Problem 4A

Group 13
GI Tract Block
 Group 13 of GIT block
Leader : Vinawine Puteri T.
Writer : Cynthia Monica
Secretary : Felix Halim
Members : Cinintya Lestari Ling
Rasita Zahrina
Giovanni Anggasta
Maria Brigitta T.
Elfarini
Budi
Clarensia
Desintha C. N.
Efi Kardiana
 Learning Objectives
1.Typhoid Fever
2.Gastroenteritis
3.Dehydration
 LO 1

Typhoid Fever
 Typhoid Fever
Definition
Is an acute infectious intestinal disease
A bacterial infection characterized by
diarrhea, systemic disease, rash, most
commonly caused by the bacteria
Salmonella typhii
Synonym: - enteric fever
- Typhus
 Epidemiology
Fig. 1. The typhoid fever
surveillance study sites

Incidence of typhoid fever

Strongly endemic
Endemic
Sporadic cases

http://www.who.int/bulletin/volumes/86/4/06-039818/en/
 Classification

SALMONELLOSIS

Enteric
Nontyphoidal
(typhoid)
Salmonellosis
fever

S.Typhi S.Typhimurium
S.Paratyphi S.Enteriditis
8
 Salmonella sp.
Structure and physiology
- Bacillus 0.5 0.8 x 1 3 - Stand in sodium
m deoxycholate, brilliant
green, sodium
- Gram negative tetrathionate
- No spore - sugar reactions:
- Fakultative anaerob fermentation of glucose
(+), mannosa (+)
- Flagel peritrich move not ferment lactose and
(+) sucrose
- Stand in the freezing - Oksidase test :
water in a long period negative, nitrate
positive, urease
negative
- TSIA : -/+, H2S (+),
without gas
 STRUCTURE
1. Flagel : movement
2. DNA : contain genetic codes to
maintain the structure of the bacterium
3. Cell wall : keep shape
4. Capsule : to protect bacterium
5. Plasma membrane : use for a way
through nutrien & waste
6. Ribosom : to produce a cell protein
 Salmonella sp.
Virulence Factors

1. Damage to host cells

2. The ability to invade cells
3. Form a coat lipopolisacharide
4. Can remove toxins
 Salmonella sp.
Antigen Structure

1. Flagella antigen (H) Ig G

2. Somatic antigen (O) Ig M
3. Vi antigen above O antigen
Capsules & prevent
phagocytosis / intracellular
destruction of bacteria
 Modes of Transmission
Person to person transmition
Rarely (bactery 10 - 10 6)
Contamination of food products
Salmonella live in the chickens
intestine
Contamination of food processing
contamination of process
equipment food presentation
 Sign & Symptoms
Typhoid fever (%) Paratyphoid A & B
KCH 2002 (n=32) (%)

Fever 89-100 100% 92-100

Headache 43-90 32% 60-100
Nausea 23-36 33-58
Vomiting 24-35 3.1% 22-45
Abdominal pain 8-52
29-92
Distension 21.8%
Diarrhea 30-57 25% 17-68
Constipation 10-79 9.3% 2-29
Cough 11-36 8.4% 10-68
Coated tongue
The 1st week

Sign &
symptoms
 The 2nd week
If you don't receive treatment for typhoid
fever, you may enter a second stage during
which you become very ill and experience

Sign &
symptoms
The 3rd week ( typhoid stage
)

Sign &
symptoms
 The 4 week th

(Improvement )
If a person survives
until the fourth week,
their symptoms will
gradually improve

