Acute diarrhea is caused by infections spread through the fecal-oral route. It affects over 1.7 billion people globally each year and causes 760,000 deaths in children under 5. The key aspects of management are fluid replacement to prevent dehydration, using oral rehydration solutions, and antimicrobial treatment only for invasive infections or immunocompromised patients to prevent antibiotic resistance. Proper sanitation and hygiene can help limit the transmission of infectious agents causing acute diarrhea.

1. Acute diarrhea&vomiting:
Professor Dr. Mohamed Alshekhani.

2. Acute diarrhea:
 Sometimes with vomiting, is the predominant symptom in infective GEitis.
 Acute diarrhoea also a symptom of other infs&non-infectious diseases.
 Stress, whether psychological or physical, can also produce loose stools.
 > 1.7 billion acute diarrhoea annually globally, with 760 000 deaths < 5.
 In developed countries, diarrhoea remains an important problem, with the
elderly being most vulnerable.
 The majority of episodes are due to infections spread by the faecal–oral
route transmitted either on fomites, on contaminated hands, food or water.
 Measures as the provision of clean drinking water, appropriate disposal of
human/ animal sewage& the application of simple principles of food
hygiene can all limit gastroenteritis.
 The clinical features of food-borne gastroenteritis vary.
 Some organisms (Bacillus cereus, Staph. Aureus& Vibrio cholerae) elute
exotoxins that cause vomiting&/or so-called ‘secretory’ diarrhoea (watery
diarrhoea without blood or faecal leucocytes reflecting SB dysfunction).

3. Acute diarrhea:
 In general, the time from ingestion to the onset of symptoms is short&
other than dehydration, little systemic upset occurs.
 Other organisms,as Shigella spp., Campylobacter spp&EHEC, may
directly invade the mucosa of the small bowel or produce cytotoxins that
cause mucosal ulceration, typically affecting the terminal SB& colon.
 The incubation period is longer& more systemic upset occurs, with
prolonged bloody diarrhoea.
 Salmonella spp. are capable of invading enterocytes& of causing both a
secretory response&invasive disease with systemic features, seen with
Salmonella Typhi& Salmonella Paratyphi (enteric fever), but may
occasionally be seen with other non-typhoidal Salmonella spp., particularly
in the immunocompromised host& the elderly.

4. Acute diarrhea:clin evaluation
 The history should address foods ingested, duration& frequency of
diarrhoea, presence of blood or steatorrhoea, abdominal pain& tenesmus,
&whether other people have been affected.
 Fever&bloody diarrhoea suggest an invasive, colitic, dysenteric process.
 An incubation period of < 18 hours suggests toxin-mediated food
poisoning,>5 days suggests diarrhoea caused by protozoa or helminths.
 Person-to-person spread suggests certain infections, as shigellosis or
cholera.
 Examination includes assessment of the degree of dehydration.
 Assessment for early signs of hypotension, such as thirst,headache, altered
skin turgor, dry mucous membranes&postural hypotension, is important,
particularly in tropical regions where dehydration progresses rapidly.
 Signs of more marked dehydration include supine hypotension &
tachycardia,decreased urinary output, delirium& sunken eyes.
 The blood pressure, pulse rate, urine output& ongoing stool losses should
be monitored closely

5. Acute diarrhea:clin evaluation
 The severity of diarrhoea may be assessed by reference to the Bristol stool
form scale (Bristol stool chart), which allows an objective assessment of
stool consistency by providing a verbal/ visual reference scale.
 The Bristol stool form scale was developed monitor patients with irritable
bowel syndrome, but its main use is to monitor hospital inpatients with
loose stool to assist in decisions on stool sampling& infection prevention
precautions, especially in relation to C. difficile.

6. Acute diarrhea:Investigations
 These include stool inspection for blood/ microscopy for leucocytes, ova,
cysts,parasites if the history indicates residence or travel to areas where
these infections are prevalent.
 Stool culture should be performed &C. difficile toxin sought.
 FBC/ serum electrolytes indicate the degree of inflammation&
dehydration.
 Where cholera is prevalent, examination of a wet film with dark-field
microscopy for darting motility may provide a diagnosis.
 In a malarious area, a blood film for malaria parasites should be obtained.
 Blood/urine cultures& a chest X-ray may identify alternative sites of
infection, particularly if the clinical features suggest a syndrome other than
gastroenteritis.

