Thedi.problem 2A

8/13/2019 Thedi.problem 2A

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Problem 2A

GIT

Thedi Darma Wijaya

405090120Group 18


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LO 1

Diarrhea


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Definition

Diarrhea is loosely defined as passage ofabnormally liquid or unformed stools at an

increased frequency.

For adults on a typical Western diet, stoolweight >200 g/d can generally be considered

diarrheal..


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Epidemiology


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Risk Factor Travelers.

most commonly due to enterotoxigenic or enteroaggregativeEscherichia colias well as to Campylobacter, Shigella,Aeromonas,norovirus, Coronavirusand Salmonella.

Consumers o f cer tain foods.

may suggest infection with Salmonella, Campylobacter, or Shigellafrom chicken; enterohemorrhagic E. coli(O157:H7) from undercooked

hamburger; Bacillus cereusfrom fried rice; Staphylococcus aureusorSalmonellafrom mayonnaise or creams; Salmonellafrom eggs; andVibriospecies, Salmonella

Imm unodefic ient p erson s.

opportunistic infections, such as by Mycobacteriumspecies, certainviruses (cytomegalovirus, adenovirus, and herpes simplex), and

protozoa (Cryptosporidium, Isospora belli, Microsporida, andBlastocystis hominis)

Daycare attendees and their family m embers.

Infections with Shigella, Giardia, Cryptosporidium, rotavirus, and otheragents are very common and should be considered.

Ins t i tut ional ized person s.

the causes are a variety of microorganisms but most commonly C.difficile.


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Classification Based on Time (WGO)

acuteif 2 weeks in duration

Based on pathophysiology Osmotic

Secretory Inflammatory

Altered motility

Malabsorption

Based on Severity Mild diarrhea

Severe diarrhea

Based on etiology

Infection Organic


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Pathophysiology

Kenneth W Simpson BVM&S, PhD, MRCVS, DipACVIM, DipECVIMCollege of Veterinary Medicine, Cornell University Ithaca NY


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Pathophysiology Osmoticdiarrhea is considered to arise as a consequence of

water retention by unabsorbed substances in the intestinallumen

e.g. secondary to maldigestion or malabsorption.

Secretorydiarrhea is caused by hypersecretion of fluids andelectrolytes by the villus crypts

e.g. in response to stimulation by E.Coli. Permeabilitydiarrhea is characterised by increased leakiness

of the intestine due to decreased mucosal integrity or increasedintestinal hydrostatic pressure

e.g. mucosal inflammation or infiltration may decrease

mucosal integrity, whereas lymphatic obstruction or portalhypertension increase hydrostatic pressure.

Motilitydisorders are poorly characterised, but diarrhea ismore often a result of decreased segmental motility, rather thanhypermotility.


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Etiology

Acute Diarrhea

More than 90% of cases of acute diarrhea arecaused by infectious agents

The remaining 10% or so are caused by

medications, toxic ingestions, ischemia, and otherconditions.

Infectious Agents acquired by fecal-oral transmission or, more commonly,

via ingestion of food or water contaminated withpathogens from human or animal feces

Disturbances of flora by antibiotics can lead to diarrheaby reducing the digestive function or by allowing theovergrowth of pathogens, such as Clostridium difficile


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Gastrointestinal Pathogens Causing Acute Diarrhea

Mechanism Locatio

n

Illness Stool Findings Examples of Pathogens

Involved

Noninflamm

atory(enterotoxin)

Proximal

smallbowel

Watery

diarrhea

No fecal leukocytes; mild or

no increase in fecallactoferrin

Vibrio cholerae, enterotoxigenic

Escherichia coli(LT and/or ST),enteroaggregative E. coli,

Clostridium perfringens, Bacillus

cereus, Staphylococcus aureus,

Aeromonas hydrophila,

Plesiomonas shigelloides,

rotavirus, norovirus, enteric

adenoviruses, Giardia lamblia,Cryptosporidiumspp.,

Cyclosporaspp., microsporidia

Inflammator

y (invasion

or cytotoxin)

