Syndrome of acute abdomen. Diagnosis, differential diagnosis and treatment tactic. Differential diagnostic of acute diseases of abdominal organs.


Acute appendicitis


Acute appendicitis is an inflammation of vermiform appendix caused by festering microflora.

Anyone can get appendicitis, but it is more common among people 10 to 30 years old. Appendicitis leads to more emergency abdominal surgeries than any other cause.


Symptoms and clinical course

The classic symptoms of appendicitis include:

        Dull pain near the navel or the upper abdomen that becomes sharp as it moves to the lower right abdomen. This is usually the first sign.

        Loss of appetite

        Nausea and/or vomiting soon after abdominal pain begins

        Abdominal swelling

        Fever of 99-102 degrees Fahrenheit

        Inability to pass gas

        Almost half the time, other symptoms of appendicitis appear, including:

        Dull or sharp pain anywhere in the upper or lower abdomen, back, or rectum

        Painful urination

        Vomiting that precedes the abdominal pain

        Severe cramps

        Constipation or diarrhea with gas


Four phases are distinguished in clinical course of acute appendicitis: 1) epigastric; 2) local symptoms; 3) calming down; 4) complications.

The disease begins with a sudden pain in the abdomen. It is localized in a right iliac area, has moderate intensity, permanent character and not irradiate. With 70 % of patients the pain arises in a epigastric area - it is an epigastric phase of acute appendicitis. In 24 hours it moves to the place of appendix existance (the Kocher's symptom). At coughing patients mark strengthening of pain in a right iliac area it is a positive cough symptom.

Pain first, vomiting next and fever last has been described as the classic presentation of acute appendicitis. Since the innervation of the appendix enters the spinal cord at the level T10, the same level as the umbilicus (belly button), the pain begins mid-abdomen. Later, as the appendix becomes more inflamed and irritates the adjoining abdominal wall, it tends to localize over several hours into the right lower quadrant, except in children under three years. This pain can be elicited through various signs and can be severe. Signs include localized findings in the right iliac fossa. The abdominal wall becomes very sensitive to gentle pressure (palpation). Also, there is severe pain on sudden release of deep pressure in the lower abdomen (rebound tenderness). In case of a retrocecal appendix (appendix localized behind the cecum), however, even deep pressure in the right lower quadrant may fail to elicit tenderness (silent appendix), the reason being that the cecum, distended with gas, protects the inflamed appendix from the pressure. Similarly, if the appendix lies entirely within the pelvis, there is usually complete absence of abdominal rigidity. In such cases, a digital rectal examination elicits tenderness in the rectovesical pouch. Coughing causes point tenderness in this area (McBurney's point) and this is the least painful way to localize the inflamed appendix. If the abdomen on palpation is also involuntarily guarded (rigid), there should be a strong suspicion of peritonitis, requiring urgent surgical intervention.


The abdominal pain usually:

Abdominal pain is the prime symptom of acute appendicitis. Classically, pain is initially diffusely centered in the lower epigastrium or umbilical area, is moderately severe, and is steady, sometimes with intermittent cramping superimposed. After a period varying from 1 to 12 hours, but usually within 4 to 6 hours, the pain localizes to the right lower quadrant. This classic pain sequence, although usual, is not invariable. In some patients, the pain of appendicitis begins in the right lower quadrant and remains there. Variations in the anatomic location of the appendix account for many of the variations in the principal locus of the somatic phase of the pain. For example, a long appendix with the inflamed tip in the left lower quadrant causes pain in that area. A retrocecal appendix may cause principally flank or back pain; a pelvic appendix, principally suprapubic pain; and a retroileal appendix, testicular pain, presumably from irritation of the spermatic artery and ureter. Intestinal malrotation also is responsible for puzzling pain patterns. The visceral component is in the normal location, but the somatic component is felt in that part of the abdomen where the cecum has been arrested in rotation.

        occurs suddenly, often causing a person to wake up at night;

        occurs before other symptoms;

        begins near the belly button and then moves lower and to the right;

        is new and unlike any pain felt before;

        gets worse in a matter of hours;

        gets worse when moving around, taking deep breaths, coughing, or sneezing.


Other symptoms of appendicitis may include

Anorexia nearly always accompanies appendicitis. It is so constant that the diagnosis should be questioned if the patient is not anorectic. Although vomiting occurs in nearly 75% of patients, it is neither prominent nor prolonged, and most patients vomit only once or twice. Vomiting is caused by both neural stimulation and the presence of ileus.

Most patients give a history of obstipation beginning before the onset of abdominal pain, and many feel that defecation would relieve their abdominal pain. Diarrhea occurs in some patients, however, particularly children, so that the pattern of bowel function is of little differential diagnostic value.

The sequence of symptom appearance has great significance for the differential diagnosis. In >95% of patients with acute appendicitis, anorexia is the first symptom, followed by abdominal pain, which is followed, in turn, by vomiting (if vomiting occurs). If vomiting precedes the onset of pain, the diagnosis of appendicitis should be questioned.

     loss of appetite



     constipation or diarrhea

     inability to pass gas

     a low-grade fever that follows other symptoms

     abdominal swelling

     the feeling that passing stool will relieve discomfort



Together with it, nausea and vomiting that have reflex character can disturb a patient. Often there is a delay of gases. The temperature of body of most patients rises, but high temperature can occur rarely and, mainly, it is a low grade fever. The general condition of patients gets worse only in case of growth of destructive changes in appendix.

