dr.farzin khorvash. dr farzin khorvash dr.farzin khorvash
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Dr.Farzin khorvash
Dr Farzin Khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Enteric Host Defenses
• Host species, genotype, and age
• Personal hygiene
• Gastric acidity and other physical barriers
• Intestinal motility
• Enteric microflora
• Specific immunity
• Phagocytic
• Humoral
• Cell–mediated
• Nonspecific protective factors and human milk
• Intestinal receptorsDr.Farzin khorvash
MICROBIAL FACTORS
• Toxins • Attachment • Invasiveness
Dr.Farzin khorvash
Gastrointestinal infections
•exception of Helicobacter pylori gastritis• noninflammatory ; syndromes of diarrhea or vomiting that tend to involve infection in the upper small bowel • inflammatory infection in the colon.• Other enteric infections and infestations cause predominantly systemic symptoms.
Dr.Farzin khorvash
MECANISM
• (1) a shift in the delicate balance of bidirectional water and electrolyte fluxes in the upper small bowel by intraluminal toxins or minimally invasive organisms
• (2) inflammatory destruction of the ileal or colonic mucosa
• (3) penetration through an intact mucosa to the reticuloendothelial system. Dr.Farzin khorvash
Infectious Doses of Enteric Pathogens
Shigella 10 to 102
Campylobacter jejuni 102 to 106
Salmonella 105
Escherichia coli 108
Vibrio cholerae 108
Giardia lamblia 10 to 102 cysts
Entamoeba histolytica 10 to 102 cysts
Cryptosporidium parvum 1 to 103 oocysts
Dr.Farzin khorvash
ACUTE NONINFLAMMATORY DIARRHEA IN ADULTS
• Rotaviruses• Norwalk-like viruses• adenoviruses• Coxsackieviruses• toxigenic Clostridium difficile • food poisoning such as Clostridium
perfringens, Bacillus cereus, or Staphylococcus aureus
• cholera • undercooked shellfish • enterotoxigenic E. coli
Dr.Farzin khorvash
ACUTE NAUSEA AND VOMITING (WINTER VOMITING DISEASE)
• acute nausea and vomiting• “intestinal flu,” or “viral
gastroenteritis” • commonly occurs in winter months
in temperate climates
Dr.Farzin khorvash
• Norwalk-like viruses (including Norwalk or Montgomery County agent and Hawaii, Snow Mountain, and Taunton agents)
• caliciviruses • astroviruses• enteroviruses (especially echovirus types 11,
14, and 18)• enteric adenoviruses • human coronaviruses • Pestiviruses• toroviruses • Picobirnaviruse
Dr.Farzin khorvash
DIFFERENTIAL DIAGNOSIS OF ACUTE NONINFLAMMATORY DIARRHEA
• osmotic diuresis nonabsorbable agents such as sorbitol , Ipecac fluid
• Heavy metal poisoning (with As, Sn, Fe, Cd, Hg, Pb)
• non–b-islet cell tumors, medullary carcinoma of the thyroid, carcinoid tumors, vasoactive intestinal polypeptide
• thyrotoxicosis and adrenal or parathyroid insufficiency
• lactase deficiency and pancreatic or biliary insufficiency
• HUS with or without enterohemorrhagic E. coli O157:H7
• dermatitis herpetiformisDr.Farzin khorvash
CHRONIC NONINFLAMMATORY DIARRHEA
• Giardiasis• tropical spruelike syndromes• syndromes of bacterial
“overgrowth,”• Cryptosporidium • I. belli infection
Dr.Farzin khorvash
ACUTE DYSENTERY
• fecal blood and pus have • frequent, small bowel movements• blood and mucus • tenesmus • pain on defecation• an inflammatory invasion of the
colonic mucosa resulting from bacterial, cytotoxic, or parasitic destruction.