Colon or

distal

small

bowel

Dysentery

or

inflammator

y diarrhea

Fecal polymorphonuclear

leukocytes; substantial

increase in fecal lactoferrin

Shigellaspp., Salmonellaspp.,

Campylobacter jejuni,

enterohemorrhagic E. coli,

enteroinvasive E. coli, Yersinia

enterocolitica, Vibrioparahaemolyticus, Clostridium

difficile, ?A. hydrophila, ?P.

shigelloides, Entamoeba

histolytica

Penetrating Distal

small

bowel

Enteric

fever

Fecal mononuclear

leukocytes

Salmonella typhi, Y.

enterocolitica, ?Campylobacter

fetus


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Association between Pathobiology of Causative Agents and Clinical Features in

Acute Infectious Diarrhea

Pathobiology/Agents Incubatio

n Period

Vo

miti

ng

Abdomi

nal Pain

F

e

v

er

Diarrhea

Toxin producers

Preformed toxin

Bacillus cereus, Staphylococcus aureus, 18 h 3

4+

12+ 0

1

+

34+, watery

Clostridium perfringens 824 h

Enterotoxin

Vibrio cholerae, enterotoxigenic Escherichia coli,

Klebsiella pneumoniae,Aeromonasspecies

872 h 2

4+

12+ 0

1

+

34+, watery

Enteroadherent

Enteropathogenic and enteroadherent E. coli,

Giardiaorganisms, cryptosporidiosis, helminths

18 d 0

1+

13+ 0

2

+

12+, watery, mushy


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Cytotoxin-producers

Clostridium difficile 13 d 0

1+

34+ 1

2

+

13+, usually watery,

occasionally bloody

Hemorrhagic E. coli 1272 h 0

1+

34+ 1

2

+

13+, initially watery,

quickly bloody

Invasive organisms

Minimal inflammation

Rotavirus and Norwalk agent 13 d 1

3+

23+ 3

4

+

13+, watery

Variable inflammation

Salmonella, Campylobacter, andAeromonas

species, Vibrio parahaemolyticus, Yersinia

12 h11 d 0

3+

24+ 3

4

+

14+, watery or bloody

Severe inflammation

Shigellaspecies, enteroinvasive E. coli,

Entamoeba histolytica

12 h8 d 0

1+

34+ 3

4

+

12+, bloody

Source:Adapted from DW Powell, in T Yamada (ed): Textbook of Gastroenterology and Hepatology, 4th

ed. Philadelphia, Lippincott Williams & Wilkins, 2003; and DR Syndman, in SL Gorbach (ed): Infectious

Diarrhea. London, Blackwell, 1986.


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Etiology

Acute Diarrhea Other Causes

Side effects from medications

Occlusive or nonocclusive ischemic colitistypically occurs

in persons >50 years colonic diverticulitisand graft-versus-host disease.

ingestion of toxins including organophosphate

insecticides, amanita and other mushrooms, arsenic, and

preformed environmental toxins in seafood, such asciguatera and scombroid.


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Etiology Chronic Diarrhea

In contrast to acute diarrhea, most of the causes of chronic diarrhea are

noninfectious

Major Causes of Chronic Diarrhea According to Predominant Pathophysiologic Mechanism

Secretory causes

Exogenous stimulant laxatives

Chronic ethanol ingestion

Other drugs and toxins

Endogenous laxatives (dihydroxy bile acids)

Idiopathic secretory diarrhea

Certain bacterial infections

Bowel resection, disease, or fistula ( decrease of absorption)

Partial bowel obstruction or fecal impaction

Hormone-producing tumors (carcinoid, VIPoma, medullary cancer of thyroid, mastocytosis,

gastrinoma, colorectal villous adenoma)

Addison's disease

Congenital electrolyte absorption defectsOsmotic causes

Osmotic laxatives (Mg2+, PO43, SO4

2)

Lactase and other disaccharide deficiencies

Nonabsorbable carbohydrates (sorbitol, lactulose, polyethylene glycol)

Steatorrheal causes

Intraluminal maldigestion (pancreatic exocrine insufficiency, bacterial overgrowth, bariatric surgery,

liver disease)

Mucosal malabsorption (celiac sprue, Whipple's disease, infections, abetalipoproteinemia, ischemia)

Post-mucosal obstruction (1 or 2 lymphatic obstruction)


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Inflammatory causes

Idiopathic inflammatory bowel disease (Crohn's, chronic ulcerative colitis)

