Osmotic Diarrhoea
• Mechanism :
-retention of water in the bowel as a result of an
accumulation of non‐absorbable water‐soluble
compounds
-cease with fasting, discontinue oral agents
• Causes :
-Purgatives like magnesium sulfate or magnesium
containing antacids
-especially associated with excessive intake of sorbitol
and mannitol.
-Disaccharide intolerance
-Generalized malabsorption
Secretory Diarrhoea
• Mechanism :
– Active intestinal secretion of fluid and electrolytes as
well as decreased absorption.
– Large volume, painless, persist with fasting
• Causes :
– Cholera enterotoxin, heat labile E.coli enterotoxin
– Vasoactive Intestinal Peptide hormone in VernerMorrison syndrome
– Bile salts in colon following ileal resection
– Laxatives like docusate sodium
– Carcinoid tumours
Inflammatory Diarrhoea
• Mechanism :
-damage to the intestinal mucosal cell leading to a loss
of fluid and blood
-pain, fever, bleeding, inflammatory manifestations
• Causes :
-- Immunodeficiency patient
– Infective conditions like Shigella dysentary
– Inflammatory conditions
• Ulcerative colitis and Crohns disease
Abnormal Motility Diarrhoea
• Mechanism :
-Increased frequency of defecation due to underlying
diseases
-large volume, signs of malabsorption (steatorrhoea)
• Causes :
–
–
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Diabetes mellitus- autonomic neuropathy
Post vagotomy
Hyperthyroid diarrhoea
Irritable Bowel Syndrome
ACUTE
GASTROENTERITIS
Acute Gastroenteritis
• Gastroenteritis is the inflammation of the lining of
stomach, small and large intestine.
• >90% of cases are infectious, although acute
gastroenteritis may follow ingestion of drugs and
chemical toxins (10%).
• Acute gastroenteritis is common among children,
elderly, and those who are immunocompromised.
Infectious Agents
• Acquired by
– fecal-oral route via direct personal contact
– ingestion of food or water contaminated with
pathogens from human or animal feces
• Acute infection occurs when the ingested
agent overwhelms the host’s mucosal
immune and non-immune (gastric acid,
digestive enzymes, mucus secretion,
peristalsis, and suppressive resident flora)
defenses.
Aetiology: Causative Pathogens
• Bacteria
• Viral
• Protozoa
Bacterial
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Campylobacter jejuni
Salmonella sp.
Shigella
Escherichia coli
Staphylococcal enterocolitis
Bacillus cereus
Clostridium perfringens
Clostridium botulinum
Gastrointestinal tuberculosis
Viral
• Rotavirus
• Norovirus
• Adenovirus
Protozoa
• Entamoeba histolytica
• Cryptosporidium
• Giardia intestinalis
• Schistosomiasis
High Risk Groups
1.
2.
3.
4.
5.
Travelers
Consumers of certain foods
Immunodeficient person
Daycare participants
Institutionalized person
1. Travelers
• Tourists to Latin America, Africa, and
Asia develop “traveler's diarrhea”
commonly due to enterotoxigenic
Escherichia coli, Campylobacter,
Shigella, and Salmonella.
• Visitors to Russia may have increase
risk of Giardia-associated diarrhea.
• Visitors to Nepal may acquire
Cyclospora.
• Campers, backpackers, and swimmers
in wilderness areas may become
infected with Giardia.
2. Consumers of Certain Food
• Diarrhea closely following food
consumption may suggest infection with
– Salmonella or Campylobacter from
chicken;
– Enterohemorrhagic Escherichia coli
(O157:H7) from undercooked hamburger
– Bacillus aureus from fried rice
– S. aureus from mayonnaise or creams
– Salmonella from eggs
– Vibro species, acute hepatitis A or B
from (raw) seafood
3. Immunodeficiency Persons
• Primary immunodeficiency
– IgA deficiency, common variable
hypogammaglobulinemia, chronic
granulomatous disease
• Secondary immunodeficiency
– AIDS, senescence, pharmacologic suppression
4. Daycare Participants
• Infections with Shigella, Giardia,
Cryptosporidium, rotavirus, and other
agents are very common and should be
considered.
5. Institutionalized Persons
• Most frequent cause of nosocomial
infections in many hospitals and long-term
care facilities
• The causes are a variety of
microorganisms but most commonly
Clostridium difficile.
