DIARRHOEA AND MALABSORPTION

SYNDROME

DR. AHMED AL-BUHAIRI

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 Stool is 60 to 90% water.

 In Western society, stool amount is 100 to 200 g/day in healthy adults depending on the amount of
unabsorbable dietary material (mainly carbohydrates).
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Definition
 Passage of more than 200 g of stool daily (Volume).
Commonly with increased “frequency” and loose or watery stools (Liquidity).
 Frequent passage of small volumes of stool, as may occur in patients with tenesmus (rectal urgency), should be
distinguished from diarrhea.
 Similarly, fecal incontinence can be confused with diarrhea. However, diarrhea can cause a marked worsening
of fecal incontinence.
 Invasive diarrhea, or dysentery, is defined as diarrhea with visible blood or mucus and commonly associated
with fever and abdominal pain, in contrast to watery diarrhea.
 Diarrhea can range in severity from an acute self-limited episode to a severe, life-threatening illness.
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Complications of diarrhoea
 Fluid loss with consequent dehydration.
 Electrolyte loss (sodium, potassium, magnesium, chloride).
 Vascular collapse can develop rapidly in patients who have severe diarrhea (eg, patients with cholera) or are
very young, very old, or debilitated.
 Bicarbonate loss can cause metabolic acidosis.
 Hypokalemia can occur when patients have severe or chronic diarrhea or if the stool contains excess mucus.
 Hypomagnesaemia after prolonged diarrhea can cause tetany.
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 In clinical practice, it is helpful to distinguish acute from chronic diarrhea, as the evaluation and
treatment are entirely different:
 Acute < 2 weeks
 Chronic > 4 weeks
 In between: Persistent diarrhea
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 Acute diarrhoea
 Most cases of acute diarrhea are due to infections and are self-limited.
 In developing countries, enteric bacteria and parasites are more prevalent than viruses and typically peak
during the summer months.
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 Escherichia coli:
 Enterotoxigenic E. coli (ETEC) causes traveler’s diarrhea.
 Enteropathogenic E. coli (EPEC) rarely causes disease in adults.
 Enteroinvasive E. coli (EIEC) causes bloody mucoid (dysentery) diarrhea; fever is common.
 Enterohemorrhagic E. coli (EHEC) causes bloody diarrhea, severe hemorrhagic colitis, and the
hemolytic uremic syndrome in 6–8% of cases; cattle are the predominant reservoir of infection.
E coli O157:H7 is a Shigatoxin– producing noninvasive organism most commonly acquired
from contaminated meat that has resulted in several outbreaks.
 EIEC and EHEC (including E. coli O157:H7) have a very low prevalence in some
developing countries .
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 Campylobacter:
 Asymptomatic infection is very common in developing countries and is associated with the
presence of cattle close to dwellings.
 Infection is associated with watery diarrhea; sometimes dysentery.
 Guillain–Barré syndrome develops in about one in 1000 of people with Campylobacter colitis.
 Poultry is an important source of Campylobacter infections.
 The presence of an animal in the cooking area is a risk factor in developing countries.
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 Shigella species:
 Most common cause of acute bloody diarrhea in developing countries.
 Hypoglycemia, associated with very high mortality occurs more frequently than in other types of
diarrheal diseases.
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 Vibrio cholerae:
 Stools are watery, colorless, and flecked with mucus; often referred to as ―ricewatery‖ stools.
 Vomiting is common; fever is typically absent.
 There is a potential for epidemic spread; any infection should be reported promptly to the
public health authorities.
 In the absence of prompt and adequate rehydration, severe dehydration leading to
hypovolemic shock and death can occur within 12–18 h after the onset of the first symptom.
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 Salmonella:
 Enteric fever — Salmonella Typhi and Paratyphi A, B, or C (typhoid fever); fever lasts for 3 weeks or
longer; patients may have normal bowel habits, constipation or diarrhea.
 Animals are the major reservoir for salmonellae.
 Humans are the only carriers of typhoidal Salmonella.
 In nontyphoidal salmonellosis (Salmonella gastroenteritis), there is an acute onset of nausea,
vomiting, and diarrhea that may be watery or dysenteric in a small fraction of cases.
 The elderly and people with immunecompromised status for any reason (e.g., hepatic and
lymphoproliferative disorders, hemolytic anemia), appear to be at the greatest risk.
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 Viral agents:
 Predominant cause of acute diarrhea, particularly in the winter season.
 Rotavirus are the leading cause of severe, dehydrating gastroenteritis among children.
 Noroviruses are the most common cause of outbreaks of gastroenteritis, affecting all age groups.
 Adenovirus infections most commonly cause illnesses of the respiratory system may cause
gastroenteritis especially in children.
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 Acute noninflammatory diarrhea

