CHAPTER I
INTRODUCTION
Typhoid fever is a systemic disease caused by Salmonella typhi. The disease is characterized by prolonged heat, the prop with bacteremia without getting involved or endokardial endothelial structure and invasion of bacteria into the cell multiplication as well as mononuclear phagocytes of the liver, spleen, lymph nodes and intestinal Peyer's patches. Until now, typhoid fever remains a public health problem, and associated with poor sanitation, especially developing countries.
In developing countries, the estimated incidence of typhoid fever varies from 10 to 540 per 100,000 population. Although the incidence of typhoid fever came down with a sanitary disposal in many developing countries, estimated that each year there are 35 million cases with 500,000 deaths in the world there. Typhoid fever in Indonesia is still an endemic disease with an incidence rate is still high. Among the diseases that are categorized as intestinal infectious diseases, typhoid fever ranks second after gastroenteritis. 1
Gastrointestinal perforation is a complex form of penetration of the wall of the stomach, small intestine, large intestine result from leakage of intestinal contents into the abdominal cavity. Perforation of the colon can potentially lead to the occurrence of bacterial contamination in the abdominal cavity (a condition known as peritonitis). Gastric perforation developed into a chemical peritonitis caused by leakage of stomach acid kedlam abdominal cavity. Perforation in any form of gastrointestinal distress is a surgical case. 3
In children, injury to the small intestine caused by blunt abdominal trauma from a very rare with 1-7% incidence. Since 30 years ago merupakn peptic ulcer perforation in a common cause. Perforated duodenal ulcer incidence is 2-3 times more than a perforated gastric ulcer. Nearly 1/3 of gastric perforation due to gastric malignancy. Approximately 10-15% of patients with acute diverticulitis can develop into free perforation. In the older patients had a mortality rate of appendicitis acuta as much as 35% and 50% morbidity. The main factors that contribute to morbidity and mortality in these patients is a severe medical conditions that accompany such appedndicitis.
Perforation of the gastrointestinal tract is often caused by diseases such as gastric ulcer, appendicitis, gastrointestinal malignancies, diverticulitis, superior mesenteric artery syndrome, trauma. 2
CHAPTER II
REVIEW REFERENCES
Digestive Anatomy
Abdominal wall containing structures musculo-aponeurosis complex. The rear structure is attached to the upper spine to the ribs, and at the bottom of the pelvis. The abdominal wall consists of various layers, from outside to inside, which consists of layers of skin and sub kutis kuitis, sub-cutaneous fat and superficial facies (facies skarpa), then the third abdominal wall muscles m. Obliquus external abdominis, m. Obliquus internus abdominis and m. The transverse abdominis, and finally layered preperitonium and peritoneum, the fascia transversalis, preperitonial fat and peritoneum. Muscles in the front middle of the rectus abdominis muscle with a pair of fascianya which are separated in the midline by the linea alba.
Abdominal wall to form the abdominal cavity that protects the contents of the abdominal cavity. Integrity of the musculo-aponeurosis layer of the abdominal wall is very important to prevent congenital hernia occurs, acquired, or iatrogenic. Another function of the abdominal wall was breathing well on the micturition and defecation by increasing intra-abdominal pressure.
Abdominal wall bleeding coming from several directions. Kraniodorsal obtained from bleeding from a branch of aa. Intercostalis VI - XII and a. superior epigastric. From the caudal there is a. iliaca a. sircumfleksa superficial, a. and external pudendal a. inferior epigastric. Vascularization wealth allows horizontal or vertical abdominal incision without causing bleeding disorders.
Innervation of the abdominal wall in segmental dipersyarafi by n.thorakalis VI - XII and n. lumbar I. 2
Gastric (stomach)
Is part and expands channels that can be most particularly in the area epigaster, consisting of the upper gastric fundus associated with osofagus through pyloric orifice, situated below the diaphragm. front of the pancreas and spleen, attached to the left fundus uteri.
Hull section comprises:
a. Ventrikuli fundus, the part that is protruding into the upper left osteum kardium and normally be filled with gas.
b. Ventrikuli corpus, as high as osteum kardiun, an indentation at the bottom of the curvature of the minor.
c. Pyloric antrum, gastric tube-shaped part has a thick muscular form spinter pylorus.
d. Curvature of the minor, there is a right side extending from osteum cardiac stomach to the pylorus.
e. Greater curvature, longer than the minor curvature extending from the left side through the fundus ventrikuli osteum kardiakum headed right up to the pylorus inferior. Gastro splenic ligament extending from the top of the greater curvature to the spleen.
f. Osteum kardiakum, a place where osofagus the abdomen into the stomach. In this section there is a pyloric orifice.
The composition of the layer from the inside out, terdin of:
• layer of mucous membrane, when the stomach is emptied, this layer will folds called rugae.
• the circular muscle layer (muscular auricular).
• oblique muscle layer (muscular oblinqus).
• the length of the muscle layer (longitudinal muscular).
• layer of connective tissue / serosa (peritoneum).
There is a relationship between the pylorus pyloric spinter.
Gastric function. consists of:
1) Accommodating food, crush and refine food by peristalsis of the stomach and gastric lymph.
2) The sap produced gastric digestion;
ð Pepsin function, break the egg whites into amino acids (albumin and peptone).
ð acid salt (HCl) function; acidify foods, as anti-septic and disinfectant, and made the atmosphere so that the acid in the pepsinogen into pepsin.