Pathophysiology
•
Infectious agents cause diarrhoea in 3
different ways as follows:
– Mucosal adherence
– Mucosa Invasion
– Toxin Production
Mucosal adherence
- Bacteria adhere to specific receptors
on the mucosa, e.g. adhesions at the
tip of the pili or fimbriae
- Mode of action: effacement of
intestinal mucosa causing lesions,
produce secretory diarrhoea as a
result of adherence
- Causing moderate watery diarrhoea
- e.g. enteropathogenic E.coli
Mucosa Invasion
- The bacteria penetrate into the intestinal
mucosa, destroying the epithelial cells and
causing dysentery
- e.g.
Shigella spp.
Enteroinvasive E.coli
Campylobacter spp
Toxin Production
i)
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ii)
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Enterotoxins
toxin produced by bacteria adhere to the intestinal epithelium,
induce excessive fluid secretion into the bowel lumen, results in
watery diarrhoea without physically damaging the mucosa.
Some enterotoxin preformed in the food can cause vomiting
e.g
Staph.aureus (enterotoxin B)
Bacillus cereus
Vibrio cholerae
Cytotoxins
damage the intestinal mucosa and sometimes vascular
endothelium, leads to bloody diarrhoea with inflammatory cells,
decreased absorptive ability.
e.g.
Salmonella spp.
Campylobacter spp.
Enterohaemorrhagic E.coli 0157
Bacterial causes of
watery diarrhoea and dysentery
Watery diarrhoea
Dysentery
- Vibrio cholerae
- Shigella spp
- Enterotoxigenic E.coli (ETEC)
- Yersinia enterocolitica
- Enteropathogenic E.coli (EPEC)
- Campylobacter spp
- Salmonella spp.
- Salmonella spp.
- Clostridium difficile
- Clostridium difficile
- Clostridium perfringens
- Enteroinvasive E.coli
- Campylobacter jejuni
- Enterohaemorrhagic
- Bacillus cereus
E.coli (EHEC)
- Staphylococus aureus + profuse vomiting
Clinical Features
• Diarrhoea
– Watery
– Bloody
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Cramping abdominal pain
Nausea, +/- Vomiting
Fever
Loss of appetite
Lethargy
Shock
Investigations
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FBC
U&E, BUN
Stool culture
Stool examination, microscopy for ova, cysts,
parasites and fecal WBC
• ELISA test
** For unresolved diarrhoea: sigmoidoscopy, rectal
biopsy and radiological studies to rule out other
organic causes
Management
Aims/Goals of management:
• Prevent, identify and treat dehydration
• Eradicate causative pathogens
– Tetracycline, Ciprofloxacin
• Prevent spread by early recognition and institution
of infection-control measures
– immunization, chemoprophylaxis, good hygiene,
improve sanitation
Prevent, Identify & Treat Dehydration
• Moderate to severe dehydration need referral to
hospital
• Oral Rehydration Solution (ORS)
– Glucose, Na, Cl, K, bicarbonate or citrate
– encourage fluid intake e.g. salt + glucose
drink to assist in co-transport of sodium into
the epithelial cells via the SGLT1 protein,
which enhances water and sodium reabsorption in small intestines.
• IV fluids (lactate Ringer’s solution) are preferred
in those with severe dehydration.