Physical findings are determined principally by what the anatomic position of the inflamed appendix is, as well as by whether the organ has already ruptured when the patient is first examined.

Vital signs are minimally changed by uncomplicated appendicitis. Temperature elevation is rarely >1C (1.8F) and the pulse rate is normal or slightly elevated. Changes of greater magnitude usually indicate that a complication has occurred or that another diagnosis should be considered.25

Patients with appendicitis usually prefer to lie supine, with the thighs, particularly the right thigh, drawn up, because any motion increases pain. If asked to move, they do so slowly and with caution.

The classic right lower quadrant physical signs are present when the inflamed appendix lies in the anterior position. Tenderness often is maximal at or near the McBurney point.8 Direct rebound tenderness usually is present. In addition, referred or indirect rebound tenderness is present. This referred tenderness is felt maximally in the right lower quadrant, which indicates localized peritoneal irritation. The Rovsing signpain in the right lower quadrant when palpatory pressure is exerted in the left lower quadrantalso indicates the site of peritoneal irritation. Cutaneous hyperesthesia in the area supplied by the spinal nerves on the right at T10, T11, and T12 frequently accompanies acute appendicitis. In patients with obvious appendicitis, this sign is superfluous, but in some early cases, it may be the first positive sign. Hyperesthesia is elicited either by needle prick or by gently picking up the skin between the forefinger and thumb.

Muscular resistance to palpation of the abdominal wall roughly parallels the severity of the inflammatory process. Early in the disease, resistance, if present, consists mainly of voluntary guarding. As peritoneal irritation progresses, muscle spasm increases and becomes largely involuntary, that is, true reflex rigidity due to contraction of muscles directly beneath the inflamed parietal peritoneum.

Anatomic variations in the position of the inflamed appendix lead to deviations in the usual physical findings. With a retrocecal appendix, the anterior abdominal findings are less striking, and tenderness may be most marked in the flank. When the inflamed appendix hangs into the pelvis, abdominal findings may be entirely absent, and the diagnosis may be missed unless the rectum is examined. As the examining finger exerts pressure on the peritoneum of Douglas' cul-de-sac, pain is felt in the suprapubic area as well as locally within the rectum. Signs of localized muscle irritation also may be present. The psoas sign indicates an irritative focus in proximity to that muscle. The test is performed by having the patient lie on the left side as the examiner slowly extends the patient's right thigh, thus stretching the iliopsoas muscle. The test result is positive if extension produces pain. Similarly, a positive obturator sign of hypogastric pain on stretching the obturator internus indicates irritation in the pelvis. The test is performed by passive internal rotation of the flexed right thigh with the patient supine.

During the examinationIt is possible to mark, that the right half of stomach falls behind in the act of breathing, and a patient wants to lie down on a right side with bound leg.

Painfulness is the basic and decisive signs of acute appendicitis during the examination by palpation in a right iliac area, tension of muscle of abdominal wall, positive symptoms of peritoneum irritation. About 100 pain symptoms characteristic of acute appendicitis are known, however only some of them have the real practical value.

The Blumberg's symptom. After gradual pressing by fingers on a front abdominal wall from the place of pain quickly, but not acutely, the hand is taken away. Strengthening of pain is considered as a positive symptom in that place. Obligatory here is tension of muscles of front abdominal wall. Slide.

The Voskresensky's symptom. By a left hand the shirt of patient is drawn downward and fixed on pubis. By the taps of 2-4 fingers of right hand epigastric area is pressed and during exhalation of patient quickly and evenly the ha nd slides in the direction of right iliac area, without taking the hand away. Thus there is an acute strengthening of pain.

The Bartomier's symptom is the increase of pain intensity during the palpation in right iliac area of patient in position on the left side. At such pose an omentum and loops of thin intestine is displaced to the left, and an appendix becomes accessible for palpation.

The Sitkovsky's symptom. A patient, that lies on left, feels the pain which arises or increases in a right iliac area. The mechanism of intensification of pain is explained by displacement of blind gut to the left, by drawing of mesentery of the inflamed appendix.

The Rovsing's symptom. By a left hand a sigmoid bowel is pressed to the back wall of stomach. By a right hand by ballotting palpation a descending bowel is pressed. Appearance of pain in a right iliac area is considered as a sign characteristic of appendicitis.

The Obrazcovs symptom. With the position of patient on the back by index and middle fingers the right iliac area of most painful place is pressed and the patient is asked to heave up the straightened right leg. At appendicitis pain increases acutely.

The Rozdolskyys symptom. At percussion there is painfulness in a right iliac area.

The general analysis of blood does not carry specific information, which would specify the presence of acute appendicitis. However, much leukocytosis and change of formula to the left in most cases can point to the present inflammatory process.


Variants of clinical course and complication

Acute appendicitis in children. With children of infancy acute appendicitis can be seen infrequently, but, quite often carries atipical character. All this is conditioned, mainly, by the features of anatomy of appendix, insufficient of plastic properties of the peritoneum, short omentum and high reactivity of child's organism. The inflammatory process in the appendix of children quickly makes progress and during the first half of days from the beginning of disease there can appear its destruction, even perforation. The child, more frequent than an adult, suffers vomiting. Its general condition gets worse quickly, and already the positive symptoms of irritation of peritoneum can show up during the first hours of a disease. The temperature reaction is also expressed considerably acuter. In the blood test there is high leukocytosis. It is necessary to remember, that during the examination of calmless children it is expedient to use a chloral hydrate enema.