Dr.Farzin khorvash
• Bacillary dysentery (Shigella dysenteriae, Shigella flexneri, Shigella sonnei, Shigella boydii; invasive Escherichia coli)
• Campylobacteriosis (Campylobacter jejuni)• Amebic dysentery (Entamoeba histolytica)• Ciliary dysentery (Balantidium coli)• Bilharzial dysentery (Schistosoma japonicum, Schistosoma
mansoni)• Other parasitic infections (Trichinella spiralis)• Vibriosis (Vibrio parahaemolyticus)• Salmonellosis (Salmonella typhimurium)• Typhoid fever (Salmonella typhi)• Enteric fever (Salmonella choleraesuis, Salmonella paratyphi)• Yersiniosis (Yersinia enterocolitica)• Spirillar dysentery (Spirillum spp.)• Proctitis• Gonococcal (Neisseria gonorrhoeae)• Herpetic (herpes simplex virus)• Chlamydial (Chlamydia trachomatis)• Syphilitic (Treponema pallidum)• Other syndromes• Necrotizing enterocolitis of the newborn• Enteritis necroticans• Pseudomembranous enterocolitis (Clostridium difficile)• Diverticulitis• Typhlitis Dr.Farzin khorvash
Syndromes without known infectious etiology
• Idiopathic ulcerative colitis• Crohn's disease• Radiation enteritis• Ischemic colitis• Allergic enteritis
Dr.Farzin khorvash
Antibiotic-Associated Colitis
• Nearly 15% of hospitalized patients receiving b-lactam antibiotics develop diarrhea
• Clostridium difficile • Staphylococcus aureus • Candida • Enterotoxigenic Clostridium
perfringens
Dr.Farzin khorvash
Dr.Farzin khorvash
CLINICAL MANIFESTATIONS
• after 5 to 10 days of antibacterial treatment or as late as 10 weeks after cessation of therapy
• may be brief and self-limited or cholera-like, resulting in more than 20 stools per day
• fever (30 to 50% of patients),leukocytosis (50 to 60%) and abdominal pain or cramping (20 to 33%)
• Nausea, malaise, anorexia, hypoalbuminemia, occult colonic bleeding, dehydration
• Infrequently, C. difficile colitis presents without diarrhea as an acute abdominal syndrome or toxic megacolon
Dr.Farzin khorvash
Dr.Farzin khorvash
Autopsy the cecum of a patient with pseudomembranous colitis.
Dr.Farzin khorvash
CHRONIC INFLAMMATORY PROCESSES
• Weight loss, fever, headache, and colicky abdominal pain ,steatorrhea , malabsorption
• Enteropathogenic and Enteroaggregative Escherichia coli
• Syphilis • Gastrointestinal Tuberculosis • Gastrointestinal Mycosis • Parasitic Enteritis
Dr.Farzin khorvash
Parasitic Enteritis
• coccidiosis • Isospora belli • Cryptosporidium• Cyclospora • G. lamblia
Dr.Farzin khorvash
differential diagnosis of chronic inflammatory diarrhea
• Idiopathic inflammatory bowel disease including regional enteritis, granulomatous colitis, and ulcerative colitis
• Sarcoidosis• lymphoma• Carcinoma• Radiation enterocolitis• ischemic colitis• diverticulitis
Dr.Farzin khorvash
Abdominal Symptoms with Fever
• (1) Enteric fever : fever, headache, abdominal pain, splenomegaly, bacteremia, and occasionally skin rash, is by several bacteria. A number of systemic bacterial, rickettsial, viral, fungal, and parasitic infections, such as malaria, may mimic enteric fever
• (2) Mesenteric adenitis, a syndrome that may mimic acute appendicitis, can be caused by several bacteria
• (3) Eosinophilia:abdominal cramps or diarrhea often accompanied by fever, parasites, usually helminths, several diseases of unknown cause, and neoplasms.
