Overview of Presentation

Definition
Types and causes Acute symptoms Chronic Pathophysiology History and examination Investigation Management Case study

Definition
Diarrhea is the abnormal passage of loose or liquid

stools more than three times daily and/or a volume of stool greater than 200 ml/day or weight of 200g/day. Diarrhoea must be distinguished from incontinence and urgency Faecal Incontinence is the involuntary voiding of faeces usually due to a pathology affecting sphincter control or loss of cognitive function. Faecal urgency

ACUTE AND CHRONIC DIARRHOEA

Diarrhoea may be defined as acute if present for less

than 2 weeks, persistent if present for 24 weeks, and chronic if greater than 4 weeks in duration

Causes of Acute Diarrhoea

Infections Viral infection:
Norovirus, rotavirus

Bacterial infection Salmonella, Campylobacter, Shigella, Escherichia coli, Clostridium difficile Parasitic infection Giardia, Entamoeba histolytica, Cryptosporidia Food poisoning Staphylococci, Bacillus cereus, Clostridium perfringens

Drugs
Laxatives, Mg-containing antacids, caffeine,

antineoplastic drugs, many antibiotics, colchicine, quinine, quinidine, prostaglandin analogs etc

Causes of chronic diarrhoea Drugs

Laxatives, Mg-containing antacids, caffeine, antineoplastic drugs, many

antibiotics, colchicine, quinine, quinidine, prostaglandin analogs etc

Functional Irritable bowel syndrome Diet Carbohydrate intolerance Inflammatory bowel disease Ulcerative colitis, Crohn's disease Surgery Intestinal or gastric bypass or resection Malabsorption syndromes Celiac sprue, Whipple's disease, pancreatic insufficiency Tumors Colon carcinoma, lymphoma, villous adenoma of the colon Endocrine disorders Vipoma, gastrinoma, carcinoid, mastocytosis, medullary carcinoma of the thyroid, hyperthyroidism, zollingar-ellison, diabetes automic neuropathy

Pathophysiology
Normally approximately 10 litres of fluid consisting of

ingested food and drink, in addition to secretions from the salivary glands, stomach, pancreas, bile ducts, and duodenum, enters the gastrointestinal tract every day. The small intestine is the major site for re-absorption. Overall, about 90% of the fluid is re-absorbed, leaving 0.1 litre to be excreted in the faeces. Diarrhoea occurs when various factors interfere with this normal process, resulting in
decreased absorption or increased secretion of fluid and electrolytes, or increase in bowel motility.

Mechanism
1. Osmotic diarrhoea
Occurs when unabsorbable, water-soluble solutes (hypertonic

substances) remain in the bowel and retain water. Examples include

Generalised malabsorption

high conc. of glucose or fructose in lumen disaccharidase deficiency or glucose galactose malabsorption magnesium sulphate hexitols (eg, sorbitol, mannitol , xylitol) Too much vitamin c

Specific absorptive defect

purgatives

Magnesium containing antacids

2. Secretory diarrhoea
This may be due to: a. Active intestinal secretion of fluid and electrolyte
Enterotoxins (eg. Cholera,E. Coli- thermolabile or thermostable toxin,

C. Difficile) which destruct the Na Various endocrine tumors produce secretagogues, including vipomas (vasoactive intestinal peptide), gastrinomas (gastrin), mastocytosis (histamine), medullary carcinoma of the thyroid (calcitonin and prostaglandins), and carcinoid tumors (histamine, serotonin, and polypeptides bile salts (in the colon) following ileal resection fatty acids(in the colon) following ileal resection

b. Decreased absorption: which may be due to decreased transit time

some laxatives eg ( docusate sodium) Carcinod tumor (eg, prostaglandins, serotonin, related compounds)

3. Inflammatory diarrhoea
Damage to intestinal mucosal cells leads to: loss of fluid and blood Defective absorption of fluid and electrolytes
This may occur in: Hypersensitivity reaction (gluten) Infective conditions(dysentery due to Shigella) inflammatory conditions(UC and Crohns disease)

4. Abnormal motility diarrhoea

This occurs in Diabetes, Post-vagotomy, hyperthyroid diarrhoea Frequency of defecation occurs

HISTORY TAKING
Demographics Age: Occupation: Residence:
extremes of age day care worker- rotavirus, astrovirus, shiggella endemic area- cholera

History of presenting complaint Onset and Duration ( within 6hr suggest preformed toxins of staph or b. cereus) Circumstances of the onset (including recent travel, food ingested, source of water), frequency Time of day (chronic usually occurs in the night and morning) Associated symptoms (Abdominal pain, nausea and vomiting, loss of weight or apetite) Fever