The establishment of a diagnosis of acute appendicitis is more difficult in young children than in the adult. The inability of young children to give an accurate history, diagnostic delays by both parents and physicians, and the frequency of GI upset in children are all contributing factors.62 In children the physical examination findings of maximal tenderness in the right lower quadrant, the inability to walk or walking with a limp, and pain with percussion, coughing, and hopping were found to have the highest sensitivity for appendicitis.63

The more rapid progression to rupture and the inability of the underdeveloped greater omentum to contain a rupture lead to significant morbidity rates in children. Children <5 years of age have a negative appendectomy rate of 25% and an appendiceal perforation rate of 45%. These rates may be compared with a negative appendectomy rate of <10% and a perforated appendix rate of 20% for children 5 to 12 years of age.13,14 The incidence of major complications after appendectomy in children is correlated with appendiceal rupture. The wound infection rate after the treatment of nonperforated appendicitis in children is 2.8% compared with a rate of 11% after the treatment of perforated appendicitis. The incidence of intra-abdominal abscess also is higher after the treatment of perforated appendicitis than after nonperforated appendicitis (6% vs. 3%).23 The treatment regimen for perforated appendicitis generally includes immediate appendectomy and irrigation of the peritoneal cavity. Antibiotic coverage is limited to 24 to 48 hours in cases of nonperforated appendicitis. For perforated appendicitis IV antibiotics usually are given until the white blood cell count is normal and the patient is afebrile for 24 hours. The use of antibiotic irrigation of the peritoneal cavity and transperitoneal drainage through the wound are controversial. Laparoscopic appendectomy has been shown to be safe and effective for the treatment of appendicitis in children

Acute appendicitis of the people of declining and old ages can be met not so often, as of the persons of middle ages and youth. This contingent of patients is hospitalized to hospital rather late: in 23 days from the beginning of a disease. Because of the promoted threshold of pain sensitiveness, the intensity of pain in such patients is small, therefore they almost do not fix attention on the epigastric phase of appendicitis. More frequent are nausea and vomiting, and the temperature reaction is expressed poorly. Tension of muscles of abdominal wall is absent or insignificant through old-age relaxation of muscles. But the symptoms of irritation of peritoneum keep the diagnostic value with this group of patients. Thus, the sclerosis of vessels of appendix results in its rapid numbness, initially-gangrenous appendicitis develops. Because of such reasons the destructive forms of appendicitis prevail, often there is appendiceal infiltrate.

With pregnant women both the bend of appendix and violation of its blood flow are causes of the origin of appendicitis. Increased in sizes uterus causes such changes. It, especially in the second half of pregnancy, displaces a blind gut together with an appendix upwards, and an overdistension abdominal wall does not create adequate tension. It is needed also to remember, that pregnant women periodically can have a moderate pain in the abdomen and changes in the blood test. Together with that, psoas-symptom and the Bartomier's symptom have a diagnostic value at pregnant women.

Appendectomy for presumed appendicitis is the most common surgical emergency during pregnancy. The incidence is approximately 1 in 766 births. Acute appendicitis can occur at any time during pregnancy.68 The overall negative appendectomy rate during pregnancy is approximately 25% and appears to be higher than the rate seen in nonpregnant women.68,69 A higher rate of negative appendectomy is seen in the second trimester, and the lowest rate is in the third trimester. The diversity of clinical presentations and the difficulty in making the diagnosis of acute appendicitis in pregnant women is well established. This is particularly true in the late second trimester and the third trimester, when many abdominal symptoms may be considered pregnancy related. In addition, during pregnancy there are anatomic changes in the appendix (Fig. 30-7) and increased abdominal laxity that may further complicate clinical evaluation. There is no association between appendectomy and subsequent fertility.

Clinical course of acute appendicitis at the atipical location (not in a right iliac area) will differ from a classic vermiform appendix .


Variants of appendix localization

1.     Appendix

2.     Appendicular artery

3.     Appendicular mesentery

4.     Ilium

5.     Caecum



Appendicitis at retrocecal and retroperitoneal location of appendiceal appendix can be with 820 % patients. Thus an appendix can be placed both in a free abdominal cavity and retroperitoneal. An atypical clinic arises, as a rule, at the retroperitoneal location. The patients complain at pain in lumbus or above the wing of right ileum. There they mark painfulness during palpation. Sometimes the pain irradiates to the pelvis and in the right thigh. The positive symptom of Rozanov painfulness during palpation in the right Pti triangle is characteristic. In transition of inflammatory process on an ureter and kidney in the urines analysis red corpuscles can be found.

Appendicitis at the pelvic location of appendix can be met in 1130 % cases. In such patients the pain is localized above the right Poupart's ligament and above pubis. At the very low placing of appendix at the beginning of disease the reaction of muscles of front abdominal wall on an inflammatory process can be absent. With transition of inflammation on an urinary bladder or rectum either the dysuric signs or diarrhea developes, mucus appears in an excrement. Distribution of process on internal genital organs provokes signs characteristic of their inflammation.

Appendicitis at the medial placing of appendix. The appendix in patients with such pathology is located between the loops of intestine, that is the large field of suction and irritation of peritoneum. At these anatomic features mesentery is pulled in the inflammatory process, acute dynamic of the intestinal obstruction develops in such patients. The pain in the abdomen is intensive, widespread, the expressed tension of muscles of abdominal wall develops, that together with symptoms of the irritation of peritoneum specify the substantial threat of peritonitis development.