Chronic Diarrhea
Causes
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Chronic Fatty Diarrhea (Diarrhea due to
Malabsorption)
Chronic Inflammatory Diarrhea
Chronic Watery Diarrhea
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Secretory Diarrhea
Osmotic Diarrhea
Drug-Induced Diarrhea
Infectious Diarrhea
Malignancy
Functional Diarrhea (diagnosis of exclusion)
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Irritable Bowel Syndrome
History
1. Age
2. Diarrhea pattern
3. Differentiating small bowel from large
bowel
4. Stool characteristics
5. Diurnal variation
6. Weight Loss
7. Medication and dietary intakes
8. Recent travel to undeveloped areas
Age
•
Young patients
– Inflammatory Bowel Disease
– Tuberculosis
– Functional bowel disorder (Irritable bowel)
•
Older patients
– Colon Cancer
– Diverticulitis
Diarrhea pattern
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Diarrhea alternates with Constipation
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Intermittent Diarrhea
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Colon Cancer
Laxative abuse
Diverticulitis
Functional bowel disorder (Irritable bowel)
Diverticulitis
Functional bowel disorder (Irritable bowel)
Malabsorption
Persistent Diarrhea
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Inflammatory Bowel Disease
Laxative abuse
Differentiating small bowel from
large bowel
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Small intestine or proximal colon
involved
– Large stool Diarrhea
– Abdominal cramping persists after
Defecation
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Distal colon involved
– Small stool Diarrhea
– Abdominal cramping relieved by Defecation
Stool characteristics
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Water: Chronic Watery Diarrhea
Blood, pus or mucus: Chronic
Inflammatory Diarrhea
Foul, bulky, greasy stools: Chronic Fatty
Diarrhea
Diurnal variation
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No relationship to time of day: Infectious
Diarrhea
Morning Diarrhea and after meals
– Gastric cause
– Functional bowel disorder (e.g. irritable
bowel)
– Inflammatory Bowel Disease
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Nocturnal Diarrhea (always organic)
– Diabetic Neuropathy
– Inflammatory Bowel Disease
Weight Loss
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Despite normal appetite
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Associated with fever
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Hyperthyroidism
Malabsorption
Inflammatory Bowel Disease
Weight loss prior to Diarrhea onset
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Pancreatic Cancer
Tuberculosis
Diabetes Mellitus
Hyperthyroidism
Malabsorption
Medication and dietary intakes
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Drug-Induced Diarrhea
Food borne Illness
Waterborne Illness
High fructose corn syrup
Excessive Sorbitol or mannitol
Excessive coffee or other caffeine
Recent travel to undeveloped
areas
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Traveler's Diarrhea
Infectious Diarrhea
Colorectal Carcinoma
• Colorectal carcinoma
– Colorectal cancer is second commonest cancer causing death in the UK
– 20,000 new cases per year in UK - 40% rectal and 60% colonic
– 3% patients present with more than one tumour (=synchronous
tumours)
– A previous colonic neoplasm increases the risk of a second tumour
(=metachronous tumour)
– Some cases are hereditary
– Most related to environmental factors - dietary red fat and animal fat
• Adenoma - carcinoma sequence
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Of all adenomas - 70% tubular, 10% villous and 20% tubulovillous
Most cancers believed to arise within pre-existing adenomas
Risk of cancer greatest in villous adenoma
Series of mutations results in epithelial changes from normality, through
dysplasia to invasion
– Important genes - APC, DCC, k-ras, p53.
Colorectal Carcinoma
• Clinical presentation
– Right-sided lesions present with
• Iron deficiency anaemia due occult GI Blood loss
• Weight loss
• Right iliac fossa mass
– Left-sided lesions present with
• Abdominal pain
• Alteration in bowel habit
• Rectal bleeding
– 40% of cancers present as a surgical emergency with
either obstruction or perforation
Colorectal Carcinoma
• Developed by Cuthbert Duke in 1932 for
rectal cancers
• Dukes staging of colorectal cancer
– Stage A - Tumour confined to the mucosa
– Stage B - Tumour infiltrating through muscle
– Stage C - Lymph node metastases present
– Five year survival - 90%, 70% and 30% for
Stages A, B and C respectively
Chronic Inflammatory Diarrhea
• Inflammatory Bowel Disease
– Ulcerative Colitis
• is a form of colitis, a disease of the intestine, specifically the large
intestine or colon
• usually present with diarrhea mixed with blood and mucus, of gradual
onset
• also may have signs of weight loss, and blood on rectal examination
– Crohn's Disease
• is an inflammatory disease which may affect any part of the
gastrointestinal tract from mouth to anus, causing a wide variety of
symptoms.
• It primarily causes abdominal pain, diarrhea (which may be bloody),
vomiting, or weight loss, but may also cause complications outside of
the gastrointestinal tract such as skin rashes, arthritis and inflammation
of the eye
– Diverticulitis
Drug-induced diarrhea
• Diarrhea - common side effect of many
classes of medications.
• Accounts for 7% of all adverse drug
effects.
• Over 700 drugs have been implicated.