ð Renin function, as the freezing of milk and yeast forms of kasinogen casein (milk protein and kasinogen).
ð layer of the stomach. The amount is a little break down fats into fatty acids which stimulate the secretion of gastric lymph.
Gastric secretion of sap began to occur at the beginning of the meal. when you see the food and the smell of food will be stimulated gastric secretion. Taste of food stimulate the secretion of the stomach due to work, causing nerve stimulation of the stomach wall nienyebabkan chemical releases a hormone called gastric secretion of sap. Gastric lymph was prevented by the sympathetic nervous system which may occur at times of emotional distress such as anger and fear.
GUT SMOOTH / intestinum MINOR
Intestinum minor is part of the digestive system foods that originate in the pylorus and ends on seikum length is about 6 m, is the longest tract where digestion and absorption of the digestive tract consisting of:
Lining the small intestine; mucosa (the inside). Circular layer (M. circular), a layer of longitudinal muscle (M. longitudinal) and serosa layers (outer)
Duodenum. Intestine is also called 12 fingers, about 25cm long horseshoe curve to the left, on this curve are the pancreas. Duodenum and the right side there are the mucous membranes that form a hill called the papilla of Vater. In the papilla of Vater it empties bile duct (ductus koledokus) and pancreatic duct (wirsungi duct / pancreatic duct)
Bile is made in the liver, to be ejected into the duodenum through a duct that functions koledokus mengemulsikan fat with the aid of lipase. The pancreas also produce amylase, which serves to digest carbohydrate disaccharides, and the function of trypsin digest protein into amino acids or albumin and polipeptika.
Duodenal mucosa lining the walls have a lot of the gland contains, called Brunner's glands, serves to produce sap intestinum.
Jejunum and Ileum, has a length of about 6 m. Two-fifths of the top is the jejunum with a length of about 2-3 m, and ileum with a length of about 4-5 m. Curvature jejunum and ileum attached to the posterior abdominal wall by means of a fan-shaped fold of peritoneum known as the mesentery.
Root of the mesentery allows the passage of the branches of the artery and superior vena mesentrika, lymph vessels and nerves into the space between two layers of peritoneum forming the mesentery. The connection between the jejunum and ileum has no clear boundary.
Lower end of the ileum associated with the mediation seikum hole called orifice ileoselkalis. Orifice is reinforced by spinter ileoselkalis and in this section there is a valve or valvula valvula seikalis baukini, serves to prevent the liquid in the column assendens not go back into the ileum.
Small bowel mucosa. Epithelial surface is very wide through the mucosal folds and microvilli facilitate digestion and absorption, is formed by folds of mucosa and sub mucosa that can enlarge the surface of the intestine.
In the cross-sectional villi lined by epithelial and kripta that produces a variety of tissue hormones and enzymes that play an active role in digestion ..
Absorption. Absorption of digested food that has been entirely takes place in the small intestine in 2 (two) channels in the capillary blood vessels and lymph channels on the inside surface of the intestinal villi.
Contains a villus lacteals, blood vessel epithelium and connective tissue in the muscle with lymphoid tissue entirely covered by a basement membrane and covered by epithelium.
Because the villi of the intestinal wall is out of contact with the liquid diet and the fat that is absorbed into the lacteals and then walk through the lymph vessels into the blood capillaries in the villi and the portal vein to the liver to have brought some changes.
SUMMARY OF ABSORPTION
The food sources of digestive organ end of the absorption
Protein
Fat
Amino acid carbon hydrates
Glycerine and fatty acids.
Monosakharida:
ð Glucose
ð Leavulosa
ð galactose from epithelium into the blood vessels and blood flow.
Epithelium of the villi into the lacteal and lymphatic flow.
Epithelium of the villi and the blood vessel walls into the bloodstream.
Bowel function, consisting of;
1) Receive substances that sudab rnakanan digested to be absorbed through blood capillaries and lymph channels.
2) Soak up the protein in the form of amino acids.
3) Carbohydrates are absorbed in the form of emulsions, fat.
In the small intestine are the intestinal lymph glands that produce the perfect food;
1) Enterokinase, activate the proteolytic enzyme.
2) Eripsin, improve digestion of proteins into amino acids.
a. Lactase Lactase transform into monosaccharides.
b. Convert maltose into monosaccharides maitosa.
c. Sucrose convert sucrose into monosaccharides.
COLON / intestinum MAJOR.
Length ±. l ½ m, width 5 - 6cm.
Layers of the colon from the inside out;
1) The mucous membranes.
2) the circular muscle layer.
3) Laplsan longitudinal muscle.
4) Connective tissue.
Bowel function, comprising:
1) It absorbs water and food.
2) Place of residence baktert coli.
3) Place the stool.
Caecum. In the appendix there caecum Vermiformis shaped like a worm that is also called the appendix, length 6 cm. Entirely covered by peritoneum, although not easy to move and have mesentenium palpable through the abdominal wall in people who are still alive.
Ascending colon length 13 cm, located in the lower abdomen to the upper right hand lengthwise down the liver and ileum. Below the heart bends to the left, the arch is called the hepatic flexure, followed by a colon tranaversum.