For the subhepatic location of appendix the pain is characteristic in right hypochondrium. During palpation painfulness and tension of musclescan be marked.

Left-side appendicitis appears infrequently and, as a rule, in case of the reverse placing of all organs, however it can occur at a mobile blind gut. In this situation all signs which characterize acute appendicitis will be exposed not on the right, as usually, but on the left.

Among complications of acute appendicitis most value have appendiceal infiltrates and abscesses.

Appendiceal infiltrate is the conglomerate of organs and tissue not densely accrete round the inflamed vermiform appendix. It develops, certainly, on 35th day from the beginning of disease. Acute pain in the stomach calms down thus, the general condition of a patient gets better. Dense, not mobile, painful, with unclear contours, formation is palpated in the right iliac area. There are different sizes of infiltrate, sometimes it occupies all right iliac area. The stomach round infiltrate during palpation is soft and unpainful.

At reverse development of infiltrate (when resorption comes) the general condition of a patient gets better, sleep and appetite recommence, activity grows, the temperature of body and indexes of blood is normalized. Pain in the right iliac area calms down, infiltrate diminishes in size. In this phase of infiltrate physiotherapeutic procedure is appointed, warmth on the iliac area.

In two months after resorption of infiltrate appendectomy is conducted.

At abscessing of infiltrate the condition of a patient gets worse, the symptoms of acute appendicitis become more expressed, the temperature of body, which in most cases gains hectic character, rises, the fever appears. Next to that, pain in the right iliac area increases. Painful formation is felt there. In the blood test high leukocytosis is present with the acutely expressed change of leukocyte formula to the left.

Local abscesses of abdominal cavity, mainly, develops as a result of the atypical placing of appendix or suppuration. More frequent from other there are pelvic abscesses. Thus a patient is disturbed by pain beneath the abcupula, there are dysuric disorders, diarrhea and tenesmus. The temperature of body rises to 38,039,0o, and rectal to considerably higher numbers. In the blood test leukocytosis, change of formula of blood is fixed to the left.

During the rectal examination the weakened sphincter of anus is found. The front wall of rectum at first is only painful, and then its overhanging is observed as dense painful infiltrate. Slide.

A subdiaphragmatic abscess develops at the high placing of appendix. The pain in the lower parts of thorax and in a upper quarter of abcupula ofn to the right, that increases at deep inhalationis except for the signs of intoxication, is characteristic of it. A patient, generally, occupies semisitting position. Swelling in an epigastric area is observed in heavy cases, smoothing and painful intercostal intervals. The abcupula ofn during palpation is soft, although tension in the area of right hypochondrium is possible. Painfulness at pressure on bottom (911) ribs is the early and permanent symptom of subdiaphragmatic abscess (the Krukovs symptom).

Roentgenologically the right half of diaphragm can fall behind from left one while breathing, and there is a present reactive exudate in the right pleura cavity. A gas bubble is considered the roentgenologic sign of subdiaphragmatic abscess with the horizontal level of liquid, which is placed under the diaphragm.

Interloop abscesses are not frequent complications of acute appendicitis. As well as all abscesses of abdominal cavity, they pass the period of infiltrate and abscess formation with the recreation of the proper clinic.

The poured festering peritonitis develops as a result of the timely unoperated appendicitis. Diagnostics of this pathology does not cause difficulties.

Pylephlebitis is a complication of both appendicitis and after-operative period of appendectomy.

The reason of this pathology is acute retrocecal appendicitis. At it development the thrombophlebitis process from the veins of appendix, passes to the veins of bowels mesentery, and then on to the portal vein. Patients complain at the expressed general weakness, pain in right hypochondrium, high hectic temperature of body, fever and strong sweating. Patients are adynamic, with expressed subicteritiousness of the scleras. During palpation painfulness is observed in the right half of abcupula ofn and the symptoms of irritation of peritoneum are not acutely expressed.

In case with rapid passing of disease the icterus appears, the liver is increased, kidney-hepatic insufficiency makes progress, and patients die in 7-10 days from the beginning of disease. At gradual subacute development of pathology the liver and spleen is increased in size, and after the septic state of organism ascites arises.


Diagnostic program

1. Anamnesis information.

2. Information of objective examination.

3. General analysis of blood and urine.

4. Vaginal examination for women.

5. Rectal examination for men.


Instrumental diagnosis

Blood and urine test.

Most people suspected of having appendicitis would be asked to do a blood test. Half of the time, the blood test is normal, so it is not that useful in diagnosing appendicitis.

Two forms of blood tests are commonly done: Full blood count (FBC), also known as complete blood count (CBC), is an inexpensive and commonly requested blood test. It involves measuring the blood for its richness in red blood cells, as well as the number of the various white blood cell constituents in it. The number of white cells in the blood is usually less than 10,000 cells per cubic millimeter. An abnormal rise in the number of white blood cells in the blood is a crude indicator of infection or inflammation going on in the body. Such a rise is not specific to appendicitis alone. If it is abnormally elevated, with a good history and examination findings pointing towards appendicitis, the likelihood of having the disease is higher. In pregnancy, elevation of white blood cells may be normal, without any infection present.