Lymphocytic and collagenous colitis

Immune-related mucosal disease (1 or 2 immunodeficiencies, food allergy,eosinophilic gastroenteritis, graft-vs-host disease)

Infections (invasive bacteria, viruses, and parasites, Brainerd diarrhea)

Radiation injury

Gastrointestinal malignancies

Dysmotile causes

Irritable bowel syndrome (including post-infectious IBS)Visceral neuromyopathies

Hyperthyroidism

Drugs (prokinetic agents)

Postvagotomy

Factitial causes

MunchausenEating disorders

Iatrogenic causes

Cholecystectomy

Ileal resection

Bariatric surgery

Vagotomy, fundoplication


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Secretory Causes

Secretory diarrheas are due to derangements in fluid andelectrolyte transport across the enterocolonic mucosa.

They are characterized clinically by watery, large-volumefecal outputs that are typically painless and persist withfasting.

Because there is no malabsorbed solute, stool osmolality isaccounted for by normal endogenous electrolytes with nofecal osmotic gap.

Osmotic Causes

Osmotic diarrhea occurs when ingested, poorly absorbable,osmotically active solutes draw enough fluid into the lumento exceed the reabsorptive capacity of the colon.

Fecal water output increases in proportion to such a soluteload. Osmotic diarrhea characteristically ceases with fastingor with discontinuation of the causative agent.


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Steatorrheal Causes Fat malabsorption may lead to greasy, foul-smelling, difficult-

to-flush diarrhea often associated with weight loss andnutritional deficiencies due to concomitant malabsorption ofamino acids and vitamins.

stool fat exceeding the normal 7 g/d; Inflammatory Causes

accompanied by pain, fever, bleeding, or othermanifestations of inflammation.

The unifying feature on stool analysis is the presence ofleukocytes or leukocyte-derived proteins such ascalprotectin.

With severe inflammation, exudative protein loss can lead toanasarca (generalized edema).


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Dysmotility Causes

Stool features often suggest a secretory diarrhea,but mild steatorrhea of up to 14 g of fat per day canbe produced by maldigestion from rapid transitalone.

The exceedingly common irritable bowel syndromeis characterized by disturbed intestinal and colonicmotor and sensory responses to various stimuli.Symptoms of stool frequency typically cease atnight, alternate with periods of constipation, areaccompanied by abdominal pain relieved withdefecation, and rarely result in weight loss or truediarrhea.


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Approach to

the Patient


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Approach to the Patient History

1.Diarrhea lasting >2 weeks is generally defined as chronic

2.Fever often implies invasive disease, although fever and diarrhea may also result frominfection outside the gastrointestinal tract, as in malaria.

3.Stools that contain blood or mucus indicate ulceration of the large bowel.

Bloody stools without fecal leukocytes should alert the laboratory to the possibility ofinfection with Shiga toxinproducing enterohemorrhagic Escherichia coli.

Bulky white stools suggest a small-intestinal process that is causing malabsorption.

Profuse "rice-water" stools suggest cholera or a similar toxigenic process.

4.Frequent stools over a given period can provide the first warning of impending dehydration.

5.Abdominal pain may be most severe in inflammatory processes like those due to Shigella,Campylobacter, and necrotizing toxins.

Painful abdominal muscle cramps, caused by electrolyte loss, can develop in severe casesof cholera.

Bloating is common in giardiasis.

An appendicitis-like syndrome should prompt a culture for Yersinia enterocoliticawith coldenrichment.

6.Tenesmus (painful rectal spasms with a strong urge to defecate but little passage of stool)may be a feature of cases with proctitis, as in shigellosis or amebiasis.

7.Vomiting implies an acute infection (e.g., a toxin-mediated illness or food poisoning) but canalso be prominent in a variety of systemic illnesses (e.g., malaria) and in intestinal obstruction.

8.Asking patients whether anyone else they know is sick is a more efficient means ofidentifying a common source than is constructing a list of recently eaten foods

9.Current antibiotic therapy or a recent history of treatment suggests Clostridium difficilediarrhea Antibiotic use may increase the risk of other infections, such as salmonellosis.


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Approach to the Patient

Physical Examination

The examination of patients for signs of dehydrationprovides essential information about the severity ofthe diarrheal illness and the need for rapid therapy.

