chapter ii thypoid
TRANSCRIPT
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
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
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
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)
D. Pathway
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
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.
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
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
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.
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)
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.
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
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
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.
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