Mild leukocytosis, ranging from 10,000 to 18,000 cells/mm3, usually is present in patients with acute, uncomplicated appendicitis and often is accompanied by a moderate polymorphonuclear predominance. White blood cell counts are variable, however. It is unusual for the white blood cell count to be >18,000 cells/mm3 in uncomplicated appendicitis. White blood cell counts above this level raise the possibility of a perforated appendix with or without an abscess. Urinalysis can be useful to rule out the urinary tract as the source of infection. Although several white or red blood cells can be present from ureteral or bladder irritation as a result of an inflamed appendix, bacteriuria in a urine specimen obtained via catheter generally is not seen in acute appendicitis.

C-reactive protein (CRP) is an acute-phase response protein produced by the liver in response to any infection or inflammatory process in the body. Again, like the FBC, it is not a specific test. It is another crude marker of infection or inflammation. Inflammation at ANY site can lead to a rise in CRP. A significant rise in CRP, with corresponding signs and symptoms of appendicitis, is a useful indicator in the diagnosis of appendicitis. If the CRP continues to be normal after 72 hours of the onset of pain, the appendicitis likely will resolve on its own without intervention. A worsening CRP with good history is a sure signal of impending perforation or rupture and abscess formation.

A urine test in appendicitis is usually normal. It may, however, show blood if the appendix is rubbing on the bladder, causing irritation. It is important to rule out an ectopic pregnancy in women of childbearing age.


Imaging studies




Plain films of the abdomen, although frequently obtained as part of the general evaluation of a patient with an acute abdomen, rarely are helpful in diagnosing acute appendicitis. However, plain radiographs can be of significant benefit in ruling out other pathology. In patients with acute appendicitis, one often sees an abnormal bowel gas pattern, which is a nonspecific finding. The presence of a fecalith is rarely noted on plain films but, if present, is highly suggestive of the diagnosis. A chest radiograph is sometimes indicated to rule out referred pain from a right lower lobe pneumonic process.



Ultrasonography and Doppler sonography provide useful means to detect appendicitis, especially in children, and shows free fluid collection in the right iliac fossa, along with a visible appendix without blood flow in color Doppler. In some cases (15% approximately), however, ultrasonography of the iliac fossa does not reveal any abnormalities despite the presence of appendicitis. This is especially true of early appendicitis before the appendix has become significantly distended and in adults where larger amounts of fat and bowel gas make actually seeing the appendix technically difficult. Despite these limitations, sonographic imaging in experienced hands can often distinguish between appendicitis and other diseases with very similar symptoms, such as inflammation of lymph nodes near the appendix or pain originating from other pelvic organs such as the ovaries or fallopian tubes.



Horseshoe shaped appendix



Case 1. Perforated appendix



Increased vascularity of the appendix

Graded compression sonography has been suggested as an accurate way to establish the diagnosis of appendicitis. The technique is inexpensive, can be performed rapidly, does not require a contrast medium, and can be used even in pregnant patients. Sonographically, the appendix is identified as a blind-ending, nonperistaltic bowel loop originating from the cecum. With maximal compression, the diameter of the appendix is measured in the anteroposterior dimension. Scan results are considered positive if a noncompressible appendix ≥6 mm in the anteroposterior direction is demonstrated. The presence of an appendicolith establishes the diagnosis. Thickening of the appendiceal wall and the presence of periappendiceal fluid is highly suggestive. Sonographic demonstration of a normal appendix, which is an easily compressible, blind-ending tubular structure measuring ≤5 mm in diameter, excludes the diagnosis of acute appendicitis. The study results are considered inconclusive if the appendix is not visualized and there is no pericecal fluid or mass. When the diagnosis of acute appendicitis is excluded by sonography, a brief survey of the remainder of the abdominal cavity should be performed to establish an alternative diagnosis. In females of childbearing age, the pelvic organs must be adequately visualized either by transabdominal or endovaginal ultrasonography to exclude gynecologic pathology as a cause of acute abdominal pain. The sonographic diagnosis of acute appendicitis has a reported sensitivity of 55 to 96% and a specificity of 85 to 98%.2830 Sonography is similarly effective in children and pregnant women, although its application is somewhat limited in late pregnancy.

A false-positive scan result can occur in the presence of periappendicitis from surrounding inflammation, a dilated fallopian tube can be mistaken for an inflamed appendix, inspissated stool can mimic an appendicolith, and, in obese patients, the appendix may not be compressible because of overlying fat. False-negative sonogram results can occur if appendicitis is confined to the appendiceal tip, the appendix is retrocecal, the appendix is markedly enlarged and mistaken for small bowel, or the appendix is perforated and therefore compressible.

Additional radiographic studies include barium enema examination and radioactively labeled leukocyte scans. If the appendix fills on barium enema, appendicitis is excluded. On the other hand, if the appendix does not fill, no determination can be made. To date, there has not been enough experience with radionuclide scans to assess their utility.


Computed tomography.

Where it is readily available, CT scan has become frequently used, especially in adults whose diagnosis is not obvious on history and physical examination. Concerns about radiation, however, tend to limit use of CT in pregnant women and children. A properly performed CT scan with modern equipment has a detection rate (sensitivity) of over 95%, and a similar specificity. Signs of appendicitis on CT scan include lack of oral contrast (oral dye) in the appendix, direct visualization of appendiceal enlargement (greater than 6 mm in cross-sectional diameter), and appendiceal wall enhancement with IV contrast (IV dye). The inflammation caused by appendicitis in the surrounding peritoneal fat (so called "fat stranding") can also be observed on CT, providing a mechanism to detect early appendicitis and a clue that appendicitis may be present even when the appendix is not well seen. Thus, diagnosis of appendicitis by CT is made more difficult in very thin patients and in children, both of whom tend to lack significant fat within the abdomen. The utility of CT scanning is made clear, however, by the impact it has had on negative appendectomy rates. For example, use of CT for diagnosis of appendicitis in Boston, MA has decreased the chance of finding a normal appendix at surgery from 20% in the pre-CT era to only 3% according to data from the Massachusetts General Hospital.