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
MESENTERIC ADENITIS
• fever • right lower quadrant pain• vomiting• diarrhea• rebound tenderness• Rectal tenderness • Leukocytosis , polymorphonuclear leukocytes • Sonographic, radiographic contrast studies or
CT examination • Stool cultures were positive in 56% • Serologic confirmation
Dr.Farzin khorvash
MESENTERIC ADENITIS
• Y. enterocolitica • Y. pseudotuberculosis• nontyphoidal Salmonella spp• S. typhi infections• tuberculous mesenteric lymphadenitis• intestinal anthrax• Penicillium marneffei infection• hemolytic streptococci • Staphylococcus aureus • Bacteroides and Clostridium spp
Dr.Farzin khorvash
Differential Diagnosis
• Tuberculosis• nontyphoidal Salmonella infections• Salmonella typhi infections• Actinomycosis• Mycobacterium avium-intracellulare
infection • P. marneffei infections • parvovirus B19 • Epstein-Barr virus • Adenovirus infection • Angiostrongylus costaricensis
Dr.Farzin khorvash
chronic enteric inflammatory
• abdominal pain, weight loss, diarrhea, or malabsorption
• gastrointestinal mycoses• Mycobacterioses• bacterial infections• certain parasitic infections such as
coccidiosis.
Dr.Farzin khorvash
SYNDROME OF ABDOMINAL PAIN OR DIARRHEA WITH EOSINOPHILIA
• NematodesStrongyloides stercoralis• Ascaris lumbricoides• small bowel)Visceral larva migrans (Toxocara canis, Toxocara cati• Trichinella spiralis• Anisakiasis • Capillaria philippinensis• Angiostrongylus costaricensis• TrematodesSchistosoma spp• Clonorchis sinensis • Opisthorchis spp• Metorchis conjunctus • Fasciola hepatica • Fasciolopsis buski • Heterophyes heterophes • Metagonimus yokogawi • Nanophyetus salmincola • CestodesEchinococcosis• ProtozoaIsospora belli• Dientamoeba fragilis• causeEosinophilic gastroenteritis• Polyarteritis nodosa and other forms of vasculitis• Inflammatory bowel disease• Malignancies
Dr.Farzin khorvash
Etiology of Traveler's Diarrhea
• Enterotoxigenic Escherichia coli• Shigella• Salmonella• Campylobacter jejuni• Vibrio parahaemolyticus• Rotavirus
Dr.Farzin khorvash
DIARRHEA IN PATIENTS WITH AIDS
• Cytomegalovirus• Cryptosporidium• Microsporidium• Entamoeba histolytica• Giardia lamblia• Salmonella spp.• Campylobacter spp.• Shigella spp.• Clostridium difficile toxin• Vibrio parahaemolyticus• Mycobacterium spp.• Isospora belli• Cyclospora• Blastocystis hominis• Candida albicans• Herpes simplex• Chlamydia trachomatis• Strongyloides• Intestinal spirochetes
Dr.Farzin khorvash
simple examination
• fresh stool specimen is mixed with a drop of methylene blue on a slide and examined for the presence of fecal leukocytes
• In most cases, no leukocytes are noted. This suggests a noninflammatory process in which diarrhea usually arises from the upper small bowel by the action of a true enterotoxin or agents such as Giardia or viruses.
• The presence of numerous polymorphonuclear leukocytes documents an inflammatory or invasive process that usually arises from the colon or distal small bowel. Dr.Farzin khorvash
Dr.Farzin khorvash
• Of greatest importance in the treatment of microbial diarrhea, regardless of the cause or category, is fluid replacement (ORT).