Though weight loss and

physical exhaustion can
continue for several
months.
Sign &
symptoms
Characteristic Typhoid fever
 Time to get the specimen

fever

blood

stool

urine

antibody

1 2 3 4 5 6 7
S.typhi in
8 week(s)
 Typhoid Fever
Pathophysiology
Salmonella Typhi

survives the acidity of the stomach

invades the Peyers Patches of the intestinal wall

macrophages (Peyers Patches)

the bacteria is within the macrophages and survives

bacteria spreads via the lymphatics while inside the

macrophages
 Diagnose
LAB
diagnose
Rutine check -SGOT and SGPT increase
-leukositosis (aneusinofilia and limfopenia)
- LED increase
WIDAL TEST Aglutination reaction between S. Typhii (antigen) with
antibody (aglutinin)
TUBEX test Detect antibody anti S.Typhi 09 in the serum of
patient
Typhidot Antibody IGM and IG G in the outer membran of
TEST salmonela typhi
IgM dipstick Antibody IGM specific S.Typhii in the whole blood
test serum
Blood culture Positive if typhoid fever but can be negative too
Widal test used to determine the existency of
aglutinin in the patients serum
- Aglutinin O (from bacterias body)
- Aglutinin H ( bacterias flagela )
- Aglutinin Vi (simpai kuman )

Factors that affect Widal test:

- Premature treatment of antibiotic
- Disability of develop antibodies and corticosteroid
treatment
- Time of blood taking
- History of vaccination
- Anamnestic reaction ( caused by past typhoid infection)
- Examination tecnic of the laboratorium
TUBEX Test
To detect antibody anti-S.typhi O9 in
patients serum
The interpretation based on the color of
the solution (redness bluish)

Lab test
Blood culture
Positif (+) result typhoid fever +
Negative (-) result possibility of
typhoid fever, because of :
Early antibiotic treatmentinhibits
growth of bacteria.
Lackness of blood volume ( 5cc of
blood)
Vaccination history
 Incubatio Wee Wee Wee Wee
n k1 k2 k3 k4
Bone marrow 90% (may decrease after 5 d of
aspirate (0.5-1 mL) antibiotics)
Blood (10-30 mL), 40%-80% ~20% Variable (20%-
stool, or duodenal 60%)
aspirate culture
Urine 25%-30%, timing unpredictable
 Specific serologic tests
Assays that identify Salmonella antibodies or antigens
support the diagnosis of typhoid fever, but these
results should be confirmed with cultures or DNA
evidence.
The Widal test was the mainstay of typhoid fever
diagnosis for decades. It is used to measure
agglutinating antibodies against H and O antigens of S
typhi
Indirect hemagglutination, indirect fluorescent Vi
antibody, and indirect enzyme-linked immunosorbent
assay (ELISA) for immunoglobulin M (IgM) and IgG
antibodies to S typhi polysaccharide, as well as
monoclonal antibodies against S typhi flagellin,37 are
promising, but the success rates of these assays vary
greatly in the literature.
 Other nonspecific laboratory studies
erythrocyte sedimentation rate (ESR),
thrombocytopenia, and relative
lymphopenia
elevated prothrombin time (PT) and
activated partial thromboplastin time
(aPTT) and decreased fibrinogen levels
Mild hyponatremia and hypokalemia are
common
 Imaging Studies
Radiography: Radiography of the
kidneys, ureters, and bladder (KUB) is
useful if bowel perforation
(symptomatic or asymptomatic) is
suspected.
CT scanning and MRI: These
studies may be warranted to
investigate for abscesses in the liver
or bones, among other sites.
 Hystologic Findings
Infiltration of tissues by macrophages (typhoid cells) that
contain bacteria, erythrocytes, and degenerated lymphocytes
In the mesenteric lymph nodes, the sinusoids are enlarged
and distended by large collections of macrophages and
reticuloendothelial cells
The spleen is enlarged, red, soft, and congested; its serosal
surface may have a fibrinous exudate. Microscopically, the red
pulp is congested and contains typhoid nodules
The gallbladder is hyperemic and may show evidence of
cholecystitis
Liver biopsy specimens from patients with typhoid fever often
show cloudy swelling, balloon degeneration with vacuolation
of hepatocytes, moderate fatty change, and focal typhoid
nodules
 Treatment
Bedrest and treatment to prevent complication and speed healing
Diet and supportive therapy restore a sense of comfort and
optimal patient health
Medication (antimicrobial) stop and prevent the spread microbial.
Chloramfenicol
Tiamfenicol
Chotrimoxazol
Amphicilin and Amoxcillin
Sefalosporin 3rd generation
Fluorokuinolon group :
Norfloxacin
Cifrofloxacin
Ofloxacin
Pefloxacin
Fleroxacin
Corticosteroid
 Antibiotic Recommendations by Origin and
Severity
Location Severity First-Line Second-Line
Antibiotics Antibiotics
South Asia, East Uncomplicated Cefixime PO Azithromycin PO
Asia45 Complicated Ceftriaxone IV or Aztreonam IV or
48,40
Cefotaxime IV Imipenem IV
Eastern Europe, Uncomplicated Ciprofloxacin PO or Cefixime PO or
Middle East, sub- Ofloxacin PO Amoxicillin PO or
Saharan Africa, TMP-SMZ PO
South America46,49 or Azithromycin PO
Complicated Ciprofloxacin IV or Ceftriaxone IV or
Ofloxacin IV Cefotaxime IV or
Ampicillin IV
or
TMP-SMZ IV
Unknown Uncomplicated Cefixime PO plus Azithromycin PO*
geographic origin or Ciprofloxacin PO or
Southeast Asia50,45 Ofloxacin PO
48,40,46,49
Complicated Ceftriaxone IV or Aztreonam IV or
Cefotaxime IV, plus Imipenem IV, plus
Ciprofloxacin IV or Ciprofloxacin IV
Ofloxacin IV or
Ofloxacin IV
Table 1: Typhoid Vaccines Available in the United States