Mild dehydration is indicated by thirst, dry mouth,decreased axillary sweat, decreased urine output,and slight weight loss.

Signs of moderate dehydration include an

orthostatic fall in blood pressure, skin tenting, andsunken eyes (or, in infants, a sunken fontanelle).

Signs of severe dehydration range fromhypotension and tachycardia to confusion and frank

shock.


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Approach to the Patient Diagnostic Approach

After the severity of illness is assessed, the clinician must distinguishbetween inflammatoryand noninflammatorydisease.

Using the history and epidemiologic features of the case as guides, theclinician can then rapidly evaluate the need for further efforts to define aspecific etiology and for therapeutic intervention.

Examination of a stool sample may supplement the narrative history. Grossly bloody or mucoid stool suggests an inflammatory process.

A test for fecal leukocytes (preparation of a thin smear of stool on a glassslide, addition of a drop of methylene blue, and examination of the wetmount) can suggest inflammatory disease in patients with diarrhea,although the predictive value of this test is still debated.

A test for fecal lactoferrin, which is a marker of fecal leukocytes, is moresensitive and is available in latex agglutination and enzyme-linkedimmunosorbent assay formats.

Approach to the


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Approach to thePatient: AcuteDiarrhea


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Approach to the Patient Laboratory Evaluation

Potentially pathogenic E. colicannot be distinguished from normal fecal flora by routine culture,and tests to detect enterotoxins are not available in most clinical laboratories.

In situations in which cholera is a concern, stool should be cultured on thiosulfatecitratebilesaltssucrose (TCBS) agar.

A latex agglutination test has made the rapid detection of rotavirus in stool practical for manylaboratories

At least three stool specimens should be examined for Giardiacysts or stained forCryptosporidiumif the level of clinical suspicion regarding the involvement of these organisms is

high. Salmonellaand Shigellacan be selected on MacConkey's agar as non-lactose-fermenting

(colorless) colonies or can be grown on Salmonella-Shigellaagar or in selenite enrichmentbroth, both of which inhibit most organisms except these pathogens.

C. difficile; stool culture for other pathogens in this setting has an extremely low yield and is notcost-effective. Toxins A and B produced by pathogenic strains of C. difficilecan be detected by rapid enzyme

immunoassays and latex agglutination tests.

Isolation of C. jejunirequires inoculation of fresh stool onto selective growth medium andincubation at 42C in a microaerophilic atmosphere.

E. coliO157:H7 is among the most common pathogens isolated from visibly bloody stools.Strains of this enterohemorrhagic serotype can be identified in specialized laboratories byserotyping but also can be identified presumptively in hospital laboratories as lactose-fermenting, indole-positive colonies of sorbitol nonfermenters (white colonies) on sorbitolMacConkey plates.

Fresh stools should be examined for amebic cysts and trophozoites.


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C. Difficile

Clostridium difficile gram-positive, anaerobic, spore-forming bacillus that is

responsible for the development of antibiotic-associated diarrheaand colitis.

C difficilewas first described in 1935 as a component of the fecal

flora of healthy newborns and was initially not thought to be apathogen.

It was named difficilebecause it grows slowly and is difficult toculture.

While early investigators noted that the bacterium produced a

potent toxin, the role of C difficilein antibiotic-associateddiarrhea and pseudomembranous colitis

C difficileinfection commonly manifests as mild-to-moderatediarrhea, occasionally with abdominal cramping


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Endoscopic visualization of pseudomembranous colitis, a characteristic

manifestation of full-blown Clostridium difficile colitis. Classic pseudomembranes are

visible as raised yellow plaques ranging from 2-10 mm in diameter and scattered

over the colorectal mucosa. Courtesy of Gregory Ginsberg, MD, University of

Pennsylvania


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Pathophysiology

C difficilecolitis results from a disturbance of the normalbacterial flora of the colon, colonization with C difficile, andrelease of toxins that cause mucosal inflammation and damage

Pathogenic strains of C difficileproduce 2 distinct toxins.

Toxin A is an enterotoxin, and toxin B is a cytotoxin. Both are highmolecular weight proteins capable of binding to

specific receptors on the intestinal mucosal cells.