Appendix (appendectomy). Part of the colon that appears like a funnel from the exit end of seikum have a narrow but still allowed to pass by some of the intestinal contents. Appendix depends on the linea terminalis crosses into the minor pelvic cavity lies horizontally behind seikum dl. As an organ of defense against infection of the appendix sometimes react violently and hyperactivity can cause perforation of the wall into the abdominal cavity. 2
DEFINITION
Typoid fever is a systemic disease of the mark with the insidious fever that lasts a long time, headache, weakness, anorexia, relative bradycardia and spenomegali.
Typoid fever is a systemic disease caused by salmonella bacteria and salmonella paratypii typii enters the human body. And is a contagious disease that attacks many people daparv and easy to cause outbreaks.
Typoid fever is an acute infectious disease that attacks the gastrointestinal tract with symptoms of fever more than a week, digestive disorders and disturbances in consciousness. 1
The peritoneum is the lining of the abdominal cavity wall and wrap some particular organ, from the diaphragm, abdominal wall, pelvic cavity, and forming the peritoneal cavity. Section attached to the abdominal wall is called the peritoneum parietale, and a wrap-called viscerale organ. Peritoneal cells derived from mesotelial basement membrane supported by connective tissue rich in blood vessels and loose.
Peritonitis is an acute or chronic inflammation in the peritoneum parietale, can occur locally (localized peritonitis) or comprehensive (general peritonitis).
Peritonitis is inflammation of the peritoneum which is a wrapper perut.2 viscera in the cavity, 3
Peritonitis is an inflammatory or suppurative response of the peritoneum caused by chemical irritation or bacterial invasion. 3
Etiology
Salmonella typhi Salmonella same as the other is a Gram-negative bacteria, have flagella, not capsulated, non-spore forming facultative anaerobes. Have a somatic antigen (O) consisting of oligosaccharides, flagelar antigen (H) consisting of protein and envelope antigen (K) comprising polysaccharides. Have makromolekular lipopolysaccharide complex that forms the outer layer of the cell wall called endotoxin da. Salmonella typhi can also obtain the R-factor plasmid associated with resistance to multiple antibiotics. Salmonella resistant to certain chemicals that inhibit other enteric bacteria. Death penalty at a temperature of 560 C is also in the dry state. In the water can hold it for 4 weeks. 1
CLASSIFICATION
Peritonitis can be classified into 2 groups based on the cause:
A. Primary peritonitis (Spontaneus)
Caused by hematogenous invasion of the peritoneal organs directly from the peritoneal cavity. Many occurred in people:
- Liver cirrhosis with ascites
- Nephroses
- SLE
- Bronkopnemonia and pulmonary tuberculosis
- Pyelonephritis
- Foreign body from the outside
2. Secondary peritonitis
Caused by acute infection of intraperitoneal organs such as:
1) chemical irritation
Perforated gastric, pancreas, gallbladder, liver, spleen, a ruptured tubal pregnancy is extra.
2) Irritation bakteriil
Perforation of the colon, small intestine, appendix, ovary cyst rupture, ruptured kidneys and jars.
Based on the pathogenesis of peritonitis can be classified as follows: 2,3,5,9
A. Primary bacterial peritonitis
Peritonitis is due to hematogenous bacterial contamination in the peritoneal cavity and no focus of infection found in the abdomen. The cause is monomikrobial, usually E. Coli, or Pneumococus Sreptococus. Primary bacterial peritonitis is divided into two, namely:
1.Spesifik: eg Tuberculosis
2.Non specific: for example non-tuberculosis pneumonia an Tonsillitis.
Risk factors that contribute to malnutrition is the existence of peritonitis, intra-abdominal malignancy, immunosuppression, and splenectomy.
High risk groups are patients with nephrotic syndrome, chronic renal failure, systemic lupus erythematosus, and hepatic cirrhosis with ascites. 3.5
2. Secondary acute bacterial peritonitis (supurativa)
Peritonitis following an acute infection or gastrointestinal perforation tractusi or urinary tract. In general, a single organism will not cause a fatal peritonitis. Synergism of multiple organisms may aggravate the occurrence of this infection. Bakterii anaerobes, especially Bacteroides species, can magnify the influence of aerobic bacteria in causing infection.
Besides a broad and long bacterial contamination can also aggravate a peritonitis. Germs can be derived from:
- Injury / trauma penetration, which carries the germs from the outside into the
peritoneal cavity.
- Perforation of the organs in the abdomen, eg peritonitis caused
by chemicals, perforation of the intestine so that stool out of the intestine.
- Complications of the inflammatory process intra-abdominal organs, such as
appendicitis.
3. Tertiary peritonitis, for example:
- Peritonitis caused by fungi
- Peritonitis is the source of the bacteria could not be found.
Peritonitis caused by a direct irritant, sepertii eg bile, gastric sap, sap pancreas, and urine.
4. Other forms of peritonitis peritonitis:
- Aseptic / sterile peritonitis.
- Granulomatous peritonitis.
- Hiperlipidemik peritonitis.
- Talc peritonitis. 3.5
Pathogenesis
The entry of the bacteria Salmonella typhi and Salmonella paratyphi going into the human body through food infected with the bacteria. Most of the bacteria will be destroyed in the stomach, but some will pass and enter the colon and multiply. When the humoral mucosal immune response (IgA) poor intestinal bacteria will penetrate the epithelial cells and subsequent to the lamina propria.