Total Time
Number of Time Needed to Minimum Booster
Vaccine How
Doses Between Set Aside Age For Needed
Name Given For
Necessary Doses Vaccination Every...
Vaccination

Ty21a
(Vivotif
Berna, 1
Swiss capsule
4 2 days 2 weeks 6 years 5 years
Serum by
and mouth
Vaccine
Institute)

ViCPS
(Typhim
Injectio
Vi, 1 N/A 2 weeks 2 years 2 years
n
Pasteur
Merieux)
Pathological Changes in
Typhoid Fever
1. The changes in the Payer's
patches from hyperplasia &
ulceration to frank ulceration &
typhoid perforation.
2. The liver may be enlarged with
fatty changes.
3. The skin may show changes with
collections of bacilli, which cause
the classical rose spots
Pathological changes in
typhoid fever
4. Cholecystitis may lead to the formation of
infected gall
stones.
5. The spleen is enlarged and soft.
6. The mesenteric glands are enlarged.
7. The kidneys show result in albuminuria.
8. Bronchitis is a usual finding on clinical
auscultation of
lungs in typhoid fever.
9. Severe case: heart may be enlarged &
affected by fatty
degeneration.
10.Finally thrombosis of the deep veins may
occur, lead to a
 Complications
Intestinal bleeding or perforation may develop
in the third week of illness. Often marked by a sudden
drop in blood pressure and shock, followed by the
appearance of blood in your stool.
Other, less common complications
- myocarditis
- Pneumonia
- pancreatitis
- Kidney or bladder infections
- osteomyelitis
- meningitis
- delirium, hallucinations and paranoid psychosis
Complications