Dr.Farzin khorvash
degree of volume depletion
• examining the turgor of the skin and mucous membranes
• by noting the amount of lacrimation
• by obtaining a history of urinary output
• changes in pulse and blood pressure
Dr.Farzin khorvash
• Electrolyte losses in severe watery diarrhea are similar to the electrolyte composition of serum, and fluid replacement should contain approximately these concentrations of electrolytes
Dr.Farzin khorvash
standard ORT regimen
• contains 3.5 g NaCl, 2.5 g NaHCO3, 1.5 g KCl, and 20 g glucose per liter of boiled water
• sodium 90, potassium 20, bicarbonate 30, chloride 80, and glucose 110 mmol/liter
• A similar solution may be prepared with 3 level tablespoons of sugar, ¾ teaspoon salt, ½ teaspoon sodium bicarbonate in 1 cup of orange juice to make up 1 liter (1.05 qt) in water.
Dr.Farzin khorvash
Therapy IV
Na+ Cl– K+ HCO3– Glucose
Intravenous solutions
Ringer's lactate 130 109 4 28* 0
Normal saline 154 154 0 0 0
WHO ORS 90 80 20 30† 111
Dr.Farzin khorvash
BRAT DIET
• Banana• Rice• Apple • Tosted bread
Dr.Farzin khorvash
ANTIMUTILITY AGENT
• Inflammatory infections: non use• non Inflammatory infections:use
Dr.Farzin khorvash
THERAPY OF ACUTE DYSENTERY
• shigellosis : fluoroquinolones • Salmonella
gastroenteritis :ciprofloxacin • C. jejuni :ciprofloxacin or
azithromycin • E. histolytica :metronidazole is
effective in eradicating hepatic amebiasis and may eradicate intestinal disease, the iodoquinol
• Schistosomal: Praziquantel Dr.Farzin khorvash
Therapy of Enteric Fever
• ampicillin, trimethoprim-sulfamethoxazole, and chloramphenicol
• Fluoroquinolones, such as ciprofloxacin or ofloxacin
• Third-generation cephalosporins, such as ceftriaxone
• aztreonam
Dr.Farzin khorvash
Therapy OF MESENTERIC ADENITIS
• self-limited • Y. enterocolitica : trimethoprim-
sulfamethoxazole, second- and third-generation cephalosporins, ciprofloxacin and other fluoroquinolones, piperacillin, imipenem, tetracycline, and chloramphenicol
• Yersinia pseudotuberculosis : tetracycline, cephalosporins, aminoglycosides and chloramphenicol
Dr.Farzin khorvash
Treatment of Clostridium difficile–Associated Diarrhea and Colitis
• 1. discontinue the offending antibiotic and/or modify the regimen to include an agent less commonly associated with C. difficile disease
• 2. Replace fluid and electrolyte losses• 3. Avoid antiperistaltic agents• 4. oral metronidazole, 250 mg qid for 10
days• 5. Do treat asymptomatic patients
colonized with C. difficile• 6. Retreat first–time recurrences with
the same regimen used to treat the initial episode
• 7. Avoid vancomycin use, if possibleDr.Farzin khorvash
• Metronidazole 250 mg qid × 10 d • 500 mg tid × 10 d • Vancomycina 500 mg tid × 10 d • 500 mg qid × 10 d • 125 mg qid × 7 d • 125 mg qid × 5 d • Teicoplanin 400 mg bid × 10 d • 100 mg bid × 10 d • Fusidic acid 500 mg tid × 10 d • Bacitracin 25,000 U qid × 10 d
Dr.Farzin khorvash
SHIGELLOSIS
•acute infectious inflammatory colitis •"bacillary dysentery,"
Dr.Farzin khorvash
ETIOLOGIC AGENT
• small, gram-negative, nonmotile bacilli
• family Enterobacteriaceae• (S. dysenteriae, S. flexneri, S.
boydii, and S. sonnei) on the basis of somatic O antigens and carbohydrate fermentation patterns.