o Watery, nonbloody, usually mild, self-limited. Caused by a virus or noninvasive bacteria.
o Periumbilical cramps, bloating, nausea, or vomiting suggests a small bowel source caused by either a
virus (rotavirus, norovirus, adenovirus), a toxin-producing bacterium (enterotoxigenic E coli,
Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, Plesiomonas shigelloides), or
another agent (Giardia) that disrupts normal absorption and secretory process in the small
intestine.
o Prominent vomiting suggests viral enteritis or S aureus food poisoning.
o Although typically mild, the diarrhea (which originates in the small intestine) can be voluminous and
result in dehydration with hypokalemia and metabolic acidosis (eg, cholera).
o Because tissue invasion does not occur, fecal leukocytes are not present.
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 Acute inflammatory diarrhea

o Blood or pus, fever. Usually caused by an invasive or toxin-producing bacterium.
o The presence of fever and bloody diarrhea (dysentery) indicates colonic tissue damage
caused by invasion (shigellosis, salmonellosis, Campylobacter ,Yersinia infection or amebiasis) a
toxin (C difficile, Aeromonas, Shiga-toxin–producing E coli), enteric viruses (e.g.
Cytomegalovirus) in immunocompromised and HIV-infected patients.
o Because these organisms predominantly involve the colon, the diarrhea is small in volume (less
than 1 L/day) and associated with left lower quadrant cramps, urgency, and tenesmus.
o Fecal leukocytes or lactoferrin usually are present in infections with invasive organisms.
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Complications of acute diarrheal disease in adults

Shigella species, Nontyphoidal Particular concern in HIV-infected

Bacteremia
Salmonella enterica, Campylobacter fetus individuals

Shiga toxins are responsible for

Shigella species, Shiga toxin-
Hemolytic-uremic syndrome damage to endothelial cells and
producing Escherichia coli
hemolytic-uremic syndrome

Guillain-Barré syndrome Campylobacter jejuni

Campylobacter species, Salmonella

Reactive arthritis
species, Shigella flexneri
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 Evaluation
 History
 Physical examination
 Laboratory tests
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 History
 Duration of symptoms, the frequency and characteristics of the stool, and associated symptoms.
 Evidence of extracellular volume depletion (eg, dark yellow or scant urine, orthostatic hypotension).
 Community outbreaks (including nursing homes, schools) suggest a viral etiology or a food source.
 Similar recent illnesses in family members suggest an infectious origin.
 Ingestion of improperly stored or prepared food implicates food poisoning.
 Consumption of unpasteurized dairy products, raw or undercooked meat or fish, the timing of symptom onset can be an
important clue to the diagnosis:
 Within six hours – suggests ingestion of a preformed toxin of Staphylococcus aureus or Bacillus cereus, particularly if nausea and vomiting
were the initial symptoms
 At 8 to 16 hours – suggests infection with Clostridium perfringens
 At more than 16 hours – suggests either viral or other bacterial infection (eg, contamination of food with enterotoxigenic or other
pathogens).
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 History
 Pregnant women have an increased risk of developing listeriosis.
 Exposure to unpurified water (camping, swimming) may result in Giardia or Cryptosporidium.
 Exposure to animals (poultry, turtles, petting zoos) has been associated with Salmonella infection.
 Recent travel abroad suggests traveler’s diarrhea.
 Antibiotic administration within the preceding several weeks increases the likelihood of C difficile colitis.
 HIV infection or sexually transmitted diseases should be determined.
 Persons are at risk for a variety of infections that cause proctitis.
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 Physical examination
Evaluating volume status and identifying complications
o Vital signs
o Findings that can suggest ileus or peritonitis (abdominal distension, pain with gentle percussion,
abdominal rigidity, or rebound tenderness).
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Assessment of severity of volume depletion