Medications commonly involved
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Antibiotics
Laxatives
Antihypertensives
Lactulose
Antineoplastics
Antiretroviral drugs
Magnesium
containing
compounds
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Anti arrhythmics
NSAIDs
Colchicine
Antacids
Acid reducing agents
Prostaglandin
analogs
Medication
Laxatives
Mechanism
Osmotic diarrhea
(osmotically active
solutes)
Stimulant laxatives
Secretory diarrhea
(excess of fluids &
electrolytes)
Erythromycin, cisapride Motility diarrhea
(shortened transit time)
Antimicrobials
Pseudomembranous
colitis (bacterial
proliferation)
Medication
Antineoplastics
NSAIDS
Alpha-glucosidase
inhibitor
Lipase inhibitors
(Orlistat)
Mechanism
Exudative diarrhea (protein
losing enteropathy)
Lymphocytic or collagenous
colitis
Malabsorption of
carbohydrates (osmotic
diarrhea)
Malabsorption of fat
(steatorrhea)
Antibiotic-induced diarrhea
• unexplained onset of diarrhea that occurs
with the administration of any antibiotic
• due to disruption of normal intestinal flora,
which leads to
• either proliferation of pathogenic
microorganisms or impairment of the
metabolic functions of the microflora
Types
• Simple antibiotic associated diarrhea
• Erythromycin induced diarrhea
• Clostridium difficile associated diarrhea
Simple antibiotic associated diarrhea
1. disturbance in the normal colonic flora, leading
to impaired fermentation of carbohydrates and
osmotic diarrhea
2. reduced production of short-chain fatty acids
which by reducing colonic absorption of fluid
causes secretory diarrhea
3. reduced digestion of bile salts by normal
colonic flora and the resultant increased colonic
concentration can stimulate secretion of fluid by
the colon and cause a secretory diarrhea
• Occurs in dose-related fashion
• more common in drugs given orally rather
than parenterally, except with drugs
excreted in the bile
• generally resolves within days of
discontinuing the offending antibiotic
• typically have a larger impact on anaerobic
bacteria in the normal fecal flora
Common antibiotics involved
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Clindamycin
Ampicillin
Amoxicillin-clavulanate
Cefixime
Cephalosporins
Fluoroquinolones
Azithromycin
Clarithromycin,
Erythromycin
Tetracyclines
Erythromycin induced diarrhea
• Caused by erythromycin
• Increased motility through stimulation of
motilin receptors
Clostridium difficile associated
diarrhea (CDAD)
• not dose related
• symptoms can last weeks to months after
the offending antibiotic has been
discontinued,
• often until treatment for the infection is
administered
antibiotic therapy
disturbance in the normal flora of the colon
colonization of the individual by the
organism (faecal-oral route)
majority
asymptomatic
Symptomatic
(1st day of antibiotic to 6 weeks after
stopping the drug)
Common antibiotics involved
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Clindamycin
Ampicillin
Amoxicillin
Quinolones
Cephalosporins
Clostridium difficile
• gram-positive bacillus
• spore-former, allowing it to survive under
harsh conditions and during antibiotic
therapy
• development of infection caused by
Clostridium difficile involves several steps
• Clostridium difficile demonstrate
production of 2 toxins
• Toxin A – bind to specific receptors in the
brush border of the intestinal epithelium
• Toxin B – site of binding has not yet been
described
Toxin A & B
Release of inflammatory mediators & cytokines
Chemotaxis of inflammatory cells
Increased fluid secretion by the epithelium
Patchy necrosis with production of an
exudate composed fibrin and neutrophils
Pseudomembrane fomation
(necrotic cellular debris, fibrin, mucin & leucocytes)
Contributing factors to CDAD
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Host susceptibility to infection
Virulence of the infecting strain
Type of antibiotic used
Timing of exposure
Spectrum of disease
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Asymptomatic colonization
Simple antibiotic associated diarrhea
Pseudomembranous colitis
Fulminant colitis
Clinical features
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Lethargy
Abdominal pain
Nausea
Anorexia
Water diarrhea
Low-grade fever
Peripheral leucocytosis
Pseudomembranous colitis – more profuse diarrhea, occult bleeding,
high fever.
