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Chapter II Thypoid

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Page 1: Chapter II Thypoid

CHAPTER II

BASICT CONCEPT

A. Definition

Typoid is a disease that causes intestinal infection in systemic

symptoms caused by salmonella typi (Carpenito, 2000)

Typoid fever is an acute infectious disease that is usually related

to the digestive tract (small intestine) with fever of more than seven

days in gastrointestinal disorders and disorders of consciousness.

(Mansjoer, 2000 : 421)

Typoid fever is a contagious disease and attacks many people it

can cause epidemic. (Widodo, 2007 : 1752)

From some definition above can be concluded that the fever is

typoid typoid is an infectious disease that occurs in the small intestine

caused by the salmonella typi with symptoms of fever for more than

seven days in gastrointestinal disorders and disorders of consciousness.

B. Etiology

The etiology of typhoid fever is Salmonella thypi. Gram-negative

bacillus hair moves with shakes, not berspora, has at least four different

antigens, namely the O antigen (somatic), H (flagella), VI, and hyaline

membrane protein (Mansjoer,2000)

Typhoid fever occur from infection by the bacterium Salmonella

group who entered the patient's body through the digestive tract. The

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main source of human infection is always release disease-causing

microorganisms, well when he was being sick or was recovering.

During recovery, patients still contain the Salmonella thypi in gall

bladder or in the kidney. As much as 5% typhoid patients will become a

while, was 2%, others will become a chronic. Most of these careers are

careers intestinal (intestinal type) while others, including urinary-type.

That a mild relapse of typhoid fever on career, especially in intestinal

type of career is difficult to know because no obvious symptoms and

complaints. (Ahyarwahyudi, 2009)

C. Patofisiology

The entry of the bacteria salmonella typhi and salmonella

paratyphi going into human body through contaminated food. Some

germs were destroyed in the stomach, partly escape into the intestine

and subsequently proliferate. When the mucosal humoral immune

responses (IgA) is less good intestinal bacteria will penetrate the

epithelial cells (particularly cell-M) and subsequently into the lamina

propia. In the lamina propia breed germs and difagosit by phagocytic

cells, primarily by macrophages. Germs can live and multiply inside

macrophages and subsequently brought to the distal ileum peyeri

Plague and then to the mesenteric lymph nodes. And than, through a

duct torasikus germs contained in these macrophages into the blood

sikulasi (leading to the first bakterimia asymptomatic) and spread

throughout the reticuloendothelial organs of the body especially the

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liver and lymph. In these organs the bacteria leave the phagocytic cells

and then multiply outside the cells or sinusoidal space and subsequent

entry into the blood circulation again resulted bakterimia the second

time accompanied by the signs and symptoms of systemic infection.

Inside the germs get into the gallbladder and the common breed

in intermittent excretion of bile into the intestinal lumen. Most remove

the germs in the faeces and partly through another entrance into the

circulation after penetrating intestinal. The same process was repeated

again, due to macrophage activation and has been hyperactive then

occur when the salmonella germs fagositosit release several

inflammatory mediators which in turn will lead to symptoms of the

inflammatory reaction which in turn will cause symptoms of systemic

inflammatory reactions such as fever, malaise, myalgia, headache, sore

abdominal, vascular instability, mental illness, and Coagulation.

In the Plague peyeri hyperactive macrophage hyperplasia

reaction network (intra S.typhi macrophages induce delayed type of

hypersensitivity reactions, tissue hyperplasia and necrosis of organs).

Tract infection bleeding can occur due to erosion of blood vessels

around the Plague peyeri which is undergoing necrosis and hiperpalsia

due to accumulation of mononuclear cells in the intestinal wall.

Limpoid tissue pathological processes can be developed until the

muscle layer, serous intestine, and can result in perforation.

Endoktosin can stick in the capillary endothelial cell receptor

with the consequent incidence of complications such as

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neuropsychiatric disorders, cardiovascular, respiratory and other organ

disorders. (Widodo,2009: 1752).