In the lamina propria then the bacteria will be eaten by a cell - macrophage cells. Macrophage cells ingested bacteria that some still survive and be carried to the distal ileum Peyer Patch and the mesenteric lymph nodes. Furthermore, through the duct toraksikus then the bacteria will be taken into the blood circulation (causing bacteremia asymptomatic) and spread throughout the reticuloendothelial organs of the body and result in bacteremia is the second time, accompanied by systemic signs and symptoms.
In the liver, the bacteria will enter the gall bladder, along with the breed and the bile is secreted into the lumen of the intestine intermittently. The same process will then be repeated, since the macrophage is activated and activated and hypertrophy of the Salmonella bacteria phagocytosis occurs when the release of several inflammatory mediators that would further systemic infection of the stomach, causing reactions such as fever, malaise, nausea, vomiting, vascular instability, mental disorders, and coagulation.
Hyperactive macrophages in the Peyer patches cause hyperplasia of the reaction network (S. thypi intramakrofag will cause slow type hypersensitivity Reski, hyperplasia of organs, and organ necrosis). GI bleeding can occur due to accumulation of mononuclear cells in the intestinal wall. The process of lymphoid tissue pathology may develop up to the muscle layer, intestinal serosa, and can lead to perforation. 1
In the Peyer patch of infected wounds or ulcers can form an oval or elongated in the axis of the intestine. When the wound penetrates the intestinal lumen and the blood vessels so there is bleeding. Furthermore when the ulcer penetrates the intestinal wall perforation may occur.
In the ileum perforation, then the liquid stool and the germs quickly mengkontaminir peritoneum and after passing the incubation period (average 6-8 hours) a new cause symptoms of peritonitis. Ileum but actually have the property "protective mechanism" that is the nature when a segment of ileum had perforated the last segment will be kaan to contract such a way that closes the hole perforations. 1
This trait lasts for 1-4 hours depending on the prevailing circumstances and also the state of the intestine itself. Suppose that patients with poor general condition (KP, kakeksia) the nature lasts 1 hour or less bahakan nothing at all. Also in the diseased intestine in typhus abdominalis suppose then this mechanism will also be reduced.
In summary concluded if the ileum is perforated, peritonitis symptoms occur after 8-12 hours later. Patients should be observed closely for at least the first 24 hours in cases of blunt abdominal trauma.
The initial reaction is a discharge of exudate peritoneal inflammation followed by formation of pus fibrinosa-attachment and attachment to melokalisisr fibrinosa infection. When the infection subsides, perlekata will disappear, but when the process will continue the peritoneal adhesions bands will get to the arch ataupu intestinal organs. Exudation of fluid can lead to excessive dehydration penumpiukan fluid in the peritoneal cavity.
Fluids and electrolytes were going to get into the intestinal lumen and cause the formation of sequestration. Accompanied by adhesions-bowel adhesions, the bowel wall into atonia. Atony of the intestinal wall causing impaired permeability of the intestinal wall resulting in dehydration, shock, circulatory disorders, oliguri. While the attachment, the attachment of causing paralytic ileus or obstruction. Ileus cause bloating, nausea, vomitting, while the inflammatory reaction causing febrile. 3
Endotoxin can be attached to the capillary endothelial cell receptor with the consequent complications such as neuropsychiatric, cardiovascular, respiratory, and other orga disorders. 1
CLINICAL MANIFESTATIONS
Period of typhoid fever shoots last between 10-14 days. Clinical symptoms that arise are very varied from mild to severe, from asymptomatic to a typical picture of the disease complicated by death. In the first week after a 10-14 day incubation period, symptoms of the disease was at first similar to other acute infectious diseases, such as prolonged high fever is as high as 39 º C to 40 º C, headache, dizziness, fatigue, anorexia, nausea , vomiting, cough, with a pulse between 80-100 times per minute, weak pulse, breathing more rapidly with the picture of catarrhal bronchitis, flatulence, and feel uncomfortable, while alternating diarrhea and constipation.
At the end of the first week, more frequent diarrhea. In patients with typical tongue is dirty in the middle, and end edges of the red and shaking or tremor. Epistaxis can be experienced by the patient while the throat was dry and inflamed. If the patient to the doctor during this period, will find a fever with the symptoms above may occur in other diseases as well. Skin rash (rash) usually occurs on the seventh day and confined to the abdomen on one side and uneven patches of ros (roseola) lasts 3-5 days, then disappear completely. Roseola occurs mainly in people with white skin type that is dark red macule 2-4 mm size, flocking, arise most commonly in the skin of the abdomen, upper arm or lower chest, looked paled when pressed. Severe infections, diffuse purpuric skin can be found. Spleen became palpable and the abdomen distends.