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 Laboratory tests
 In acute noninflammatory diarrhea diagnostic investigation is unnecessary except in:
 Suspected outbreaks,
 Patients at high risk for spreading infection to others
 Persistent diarrhea beyond 7 days.
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 In general, initial evaluation is indicated in the following situations:

(1) signs of inflammatory diarrhea manifested by any of the following: fever (higher than 38.5°C), bloody diarrhea,
severe abdominal pain or WBC 15,000/mcL or more.
(2) the passage of six or more unformed stools in24 hours.
(3) profuse watery diarrhea and dehydration.
(4) frail older patients or nursing home residents.
(5) immunocompromised patients (AIDS, posttransplantation).
(6) exposure to antibiotics or hospital-acquired diarrhea (onset following at least 3 days of hospitalization).
(8) systemic illness.
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 Laboratory tests
o CBC
• Helpful in suggesting severe disease or potential complications. A low platelet count may prompt concern for
the development of the hemolytic-uremic syndrome, and a leukemoid reaction is consistent with the diagnosis
of C. difficile infection.
o Creatinine, urea, K, Na.
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 Laboratory tests
o Stool specimens for
o Microscopy.
o In case of bloody diarrhea test for shiga toxin producing E. coli (an outbreak or in an afebrile patient) and for
Entamoeba.
o Test for C difficile. in patients who are hospitalized or who have a history of antibiotic exposure.
o Bacterial cultures.
o Multiplex molecular techniques with nucleic acid amplification (eg, polymerase chain reaction [PCR] assays) that screen
for a panel of pathogens, including viruses, protozoa, and bacteria and can detect potential pathogens in 35–54% of
specimens within 1–4 hours.
o Blood cultures should be obtained in patients with high fevers or who appear systemically ill.
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Treatment
 In over 90% of patients with acute noninflammatory diarrhea, the illness is mild and self-limited, responding within
days to simple rehydration therapy or antidiarrheal agents.
 Hospitalization is required in patients with:
 Severe dehydration for intravenous fluids, especially if vomiting or unable to maintain sufficient oral fluid intake.
 Organ failure, or altered mental status.
 Bloody diarrhea that is severe or worsening in order to distinguish infectious versus noninfectious cause (IBD or intestinal
ischemia).
 Severe abdominal pain, worrisome for toxic colitis, IBD, intestinal ischemia, or surgical abdomen.
 Signs of severe infection or sepsis (temperature higher than 39.5°C, leukocytosis, rash).
 Severe or worsening diarrhea in patients who are older than 70 years or immunocompromised.
 Signs of hemolytic-uremic syndrome (acute kidney injury, thrombocytopenia, hemolytic anemia).
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 Treatment
 Diet
 Mild diarrhea need adequate oral fluids containing carbohydrates and electrolytes.
 Patients find it more comfortable to rest the bowel by avoiding high-fiber foods, fats, milk products, caffeine, and
alcohol.
 Frequent feedings of tea, carbonated beverages, and soft, easily digested foods (eg, soups, crackers, bananas,
applesauce, rice, toast) are encouraged.
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 Rehydration
In more severe diarrhea, dehydration can occur quickly, especially in children and frail older adults.
 Oral rehydration with fluids containing glucose, Na+, K+, Cl–, and bicarbonate or citrate is preferred
when feasible.
 A convenient mixture is ½ tsp salt (3.5 g), 1 tsp baking soda (2.5 g NaHCO3), 8 tsp sugar (40 g), and 8
oz orange juice (1.5 g KCl), diluted to 1 L with water.
 Alternatively, oral electrolyte solutions (eg, Pedialyte, Gatorade) are readily available.
 Fluids should be given at rates of 50–200 mL/kg/24 h depending on the hydration status.
 Intravenous fluids (lactated ringer injection) are preferred in patients with severe dehydration.
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 Antidiarrheal Agents
o They should not be used in patients with inflammatory diarrhoea (bloody diarrhea, high fever, or systemic
toxicity) and should be discontinued in patients whose diarrhea is worsening despite therapy.
o Antidiarrheal agents may be used in mild to moderate non-inflammatory diarrhoea diarrheal illnesses to
improve patient comfort.
o Loperamide is preferred.
o Bismuth subsalicylate reduces symptoms in patients with traveler’s diarrhea.
o Anticholinergic agents (eg, diphenoxylate with atropine) are contraindicated in acute diarrhea because of the rare
precipitation of toxic megacolon.
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 Antibiotic Therapy
 1. Empiric treatment (before culture)
o Empiric treatment may be considered while the stool bacterial culture is incubating in certain patients:
• Severe disease (fever, more than six stools per day, volume depletion warranting hospitalization)
• Features suggestive of invasive bacterial infection, such as bloody or mucoid stools (except in cases of nonsevere
disease when fever is low or absent and no suspicion of infection with STEC)
• Host factors that increase the risk for complications, including age >70 years old and comorbidities such as cardiac
disease and immunocompromising conditions.
o The oral drugs of choice for empiric treatment are the fluoroquinolones , alternatives include trimethoprim-
sulfamethoxazole; or doxycycline.
o Macrolides and penicillins are not recommended (microbial resistance to these agents).
o Rifaximin and azithromycin are approved for empiric treatment of noninflammatory traveler’s diarrhea.
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 2. Specific antimicrobial treatment (after culture)