Typhoid Pneumonia with Empyema

 Differential Diagnoses
Abdominal Abscess
Amebic Hepatic Abscess
Appendicitis
Dengue Fever
Malaria
Rickettsial diseases
 Preventions
Hand washing with soap and water before eating.
Avoid foods and beverages from street vendors.
Drink by buy it bottled or bring it to a rolling boil for 1 minute
before you drink it. Bottled carbonated water is safer than
uncarbonated water.
Ask for drinks without ice unless the ice is made from bottled or
boiled water.
Eat foods that have been thoroughly cooked and that are still
hot & steaming.
Avoid vegetables like lettuce are easily contaminated and are
very hard to wash well.
When you eat raw fruit or vegetables that can be peeled, peel
them yourself. (Wash your hands with soap first.) Do not eat
the peelings.
 Tips to Reduce Your Risk of
Salmonella from Eggs
Keep eggs refrigerated at 45 F (7 C) at all times.
Discard cracked or dirty eggs.
Wash hands, cooking utensils, and food preparation surfaces with soap
and water after contact with raw eggs.
Eggs should be cooked until both the white and the yolk are firm and
eaten promptly after cooking.
Do not keep eggs warm or at room temperature for more than 2 hours.
Refrigerate unused or leftover egg-containing foods promptly.
Avoid eating raw eggs.
Avoid restaurant dishes made with raw or undercooked, unpasteurized
eggs. Restaurants should use pasteurized eggs in any recipe (such as
Hollandaise sauce or Caesar salad dressing) that calls for raw eggs.
Consumption of raw or undercooked eggs should be avoided,
especially by young children, elderly persons, and persons with
weakened immune systems or debilitating illness.
 LO 2

Gastroenteritis
 Definition
Inflammation of the mucous membrane of
both stomach and intestine. (Source:
Stedman's Medical Spellchecker,
2006 Lippincott Williams & Wilkins)
 Risk Factors
Overcrowding
Poverty
Poor sanitation
International travel
For Children :
Young age
Immune deficiency
Measles
Malnutrition
Lack of exclusive breast feeding
 Risk Factors
1. Consumers of certain foods :
Dairy food-Campylobacter and Salmonella species
Eggs -Salmonella species
Meats -C perfringens and Aeromonas, Campylobacter,
and Salmonella species
Ground beef - Enterohemorrhagic E coli
Poultry -Campylobacter species
Pork-C perfringens, Y enterocolitica
Seafood - Astrovirus and Aeromonas, Plesiomonas, and
Vibrio species
Oysters - Calicivirus and Plesiomonas and Vibrio species
Vegetables -Aeromonas species and C perfringens
2. Immunodeficient persons

3. Daycare attendees and their family

members:
rotavirus; astrovirus; calicivirus; and
Campylobacter, Shigella, Giardia, and
Cryptosporidium species
4. Animal exposure :
Exposure to young dogs or cats
Campylobacter organisms.
Exposure to turtles Salmonella
organisms.
5. Water exposure :
Swimming pools have been associated with
outbreaks of infection with Shigella species
Aeromonas organisms are associated with
exposure to the marine environment.
Giardia, Cryptosporidium, and Entamoeba
organisms are resistant to water chlorination

6. Certain medical conditions predispose

patients to infection, including the following :
C difficile - Hospitalization, antibiotic
administration
Plesiomonas species - Liver diseases or
malignancy
Transmitted of the
disease

http://activity.ntsec.gov.tw/lifeworld/english/content/images/en_dis_c
Signs & Symptoms
 Signs & Symptoms
Common symptoms
Low grade fever (99F)
Nausea with or without vomiting
Mild-to-moderate diarrhea: May range from 2-4 loose stools per day
for adolescents and adults to stools that run out of the diaper in
infants.
Crampy painful bloating
Vomiting
More serious symptoms
Blood in vomit or stool
Vomiting more than 48 hours
Fever higher than 101F
Swollen abdomen or abdominal pain coming from the right lower
side
Dehydration - Little to no urination, extreme thirst, lack of tears, and
dry mouth (dry diapers in infants)
 Diarrhea
Rapid movement of fecal matter through
the intestines resulting in poor absorption
of water, nutritive elements, and
electrolytes and producing abnormally
frequent watery bowel
movements.(dorland)
Increased stooling, with stool consistency
less solid than normal, constitutes a
satisfactory, if somewhat imprecise
(clevelandclinic)
Types of diarrhea
 Acute, persistent, &
chronic diarrhea
Acute diarrhea is defined as a greater
number of stools of decreased form
from the normal lasting for less than
14 days.
If the illness persists for more than 14
days, it is called persistent.
If the duration of symptoms is longer
than 1 month, it is considered chronic
diarrhea.
Osmotic diarrhea
osmotic force that acts in the lumen
to drive water into the gut (caused by
hyperosmotic drugs (MgSO4, Mg(OH)2),
malabsorption, defect in mucosal
absorption (disacharide deficiency,
glucose/galactose malabsorption)
 Mechanism
Osmotic
 Mechanism
Osmotic
Lactase Deficiency (Gastroenteritis)
ingested lactose remains osmotic load
Laxative