High-resolution helical CT also has been used to diagnose appendicitis. On CT scan, the inflamed appendix appears dilated (>5 cm) and the wall is thickened. There is usually evidence of inflammation, with "dirty fat," thickened mesoappendix, and even an obvious phlegmon. Fecaliths can be easily visualized, but their presence is not necessarily pathognomonic of appendicitis. An important suggestive abnormality is the arrowhead sign. This is caused by thickening of the cecum, which funnels contrast agent toward the orifice of the inflamed appendix. CT scanning is also an excellent technique for identifying other inflammatory processes masquerading as appendicitis.

Several CT techniques have been used, including focused and nonfocused CT scans and enhanced and nonenhanced helical CT scanning. Nonenhanced helical CT scanning is important, because one of the disadvantages of using CT scanning in the evaluation of right lower quadrant pain is dye allergy. Surprisingly, all of these techniques have yielded essentially identical rates of diagnostic accuracy: 92 to 97% sensitivity, 85 to 94% specificity, 90 to 98% accuracy, and 75 to 95% positive and 95 to 99% negative predictive values. The additional use of a rectally administered contrast agent did not improve the results of CT scanning.


Pic. Acute uncomplicated appendicitis


Fig. Transverse CT images in 62-year-old man with perforated appendicitis. The appendix (arrowheads) is traceable. (a)Image shows defect (straight arrow) of appendiceal wall enhancement, abscess (Ab), and extraluminal air (curved arrow). (b) Image shows abscess (Ab) and extraluminal appendicolith (arrow).


Laparoscopy can serve as both a diagnostic and therapeutic maneuver for patients with acute abdominal pain and suspected acute appendicitis. Laparoscopy is probably most useful in the evaluation of females with lower abdominal complaints, because appendectomy is performed on a normal appendix in as many as 30 to 40% of these patients. Differentiating acute gynecologic pathology from acute appendicitis can be effectively accomplished using the laparoscope.


Table. Alvarado Scale for the Diagnosis of Appendicitis





Migration of pain





Nausea and/or vomiting

Right lower quadrant tenderness




Laboratory values


Elevated temperature Leukocytosis

Left shift in leukocyte count





Total points 10


Differential diagnostics

Acute appendicitis is differentiated with the diseases which are accompanied by pain in the abcupula ofn.

The differential diagnosis of acute appendicitis is essentially the diagnosis of the acute abdomen. This is because clinical manifestations are not specific for a given disease but are specific for disturbance of a given physiologic function or functions. Thus, an essentially identical clinical picture can result from a wide variety of acute processes within the peritoneal cavity that produce the same alterations of function as does acute appendicitis.

The accuracy of preoperative diagnosis should be approximately 85%. If it is consistently less, it is likely that some unnecessary operations are being performed, and a more rigorous preoperative differential diagnosis is in order. A diagnostic accuracy rate that is consistently >90% should also cause concern, because this may mean that some patients with atypical, but bona fide, cases of acute appendicitis are being "observed" when they should receive prompt surgical intervention. The Haller group, however, has shown that this is not invariably true. Before that group's study, the perforation rate at the hospital at which the study took place was 26.7%, and acute appendicitis was found in 80% of the patients undergoing operation. By implementing a policy of intensive inhospital observation when the diagnosis of appendicitis was unclear, the group raised the rate of acute appendicitis found at operation to 94%, but the perforation rate remained unchanged at 27.5%. The rate of false-negative appendectomies is highest in young adult females. A normal appendix is found in 32 to 45% of appendectomies performed in women 15 to 45 years of age.

A common error is to make a preoperative diagnosis of acute appendicitis only to find some other condition (or nothing) at operation.

Food toxicoinfection.

Complaints for pain in the epigastric area of the intermittent character, nausea, vomiting and liquid emptying are the first signs of disease. The state of patients progressively gets worse from the beginning. Next to that, it is succeeded to expose that a patient used meal of poor quality. However, here patients do not have phase passing, which is characteristic of acute appendicitis, and clear localization of pain. Defining the symptoms of irritation of peritoneum is not succeeded, the peristalsis of intestine is, as a rule, increased.

Acute gastroenteritis.

Acute gastroenteritis is common but usually can be easily distinguished from acute appendicitis. Gastroenteritis is characterized by profuse diarrhea, nausea, and vomiting. Hyperperistaltic abdominal cramps precede the watery stools. The abdomen is relaxed between cramps, and there are no localizing signs. Laboratory values vary with the specific cause.

Acute pancreatitis.

In anamnesis in patients with this pathology there is a gallstone disease, violation of diet and use of alcohol. Their condition from the beginning of a disease is heavy. Pain is considerably more intensive, than during appendicitis, and is concentrated in the upper half of abcupula ofn. Vomiting is frequent and does not bring to the recovery of patients.

Perforative peptic and duodenum ulcer.