Fulminant colitis
• 1-3% of patients with Clostridium difficile
infection
• Presentation –severe abdominal pain,
distension, high fever, marked
leucocytosis
• Complications – colonic perforation, toxic
megacolon
Diagnosis of Clostridium difficile
infection
• Tissue culture assay for toxin B
• ELISA for toxin A/B
• Latex agglutination assays (detect enzyme
glutamate dehydrogenase)
Treatment of CDAD
• Discontinuation of the offending antibiotic
• Supportive fluids and electrolytes
replacement
• Enteric isolation precautions
• Aviod antiperistaltic agents and opiates
• Antibiotic is indicated for moderate to severe
cases
• 1st line : Vancomycin 125mg qds and
metronidazole 250mg tds or
bacitracin 25,000 units qds
• Parenteral metronidazole 500mg qds may be
used if oral agents are not tolerated
• Used of probiotics in recurrent relapses of
Clostridium difficile infection
• Saccharomyces boulardii 1g od during
concurrent antibiotic treatment
Endocrine causes
• Diabetic autonomic neuropathy
• Thyrotoxicosis
• Neuroendocrine tumours
~ Zollinger Ellison syndrome
~ VIPoma
~ Somatostatinoma
~ Carcinoid syndrome
~ Medullary carcinoma of thyroid
Diabetic autonomic neuropathy
• Reduces small bowel motility
&
• affects enterocyte secretion
Bacterial overgrowth
Watery, continuous/interrupted by constipation
diarrhoea, worse at night(nocturnal diarrhoea)
Other clinical features
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Postural hypotension
Gastroparesis ( nausea and vomitting)
Difficulty in micturition ( bladder atony)
Erectile dysfunction
Gustatory sweating
Treatment
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Broad spectrum antibiotics
Antidiarrhoeal- Loperamide
Alpha 2 adrenergic agonist- Clonidine
Somatostatin analogue- Octreotide
Thyrotoxicosis
• Increase motility of GIT
• Shortened transit time
• Reduced time for action of bile on fat
digestion
• Malabsorption of nutrients
Increased bowel movement, diarrhoea, mild
steatorrhoea
Other clinical features
Symptoms
• Weight loss
• Increase appetitite
• Heat intolerance
• Palpitations
• Tremor
• Irritability
Signs
• Tachycardia
• Goitre
• Lid retraction
• Lid lag
Graves’
+ ophthalmoplegia (diplopia)
+ pretibial myxoedema
+ thyroid acropachy
Investigations
• Serum T4 & TSH
Treatment
• Carbimazole
• Propranolol
Neuroendocrine tumours of
pancreas
Zollinger Ellison syndrome
1. Severe peptic ulceration
2. Gastric acid hypersecretion
3. Non beta cell islet tumour of pancreas
(gastrinoma)
Gastrinoma
• Increase gastrin levels
• Increase acid production by parietal cells of
stomach
• Small intestine pH low &acidic
• Pancreatic lipase inactivated, bile acids
precipitated
• Diarrhoea & steatorrhoea
Treatment: High dose proton pump inhibitors
VIPoma
• Vasoactive intestinal peptide (VIP)
• Stimulate adenyl cyclase in enterocytes
(stimulate secretion of water and electrolytes)
• Secretory diarrhoea
Clinical syndrome: watery diarrhoea, hypokalemia,
metabolic acidosis
Somatostatinoma
• Function of somatostatin: suppress GI
hormones, pancreatic hormones,
pancreatic enzymes
• Increase levels of somatostatin
• Diabetes mellitus and
diarrhoea/steatorrhoea
Investigations
• Fasting blood sample for:
~ Chromogranin A
~ Hormones ( gastrin, VIP, somatostatin)
• Ultrasound scan, CT, MRI to look for
tumours
Treatment
• Surgically resect solitary tumours
• Somatostatin analogue (Octreotide)
Carcinoid tumour
• Most commonly found in small bowel
• Local mass effect (obstruction,
appendicitis) or
• Hormone excess
~ ectopic ACTH or 5-HT (serotonin)
Carcinoid syndrome- when vasoactive
hormones reach systemic circulation
Carcinoid syndrome
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Flushing
Wheezing ( bronchoconstriction)
Diarrhoea
Facial telangiectasia
Cardiac involvement
Investigations
• 24 hour urine collection of 5HIAA (5
hydroxyindoleacetic acid)
Medullary carcinoma of thyroid
• Parafollicular C cells
• Produce calcitonin & also 5HT
• diarrhoea
Post Gut Resection
Diarrhoea
Pathophysiology
Mesenteric
vascular
occlusion
Crohn’s
disease
Necrotising
enterocolitis
Volvulus
Gut resection
Injury/
trauma
to the
gut
Tumours
of the
small
intestine