o Not recommended in patients with nontyphoid Salmonella, Campylobacter, Aeromonas, or Yersinia,
except in severe disease, because they do not hasten recovery or reduce the period of fecal
bacterial excretion.
o The infectious bacterial diarrheas for which treatment is recommended are shigellosis, cholera,
extraintestinal salmonellosis, listeriosis, and C. difficile.
o The parasitic infections for which treatment is indicated are amebiasis, giardiasis,
cryptosporidiosis, and cyclosporiasis.
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 Chronic Diarrhea
 Diarrhea present for longer than 4 weeks.
 The causes of chronic diarrhea may be grouped into the following major pathophysiologic categories:
medications, osmotic diarrheas, secretory conditions, inflammatory conditions, malabsorptive
conditions, motility disorders, chronic infections, and systemic disorders.
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 Medications
 All medications should be carefully reviewed. Common offenders include cholinesterase inhibitors, SSRIs,
ARBs, PPI, NSAIDs, metformin, allopurinol, and orlistat.
 Chronic Infections
 Chronic parasitic infections may cause diarrhea through a number of mechanisms. Commonly include the
protozoans Giardia, amebiasis and Cyclospora as well as the intestinal nematodes.
 Strongyloidiasis and capillariasis in endemic regions, especially in the presence of eosinophilia.
 Bacterial infections with C difficile and, uncommonly, Aeromonas and Plesiomonas may cause chronic diarrhea.
 Immunocompromised patients are susceptible to infectious organisms that can cause acute or chronic
diarrhea, including microsporidia, Cryptosporidium, CMV, Cystoisospora belli (formerly Isospora belli),
Cyclospora, and Mycobacterium avium complex.
 Systemic Conditions
 Chronic systemic conditions, such as thyroid disease, diabetes, and collagen vascular disorders, may cause
diarrhea through alterations in motility or intestinal absorption.
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Osmotic gap
 As stool leaves the colon, fecal osmolality is equal to the serum osmolality, ie, approximately 290
mOsm/kg.
 The stool osmolality may be estimated by multiplying the stool (Na + K) × 2.
 The osmotic gap is the difference between the measured osmolality of the stool (or serum) and the
estimated stool osmolality and is normally less than 50 mOsm/kg. Osmotic gap = 290-2(stool Na +
stool K).
 An increased osmotic gap (greater than 75 mOsm/kg) implies that the diarrhea is caused by ingestion
or malabsorption of an osmotically active substance.
 The most common causes are carbohydrate malabsorption (lactose, fructose, sorbitol), laxative
abuse and malabsorption syndromes.
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Osmotic Secretory Inflammatory Malabsorptive Altered motility