Diagnostic difficulties during this pathology arise up only on occasion. They can be in patients with the covered perforation, when portion of gastric juice flows out in an abdominal cavity and stays too long in the right iliac area, or in case of atypical perforations. Taking it into account, it is needed to remember, that the pain in the perforative ulcer is considerably more intensive in epigastric, instead of in the right iliac area. On the survey roentgenogram of organs of abdominal cavity under the right cupula of diaphragms free gases can be found.


Gynecologic disorders

Diseases of the female internal reproductive organs that may erroneously be diagnosed as appendicitis are, in approximate descending order of frequency, pelvic inflammatory disease, ruptured graafian follicle, twisted ovarian cyst or tumor, endometriosis, and ruptured ectopic pregnancy.

Pelvic Inflammatory Disease.

In pelvic inflammatory disease the infection usually is bilateral but, if confined to the right tube, may mimic acute appendicitis. Nausea and vomiting are present in patients with appendicitis, but in only approximately 50% of those with pelvic inflammatory disease. Pain and tenderness are usually lower, and motion of the cervix is exquisitely painful. Intracellular diplococci may be demonstrable on smear of the purulent vaginal discharge. The ratio of cases of appendicitis to cases of pelvic inflammatory disease is low in females in the early phase of the menstrual cycle and high during the luteal phase. The careful clinical use of these features has reduced the incidence of negative findings on laparoscopy in young women to 15%.

Ruptured Graafian Follicle. Ovulation commonly results in the spillage of sufficient amounts of blood and follicular fluid to produce brief, mild lower abdominal pain. If the amount of fluid is unusually copious and is from the right ovary, appendicitis may be simulated. Pain and tenderness are rather diffuse. Leukocytosis and fever are minimal or absent. Because this pain occurs at the midpoint of the menstrual cycle, it is often called mittelschmerz.

Twisted Ovarian Cyst.

Serous cysts of the ovary are common and generally remain asymptomatic. When right-sided cysts rupture or undergo torsion, the manifestations are similar to those of appendicitis. Patients develop right lower quadrant pain, tenderness, rebound, fever, and leukocytosis. If the mass is palpable on physical examination, the diagnosis can be made easily. Both transvaginal ultrasonography and CT scanning can be diagnostic if a mass is not palpable.

Torsion requires emergent operative treatment. If the torsion is complete or longstanding, the pedicle undergoes thrombosis, and the ovary and tube become gangrenous and require resection. Leakage of ovarian cysts resolves spontaneously, however, and is best treated nonoperatively.

Ruptured Ectopic Pregnancy.

Blastocysts may implant in the fallopian tube (usually the ampullary portion) and in the ovary. Rupture of right tubal or ovarian pregnancies can mimic appendicitis. Patients may give a history of abnormal menses, either missing one or two periods or noting only slight vaginal bleeding. Unfortunately, patients do not always realize they are pregnant. The development of right lower quadrant or pelvic pain may be the first symptom. The diagnosis of ruptured ectopic pregnancy should be relatively easy. The presence of a pelvic mass and elevated levels of chorionic gonadotropin are characteristic. Although the leukocyte count rises slightly (to approximately 14,000 cells/mm3), the hematocrit level falls as a consequence of the intra-abdominal hemorrhage. Vaginal examination reveals cervical motion and adnexal tenderness, and a more definitive diagnosis can be established by culdocentesis. The presence of blood and particularly decidual tissue is pathognomonic. The treatment of ruptured ectopic pregnancy is emergency surgery.

The apoplexy of ovary more frequent is with young women and, as a rule, on 10-14 day after menstruation. Pain appears suddenly and irradiate in the thigh and perineum. At the beginning of disease there can be a collapse. However, the general condition of patients suffers insignificantly. When not enough blood was passed in the abdominal cavity, all signs of pathology of abdominal cavity organs calm down after some time. Signs, which are characteristic of acute anemia, appear at considerable hemorrhage. Abdomen more frequent is soft and painful down, (positive Kulenkampff's symptom: acute pain during palpation of stomach and absent tension of muscles of the front abdominal wall).

During paracentesis of back fornix the blood which does not convolve is got.

Extra-uterine pregnancy.

A necessity to differentiate acute appendicitis with the interrupted extra-uterine pregnancy arises, when during the examination the patient complains at the pain only down in the stomack, more to the right. Taking it into account, it is needed to remember, that at extra-uterine pregnancy a few days before there can be intermittent pain in the lower part of the abdomen, sometimes excretions of coffee colour appear from vagina. In anamnesis often there are the present gynaecological diseases, abortions and pathological passing of pregnancy. For the clinical picture of such patient inherent sudden appearance of intensive pain in lower part of the abdomen. Often there is a brief loss of consciousness. During palpation considerable painfulness is localized lower, than at appendicitis, the abdomen is soft, the positive Kulenkampff's symptom is determined. Violations of menstrual cycle testify for pregnancy, characteristic changes are in milk glands, vagina and uterus. During the vaginal examination it is sometimes possible to palpate increased tube of uterus. The temperature of body more frequently is normal. If hemorrhage is small, the changes in the blood test are not present. The convincing proof of the broken extra-uterine pregnancy is the dark colour of blood, taken at punction of back fornix of vagina.

Acute cholecystitis.