Dr.Farzin khorvash
EPIDEMIOLOGY
• high rate of secondary household transmission
• often symptomatic in children • asymptomatic in adults
Dr.Farzin khorvash
PATHOGENESIS AND PATHOLOGY
• extensive ulceration of the epithelial surface of the colonic mucosa
• exudate consisting of desquamated colonic cells, PMNs, and erythrocytes that may resemble a pseudomembrane
Dr.Farzin khorvash
CLINICAL MANIFESTATIONS
• is typically a pediatric ambulatory disease
• presenting as a self-limited nonbloody but inflammatory watery diarrhea containing many neutrophils.
• over the first 24 to 48 h, one-fourth developed transient fever
• one-fourth had fever and self-limited watery diarrhea
• the remaining one-fourth had fever and watery diarrhea that progressed to bloody diarrhea and dysentery
Dr.Farzin khorvash
• In young children in particular fever 40° to 41°C
• sometimes resulting in generalized seizures
Dr.Farzin khorvash
Severe dysentery
• due to S. dysenteriae type 1, occurs less commonly with S. flexneri, and is least likely with S. sonnei or S. boydii
• mild disease generally recover without specific therapy in a few days to a week
• Severe shigellosis can progress to toxic dilatation and colonic perforation Dr.Farzin khorvash
Endoscopy
• shows the mucosa to be hemorrhagic, with mucous discharge and focal ulcerations
• sometimes an overlying exudate resembling a pseudomembrane.
• The majority of lesions are in the distal colon
Dr.Farzin khorvash
• Mild dehydration is common • severe dehydration is very rare• protein-losing enteropathy can
occur • extraintestinal complications of
shigellosis arise in patients in developing countries caused by S. dysenteriae type 1 and S. flexneri and to the poor nutritional state of the hosts.
Dr.Farzin khorvash
HUS
• with S. dysenteriae type 1• STEC strains (such as E. coli O157:H7) • usually develop toward the end of the first
week of shigellosis, when dysentery is already resolving
• Oliguria and a marked drop in hematocrit (by as much as 10% within 24 h) are the first signs
• may progress to anuria with renal failure and to severe anemia with congestive heart failure
• Even with advanced therapy, 5 to 10% of patients with HUS die of the acute illness.
Dr.Farzin khorvash
HUS
• Leukemoid reactions• with leukocyte counts of <50,000/uL• thrombocytopenia, with 30,000 to
100,000 platelets/uL, is common and in adults can lead to TTP
• profound hyponatremia and severe hypoglycemia
• may underlie central nervous system abnormalities such as seizures and altered consciousness.
Dr.Farzin khorvash
Ikari syndrome
• S. flexneri is associated with a rare toxic encephalopathy that is manifested by bizarre posturing and lethal cerebral edema
Dr.Farzin khorvash
Reactive arthritis
• with S. flexneri • antigen HLA-B27• the full triad of Reiter's syndrome
sometimes develops weeks to months after diarrheal illness
• Pneumonia, meningitis, vaginitis (in prepubertal girls), keratoconjunctivitis, and "rose spot" rashes are rare events
Dr.Farzin khorvash
DIAGNOSIS AND LABORATORY FINDINGS
• The specific :culture of Shigella from the stool
• PCR have been developed but are not yet widely available
• enzyme immunoassay to detect Shiga-family toxins in stool : S. dysenteriae type 1
• More than one differential selective medium should be used for culture— i.e., MacConkey and one other medium, such as Hektoen enteric or xylose-lysine-deoxycholate.
Dr.Farzin khorvash
TREATMENT
• The mild to moderate dehydration in shigellosis is readily corrected with oral rehydration solutions
• Since S. sonnei infection is usually self-limited, culture results generally do not become available until the patient is better and there is little clinical need for further therapy.
