By Semester 6 and Smester 7

By Semester 6 and Smester 7
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 Chronic Diarrhoea Persistent 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 Sudden onset of bowel frequency
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 Dirrhoea- Pathophysiologic 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
Osmotic Diarrhoea Secretory Diarrhoea Inflammatory Diarrhoea Abnormal Motility Diarrhoea

Osmotic Diarrhoea Mechanism : Causes :
-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 : Causes :
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 Verner-Morrison 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 : 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 Campylobacter jejuni Salmonella sp. Shigella
Escherichia coli Staphylococcal enterocolitis Bacillus cereus Clostridium perfringens Clostridium botulinum Gastrointestinal tuberculosis

Viral Protozoa Rotavirus Norovirus Adenovirus Entamoeba histolytica
Cryptosporidium Giardia intestinalis Schistosomiasis

High Risk Groups 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 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 Cramping abdominal pain
Watery Bloody Cramping abdominal pain Nausea, +/- Vomiting Fever Loss of appetite Lethargy Shock

Investigations 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 re-absorption in small intestines. IV fluids (lactate Ringer’s solution) are preferred in those with severe dehydration.

Chronic Diarrhea

Causes Chronic Fatty Diarrhea (Diarrhea due to Malabsorption)
Chronic Inflammatory Diarrhea Chronic Watery Diarrhea Secretory Diarrhea Osmotic Diarrhea Drug-Induced Diarrhea Infectious Diarrhea Malignancy Functional Diarrhea (diagnosis of exclusion) Irritable Bowel Syndrome

History Age Diarrhea pattern
Differentiating small bowel from large bowel Stool characteristics Diurnal variation Weight Loss Medication and dietary intakes Recent travel to undeveloped areas

Age Young patients Older patients Inflammatory Bowel Disease
Tuberculosis Functional bowel disorder (Irritable bowel) Older patients Colon Cancer Diverticulitis

Diarrhea pattern Diarrhea alternates with Constipation
Colon Cancer Laxative abuse Diverticulitis Functional bowel disorder (Irritable bowel) Intermittent Diarrhea Malabsorption Persistent Diarrhea Inflammatory Bowel Disease

Differentiating small bowel from large bowel
Small intestine or proximal colon involved Large stool Diarrhea Abdominal cramping persists after Defecation Distal colon involved Small stool Diarrhea Abdominal cramping relieved by Defecation

Stool characteristics
Water: Chronic Watery Diarrhea Blood, pus or mucus: Chronic Inflammatory Diarrhea Foul, bulky, greasy stools: Chronic Fatty Diarrhea

Diurnal variation 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 Nocturnal Diarrhea (always organic) Diabetic Neuropathy

Weight Loss Despite normal appetite Associated with fever
Hyperthyroidism Malabsorption Associated with fever Inflammatory Bowel Disease Weight loss prior to Diarrhea onset Pancreatic Cancer Tuberculosis Diabetes Mellitus

Medication and dietary intakes
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
Traveler's Diarrhea Infectious Diarrhea

Colorectal Carcinoma Colorectal carcinoma Adenoma - carcinoma sequence
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 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
Antibiotics Laxatives Antihypertensives Lactulose Antineoplastics Antiretroviral drugs Magnesium containing compounds Anti arrhythmics NSAIDs Colchicine Antacids Acid reducing agents Prostaglandin analogs

Medication Mechanism Laxatives 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 Mechanism Antineoplastics Exudative diarrhea (protein losing enteropathy) NSAIDS Lymphocytic or collagenous colitis Alpha-glucosidase inhibitor Malabsorption of carbohydrates (osmotic diarrhea) Lipase inhibitors (Orlistat) 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
disturbance in the normal colonic flora, leading to impaired fermentation of carbohydrates and osmotic diarrhea reduced production of short-chain fatty acids which by reducing colonic absorption of fluid causes secretory diarrhea 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
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

disturbance in the normal flora of the colon
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
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

Release of inflammatory mediators & cytokines
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
Host susceptibility to infection Virulence of the infecting strain Type of antibiotic used Timing of exposure

Spectrum of disease Asymptomatic colonization
Simple antibiotic associated diarrhea Pseudomembranous colitis Fulminant colitis

Clinical features 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
Postural hypotension Gastroparesis ( nausea and vomitting) Difficulty in micturition ( bladder atony) Erectile dysfunction Gustatory sweating

Treatment 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 Severe peptic ulceration Gastric acid hypersecretion 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 Treatment 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 Investigations 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 Gut resection Mesenteric vascular occlusion
Crohn’s disease Injury/ trauma to the gut Tumours of the small intestine Necrotising enterocolitis Volvulus Gut resection

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 diarrhoea- No 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 FOODS. MANY PEOPLE FIND THAT THEIR SIGNS AND SYMPTOMS WORSEN WHEN THEY EAT CERTAIN FOODS. FOR INSTANCE, CHOCOLATE, MILK AND ALCOHOL MIGHT CAUSE CONSTIPATION OR DIARRHEA. CARBONATED BEVERAGES AND SOME FRUITS AND VEGETABLES MAY LEAD TO MORE BLOATING AND DISCOMFORT IN SOME PEOPLE WITH IBS. THE ROLE OF FOOD ALLERGY OR INTOLERANCE IN IRRITABLE BOWEL SYNDROME HASN'T BEEN WELL STUDIED. IF YOU EXPERIENCE CRAMPING AND BLOATING MAINLY AFTER EATING DAIRY PRODUCTS, FOOD WITH CAFFEINE, OR SUGAR-FREE GUM OR CANDIES, THE PROBLEM MAY NOT BE IRRITABLE BOWEL SYNDROME. INSTEAD, YOUR BODY MAY NOT BE ABLE TO TOLERATE THE SUGAR (LACTOSE) IN DAIRY PRODUCTS, CAFFEINE OR THE ARTIFICIAL SWEETENER SORBITOL. Stress. If you're like most people with IBS, you probably find that your signs and symptoms are worse or more frequent during stressful events, such as a change in your daily routine or family arguments. But while stress may aggravate symptoms, it doesn't cause them. Other illnesses. Sometimes another illness, such as an acute episode of infectious diarrhea (gastroenteritis), can trigger IBS.

Management Exclusion diet Fiber supplements Laxatives
Anti-diarrhoea medication Antispasmodic Antidepressants Exclusion diet for example for lactose intolerance pt. Fiber supplements and laxatives can relieve the constipation-predominant irritable bowel. Antidiarrhoeals such as loperamide can relieve diarrhoea Antispasmodic for colic and bloating. Antidepressants such as amitryptiline if the patient has pain ass wif depression.

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
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: 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

Hypokalaemia Depletional hyponatraemia Hypernatraemia Hypophosphataemia Hypomagnesemia Dehydration Hypovolaemic shock

Principles of Management of Acute Diarrhoea

Acute Diarrhoea : Management
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 g Trisodium citrate dehydrate 2.9 g (or sodium bicarbonate 2.5g) Potassium chloride 1.5g Glucose 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 : ml/kg/24 hours Second 10 kg : 50 ml/kg/24 hours Subsequent kg : 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 Intravenous 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
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 Kochar’s Clinical Medicine for Students, Fifth edition.pg41-47 Murtagh’s Family Practicespg

References http://www.patient.co.uk/showdoc/40025020/
Emedicinehealth.Dehydration Medication Induced Constipation and Diarrhea; May 2008 issue; Practical Gastroenterology

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