S. typhi enter the human body through contaminated food and

water. Some germs destroyed by stomach acid and partially into the

intestine and reach the lymphoid tissue in the terminal ileum Plaque

Peyeri that hypertrophy. In the event of bleeding complications and

peforasi intestianal, bacteria penetrate the lamina propia, incoming flow

mesenterial lymph into lymph nodes, and enter the blood stream

through the duct torasikus. S typhi others can reach the liver through the

portal circulation from the intestine. typhi nesting Plaque Peyeri,

spleen, liver, and other parts of reticuloendothelial system. Endotoxin S.

Typhi role in local inflammatory processes in the tissue where the

bacteria multiply. S typhi and endotoksinnya stimulates synthesis and

release of pyrogen substance and leukocytes in the inflamed tissue,

resulting a fever. (Mansjoer,2009: 422)

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D. Pathway

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E. Clinical Manifestation

The symptoms that ocur is variety. In the first week of

complaints and symptoms are similar to acute infectious diseases in

general are fever, headache, dizziness, muscle pain, anorexia, nausea,

vomiting, or diarrhea obstipation, uneasy feeling in the stomach, cough

and epistaxis. On physical examination found only at body temperature

increase.

In the second week of the symptoms become more obvious form

of fever, bradikardi relative, typhoid tongue dirty in the middle, edge

and red edge and tremors, hepatomegaly, spelnomegali, meteorismus,

disturbance of consciousness until coma somnolen, while roseolae

rarely found in Indonesian people. (Mansjoer,2009: 422)

Early bud typhoid fever lasts between 10-14 days. Clinical

symptoms occur varies from mild to hard, from asymptomatic until the

disease is a typical accompanied suffered complications up to death.

In the first week of clinical symptoms of the disease found in the

complaints and symptoms similar to acute infectious diseases in general

are fever, headache, dizziness, muscle pain, anorexia, nausea, vomiting,

or diarrhea obstipation, uneasy feeling in the stomach, cough and

epistaxis. On physical examination only showed increased body

temperature. The characteristic of fever is increasing slowly and

especially on the afternoon till night. In the second week of the

symptoms become more obvious form of fever, the relative bradiarkia

(bradiarkia the relative is not followed 1oC temperature increase with

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increasing pulse 8 times per min), webbed tongue (gross in the middle,

edge and red edge, and tremors), hepatomegaly, splenomegali,

meteroismus, mental disorders such as somnollen, strupor, coma,

delirium, or psychosis. Roseolae rarely found in Indonesian people.

(Widodo, 2007: 1753)

The biggest risk factor in this disease are those who have clean

habits in consuming less food, because thypi disease can be transmitted

through contaminated food and drink with germs thypi. Data show that

thypi many children aged 12-13 years to attack (70% -80%), aged 30-

40 years (10% -20%) and in children over the age of 12-13 years (5% -

10% ) (Zulkoni, 2010; 42)

F. Supporting Examination

1. Peripheral blood examination: leukofenia, limfositosis,

aneosinofilia, anemia, thrombocytopenia.

2. Bone marrow examination showed hyperactive bone marrow

picture.

3. Examination showed Widal titer against antigen 0 1 / 200 or more,

while the titer H antigen, although high but not significant for

diagnosis because could remain high titer H after immunization is

done or the patient has long recovered. (Murwani, Arita. 2008)

4. Examination of SGPT and SGOT

SGOT and SGPT after fever typoid often increased but may be back

to normal after recovering his typoid. Increased SGOT and SGPT

does not require special threatmen.

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5. Blood Culture Examination

Positive blood culture results confirm the diagnosis typoid fever,

but a negative result does not exclude typoid fever, because

probably caused by some of the following:

a. Have received antibiotic therapy. If the patient prior to blood

culture has received antibiotics, the bacterial growth inhibition

in culture media was negative and the results may.

b. Less blood volume (needed for approximately 5 cc of blood). If

blood culture is too little, then the result could be negative.

Blood drawn directly bedside should be incorporated into the

liquid media bile (oxygall) for bacterial growth.

c. Vaccination history. Vaccination in the past causing antibiotic in

the patient's blood. Antibiotics (Aglutinin) so that it can

suppress bacteremia can be a negative blood culture.

d. When the blood sampling after the first week, at which time it

increases aglutinin.

(Widiastuti, 2001)

G. Management

1. Medical

Giving antibiotics to stop and eradicate the spread of germs.