Receptor-bound toxins gain intracellular entry where they

catalyze a specific alteration of Rho proteins, small glutamyltranspeptidase (GTP)binding proteins that assist in actinpolymerization, cytoskeletal architecture, and cell movement.

Both toxin A and toxin B appear to play a role in thepathogenesis of C difficilecolitis in humans.


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Signs and Symptoms

Usually occurs approx 5-10 days after

ant ib iot ic use but can be anywhere from 1

day to 2 months Mild-to-moderate watery diarrhea that is rarely

bloody

Cramping abdominal pain

Nausea and vom it ing is rare

Sepsis (rare)

Acute abdomen (rarer)


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Physical Physical examination may reveal the following:

Fever

Dehydration

Lower abdominal tenderness

Rebound tenderness - Raises the possibility of colonic perforationand peritonitis

Laboratory Studies CBC count

Leukocytosis may be present.

Stool examination Stool may be hemoccult positive in severe colitis, but grossly bloody

stools are unusual.

Fecal leukocytes are present in about half of the cases.

Enzyme immunoassay for detecting toxins A and B is usedin most labs. The sensitivity is moderate (79-80%) andspecificity is excellent (98%)


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Post-Diarrhea ComplicationsPost-Diarrhea Complications of Acute Infectious Diarrheal Illness

Complication Comments

Chronic diarrhea Occurs in ~1% of travelers with acute diarrhea

Lactase deficiency

Small-bowel bacterial overgrowth Protozoa account for ~ of cases

Malabsorption syndromes (tropical and

celiac sprue)

Initial presentation or exacerbation of inflammatory

bowel disease

May be precipitated by traveler's diarrhea

Irritable bowel syndrome Occurs in ~10% of travelers with traveler's diarrhea

Reiter's syndrome (reactive arthritis) Particularly likely after infection with invasive

organisms (Shigella, Salmonella, Campylobacter)

Hemolytic-uremic syndrome (hemolytic anemia,

thrombocytopenia, and renal failure)

Follows infection with Shiga toxinproducing bacteria

(Shigella dysenteriaetype 1 and enterohemorrhagic

Escherichia coli)


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Treatment Acute Diarrhea: Treatment

Fluid and electrolyte replacement are of central importance to all forms ofacute diarrhea.

In moderately severe nonfebrile and nonbloody diarrhea, antimotility andantisecretory agents such as loperamide can be useful adjuncts to controlsymptoms.

Bismuth subsalicylate may reduce symptoms of vomiting and diarrhea

Judicious use of antibiotics is appropriate in selected instances of acutediarrhea and may reduce its severity and duration

Many physicians treat moderately to severely ill patients with febriledysentery empirically without diagnostic evaluation using a quinolone, suchas ciprofloxacin (500 mg bid for 35 d).

Empirical treatment can also be considered for suspected giardiasis with

metronidazole (250 mg qid for 7 d). Antibiotic prophylaxis is indicated for certain patients traveling to high-risk

countries in whom the likelihood or seriousness of acquired diarrhea wouldbe especially high, including those with immunocompromise, IBD,hemochromatosis, or gastric achlorhydria. Use oftrimethoprim/sulfamethoxazole, ciprofloxacin, or rifaximin may reducebacterial diarrhea in such travelers by 90%, though rifaximin may not besuitable for invasive disease..


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Chronic Diarrhea: Treatment

Treatment of chronic diarrhea depends on the specific etiologyand may be curative, suppressive, or empirical.

Resection of a colorectal cancer, antibiotic administration forWhipple's disease, or discontinuation of a drug.

Elimination of dietary lactose for lactase deficiency or gluten forceliac sprue, use of glucocorticoids or other anti-inflammatoryagents for idiopathic IBDs, adsorptive agents such ascholestyramine for ileal bile acid malabsorption, proton pumpinhibitors such as omeprazole for the gastric hypersecretion of

gastrinomas, somatostatin analogues such as octreotide formalignant carcinoid syndrome, prostaglandin inhibitors such asindomethacin for medullary carcinoma of the thyroid, andpancreatic enzyme replacement for pancreatic insufficiency


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Prophylaxis Improvements in hygiene to limit fecal-oral spread of enteric

pathogens Travelers can reduce their risk of diarrhea by eating only hot,

freshly cooked food; by avoiding raw vegetables, salads, andunpeeled fruit; and by drinking only boiled or treated water andavoiding ice. Historically, few travelers to tourist destinations

adhere to these dietary restrictions. Bismuth subsalicylate is an inexpensive agent for theprophylaxis of traveler's diarrhea; it is taken at a dosage of 2tablets (525 mg) four times a day.