Food Sweetener (Hexitols,Sorbitol,etc)

IBS
Secretory diarrhea
increase in the active secretion
inhibition of absorption.
The most common cause of this type
of diarrhea is a cholera toxin that
stimulates the secretion of anions,
especially chloride ions.
 Mechanism
Secretory
 Mechanism
Secretory
Vibrio Cholerae Cholera Toxin A
cAMP

Cl- + H2O + Na (by CFTR)

Bacterial Toxin/Hormones (Tumours)

secrete fluid and mucus
Mechanism of Diarrhea
 Inflammatory
diarrhea
Damage to the mucosal lining or brush borderpassive
loss of protein-rich fluids, and a decreased ability to
absorb these lost fluids.

Features of all three of the other types of diarrhea can

be found in this type of diarrhea.
It can be caused by bacterial infections, viral infections,
parasitic infections, or autoimmune problems such as
inflammatory bowel diseases.
It can also be caused by tuberculosis, colon cancer, and
enteritis.
 Traveler diarrhea
The majority of episodes of travelers diarrhea
are self- limiting and last no longer than 5 days,
but some episodes may result in significant
discomfort and even dehydration. Travelers
diarrhea is usually categorized into three forms:
Classic passage of three or more unformed stools
in a 24-h period plus at least one of the following
symptoms or signs: nausea, vomiting, abdominal
pain or cramps, fever, bloody stools.
 Traveler diarrhea
Moderate passage of one or two unformed
stools in a 24-h period plus at least one of the
above symptoms or signs, or three or more
unformed stools without any of the above
symptoms or signs.
Mild passage of one or two unformed stools in
a 24-h period without any of the above
symptoms [12].
Most episodes occur between 4 days and 14
days after arrival but they can occur sooner if a
high concentration of bacteria is ingested.
 Etiology (infectious)
Host Cause

E. coli and viruses such as rotavirus, Minimal to moderate mucosal inflammation

Norwalk agent, and HIV

Shigella, enteroinvasive E. coli Bacteria that destroy entherocytes

Entamoeba Histolytica, Salmonella, that penetrate the mucosa, result in

Campylobacter jejuni, and Yersinia moderate to severe inflammation with or
enterocolitica without ulceration.
B. cereus, S. aureus, and Clostridium Ingestion of preformed toxin produced by
perfringens bacteria can result in acute jejunitis.

Aeromonas, Shigella, and Vibrio spp. (e.g., produce enterotoxins and also invade the
V. parahaemolyticus) intestinal mucosa.

Clostridium difficile and hemorrhagic E. coli produce inflammation from cytotoxins

0157:H7
 Etiology (noninfectious)
Inflammatory bowel disease
Irritable bowel syndrome
Ischemic bowel disease
Partial small bowel obstruction
Pelvic abscess in the rectosigmoid area
Fecal impaction
The ingestion of poorly absorbable sugars,
such as lactulose and acute alcohol
ingestion.
Etiology (noninfection)
 Bacteri Shigella, Salmonella, E.Coli, Gol. Vibrio, Bacillus cereus
E Clostridium perfringens, Stafilokokus aureus, Campylobacter
T
H Infection Viral Rotavirus, Norwalk/Norwalk like agent, Adenovirus
Protozoa, Entamoeba histolytica, Giardia lamblia, Balantidum
I
O Parasite Cacing perut, Ascaris, Trichiuris, Strongyloides
L Jamur, Candida

O
G
Carbohydrate Disakarida (laktosa, maltosa, sukrosa)
Y Monosakarida ( glucosa, fructosa, galactosa)
Malabsorpsi Fat Especially Long Chain trigyceride
O
F Asam amino, B lactoglobulin
Protein