Antibiotics can be used:

a Cloramfenicol: dose the first day of 4 x 250 Mg, second day 4 x

500 Mg, given during the fever continued until two days free of

fever. Then the dose was reduced to 4 x250 Mg during five days

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later. Recent research (Nekwan, et al at the Friendship Hospital)

cloromfenicol usage still shows the results of a four-day drop in

temperature, the same as the latest drugs of this type of

quinolones.

b Ampisillin / amoxicillin: dose 50-150 mg / kg BW, was given a

two-week.

c Cofrimoksazol: 2 x 2 tablets (one tablet containing 400 Mg 80

Mg sulfametaksazol trimethoprim also given for two weeks).

d II and III generation cephalosporins. In sub-section of tropical

and infectious diseases FKUI RSCM. Giving cephalosporin

successfully overcome with good typhoid fever. Fever generally

subsided day-to-3 or before the day-to-4.

Regimens are in use is:

1) Cektriakson 4 g / day for 3 days.

2) Norfloxacin 2 x 400 Mg / day for 14 days.

3) Skiprofloksasin 600 Mg / day for 6 days.

4) Ofloksasin 600 Mg/day for 7 days.

5) Pefloksasin 400 Mg/day for 7 days.

6) Fleroksasin 400 Mg/ day for 7 days.

2. Nursing

Aims to prevent complications and speed healing. Patients

should be an absolute bed rest until at least 7 days or more or less

free of fever for 14 days. Mobilization phase conducted in

accordance with the patient recovers his strengthn very guarded

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higine care needs of individuals, cleanliness of the bed, clothes and

equipment used by patients. Patients with decreased consciousness

of her position should be altered to prevent decubitus and

pneumonia hypostatic, defecation and waste water need to be

considered for occasional constipation and urine retention.

3. Diet

The first patient was given a diet slurry filter, and then coarse

slurry, and finally the rice according to the level of patient recovery.

However, some research shows that giving solid food early, ie rice

with side dishes, low-cellulose (abstinence vegetables with coarse

fibers) could be given safely. (Mansjoer, 2000)

H. Assesment

1. Activity/ Rest.

Symptoms: weakness / fatigue / malaise, insomnia, diarrhea,

restrictions on activities relating to the effects of the disease

process.

2. Circulation.

Signs: tachycardia, reddish area ecchymoses, blood pressure,

hypotension, including postural.

3. Elimination.

Symptoms: Stool textures vary from soft to shape odor or watery.

Signs: lower bowel sounds, no intestinal peristalsis can be seen.

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4. Food/ Fluid.

Symptoms: anorexia, nausea, vomiting, decreased body weight,

intolerance to dietary / sensitive eg fresh fruit / vegetables, dairy

products, fatty food.

Signs: reduction of subcutaneous fat, weakness, muscle tone and

bad skin turgor, pale mucous membranes, wounds, inflammation,

oral cavity.

5. Pain/ Comfortable.

Symptoms: tender on the outside and bottom left.

Signs: tenderness or distension abdoment.

(Doenges, 2000 : 471)

I. Nursing Diagnosis

1 Hipertermi related to salmonella thypi infection process

2 Intolerance activity related to bed rest thirst.

3 The risk of fluid volume deficit related to the inclusion of the loss,

nausea, vomiting / excessive spending, diarrhea, body temperature.

4 Imbalance nutrition less than body requirement related to intek less

due to nausea, vomiting, anorexia, or diarrhea due to excessive

output.

5 Diarrhea related to inflammation of the intestine wall.

6 acute pain related to inflammation in the small intestine.

7 Lack of knowledge about disease conditions, needs treatment, and

prognosis related to a lack of information or inadequate information

(Nanda, 2007-2008)

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J. Intervention

1. Hipertermi related to salmonella thypi infection process.

Criteria outcome:

a. Body temperature normal

b. Pulse and respiratory rate are normal

c. No change in skin color and no headache.

Intervention :

a. Monitoring body temperature oftenly

b. Monitoring IWL

c. Monitoring skin color and skin temperature

d. Monitoring blood prresure, pulse, and RR

e. Monitoring decreasing of alert

f. Monitoring WBC, Hb, HCt,

g. Give Antipiretic

h. Give warm compres.