The possibility of exerting a major impact on the worldwide

morbidity and mortality associated with diarrheal diseases hasled to intense efforts to develop effective vaccines against thecommon bacterial and viral enteric pathogens.

Recent research has yielded promising advances in thedevelopment of vaccines against rotavirus, Shigella, V.cholerae, S. typhi, and enterotoxigenic E. coli.


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LO 2

Dehydration


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Background

Dehydration describes a state of negative fluid

balance that may be caused by numerous

disease entities.

Diarrheal illnesses are the most common

etiologies.

Worldwide, dehydration secondary to diarrheal

illness is the leading cause of infant and child

mortality.


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Epidemiology

International

Diarrheal illnesses with subsequent dehydration

account for nearly 4 million deaths per year in

infants and children.

The overwhelming majority of these deaths

occur in developing nations.

Age

Children younger than 5 years are at the

highest risk.


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Causes

Common causes

Gastroenteritis: This is the most common cause of

dehydration

Stomatitis: Pain may severely limit oral intake.

Diabetic ketoacidosis (DKA): Dehydration is caused

by osmotic diuresis.

Febrile illness: Fever causes increased insensible

fluid losses and may affect appetite. Pharyngitis: This may decrease oral intake.


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Causes Life-threatening causes

Gastroenteritis DKA

Burns: Fluid losses may be extreme. Very aggressive fluidmanagement is required

GI obstruction: This is often associated with poor intake andemesis. Bowel ischemia can result in extensive capillary leakand shock.

Heat stroke: Hyperpyrexia, dry skin, and mental statuschanges may occur.

Cystic fibrosis: This results in excessive sodium and chloridelosses in sweat, placing patients at risk for severehyponatremic hypochloremic dehydration.

Diabetes insipidus: Excessive output of very dilute urine canresult in large free water losses and severe hypernatremicdehydration.


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Hormonal regulation of body water


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Pathophysiology

The negative fluid balance that causes dehydration results from

decreased intake, increased output (renal, GI, or insensiblelosses), or fluid shift (ascites, effusions, and capillary leak

states such as burns and sepsis).

The decrease in total body water causes reductions in both the

intracellular and extracellular fluid volumes. Young children are more susceptible to dehydration due to

larger body water content, renal immaturity, and inability to

meet their own needs independently.

Older children show signs of dehydration sooner than infantsdue to lower levels of extracellular fluid (ECF).


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Classification Based on pathophysiology, dehydration can be categorized

according to osmolarity and severity. According to osmolarity:

isonatremic (130-150 mEq/L),

occurs when the lost fluid is similar in sodium concentration to the blood.Sodium and water losses are of the same relative magnitude in both the

intravascular and extravascular fluid compartments. hyponatremic (< 130 mEq/L),

occurs when the lost fluid contains more sodium than the blood (loss ofhypertonic fluid). Relatively more sodium than water is lost.

Because the serum sodium is low, intravascular water shifts to theextravascular space, exaggerating intravascular volume depletion for a given

amount of total body water loss. hypernatremic (>150 mEq/L).

occurs when the lost fluid contains less sodium than the blood (loss ofhypotonic fluid). Relatively less sodium than water is lost.

Because the serum sodium is high, extravascular water shifts to theintravascular space, minimizing intravascular volume depletion for a givenamount of total body water loss.