If the first week, the body temperature gradually increased each
day, which usually decreases in the morning then increasing in the afternoon or evening. Therefore, in the second week the patient's body temperature constant in the high state (fever). High body temperature, with a slight drop in the morning last. Relative slowing the patient's pulse. The proper pulse increases with increasing temperature, pulse current is relatively slower than the increase in body temperature. Symptoms of more severe septicemia which is characterized by patients who experience a state of delirium. Hearing loss usually occurs, the tongue was dry, shiny red, whereas the faster the pulse decreased blood pressure, diarrhea, dark rose, enlarged liver and spleen, stomach bloating and frequent reads, impaired consciousness, drowsiness continuously, and began a mess when communicating . 1
In the third week of the body temperature gradually decreased, and the normal return at the end of the week. It happens if no complications or successfully treated. When things got better, the symptoms will be reduced and the temperature begins to drop. Yet it is precisely at this moment bleeding complications and perforation tends to occur, due to loss of crust from the ulcer. Conversely, if the situation continued to deteriorate, with septicemia become heavy with the typical signs of delirium or stupor, the muscles to move on, alvi incontinence and urinary incontinence. Meteorisme and timpani are still happening, is also greatly increased abdominal pressure followed by abdominal pain. Patients then collapses. If the pulse is increased accompanied by a local or general peritonitis, then this indicates the occurrence of intestinal perforation while sweating, restlessness, difficulty breathing, and collapse of a palpable pulse beat gives an overview of bleeding. Toxic myocardial degeneration is a common cause of death of patients with typhoid fever during the third week. 1
Acute abdomen due to gravity describe the clinical circumstances in which the abdominal cavity usually begins suddenly with pain as main complaint. This situation requires immediate countermeasures are often in the form of surgery, such as perforation, intra-abdominal bleeding, infection, and obstruction. Bowel perforation is a serious complication, occurring in 1-3% of cases. There are holes in the intestines, resulting in intestinal contents can be entered into the abdominal cavity and cause symptoms. Signs of bowel perforation is abdominal pain that is unbearable (acute abdomen), or abdominal pain that had existed before experiencing exacerbations, increased pulse rate and blood pressure dropped suddenly. Acute abdomen requires immediate treatment. 2
Intestinal perforation can be divided into:
A. Non-traumatic perforation, eg peptic ulcer, typhoid and appendicitis.
2. Perforation by trauma (sharp and blunt)
The presence of blood or fluid in the peritoneum cavity would give a sign - a sign stimulus peritoneum. Peritoneum causing stimulation and defans muscular tenderness, liver dullness may disappear due to the free air under the diaphragm. Decreases peristaltic lost due to temporary paralysis usus.1
When bacterial peritonitis has occurred, the patient's body temperature will rise and there is tachycardia, hypotension and the patient was lethargic and syok.1
This stimulation causes pain on any movement that causes a shift in the peritoneum peritoneum. Pain is a subjective form of pain when the patient moves, such as roads, breathing, coughing, or straining. Pain is a pain if the objective is moved such as palpation, tenderness loose, psoas test, or test lainnya.3, 5
Sunday is the fourth stage of healing although at the beginning of this week can be found lobar pneumonia, or thrombophlebitis of femoral vein. In those who get a mild infection thus produced only a weak immune, relapse can occur and take place in a short time. Recurrence may be lighter than the primary attack but can cause more severe symptoms than the primary infection. Ten percent of untreated typhoid fever will lead to relapse. 1
DIAGNOSIS
Clinical picture of typhoid fever diseases vary widely from only a mild illness is not diagnosed until the disease with a typical picture of complications and death. Therefore, early diagnosis is very rewarding to be given appropriate therapy and minimize complications. Knowledge of the clinical picture of this disease is very important to help detect early. Although in some cases required additional tests to help establish the diagnosis. The diagnosis of typhoid fever is still not complete when it has not been supported by the clinical microbiology laboratory diagnosis, but conventional laboratory diagnosis can be made through the identification of the antigen / antibody in the sample and through a culture of microorganisms.
Diagnosis of typhoid fever can be taken with a history of fever, gastrointestinal disorders, and may be accompanied by disturbances of consciousness. Differential diagnosis of typhoid fever is a viral gastroenteritis, enteritis due to Salmonella bacteria in addition, pseudomembranous colitis, appendicitis, and cholecystitis. 1
Diagnosis of peritonitis can be enforced by the clinical picture, laboratory tests and X-Ray. The clinical features depend on the extent of peritonitis, severe peritonitis and type of organisms responsible. Peritonitis can be local, spread, or the public. On examination will be obtained in the form of severe abdominal pain (pain in the entire field will complete abdomen in case of generalized peritonitis), nausea, vomiting, and fever. However, the symptoms in each person can vary greatly. 3
At follow-up of symptoms, the stomach becomes bloated, there are signs of ileus until the shock. And hypotension. Clinical picture which is common in primary bacterial peritonitis is the existence of abdominal pain, fever, pain and bowel sounds off the press and the decline or disappear. While the clinical picture of bacterial peritonitis secondary to the presence of acute abdominal pain. 1.2
On physical examination systematically the physical examination will reveal abdominal inspection: left abdominal breathing or paralyzed with pain, palpation: Defans muscular, muscle tenderness throughout the abdomen, percussion: the whole word of abdominal pain, liver dullness disappears, auscultation: decreased bowel sounds to disappear. 2
DIAGNOSIS
The differential diagnosis of peritonitis adalah appendicitis, pancreatitis, gastroenteritis, cholecystitis, salpingitis, ruptured ectopic pregnancy. 2
Examination support
Laboratory examination fever typoid
Laboratory examination includes examination of hematology, urinalis, clinical chemistry, imunoreologi, microbiology, and molecular biology. This examination is intended to help establish the diagnosis (sometimes even a decisive diagnosis), establishing prognosis, monitoring the course of the disease and results of treatment and the emergence of penyulit.
Hematology
Hemoglobin levels can be normal or decreased if there is complicating intestinal bleeding or perforation. Often low white cell count (leukopenia), but can also be normal or high. Leukocyte counts: frequent neutropenia with relative lymphocytosis. LED (erythrocyte sedimentation rate): Increase or decrease the normal platelet count (thrombocytopenia).