2. Intolerance activity related to bed rest thirst.

Criteria outcome :

a. Needs a bath, eating, drinking, elimination, dressing, oral

hygiene, hair, nails and genetal fulfilled.

b. Client cooperative to bedrest.

c. Client mobilisation step by step.

Intervention :

a. Help on ADL fullfilled like feeding, drinking, dressing, and

attention on oral hygiene, hair, nail, and genetal.

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b. Involved family on ADL fullfilled

c. Explain bedrest purpose to prevent complication and increas

recovery process.

3. The risk of fluid volume deficit related to the inclusion of the loss,

nausea, vomiting / excessive spending, diarrhea, body temperature.

Criteria outcome :

a. BP, body temperature are normal

b. No shymptomps of dehydration, good of skin turgor, mucus

membrane is wet no over thirsty desire.

Intervention :

a. Maintain accurate intake and output

b. Monitoring hydration status (Moisture mucosa, adequate pulse,

blood pressure orthostatic) if necessary.

c. Monitoring vital sign

d. Monitoring food/fluid intake and account daily calory intake .

e. Collaboration with docter if fluid output is getting wort.

4. Imbalance nutrition less than body requirement related to intek less

due to nausea, vomiting, anorexia, or diarrhea due to excessive

output.

Criteria outcome :

a. Increasing of body weight whereas purpose

b. Body weight is ideal where as tall

c. Can identify nutririon needed

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d. No malnutrion shymptomp

e. No decreasing of body weight.

Intervention :

a. Assest any food alergy

b. Colaboration with Kolaborasi dengan nutritionists to specify

the number of calories and nutrients that are in need of patients,

c. Make sure that contain high fiber diet to prevent constipation.

d. Monitoring of skin turgor

e. Monitoring of body weight decreasing .

5. Diarrhea related to inflammation of the intestine wall.

Criteria outcome :

a. Soloid stool, and bowel elimination 3 times a days

b. Maintain rectal areas from irritation

c. No diarrhea

d. Explain caused of diarhea

e. Maintain skin turgor

Intervention :

a. Evaluation food intake

b. Identify diarrhea cause

c. Monitoring sign and shymptomp of diarrhea

d. Instruct patient to eat low fiber food, high protein, and high

calori.

e. Monitoring of safe food preparation

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6. Acute pain related to inflammation in the small intestine.

Criteria outcome :

a. Report that pain occur and controlled

b. Looked relaxed and seemed to sleep or rest adequately.

Intervention :

a. Assess the level of pain, duration, location, intensity and

characteristics of pain.

b. The review of factors that increase the pain and reduce pain give

a warm compress on the painful area.

c. Collaboration with the medical team in the administration of

drugs Analgesic.

7. Lack of knowledge about disease conditions, needs treatment, and

prognosis related to a lack of information or inadequate information

(Nanda, 2007).

Criteria outcome :

The family of patient understand about patient disease.

Intervention :

a. Assess the extent of knowledge about the client's family of client

diseases.

b. Give health education about the disease and treatment of clients.

c. Give families the opportunity to ask questions when something

is poorly understood.

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Salmonella Typhi

MulutLambung HCLMual-muntah Melalui barier asam lambung

Masuk ke usus halus

Masuk ke folokel limfoid intestine atau nodus fever

Reaksi inflamasi

Anoreksia

Perubahan nutrisi kurang dari kebutuhan tubuh Menstimulasi Makrofan

Memproduksi sitiokinin

Retikuloendolial menyebar di hati atau limfa

Hepatomegali spenomegali

Nyeri

Vasodilatasi dari capsulla di permukaan

hati dan limfaDi hasilkan braditinnin histamin serotonin

Stimulasi nyeri

Konalsi PH rendah

Mikroba mati

Hipertermi

Penyabaran seraprogrsp

Pasien mendapat perawatan rumah

sakitEfek hospitalisasi

Prosedur

Pasien cemas

Peningkatan tekanan osmotik

Peningkatan kontraksi usus halus

Penurunan reabsorbsi usus

Diare

Output berlebih

Resiko kekurangan volume cairan

Input berkurang

Kelemahan fisik

Intoleran aktifitas