Example Dairy (lactose), fruits and
artificial sweeteners
(fructose and sorbitol),
processed foods and soft
drinks (high-fructose corn
syrup), and alcohol,
Magnesium- or phosphate-
containing compounds
(laxatives, antacids).
Abdominal distention,
bloating, and flatulence.
Volume (Liters/day) < 1L/d
Fasting Stops
Besacodyl, Villous adenoma
Neuroendocrine Tumors
(stimulating intestinal or
pancreatic secretion)
Bile salt malabsorption
(stimulating colonic
secretion)
Microscopic colitis.
Dehydration and electrolyte
imbalance.
>1L/d
(Liters/d)
No effect
IBD Mucosal intestinal IBS (most common)
Ischemic colitis diseases (Coeliac), Small Abnormal intestinal motility
C diff intestinal bacterial secondary to systemic
overgrowth disorders (diabetic
Short Bowel Syn, neuropathy). Radiation
Pancreatic Insufficiency, enteritis, or surgery
(ch. Pancreatitis), (vagotomy) due to rapid
Mesenteric insufficiency transit or to stasis of
Lymphatic obstruction intestinal contents with
bacterial overgrowth,
Abdominal pain, fever, Weight loss, osmotic IBS (lower
weight loss, and diarrhea, steatorrhea,, abdominal pain and altered
hematochezia. nutritional deficiencies. bowel habits).
< 1L/d < 1L/d < 1L/d
No effect Stops Reduces

Osmotic gap Increased Normal Variable Increased Normal

Blood & mucus Absent Absent Present Absent Absent

Possible clue Laxative use Dehydration Fever, pain Malnutrition Surgery

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 Diagnosis
Hx
 Relationship to meals (postprandial diarrhea in osmotic diarrhoea).
 Whether it occurs at night (organic cause, not functional) or during fasting (non-osmotic).
 Malabsorption disorder (steatorrhoea), inflammatory disorder (containing
 blood or pus), or a osmotic or secretory process (watery).
 Abdominal pain suggests IBS or IBD.
 Medications and diet should be reviewed.
 Recent psychosocial stressors should be reviewed (IBS).
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 Diagnosis
 Review of systems should seek symptoms suggesting possible causes, including joint pains
(inflammatory bowel disease, celiac disease), flushing (carcinoid, vipoma, mastocytosis), chronic
abdominal pain (irritable bowel, inflammatory bowel disease, gastrinoma), and GI bleeding (ulcerative
colitis, tumor).
 Past medical history should identify known risk factors for diarrhea, including inflammatory bowel
disease, irritable bowel syndrome, HIV infection, and previous GI surgical procedures (eg, intestinal or
gastric bypass or resection, pancreatic resection). Family and social history.
 Physical examination should assess for signs of malnutrition, dehydration, and IBD.
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Interpretation of findings
 In the absence of laxative use, large-volume watery diarrhea (eg, daily stool volume > 1 L/day)
strongly suggests an endocrine tumor cause in patients with normal GI anatomy. A history of oil
droplets in stool, particularly if associated with weight loss, suggests malabsorption.
 Recurrent bouts of bloody diarrhea in a younger person suggest inflammatory bowel disease.
Diverticular bleeding and ischemic colitis also manifest with acute bloody diarrhea.
 Diarrhea that consistently follows ingestion of certain foods suggests food intolerance.
 Diarrhea with green or orange stools suggests impaired absorption of bile salts.
 The symptoms can help identify the affected part of the bowel. Generally, in small-bowel diseases,
stools are voluminous and watery or fatty. In colonic diseases, stools are frequent, sometimes small in
volume, and possibly accompanied by blood, mucus, pus, and abdominal discomfort.
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Interpretation of findings
 In irritable bowel syndrome (IBS), abdominal pain is related to defecation, associated with changes in
stool frequency or consistency, or both. However, these symptoms alone do not discriminate IBS from
other diseases (eg, inflammatory bowel disease). Functional diarrhea is characterized by loose or
watery stools with onset at least 6 months before diagnosis and present during the previous 3 months.
These patients do not meet the criteria for IBS; they may have abdominal pain and/or bloating, but
these are not predominant symptoms.
 Extra-abdominal findings that suggest an etiology include skin lesions or flushing (mastocytosis),
thyroid nodules (medullary carcinoma of the thyroid), right-sided heart murmur (carcinoid),
lymphadenopathy (lymphoma, AIDS), and arthritis (inflammatory bowel disease, celiac disease).
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Evaluation
 Chronic diarrhea (> 4 weeks) requires evaluation, as does a shorter (1 to 3 weeks) bout of diarrhea in
immunocompromised (e.g. AIDS-associated diarrhea) patients or those who appear significantly ill.
 Diagnostic evaluation should be directed by the history and physical examination when possible. If this
approach does not provide a diagnosis or direction, a broader approach is needed.
 Common causes should be excluded, including medications, chronic infections, and irritable bowel
syndrome.
 The presence of nocturnal diarrhea, weight loss, anemia, or positive results on FOBT are inconsistent
with functional bowel disorders and warrant further evaluation.
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Initial Diagnostic Tests