Urinalis
Protein: varies from negative to positive (from fever) normal leukocytes and erythrocytes; if the increased possibility of complications.
Clinical Chemistry
Liver enzymes (SGOT, SGPT) often increases with the picture of inflammation to acute hepatitis.
Imunorologi
Widal serology aimed at detecting the antibody (in blood) to the antigen bacteria Salmonella typhi / paratyphi (reagent). This test is a test that is still very popular ancient and the most frequently asked, especially in countries where the disease is endemic such as in Indonesia. As a quick test (rapitd test) results can be immediately known. Positive results expressed by
the agglutination. Therefore, this type of antibody known as febrile agglutinin. The test results are affected by many factors that can give false positives or false negatives. False-positive results can be caused by factors, among others, had to get vaccinated, cross-reaction with other species (Enterobacteriaceae sp), the reaction anamnestik (never sick), and the presence of rheumatoid factor (RF). False negative results can be caused by, among others, the patient was getting antibiotic therapy, blood sampling time is less than 1 week of illness, patient's general condition is poor, and the presence of other immunological diseases.
Diagnosis of Typhoid fever / paratyphoid declared when a / O titer = 1/160, maybe even once a threshold value should be higher given the illness of typhoid fever is endemic in Indonesia. O titer increased after the end of the week. See things on the test request this widal on new patients suffering from fever a few days is not quite right. When the reactive (positive) it is most likely not caused by the disease at that time but from previous contacts. Elisa examination Salmonella typhi / paratyphi LGG and lgM is a newer immunologic tests, which are considered more sensitive and specific than the Widal test for detecting typhoid fever / paratyphoid. As a quick test (Rapid Test) results can also be in the know. Diagnosis of Typhoid fever / paratyphoid stated 1 / if positive lgM indicating acute infection; 2 / if it indicates a positive LGG had contact / have been infected / reinfection / endemic areas.
Microbiology
Culture is the gold standard test (gold standard) for the examination of Typhoid fever / paratyphoid. Interpretation of results: if the result is positive, a definitive diagnosis for typhoid fever / paratyphoid. The opposite if results negativity, yet certainly not the Typhoid fever / paratyphoid, because false-negative culture results can be caused by several factors, including the amount of blood that is too little less than 2 ml), blood is not immediately inserted into the medial Gall (left to freeze the blood in the syringe so that bacteria trapped in the clot), when blood sampling in week-1 is still sick, had to get antibiotic therapy, and have received vaccinations. Disadvantages of this test was the result can not immediately known because it requires time for growth of bacteria (positive is usually between 2-7 days, when there is no colony growth anticipated to 7 days). Choice of materials used in the initial specimen is sick of blood, then to an advanced stage / carrier used urine and feces.
Molecular biology.
PCR (Polymerase Chain Reaction) method is widely used starting. On the way to do this in the multiplication of bacteria DNA is then identified with a specific DNA probe. Advantages of this test can detect bacteria present in small amounts (high sensitivity) and the uniqueness (specificity) is high as well. Specimens can be used blood, urine, other body fluids and tissue biopsy.
Diagnostic criteria commonly used are:
positive stool supporting the clinical diagnosis of typhoid fever.
A. Ensure a positive blood culture of typhoid fever but negative blood cultures do not rule out typhoid fever.
2. Increasing culture test widal titer 4-fold for 2-3 weeks to make sure
3. diagnosis of typhoid fever.
4. Single widal reaction with O antigen antibody titer 1: 320 or antigen titer
5. H 1: 640 to support the diagnosis of typhoid fever in a patient with typical clinical picture.
6. In some patients, the test remains negative widal although the re-examination of positive blood cultures. 1
Laboratory tests on peritonitis
On laboratory examination found the lekositosis, increased hematocrit and metabolic acidosis.
On radiological examination will show diustensi BOF colon and small intestine with the liquid surface. Photos will be found in the diaphragm sickle cell water under the right diaphragm (30% false negative). 2
Radiological examination: Plain photo abdomen performed 3 position results obtained Preperitoneal fat disappear Line, Ground Glass Appearance (+), intestinal distension (-), Air fluid level WNL, pneumoperitoneum (-). Air will look relatively much fills the lumen of the stomach and colon , while a small amount will fill some of the small intestine. A bit of air and fluid also fills the lumen of the intestine and water is minimal fluid level is not a pathological picture. Air fluid levels can also be found in the lumen of the colon, and three to five fluid levels with a length of 2.5 cm was within normal limits and is often found in the lower right quadrant. Two water fluid level or more in diameter over 2.5 cm (5-8 cm other literature) in length or caliber (dilation) is an abnormal condition and is always associated with the sign of either obstructive or paralytic illeus. Air fluid level in the small intestine will be shaped in short, if there is transudation of fluid in the gut that will show you a picture terdistensi step ladder appearance (like a picture of the stairs). Air fluid level in the colon will show a long-term. On a plain photo abdomen 3 position of the patient is not found a picture of the water fluid level, or step-ladder appearance.