D Food : spoiled food

I
A Poisoned : poisounous food (bacteri : Clostridium botulinum, S
R mixture food poison (chemical)
R Konstitution : Kwashiorkor, Marasmus
H Allergic : milk allergy, food allergy, cows milk protein sensiti
E
Imunodeficiency
A
Other reason (psikis)
Pathogenesis of infectious diarrhea
Pathogenesis diarrhea-antibiotic
cause
 How is the cause of diarrhea
diagnosed?
Diagnostic tests to find the cause of diarrhea
may include the following:
Medical history and physical
examination. The doctor will ask you about
your eating habits and medication use and
will examine you for signs of illness.
Stool culture. A sample of stool is analyzed
in a laboratory to check for bacteria,
parasites, or other signs of disease and
infection.
Blood tests. Blood tests can be helpful in
ruling out certain diseases.
 Fasting tests. To find out if a food intolerance
or allergy is causing the diarrhea, the doctor may
ask you to avoid lactose, carbohydrates, wheat,
or other foods to see whether the diarrhea
responds to a change in diet.
Sigmoidoscopy. For this test, the doctor uses a
special instrument to look at the inside of the
rectum and lower part of the colon.
Colonoscopy. This test is similar to a
sigmoidoscopy, but it allows the doctor to view
the entire colon.
Imaging tests. These tests can rule out
structural abnormalities as the cause of diarrhea.
 Treatment and therapy acute
diarrhea
Antidiarrheal medication are ineffective (kaolin-
pectin combination) or even dangerous
(Loperamid, tincture of opium, diphenoxylate
with atropin)
Bismuth subsalycilate preparation may reduce
stool volume but are not critical to recovery.
(for travellers diarrhea)
Oral immunoglobulin or specific antiviral agents
have occasionally been useful in limiting
duration of disease in immunocompromised
patients.
Therapy
Therapy
Oral rehydration therapy : ORT
 Complication of Diarrhea
Hypernatremia
Hyponatremia
Fever
Oedem/overhydration
Asidosis
Hypokalemia
Paralyticus ileus
Cramp
Lactose Intolerance
Glucose Malabsorption
Renal failure
 Prevention of Diarrhea
Breastfeeding
Improved feeding practices
Use of safe water
Handwashing
Food safety
Use of latrines and safe disposal of
stools
Measles immunization
Clinical
algorithm
Prognosis
 LO 3

Dehydration
 Dehydration
Dehydration is a condition that
occurs when the loss of body fluids,
mostly water, exceeds the amount
that is taken in
 Symptoms
Dry or sticky mouth
Low or no urine output; concentrated
urine appears dark yellow
Not producing tears
Sunken eyes
Markedly sunken fontanelles (the soft
spot on the top of the head) in an
infant
Lethargic or comatose (with severe
dehydration)
Muscle cramps
Nausea and vomiting
Heart palpitations
 Causes of dehydration
Diarrhea : Worldwide, more than four million children
die each year because of dehydration from diarrhea.
Vomiting
Sweat
Diabetes:In people withdiabetes, elevated blood
sugar levels cause sugar to spill into the urine and
water then follows,frequent urinationand excessive
thirst are among the early symptoms of diabetes.
Burns:The skin acts as a protective barrier for the
body and is also responsible for regulating fluid loss.
Inability to drink fluids
Dehydration Rate
a.Mild dehydration
Fluid lost 2-5% of body weight with clinical
picture is less elastic skin turgor,
hoarseness, the client has not fallen on the
state of shock.
b.Moderate dehydration
Fluid lost 5-8% of body weight with poor
clinical skin turgor, hoarseness, rapid pulse
and in presyok.
c.Severe dehydration
Loss of fluid 80-10% of body weight with
such clinical signs of dehydration is
coupled with decreased consciousness,
apathy to coma, stiff muscles until
cyanosis.
Level of dehydration Estimated fluid loss Signs
and Symptoms in Children
Level of Estimate
dehydrat d fluid Signs and symptoms
ion loss
<3% of
Minimal body none
weight
Fussy, tired, irritable child. Dry
mucous membranes (mouth,
Mild to <10% of
tongue), increased heart rate,
moderat body
increased breathing rate,
e weight
decreased urine output,
increased thirst
Listless, lethargic, unconscious.
Too weak to cry. Sunken eyes,
sunken fontanelle (soft spot of
10% of
skull). Increased heart rate,
body
Severe weak pulses, and rapid shallow
weight or
breathing. Cool, mottled skin.
more
No urine output (dry diapers).
Too weak to suckle or drink
Based on tonicity of fluid
Isotonis Dehydration
Loss water and Na within same
proportion.
Caused by diarrhea
Signvery rapid, thirsty ,cold extremity
and sweaty, consciousness goes down
and appears hypovolemik shock
Hypertonis Dehydration
Loss water and Na ,but the proportion
of lossing water is more than lossing
Na (Na >150 mmol/L)
Sign very thirsty,irritable
Hypotonis dehydration
Loss water and Na ,but the proportion
of lossing Na is more than lossing
water (Na >130 mmol/L)
sign letargi, spasm
 Physical exam
Low blood pressure
Blood pressure that drops when
you go from lying down to standing
Rapid heart rate
Poor skin turgor-- the skin may lack
its normal elasticity and sag back
into position slowly when pinched
up into a fold by the doctor;
normally, skin springs right back
into position
Delayed capillary refill
Shock
 Scoring System
Degree of dehydration