 Stool xtics Consistency (watery, semi-solid or solid) Colour (pale, black tarry) Blood ( cancers, campylobactor, amoebiasis) mucous (colorectal cancers, polyps and IBS), pus ( IBD, diverticulitis) Odour (foul in parasitic infections) Tenesmus, incontinence

urgency

 Past medical and surgical history Lactose intolerance Chronic infections -HIV Gut resection (Short bowel syndrome) Hyperthyroidism Pancreatic disorders (diabetes)
Drug history Magnesium containing antacids Antibiotics (Neomycin and erythromycin)

Pseudomembraneous colitis

Cytotoxic drugs
NSAIDS PPI

 Family history IBS, Diabetes GI tumors

Social history Source of drinking water Toilet facilities Travelling alcohol

Examination
Clubbing Palor Dehydration Lethargy, dry mucous membranes, sunken eyes, poor skin turgor, delayed capillary refill Pyrexia Goitre Wasting (malnutrition) Abdominal signs Rebound tendernes, Bowel sound, increased or normal Digital rectal examination Xtics of the stool Colorectal faeces Impacted faeces

Investigations
Basic blood tests Stool test Small & large bowel investigations Endoscopic & histological assessment small bowel imaging(barium enema) and enteroscopy Tests for malabsorption Investigations for specific conditions

Basic Blood Tests

For evidence of malabsorption electrolytes FBC, urea and electrolytes electrolytes (K+ levels are decreased liver function tests- albumin and PPT vitamin B12, folate, calcium, ferritin, Erythrocyte sedimentation rate (increased in cancer and IBD), a C reactive protein (increased in infections and IBD).

Thyroid function tests if hyperthyroidism suspected

Serological test for coeliac disease +ve antiendomysium

Stool investigations
Cultures Stool cultures are not routinely indicated in acute diarrhoea. Performed in patients with severe diarrhea and fever and also in prolonged (greater than 14 days) diarrheal illness.

Macroscopy
Consistency (watery, semi-solid or solid) Colour (pale, black tarry)

Blood ( cancers, campylobactor, amoebiasis)

mucous (colorectal cancers, polyps and IBS), pus ( IBD, diverticulitis) Odour (foul in parasitic infections)

Microscopy
1. Bacteria ; gram staining (a) Specific coliform -scanty pus cells (b) Shigellae -pus cells in aboundance with or without RBC. (c) Salmonellae -pus cells in abundace with or without RBC (d) Overgrowth of Commensals-- pus cells

2. Fungi Monilia

--

profuse budding yeasts, hyphae.

3. Protozoa (a) Giardia lamblia -typical cysts (b) Trichomonas hominis -- motile flagellates (c) Entamoeba Histolytica -- motile amoeba , cysts, pus cells, RBC.

4. worms Trichuris trichiura

--

typical ova

Small and large bowel investigations

Endoscopy and Biopsy Sigmoidoscopy and colonoscopy

allow assessment of the colon ; neoplasia, IBD

Biopsy
colonic

mucosa for histological examination Distal duodenal biopsy in those with small bowel enteropathy in the absence of +ve antiendomysium antibodies

Imaging Small bowel imaging should be reserved for cases where small bowel malabsorption is suspected & histology is normal. Barium enema

Test for malabsorption

Serology for coeliac disease
Endoscopic duodenal biopsy to exclude other rare

forms
Pancreatic malabsoption 90% of the pancreatic acinar tissue must be destroyed before symptoms of malabsorption become evident

Invasive pancreatic function testing Pancreatic imaging Non-Invasive pancreatic function testing

Investigations for specific conditions

Diarrhoea due to bacterial overgrowth Culture of
jejunal aspirates unwashed small bowel biopsies

Intestinal inflammation Tc-HMPAO labelled white cell scanning

non invasive useful technique in absence of endoscopic ileal access

Complications
Dehydration Electrolyte imbalance Reactive complications arthritis, skin and eye inflammation NB: uncommon if a virus is the causative agent Systemic spread of the infection bones, joints, or the meninges. more likely if Salmonella infection. Persistent diarrhoea syndromes Trigger for IBS Secondary lactose intolerance

Haemolytic uraemic syndrome It is more common in children E.coli O157:H7 Xtd by

Haemolytic anaemia, low platelet count kidney failure

Reduced effectiveness of some drugs.

Due to malabsoption of the drugs

Management
The underlying cause of the diarrhoea must be treated and not the just the symptoms

Fluid therapy
The aim is to prevent dehydration, or to treat dehydration

if it has developed. Oral Drink at least 200 mls after each bout of diarrhoea If there is vomitting, wait 5-10 minutes and then start drinking again, but more slowly. Salted rice water, salted vegetable or chicken soup, Oral rehydration therapy
mouth

consists of solution of salts and sugars that is taken by the

Intravenous fluid eg.