Dr.Farzin khorvash
• Trimethoprim-sulfamethoxazole 10/50 mg/kg bid × 3-5 d
• Ciprofloxacin 15 mg/kg q12h × 3-5 d; 500 mg max/dose 500 mg bid × 3 d
• Azithromycin 12 mg/kg on day 1 (max, 500 mg), 6 mg/kg on days 2-5 (max,250 mg/d) ,1 g (single dose)
• Cefiximeb 8 mg/kg (max, 400 mg) once daily × 5 d ,400 mg/d × 5 dDr.Farzin khorvash
HUS
• often requires dialysis
Dr.Farzin khorvash
Dr.Farzin khorvash
Cholera
Dr.Farzin khorvash
VIBRIO
• 1. Aerobic, motile Gram negative rods
• 2.a profuse watery diarrhea that is potentially fatal
Dr.Farzin khorvash
Dr.Farzin khorvash
Vibrio choleraeMicrobiology: Gram stain
• Comma-shaped, curved Gram negative rod
• Can’t differentiate from other Gram negative rods
Dr.Farzin khorvash
Dr.Farzin khorvash
LAB DIAGNOSIS
Organism can be seen in stool by direct microscopy after gram stain and dark field illumination
Cholera can be cultured on special alkaline media like triple sugar agar or TCBS agar.
Serologic tests are available to define strains, but this is needed only during epidemics to trace the source of infection.
Dr.Farzin khorvash
OTHER LAB FINDINGS
Dehydration leads to high blood urea & serum creatinine. Hematocrit & WBC will also be high due to hemoconcentration.
Dehydration & bicarbonate loss in stool leads to metabolic acidosis with wide-anion gap.
Total body potassium is depleted, but serum level may be normal due to effect of acidosis.
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
Cholera:‘Rice water’ stool
Dr.Farzin khorvash
نقش مواد غذایی در انتقال ویبریوکلره:
استفاده از آب آلوده در پخت برنجآب میوه رقیق شده با آب آلودهشستشوی میوه و سبزی با آب آلوده مواد غذایی دریایی (خرچنگ، میگو و
ماهی خام)گوشت خوک پخته نشدهفرنی گندمغذاهای خیابانیشیر نارگیل فریز شدهDr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
CHOLERAClinical manifestation
&Assessment of dehydration
Dr.Farzin khorvash
PATHOPHYSIOLOGY
• Non inflammatory
• Enterotoxin induced diarrhea
Dr.Farzin khorvash
PATHOPHYSIOLOGY
• Infective doseNormal condition
Abnormal condition
• Enterotoxin structureComponent A
Component B
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
CLINICAL MANIFESTATION
• Depends on :biotypeagenumber of bacteriastatus of immunityblood group O ?
Dr.Farzin khorvash
CLINICAL MANIFESTATION
• Sub clinical• Clinical :
profuse , watery diarrhea “rice water”
vomitingleg cramps
convulsion,fever,hypoglycemia(children)sometimes “cholera sica”
Dr.Farzin khorvash
LABORATORY FINDINGS
• Hemoconcentration• Leuckocytosis• Hyperglycemia• Hypocalemia• Increased protein , phosphate ,
lactate• Increased BUN , Cr• Metabolic acidosis
Dr.Farzin khorvash
CLINICAL MANIFESTATION
• Dehydration
some dehydration
severe dehydration
Dr.Farzin khorvash
CLINICAL MANIFESTATION
• Some dehydration
Restlessness and irritability Sunken eyes Dry mouth and tongue Increased thirst
Skin goes back slowly when
pinched
Dr.Farzin khorvash
CLINICAL MANIFESTATION
• Severe dehydration
Lethargy or unconsciousness Very dry mouth and tongue Skin goes back slowly when
pinched Weak or absent pulse
Low blood pressure
Dr.Farzin khorvash
ASSESSMENT OF DIARRHEA PATIENTS FOR DEHYDRATION
SEVER DEHYDRATION
SOME DEHYDRATION
NO DEHYDRATION
LETHARGIC OR UNCONSCIOUS,FLOPPY RESTLESS , IRRITABLE WELL,ALLERT
CONDITION
VERY SUNKEN ANDDRY SUNKEN NORMAL
EYE
ABSENT ABSENT PRESENTTEARS
VERY DRY DRY MOISTMOUTH&TONGUE
DRINK POORLY ORNOT ABLE TO DRINK
THIRSTYDRINK EAGERLY
NOT THIRSTYDRINK NORMALLY
THIRST
GOES BACK VERY SLOWLY
GOES BACK SLOWLY GOES BACK QUICKLYSKIN PINCH
Dr.Farzin khorvash
Dr.Farzin khorvash
Dr.Farzin khorvash
The goal of therapy
• to restore the fluid losses caused by diarrhea and vomiting
Dr.Farzin khorvash
• treatment of patients without severe dehydration is easy
• treatment of patients with severe dehydration requires experience and proper training.