Pneumoperitoneum refers to the presence of free air in peritoneal cavity. Pneumoperitoneum can be demonstrated by plain photo abdomen. Pneumoperitoneum is most often caused due to perforation of hollow abdominal organs and can cause a medical emergency. The most frequent area is usually under the cupola (dome) the right diaphragm. Free air usually appear 1-2 hours after perforation of the intestine. Absence of free air in peritoneal cavity does not just get rid of the perforation, because it does not appear in 25% of cases of duodenal ulcer perforation (depending on the shape, size, and position of the perforation). On a plain photo abdomen in three position patient shows no such picture. 4
COMPLICATIONS
Early complications: septicemia and septic shock, hypovolemic shock, recurrent intra-abdominal sepsis can not be controlled by multi-system failure, residual intraperitoneal abscesses, portal Pyemia (eg, hepatic abscess)
Complications: Adhesion, recurrent intestinal obstruction. 2
MANAGEMENT
Administration of Typhoid Fever
Is still adhered to the management of typhoid fever trilogy, namely: Rest and maintenance, dietary and adjunctive therapy (symptomatic and supportive), and the provision of medical. Breaks in the form of bed rest and professional care aims to prevent complications. While diet and adjunctive therapy is of considerable significance in the process of healing diseases, typhoid fever, due to lack of food will lower the general condition and nutrition of patients will increasingly fall and will be a long healing process. Medical administration of typhoid fever may include antibiotics, antipyretics, and steroids. Antimicrobial drugs are often given chloramphenicol, tiamfenikol, cotrimoxazole, third-generation cephalosporins, ampicillin, and amoxicillin.
Chloramphenicol is the drug of choice to treat typhoid fever. Chloramphenicol has a biological availability of 80% on iv administration. 3-hour plasma half-life in newborns, and in case of liver cirrhosis was extended to 6 hours. The dose administered orally in adults is 20-30 (40) mg / kg / day. In children aged 6-12 years require a dose 40-50 mg / kg / day. In children aged 1-3 years require doses 50-100 mg / kg / day. On intravenous administration requires 40-80 mg / kg / day for adults, 50-80 mg / kg / day for children aged 7-12 years, and 50-100 mg / kg / day for children aged 2-6 years. Forms are available in the form of capsules 250 mg, 500 mg, suspension of 125 mg / 5 ml, 125 ml/5ml syrup, powder injection of 1 g / Vail. Intramuscular inoculation is not recommended because this ester hirolisis unpredictable and injection site pain. From the experience of these drugs can reduce the average 7.2 days of fever. To avoid the Jarisch-Herxheimer reaction in the treatment of typhoid fever with chloramphenicol, the dose is as follows: day 1: 1g, Day 2: 2 g, day 3: 3 g, 3 g day and then forwarded to the normal body temperature. Some side effects that may arise in the provision of chloramphenicol are nausea, vomiting, diarrhea, dry mouth, stomatitis, pruritus ani, inhibition of erythropoiesis, Gray-Syndrome in newborns, hemolytic anemia, exanthema, urticaria, fever, hives, anaphylaxis, and Stevens-Johnson Syndrome sometimes. Reaction to chloramphenicol interaction with paracetamol would extend the plasma half-life of chloramphenicol. Drug interactions with sitostatika will increase the risk of a bone marrow damage.
Tiamfenikol have the dosage and effectiveness similar to chloramphenicol, but hematologic complications such as likelihood of aplastic anemia is lower in comparison with chloramphenicol. Tiamfenikol dose for adults is 500 mg every 8 hours, and for children 30-50 mg / kg / day divided into 4 times a day administration. Forms are available in the form of capsules 500 mg. Some side effects that may arise in the provision of chloramphenicol are nausea, vomiting, diarrhea, bone marrow depression that is reversible, optical neuritis and peripheral, and can lead to Gray baby syndrome. Tiamfenikol interactions with rifampicin and will speed up your metabolism fenobarbiton tiamfenikol. With typhoid fever in tiamfenikol may fall after 5-6 days.
Cotrimoxazole is a combination of two antibiotics, namely trimetroprim and sulfamethoxazole. This drug combination also known as TMP / SMX, and circulated in the community with several trademark names such as Bactrim. These drugs have biological availability of 100%. Plasma half-life of 11 hours. The dose for oral administration in adults and children are trimetroprim 320 mg / day, sufametoksazol 1600 mg / day. In children 6 years trimetroprim 160 mg / day, sufametoksazol 800 mg / day. At best intravenous infusion given briefly in the delivery of 8-12 hours. Some possible side effects are pain, thromboplebitis, nausea, vomiting, abdominal pain, diarrhea, esophageal ulceration, leucopenia, thrombopenia, megaloblastic anemia, elevated serum creatinine, exanthema, urticaria, itching, fever, and hypersensitivity reactions due to the fluid content of Natriumdisulfit infusion. Antacids reduce the interaction of cotrimoxazole degan resorbsi sulfonamides. At the same time with diuretics pemberiaan thiazid will increase the incidence of thrombopenia, especially in older patients.