7. Acute diarrhea:Management
 All patients with acute, potentially infective diarrhoea should be
appropriately isolated to minimise person-to-person spread of infection.
 If the history suggests a food-borne source, public health measures must be
implemented to identify the source& to establish whether other linked
cases exist.

8. Acute diarrhea:Management
 Fluid replacement:
 Replacement of fluid losses in diarrhoeal illness is crucial& life-saving.
 Although normal daily fluid intake in an adult is only 1–2 L, there is
considerable additional fluid movement in/ out of the gut in secretions.
 Altered gut resorption with diarrhoea can result in substantial fluid loss;
for example, 10–20 L of fluid may be lost in 24 hours in cholera.
 The fluid lost in diarrhoea is isotonic, so both water/ electrolytes need to be
replaced.
 Absorption of electrolytes from gut is active process requiring energy.
 Infected mucosa is capable of very rapid fluid/ electrolyte transport if
carbohydrate is available as an energy source.

9. Acute diarrhea:Management
 Oral rehydration solutions (ORS)
 Contain sugars, water& electrolytes
 ORS can be just as effective as IV replacement fluid, even in the
management of cholera.
 In mild to moderate GEitis, adults should be encouraged to drink fluids, if
possible, continue normal dietary food intake.
 If this is impossible – due to vomiting, for example – IVF will be required.
 In very sick patients or those with cardiac or renal disease, monitoring of
UO&CVP may be necessary.
 The volume of fluid replacement required should be estimated based on
the following considerations:
 Replacement of established deficit:After 48 hs of moderate diarrhoea (6–10
stools/24 hrs), the average adult will be 2–4 L depleted from diarrhoea
alone &associated vomiting will compound this.

10. Acute diarrhea:Management
 Adults with this symptomatology should therefore be given rapid
replacement of 1–1.5 L, either orally ORS or by IV infusion (normal
saline), within the first 2–4 hours of presentation.
 Longer symptomatology or more persistent/severe diarrhoea rapidly
produces fluid losses comparable to diabetic ketoacidosis& a metabolic
emergency requiring active intervention.
 Replacement of ongoing losses.
 The average adult’s diarrhoeal stool accounts for a loss of 200 mL of
isotonic fluid.
 Stool losses should be carefully charted&estimate of ongoing replacement
fluid calculated.
 Commercially available rehydration sachets are conveniently produced to
provide 200 mL of ORS; one sachet per diarrhoea stool is an appropriate
estimate of supplementary replacement requirements.
 Replacement of normal daily req:The average adult has a daily 1–1.5 L of
fluid+ calculations above, increased substantially in fever or a hot envir.

11. Acute diarrhea:Management
 Antimicrobials: non-specific gastroenteritis, routine use of antimicrobials
does not improve outcome& lead to antimicrobial resistance or side-effects.
 They are usually used where there is systemic involvement, a host with
immunocompromise or significant comorbidity.
 Evidence suggests that, in EHEC infections, the use of antibiotics may
make the complication of HUS more likely due to increased toxin release.
 Conversely, antibiotics are indicated in Shigella dysenteriae infection& in
invasive salmonellosis – in particular, typhoid fever.
 Antibiotics may also be advantageous in cholera epidemics, reducing
infectivity& controlling the spread of infection.

12. Acute diarrhea:Management
 Antimicrobial-associated diarrhoea (AAD) is a common complication of
antimicrobial therapy, especially with broad spectrum agents.
 It is most common in the elderly but can occur at all ages.
 Although the specific mechanism is unknown in most cases of AAD, C.
difficile is implicated in 20–25% of cases& is the most common cause
among patients with evidence of colitis.
 C. perfringens is a rarer cause that usually remains undiagnosed&
Klebsiella oxytoca may also cause antibiotic-associated haemorrhagic
colitis.