Dr.Farzin khorvash
Basic training
• in how to recognize the degree of dehydration
• how to select the proper intravenous solution
• how rapidly to rehydrate the patient is crucial
Dr.Farzin khorvash
• Guidelines to rehydrate cholera patients have been written and reviewed elsewhere
Dr.Farzin khorvash
intravenous route
• should be restricted to patients with moderate dehydration who do not tolerate the oral route
• those who purge more than 10 to 20 ml/kg/hour
• patients with severe dehydration.
Dr.Farzin khorvash
Rehydration
• should be accomplished in two phases
• rehydration phase • maintenance phase
Dr.Farzin khorvash
The purpose of the rehydration phase
• is to restore normal hydration status
• it should last no more than 4 hours
Dr.Farzin khorvash
Intravenous fluids
• should be infused at a rate of 50 to 100 ml/kg/hour in severely dehydrated patients.
• Ringer's lactate solution is the most frequently recommended solution
Dr.Farzin khorvash
Electrolyte Concentration of Cholera Stools and Common Solutions Used for Treatment
Electrolyte and Glucose Concentration (mmol/L)
Na+ Cl– K+ HCO3– Glucose
Cholera stool
Adults 130 100 20 44
Children 100 90 33 30
Intravenous solutions
Ringer's lactate 130 109 4 28* 0
Normal saline 154 154 0 0 0
WHO ORS 90 80 20 30† 111
*Ringer's lactate does not contain HCO3–; it has lactate instead.
†Bicarbonate is replaced by trisodium citrate, which persists longer than bicarbonate in sachets. Abbreviation: WHO ORS, World Health Organization oral rehydration solution.
Copyright © 2000, 1995, 1990, 1985, 1979 by Churchill Livingstone
Dr.Farzin khorvash
• Normal saline solution is not recommended because it does not correct the metabolic acidosis.
Dr.Farzin khorvash
• When intravenous access proves difficult
• nasogastric tubes • or intraosseous catheters can be
used
Dr.Farzin khorvash
finishing the rehydration
• all signs of dehydration should have abated
• the patient should pass urine at a rate of 0.5 ml/kg/hour or greater
• Then starts the maintenance phase.
Dr.Farzin khorvash
maintenance phase
• During this phase the objective is to maintain normal hydration status by replacing ongoing losses
• The oral route is preferred during this phase
• use of oral rehydration solutions at a rate of 500 to 1000 ml/hour is highly recommended
Dr.Farzin khorvash
Oral rehydration therapy
• uses the principle of common transportation of solutes, electrolytes, and water by the intestine not affected by the cholera toxin
• People with diarrhea can undergo successful rehydration with simple solutions containing glucose and electrolytes that may be prepared at home.
Dr.Farzin khorvash
Evaluation of rehydration status• accurate recording of intake and
output volumes are essential• Patients without severe
dehydration who tolerate the oral route can be rehydrated with oral rehydration solutions exclusively and discharged promptly from the health center
Dr.Farzin khorvash
Discharge patients
• urine volume higher than 40 ml/hour
• diarrhea output below 400 ml/hour
• oral ingestion of rehydration solutions between 600 and 800 ml/hour
Dr.Farzin khorvash
Case-fatality rate
• during epidemics may be reduced to values below 1% even in disaster situations, provided that adequate access to health care centers and proper management of patients can be ensured
• Figures as high as 10% have been reported in epidemic settings when patients had no access to health care or received improper treatment
Dr.Farzin khorvash
Antimicrobial agents
• play a secondary role in the treatment of cholera
• patients with severe dehydration are given antibiotics
• duration of diarrhea is decreased • volume of stool is reduced by nearly
half• Early discharge and lessened hydration
decrease hospital expense• These benefits are critical in epidemic
conditions.