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Approach to the Patient History

The following should be considered in patients with dehydration: Intake of fluids, including the volume, type (hypertonic or hypotonic), andfrequency

Urine output, including the frequency of voiding (last wet diaper), presence ofconcentrated or dilute urine, hematuria

Stool output, frequency of stools, stool consistency, presence of blood or mucusin stools

Emesis, including frequency and volume and whether bilious or nonbilious,hematemesis

Contact with ill people, especially others with gastroenteritis, use of daycare

Underlying illnesses, especially cystic fibrosis, diabetes mellitus, hyperthyroidism,renal disease

Fever

Appetite patterns Weight loss

Travel

Recent antibiotic use

Possible ingestions


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Clinical Findings of Dehydration

Symptom/Sign Mild Dehydration Moderate Dehydration Severe Dehydration

level of consciousness Alert Lethargic Obtunded

Capillary refill* 2 s 2-4 s >4 s, cool limbs

Mucous membranes Normal Dry Parched, crackedTears Normal Decreased Absent

Heart rate Slightly increased Increased Very increased

Respiratory rate/pattern* Normal Increased Increased and hyperpnea

Blood pressure Normal Normal, but orthostasis Decreased

Pulse Normal Thready Faint or impalpable

Skin turgor* Normal Slow Tenting

Fontanel Normal Depressed Sunken

Eyes Normal Sunken Very sunken

Urine output Decreased Oliguria Oliguria/anuria


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Estimated Fluid Deficit

Severity Infants (weight < 10 kg) Children (weight >10 kg)

Mild dehydration 5% or 50 mL/kg 3% or 30 mL/kg

Moderate dehydration 10% or 100 mL/kg 6% or 60 mL/kg

Severe dehydration 15% or 150 mL/kg 9% or 90 mL/kg


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J.Fortin & M.A. Parent.

Tropical Pediatrics &

Environmental ChildHealth.pg 110

A h h P i


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Procedures

Intravenous line

If severe dehydration is present, peripheral intravenous line insertion

may be difficult.

The preferred sites for initial insertion attempts include the basilic and

cephalic veins in the antecubital fossa and the saphenous veins nearthe ankle.

If peripheral intravenous access cannot be rapidly achieved (< 90 s)

in a child with severe dehydration and shock, intraosseous

cannulation should be attempted.

Orogastric/nasogastric tube: An orogastric/nasogastric tube may be inserted to facilitate enteral

rehydration in children with mild-to-moderate dehydration.

These tubes should be considered to assist in the nutritional recovery

of children who are critically ill or severely dehydrated.


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intraosseous cannulation

T t t


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Treatment Oral rehydration solutionsComposition of Appropriate Oral Rehydration Solutions

SolutionCarbohydrate

(g/dL)

Sodium

(mEq/L)

Potassium

(mEq/L)

Base

(mEq/L)

Osmolali

ty

Pedialyte 2.5 45 20 30 250

Infalyte 3 50 25 30 200

Rehydralyte 2.5 75 20 30 310

WHO/UNICE

F*

2 90 20 30 310

Composition of Inappropriate Oral Rehydration Solutions

SolutionCarbohydrate

(g/dL)

Sodium

(mEq/L)

Potassium

(mEq/L)

Base

(mEq/L)

Osmolal

ityApple juice 12 0.4 26 0 700

Ginger ale 9 3.5 0.1 3.6 565

Milk 4.9 22 36 30 260

Chicken

broth

0 2 3 3 330


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Rehydration protocols:

Mild: 50cc/kg of ORS plus replacement over 4 hours**

begin with 5cc aliquots q1-2 min with volumes increasing as tolerated

Moderate: 100cc/kg of ORS plus replacement over 4 hours

As for mild, but should be in supervised setting

Severe: 20cc/kg of isotonic IV fluids over one hour

Repeat as necessary

Continue replacement for stools

** ongoing losses can be matched at approximately 10cc/kg foreach stool


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Diet

Breast-feeding should be resumed as soon as possible.

Foods that contain complex carbohydrates (eg, rice, wheat,potatoes, bread, cereals), lean meats, fruits, and vegetablesare encouraged.

Fatty foods and simple carbohydrates should be avoided. Probiotics

Normally, gut flora (saccharolytic bacteria) ferment dietarycarbohydrates that have not been absorbed. Diarrhea

reduces fecal flora. Probiotics (e.g. Lactobacillus GG) alter the composition of

gut flora and assist in restoring normal gut function.

More studies are supporting the use of probiotics,specifically Lactobacillus GG, as an adjuvant therapy in

AGE.


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Fauci, Braunwald,Lipincolt,etc.Harrisons

Principle Internal Medicine.17thed.chpter

40&122

http://pediatrics.uchicago.edu/chiefs/inpatient/A

cuteGE.htm

http://emedicine.medscape.com/
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