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 3040 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 Mulut Lambung HCL Konalsi PH rendah Mikroba mati Menstimulasi Makrofan Memproduksi sitiokinin Reaksi inflamasi Hipertermi

Mual-muntah Anoreksia Perubahan nutrisi kurang dari kebutuhan tubuh Input berkurang Kelemahan fisik Intoleran aktifitas

Melalui barier asam lambung Masuk ke usus halus Masuk ke folokel limfoid intestine atau nodus fever Retikuloendolial menyebar di hati atau limfa Hepatomegali spenomegali Nyeri Vasodilatasi dari capsulla di permukaan hati dan limfa Di hasilkan braditinnin histamin serotonin Stimulasi nyeri

Penyabaran seraprogrsp Pasien mendapat perawatan rumah sakit Efek hospitalisasi Prosedur Pasien cemas

Peningkatan tekanan osmotik Peningkatan kontraksi usus halus Penurunan reabsorbsi usus Diare Output berlebih Resiko kekurangan volume cairan