 Stool for:
 Microscopic examination for ova and parasites.
 Parasitic infections (Giardia, E histolytica, Cryptosporidia, and Cyclospora) may be diagnosed with stool antigen assays or
microscopy with special stains.
 C. difficile in patients with recent antibiotic exposure or suspected C. difficile infection.
 Occult blood.
 Fat (by Sudan stain or fecal elastase) if suspicion of malabsorption.
 Electrolytes (to calculate the stool osmotic gap) in chronic watery diarrhea.
 Fecal calprotectin or fecal lactoferrin (to screen for IBD).

 Complete blood count with differential.

 Celiac serology (IgA tissue transglutaminase).
 Thyroid-stimulating hormone (TSH) and free thyroxine (T4).
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o An increased osmotic gap suggests an osmotic diarrhea or disorder of malabsorption.

o A positive fecal fat stain suggests a disorder of malabsorption.
o The presence of fecal leukocytes or lactoferrin may suggest IBD.
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 3. Endoscopic examination and mucosal biopsy

 Colonoscopy with mucosal biopsy from the colon and terminal ileum to exclude IBD, microscopic
colitis, and colonic neoplasia.

 Upper endoscopy with small bowel biopsy is performed when a small intestinal malabsorptive
disorder is suspected (Coeliac disease, Whipple disease).
 It may also be done in patients with advanced AIDS to document Cryptosporidium, microsporidia, and Mavium-
intracellulare infection.
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 Further Studies
If the cause of diarrhea is still not apparent, further studies may be warranted.
 24-hour stool collection quantification of total weight and fat:
o A stool weight of less than 200 g/24 h excludes diarrhea and suggests a functional disorder such as IBS.
o A weight greater than 1000–1500 g suggests a significant secretory process including neuroendocrine tumors.
o A fecal fat determination in excess of 10 g/24 h confirms a malabsorptive disorder.

 Fecal elastase less than 100 mcg/g may be caused by pancreatic insufficiency.
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 2. Imaging studies
o Calcification on a plain abdominal radiograph confirms a diagnosis of chronic pancreatitis, although
abdominal CT and endoscopic ultrasonography are more sensitive for the diagnosis of chronic
pancreatitis as well as pancreatic cancer.
o Small intestinal imaging with CT or MRI enterography is helpful in the diagnosis of Crohn disease,
small bowel lymphoma, carcinoid, and jejunal diverticula.
o Somatostatin receptor scintigraphy for localized neuroendocrine tumors.
o 75Se HCAT scintigraphy for bile salt malabsorption.
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 3. Further laboratory tests

o A. Serologic tests for neuroendocrine tumors
 Serum chromogranin A (pancreatic neuroendocrine tumors), vasoactive intestinal peptide (vipoma),
calcitonin (medullary thyroid carcinoma), gastrin (zollinger-ellison syndrome), and urinary 5-
hydroxyindoleacetic acid (5-HIAA) (carcinoid).

o B. Breath test
 The diagnosis of small bowel bacterial overgrowth is suggested by a noninvasive breath tests (glucose
or lactulose); however, a high rate of false-positive test results limits the utility of these tests.
 A definitive diagnosis of bacterial overgrowth is determined by aspirate of small intestinal contents for
quantitative aerobic and anaerobic bacterial culture.
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 Treatment
 All medications should be carefully reviewed, and discontinuation of potential culprits should be considered.
 Treatment of the cause.
 Antidiarrheal agents may be used in certain patients with chronic diarrheal conditions
 Opioids are safe in most patients with chronic, stable symptoms. Loperamide.
 Diphenoxylate with atropine.
 Codeine and deodorized tincture of opium: Because of potential habituation, these drugs are avoided except in cases
of chronic, intractable diarrhea.
 Clonidine: May help in patients with secretory diarrheas, diabetic diarrhea, or cryptosporidiosis.

 Octreotide: For secretory diarrheas due to neuroendocrine tumors (VIPomas, carcinoid).

 Bile salt binders: Cholestyramine or colestipol or colesevelam may be useful in patients with bile salt-induced
diarrhea.
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