Dr.Farzin khorvash
• Oral tetracycline and doxycycline are the agents of choice in areas of the globe where sensitive strains predominate
• A single dose of doxycycline (300 mg) is the preferred regimen
• Tetracyclines are not safe in children younger than 7 years
• alternatives such as trimethoprim-sulfamethoxazole, erythromycin, and furazolidone are preferred over tetracyclines
• Pregnant women can be treated with erythromycin or furazolidone Dr.Farzin khorvash
• In the last 2 decades the appearance of strains resistant to tetracyclines and other antimicrobial agents
• New agents :with quinolones being the most effective
• Ciprofloxacin has been more extensively studied than other quinolones.
Dr.Farzin khorvash
• Two regimens of ciprofloxacin • a single dose of 1 g • once-daily regimens of 250 mg for
3 days.
Dr.Farzin khorvash
Therapy of Cholera
1.Evaluate the degree of dehydration on arrival
2.Rehydrate the patients in two phases:
Rehydration phase: lasts 2–4 h
Maintenance phase: lasts until diarrhea abates
3.Register output and intake volumes in predesigned charts and periodically review the data
4.Use the intravenous route only for
Severely dehydrated patients during the rehydration phase, in whom an infusion rate of 50–100 ml/kg/h is advised
Moderately dehydrated patients who do not tolerate the oral route High stool purgers (>10 ml/kg/h) during the maintenance phase
5.Use ORS for patients during the maintenance phase at a rate of 800–1000 ml/h, matching ongoing losses with ORS
6.Discharge patients to the treatment center if the following conditions are fulfilled:
Oral tolerance, ³1000 ml/h
Urine volume, ³40 ml/h
Stool volume, £400 ml/h
Dr.Farzin khorvash
Dr.Farzin khorvash
Prevention
• V. Cholerae is spread through contaminated food and water, therefore, prevention depends upon the interruption of fecal-oral transmission
• Anti-biotic prophylaxis, vaccines and surveillance of new cases are the answer to preventing the spread of disease.
Dr.Farzin khorvash
Cholera is not transmissible person-to-person, but can easily be spread through contaminated food and waterDr.Farzin khorvash
Sari Cloth Filtration:Preventative Measure
Using Sari cloth to filterWater
Dr.Farzin khorvash
Vaccines
• Two types of cholera vaccines are currently approved for use in humans.– Killed-whole-cell formulation: killed
bacterial cells from both biovars of serovar 01 and purified B subunit of the cholera toxin.
Provides immunity to only 50% of adult victims and to less than 25% of child victims.
– Live-attenuated vaccine, genetically engineered
Provides >90% protection against classical biovar and 65-80% agaisnt E1Tor biovar.Dr.Farzin khorvash
Vaccines: Problems
• The live vaccine is associated with certain problems:• Side Effects:
• Cause mild diarrhea, abdominal cramping and slight fever
• Possible virulence of live strain• Upon infection of the vaccine strain by
cholera toxin
Dr.Farzin khorvash
Chemoprophylaxis of household contacts
• published data do not support this concept
• More recently it has been shown that when transmission of the disease is low, as occurs in endemic areas, the utility of chemoprophylaxis is not significant
• Prophylaxis with antibiotics might be considered in situations in which the rate of transmission of the disease is high, along with other measures to curtail transmission
Dr.Farzin khorvash
Dr.Farzin khorvash