Short Bowel Syndrome (SBS)
Impaired absorption of fluid and
nutrients
Diarrhoea
* Normally, length of small intestine: 6m; in SBS, <2m *
Factitious diarrhoea
• 1. Purgative abuse
• High diarrhoea volume, low serum potassium
• Sigmoidoscope shows pigmented mucosa
(melanosis coli)
• Barium enema shows dilated colon
• May be associated with eating disorders
2. Dilutional diarrhoea
• dilute stools on purpose
• Check stool osmolality and electrolytes
Investigation of diarrhoea
• Acute-self limiting diarrhoeaNo investigations are necessary
• Investigations are indicated when:
-Signs of Dehydration (electrolytes imbalances)
-Chronic or persistent diarrhoea
-Bloody Diarrhoea
-Anemia, Weight loss, abdominal mass or
suspicion of neoplasia
-Patients with IBS with significant change of
symptoms
Irritable Bowel Syndrome
• Functional bowel disorder
• Absence of any organic causes
Epidemiology
• Young
• <35 years old
• Female
Clinical Features
• Abdominal pain or discomfort
• Abdominal bloating/ distension
• Change in bowel habits (constipation
alternating with diarrhoea)
• Urgency of bowel movements
• Tenesmus
Diagnosis
• no specific laboratory or imaging test
• Diagnosis of exclusion
• Rome Criteria
Rome III Criteria (2006)
• Recurrent abdominal pain or discomfort at
least 3 days per month during the previous
3 months that is associated with 2 or more
of the following:
– Relieved by defecation
– Onset associated with a change in stool
frequency
– Onset associated with a change in stool form
or apperance.
Cont.
• Supporting symptoms:
– Altered stool frequency
– Altered stool form
– Altered stool passage (straining and/or
urgency)
– Mucorrhoea
– Abdominal bloating or subjective distention
Etiology
• Currently unknown.
• Thought to result from
– an interplay of abnormal gastrointestinal(GI)
tract movements
– Increased awareness of normal bodily
functions
– Change in the nervous system
communication between the brain and the GI
tract,
Cont.
• Has also developed after episodes of
gastroenteritis
• Dietary allergies or food sensitivities (not
yet proven)
• Symptoms worsen during periods of stress
or menses
Management
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Exclusion diet
Fiber supplements
Laxatives
Anti-diarrhoea medication
Antispasmodic
Antidepressants
Blood Tests
1. Full Blood Count
- Anemia? MCH? (iron deficiency? Anemia
of chronic illness?)
- MCV (inc in Crohn’s, celiac disease; dec
in iron defi anemia)
2. Renal Profile
- Electrolyte imbalances (dec K)
3. Arterial Blood Gas
- Acid-Base balance (loss of alkali in
diarrhoea)
4. HIV serology (opportunistic infection of the
gutchronic diarrhoea)
5. ESR (cancer, IBD)
6. CRP (IBD)
7. Thyroid function test (hyperthyroidism)
8. Celiac Serology
9. Tumor Markers (eg: CEA)
……
Depends on your differential diagnosis~
Stool
•
( must be collected fresh on three
occasions)
– Microscopy for parasites and red and white
cells ( warm specimen for amoebiasis)
– Cultures: Pathogens, Campylobacter sp.,
C.difficile (pseudomembranous colitis,
Yersinia, sp
Stool
– For occult blood
– For ova and cyst (eg: Cryptosporidiosis,
Blastocystis)
– For fat excretion (steatorrhoea)
Imaging and Scope:
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Barium Studies: Barium enema, Barium
follow-through
Ultrasound
Abdominal X-Ray (chronic pancreatitis)
CT scan
MRI
Imaging and Scope:
• Small Bowel Endoscopy (for
malabsorption disorders) and Capsule
Endoscopy
• Colonoscopy/ Barium enema
– To exclude malignancy and in colitis
• Rigid / Flexible sigmoidoscopy
– Biopsy of normal and abnormal looking
mucosa
Complications of
Diarrhoea
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Hypokalaemia
Depletional hyponatraemia
Hypernatraemia
Hypophosphataemia
Hypomagnesemia
Dehydration
Hypovolaemic shock
Principles of Management
of Acute Diarrhoea
Acute Diarrhoea : Management
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Access Hydration Status
Encourage fluids intake
Consider antibiotics if ill or frail
Consider referring if very ill, diabetic on
insulin or metformin
• Symptomatic relief with antimotility drugs
• Advice on how to reduce spread by hand
washing.