Ampicillin and amoxicillin have the ability to reduce the fever is lower compared to chloramphenicol. These drugs have biological availability: 60%. Plasma half-life of 1.5 hours (the newborn: 3.5
hours). The dose for oral administration in an empty stomach is divided every 6-8 hours in the delivery of approximately 1/2 hour before meals. For adults 2-8 g / day, whereas children 100-200 mg / kg / day. At best pemberiaan intravenously administered with a short infusion, divided into pemberiaan every 6-8 hours. For adults 2-8 g / day, whereas children 100-200 mg / kg / day. Forms are available in the form of capsules 250 mg, 500 mg; Kaptab 250 mg, 500 mg; powder Inj.250 mg / vial, 500 mg / vial, 1g/vial, 2 g / vial; Syrup 125 mg / 5 ml, 250 mg / 5 ml; Tablets 250 mg, 500 mg. Some side effects that may occur are pain, thrombophlebitis, diarrhea, nausea, vomiting, stomach burning, epigastric pain, neuromuscular irritation, hallucinations, toxic neutropenia, hemolytic anemia, macular exanthema, and some allergic manifestations. Interaction with allopurinol may facilitate the emergence of an allergic skin reaction. Ampicillin elimination is slowed at the same time giving the urikosuria (eg probenezid), diuretics, and drugs with a weak acid.
The third-generation cephalosporins (Sefuroksin, Moksalaktan, cefotaxime, and Seftizoksim) which to date has been proven effective for typhoid fever is ceftriaxone. Antibiotics should only be used for the treatment of severe infections or who can not be treated with other antimicrobials, according to its antibacterial spectrum. This is because it was expensive but also has a high antibacterial potency recommended dosage is between 3-4 grams in 100 cc of dextrose administered over 1/2 hours perinfus once daily, administered for 3 to 5 days. increased BUN, kanidiasis, creatinine increase, eusinophilila, erythema multiforme, fever, headache, interstitial nephritis, neutropenia, phlebitis, pseudomembranous colitis, Stevens-Johnson syndrome, thrombocytopenia, transaminases increased, toxic epidermal necrolysis, urticaria, vaginitis. ESO also reported the reaction of other cephalosporins: agranulocytosis, hemolytic anemia, bleeding, Pancytopenia, renal dysfunction, dizziness, superinfection, toxic nephropathy.
Peritonitis on the general principles of therapy is the replacement of lost fluids and electrolytes intravenously done, great resuscitation with isotonic saline solution is important. Return of intravascular volume to improve tissue perfusion and oxygen delivery, nutrition, and defense mechanisms. Urine output of central venous pressure, and blood pressure should be monitored to assess the adequacy of resuscitation. 1
Antibiotic therapy should be administered as soon as the diagnosis of bacterial peritonitis was made. Broad-spectrum antibiotics are given empirically, and then changed its kind after the culture results came out. Choice of antibiotics based on the organisms which are suspected to be the cause. Broad-spectrum antibiotics are also additional surgical drainage. Adequate doses should be available at the time of surgery, because bacteremia will develop during the operation.
Disposal of septic focus or other inflammatory done with laparotomy surgery. The incision chosen was a vertical incision was underlined that generates the entrance to the entire abdomen and easily opened and closed. If peritonitis is localized, targeted incision above the place of inflammation. Operating techniques are used to control the contamination depends on the location and pathological nature of the gastrointestinal tract. In general, continuous peritoneal contamination can be prevented by closing, mengeksklusi, or a perforated viscus mereseksi. 4
Lavase peritoneum performed on the diffuse peritonitis, which is using crystalloid solution (saline). To avoid the spread of infection to the place that is not contaminated, it can be given antibiotics (eg cephalosporins) or antiseptic (eg povidone iodine) in the irrigation fluid. When peritonitisnya localized, lavase peritoneum should not be done, because this will cause bacteria to spread elsewhere. 2.3
Drainage (drainage) in general peritonitis is not recommended, because the drain pipe that will immediately isolated / separated from the peritoneal cavity, and can be a place of entry for exogenous contaminants. Drainage is useful in circumstances where there is a continuous contamination (eg fistula) and is indicated for localized peritonitis that can not be resected. 1, 3
Prognosis
Prognosis for mild local peritonitis is good, while the general prognosis is lethal peritonitis caused by virulent organisms. 2
CONCLUSION
Gastrointestinal perforation is a complex form of penetration of the wall of the stomach, small intestine, large intestine result from leakage of intestinal contents into the abdominal cavity. Perforation of the colon can potentially lead to the occurrence of bacterial contamination in the abdominal cavity (a condition known as peritonitis).
Perforation of the gastrointestinal tract is often caused by diseases such as gastric ulcer, appendicitis, gastrointestinal malignancies, diverticulitis, superior mesenteric artery syndrome, trauma.
Penatalaksaan depending on the underlying disease. Surgical intervention is almost always required in the form of exploration laparotomy and closure of the perforation by washing the peritoneal cavity (medical evacuasi). Conservative therapy is indicated in cases of patients with clinically non-toxic and generally stable condition and is usually given intravenous fluids, antibiotics, aspiration NGT, and fasted patients
REFERENCE
1. Ilmu penyakit dalam. Edisi II. Jakarta. 2006. Balai penerbitan FKUI.
2. Schwartz, Seymour I, Intisari Prinsip-prinsip Ilmu Bedah, EGC, Jakarta, 2000
3. Lee JA, Peritonitis, last update Juli 2006, Available from URL : http://www.nlm.nih.gov/medlineplus/ency/article/0006487.htm
4. Rasad S, Kartoleksono S, Ekayuda I, 1999, Abdomen Akut, dalam Radiologi Diagnostik, p 256-257, Gaya Baru, jakarta.
5. Peritonitis, last update 2004 available from URL: http://www.medicastore.com/arsip.html
No comments:
Post a Comment