Normal saline , dextose, ringers lactate

 Treatment of symptoms loperamide, bismuthsubsalicylate

Antibiotics
Evaluate for likely cause and treat as needed Travellers diarrhoeaquinolone Bloody diarrhoeaquinolones Shigella ciprofloxacin or azithromycin Campylobacter floroquinolones Samonella non-typhi floroquinolones or ceftriaxone Ecoli Floroquinolones Toxigenic C.difficile vancomycin, metronidazole Giadia metronidazole Cryptosporidium paramomycin+ azithromycin Isospora or cyclospora trimethoprim/sulphamethoxazole

CASE 1
A 52-year-old woman presents with left-sided abdominal

pain and severe diarrhea. Her abdominal pain was cramping and mildly relieved by food, but not with defecation. Her diarrhea was watery, she had >4 bowel movements each day. There was no hematemesis or melena. Her symptoms persisted with varying severity and no relief with over-the counter medications. In August of 1999, she underwent an upper endoscopy that revealed multiple ulcers in the stomach and duodenum. A biopsy for Helicobacter pylori was negative. She was started on Omeprazole with resolution of her abdominal pain and diarrhea. When the proton pump inhibitor was discontinued several months later, her diarrhea and abdominal discomfort returned.

 During August of 2000, an upper GI series again

demonstrated a duodenal ulcer. A serum gastrin level was normal. Her stool was negative for WBCs, ova, parasites, or C. difficile. An abdominal MRI was reportedly negative. She was restarted on Omeprazole and followed. During 2002, an abdominal MRI reportedly demonstrated a solitary lesion in the medial segment of the left lobe of the liver. No other upper GI abnormalities were noted by imaging studies. In April of 2002, the patient underwent an unremarkable upper endoscopy. No ulcers were seen.

 Review of Systems:Notable for paresthesias of the left hand, anxiety,

and intermittent vaginal spotting. spontaneous vaginal deliveries. adenoidectomy as a child.

Past Medical History:Borderline hypertension and three normal Past Surgical History:She is status post tonsillectomy and Social History:She is married with three grown children, and works

as a homemaker. She denies alcohol or tobacco use. She has not traveled overseas in over 5 years. She lives in a suburban setting and has no contact with farm animals or products. She eats a normal diet. Family History:Her father had cardiac disease and hypertension, and died of a myocardial infarction. Her mother is alive with thyroid disease. Her three siblings are healthy. There is no family history of cancer or diabetes mellitus.
Allergies:No known drug allergies. No known allergies to latex.

 Physical Examination: The patient is a well-developed, well-nourished white female

in no acute distress. Vital signs reveal blood pressure 144/83, pulse 85, respiratory rate 18, O2 sat 99% on room air, and temperature 35.7oC. Head and neck exam reveals no thyromegaly or lymphadenopathy. Lungs are clear to auscultation bilaterally. Cardiac exam is unremarkable with no murmurs, gallops, or rubs appreciated. Abdomen is soft, nontender, and nondistended. Rectal examination was normal, with hemoccult negative stool. There is no hepatosplenomegaly or periumbilical adenopathy. Neurological exam is unremarkable.

Laboratory Studies: CBC: WBC 6100/mm3 , HgB 13.6 g/dL, Hct 39.5%, MCV 90.4fL, RDW 13.4%, platelets 268,000/mm3 Basic metabolic panel showed the following results: Sodium 140 mEq/L, potassium 3.8 mEq/L, chloride 101 mEq/L, BUN 10 mg/dL, creatinine 0.7 mg/dL, glucose 95 mg/dL, bicarbonate 26 mEq/L Liver function tests demonstrated the following: Total protein 7.8 g/dL, albumin 4.5 g/dL, total bilirubin 0.5 mg/dL, ALT 11 IU/L, AST 17 IU/L, alkaline phosphatase 73 IU/LAmylase 54 IU/L, Lipase 27 IU/dLCa2+ 10.1 mg/dLCA 19-9 = 40.4 U/mL (1-36)

 What is your differential diagnosis?

How would you proceed?

Case 2
Mr. Eric Ansah, 22yr old political science student of KNUST

present to the hospital with a 2 day history of diarrhoea. He said the diarrhoea begun the first day as just watery diarrhoea which had a frequency of 5 during the day. Latter that evening, he started passing blood and mucous stained watery stool. The diarrhoea was associated with crumpy abdominal pain, flatulence and tenesmus. The symptoms became severe that he had to stay away from lectures the following day. However there was no fever. When asked about what could be causing the symptoms, the patient said I think my symptoms were because the kebab I took 3 days ago contained a lot of papper

 What are the differencial diagnosis?

What other investigations would you do? How would you manage the patient?