• Food-handlers and staff in health care
services should be symptom free for 48
hours before return.
• Drink glucose containing liquids and soups
• Carbohydrates e.g. pasta and bread,
assist the co-transport of glucose and
sodium, so the amount of diarrhoea lost
will be less than if water is used alone
Particular care should be taken when
dealing with the following patients:
• The very young or elderly
• Those with co-morbidity e.g.diabetes,
immunodeficiency, inflammatory bowel
disorder or gastric hypochlorhydria
• Patients taking systemic corticosteroids,
ACE-inhibitors, diuretics or acid
suppressants
• Antibiotic therapy is usually only indicated
for patients with positive stool cultures,
who are systemically unwell and whose
condition fails to improve within a few
days.
Dehydration: Management
• Children and Elderly are especially prone
to dehydration.
• A child should be encouraged by their
preferred diet.
• Breastfeeding should be continued and
alternate with ORS
Oral Rehydration Therapy
• The use of Oral Rehydration Therapy
(ORT) is advisable for all cases with
dehydration seen.
– Oral Rehydration Salt –standard or reduced
osmolarity
– Home solutions
Oral Rehydration Therapy
– Sodium chloride
3.5 g
– Trisodium citrate dehydrate
2.9 g
(or sodium bicarbonate 2.5g)
– Potassium chloride
1.5g
– Glucose
20 g
– To be dissolved in one litre of clean drinking water
– encourage fluid intake e.g. salt + glucose drink to
assist in co-transport of sodium into the epithelial cells
via the SGLT1 protein, which enhances water and
sodium re-absorption in small intestines.
• Adults should receive 2 litres of ORT in the
first 24 hours, followed by unrestricted
normal fluids with 200 ml of ORT for every
loose stool or vomit.
• Mild dehydration (<5%) can be treated in a
primary care, by giving ORS.
• Moderate (5-10%) or severe (greater than
10%)dehydration is an indication for
admission.
Fluid management of Moderate to
Severe Dehydration
Treat Shock
Rehydrate
Maintainance
Ongoing Losses
• Treat Shock:
20 ml /kg 0.9% saline over 10 to 15 mins
• Rehydration
fluid deficit: % of dehydration X body
weight
0.45% saline/2.5 % dextrose
over 24 hours-low or normal plasma
sodium
over 48 hours-high plasma sodium
• Maintenance :
First 10 kg
Second 10 kg
Subsequent kg
: 100 ml/kg/24 hours
: 50 ml/kg/24 hours
: 20 ml/kg/24 hours
• Close monitoring : clinical condition
(vomiting, diarrhoea), plasma creatinine,
and electrolytes.
Principles of Management
of Chronic Diarrhoea
1. Rehydration
• Oral rehydration therapy
– Oral Rehydration Salt –standard or reduced
osmolarity
– Home solutions
• Intravenous therapy
– Ringer’s Lactate solution (Hartmann’s soln)
– Normal saline/ Half normal saline with 5-10%
glucose
– Half strength Darrow’s soln
2. Stop diarrhoea
• Anti-motility agents: Codeine, Loperamide,
Diphenoxylate, Bismuth subsalicylate
• Adsorbents: Zaldaride Maleate
• Anti-spasmodic agents: Propantheline,
Dicyclomine, Mebeverine
• Antibiotics? Cholera, Dysentery, Giardiasis
3. Treat the underlying cause
4. Symptomatic Management
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Blood transfusion
Analgesics
Rehydration and electrolyte replacement
Diet modification (malabsorption
disorders)
Treat accordingly~
References
• Harrison’s Principal of Internal
Medicine.2005, pg 225-233
• Kumar and Clark,
• Rehydration Project
• http://rehydrate.org/diarrhoea/tmsdd/1med
.htm#intro
• Kochar’s Clinical Medicine for Students,
Fifth edition.pg41-47
• Murtagh’s Family Practicespg467-483
References
• http://www.patient.co.uk/showdoc/4002502
0/
• Emedicinehealth.Dehydration
• Medication Induced Constipation and
Diarrhea; May 2008 issue; Practical
Gastroenterology
• Medication Induced Constipation and
Diarrhea; May 2008 issue; Practical
Gastroenterology