Score 0 1 2
General condition Healthy Irritability, Delirium, coma
sleepy, or shock
apathy Very
Skin elasticity Normal
Decreased decreased
Eye Normal
Sunken(ckun Very sunken
Fontanel (ubun2) Normal
g) Very sunken
Mouth Normal
Sunken Dry & cyanotic
Pulse Normal
Dry > 140
120-140
Amount of score: 0- 2 Mild dehydration
3- 6 Moderate dehydration
7-12 Severe dehydration
 Plan A
(to prevent dehydration)
1. Give patients more liquid than usual, such as:
Oralite,dll
Keep breastfeeding and give formula milk
2. Continue give meals
Porridge with meats or fish.
Bananas/ juices to additional Kalium.
Give foods every 3-4 hours (6x a day).
 Plan A
(to prevent dehydration)
3. Bring patient to medical centre if:
Often defecation
Very thristy
Sunken eyes
Fever
Anorexia
Bloody stools
4. Give oralite
<2 years : 50-100 ml (1/4 -1/2 cup)
2-5 years : 100-200 ml (1/2-1 cup)
 Plan B
(for mild/ moderate dehydration)

1. Use this table for plots:

Add age of patient if weight not known

Give oralite in off
 Plan C
(for severe dehydration)
1. Give liquid intravena
Are you give intravena to Yes 2. After 1-3 hour recheck
patient? again and choice suitable
about treatment
no
Yes
Patient can drink? 1. Begin to give oralitr

no 20-25% liquid must given

Are you have a skill to Yes
installed a tools?
no
Suggested to give liquid
intravena
IV Dose for patient :
First 1 hour: 30 ml/kg
2 hour : 40 ml/kg
in one hour
1. Begin rehydration with
NGT
2. If IV threatment
available, suggest to the
nearest medical centre.
Dose of liquid/ NGT:
20 ml/kg/Hour
 Complications
Kidney failure
Coma
Shock
Heat-related illnesses & associated
complications
Electrolyte abnormalities
In dehydration, electrolyte abnormalities
may occur since important chemicals (like
sodium and potassium) are lost from the
body through sweat.
If rehydration is done too slowly :
--> hypotensive & in shock for too long
If done too quickly :
--> water and electrolyte concentrations
within organ cells can be negatively
affected --> causing cells to swell --> die.
 Conclusion
Maybe this woman has been
infected by Salmonella typhi
 Advise
Need more spesific examination
(like Tubex test) and Give Oral
rehidration, bed rest, & smooth
foods