The high placing of vermiform appendix in the right half of abdomen during its inflammation can cause the clinic somewhat similar to acute cholecystitis. But unlike appendicitis, in patients with cholecystitis the pain is more intensive, has cramp-like character, is localized in right hypochondrium and irradiate in the right shoulder and shoulder-blade. Also the epigastric phase is absent. The attack of pain can arise after the reception of spicy food and, is accompanied by nausea and frequent vomiting by bile. In anamnesis patients often have information about a gallstone disease. During examination intensive painfulness is observed in right hypochondrium, increased gall-bladder and positive symptoms Murphy's and Ortner's.

Right-side kidney colic.

For this disease tormina at the level of kidney and in lumbus is inherent, hematuria and dysuric signs which can take place at the irritation of ureter by the inflamed appendix. Intensity of pain in kidney colic is one of the basic differences from acute appendicitis. Pain at first appears in lumbus and irradiate downward after passing of ureter in genital organs and front surface of the thigh. In diagnostics urogram survey is important, and if necessary chromocystoscopy. Absence of function of right kidney to some extent allows to eliminate the diagnosis of acute appendicitis.

Acute mesenteric adenitis.

Acute mesenteric adenitis is the disease most often confused with acute appendicitis in children. Almost invariably, an upper respiratory tract infection is present or has recently subsided. The pain usually is diffuse, and tenderness is not as sharply localized as in appendicitis. Voluntary guarding is sometimes present, but true rigidity is rare. Generalized lymphadenopathy may be noted. Laboratory procedures are of little help in arriving at the correct diagnosis, although a relative lymphocytosis, when present, suggests mesenteric adenitis. Observation for several hours is in order if the diagnosis of mesenteric adenitis seems likely, because it is a self-limited disease. However, if the differentiation remains in doubt, immediate exploration is the safest course of action.

Human infection with Yersinia enterocolitica or Yersinia pseudotuberculosis, transmitted through food contaminated by feces or urine, causes mesenteric adenitis as well as ileitis, colitis, and acute appendicitis. Many of the infections are mild and self limited, but they may lead to systemic disease with a high fatality rate if untreated. The organisms are usually sensitive to tetracyclines, streptomycin, ampicillin, and kanamycin. A preoperative suspicion of the diagnosis should not delay operative intervention, because appendicitis caused by Yersinia cannot be clinically distinguished from appendicitis due to other causes. Approximately 6% of cases of mesenteric adenitis are caused by Yersinia infection.

Salmonella typhimurium infection causes mesenteric adenitis and paralytic ileus with symptoms similar to those of appendicitis. The diagnosis can be established by serologic testing. Campylobacter jejuni causes diarrhea and pain that mimics that of appendicitis. The organism can be cultured from stool.


Other intestinal disorders


Meckel's Diverticulitis.

Meckel's diverticulitis gives rise to a clinical picture similar to that of acute appendicitis. Meckel's diverticulum is located within the distal 2 ft of the ileum. Meckel's diverticulitis is associated with the same complications as appendicitis and requires the same treatmentprompt surgical intervention. Resection of the segment of ileum bearing the diverticulum with end-to-end anastomosis can nearly always be done through a McBurney incision, extended if necessary, or laparoscopically.

Crohn's Enteritis.

The manifestations of acute regional enteritisfever, right lower quadrant pain and tenderness, and leukocytosisoften simulate acute appendicitis. The presence of diarrhea and the absence of anorexia, nausea, and vomiting favor a diagnosis of enteritis, but this is not sufficient to exclude acute appendicitis. In an appreciable percentage of patients with chronic regional enteritis, the diagnosis is first made at the time of operation for presumed acute appendicitis. In cases of an acutely inflamed distal ileum with no cecal involvement and a normal appendix, appendectomy is indicated. Progression to chronic Crohn's ileitis is uncommon.

Colonic Lesions.

Diverticulitis or perforating carcinoma of the cecum, or of that portion of the sigmoid that lies in the right side, may be impossible to distinguish from appendicitis. These entities should be considered in older patients. CT scanning is often helpful in making a diagnosis in older patients with right lower quadrant pain and atypical clinical presentations.

Epiploic appendagitis probably results from infarction of the colonic appendage(s) secondary to torsion. Symptoms may be minimal, or there may be continuous abdominal pain in an area corresponding to the contour of the colon, lasting several days. Pain shift is unusual, and there is no diagnostic sequence of symptoms. The patient does not look ill, nausea and vomiting are unusual, and appetite generally is unaffected. Localized tenderness over the site is usual and often is associated with rebound without rigidity. In 25% of reported cases, pain persists or recurs until the infarcted epiploic appendage is removed.



Acute cholecystitis is inflammation of gall-bladder. After frequency this disease takes second place after appendicitis and makes about 10 % in relation to all acute surgical diseases of organs of abdominal cavity.


Symptoms and clinical passing

The disease, as a rule, begins after violation of diet: reception of plenty of rich, meat food, especially in combination with strong drinks.

Pain syndrome. Characteristic for it is great arching pain in right hypochondrium and epigastric area with an irradiation in right supraclavicular area and right shoulder. If pain syndrome has the strongly expressed cramp-like character, it is named hepatic colic.

Cholecystitis usually presents as a pain in the right upper quadrant. This is known as biliary colic. This is initially intermittent, but later usually presents as a constant, severe pain. During the initial stages, the pain may be felt in an area totally separate from the site of pathology, known as referred pain. The pain is originally located in the right upper quadrant but the referred pain may occur in the right scapula region (Boas' sign).

This may also present with the above mentioned pain after eating greasy or fatty foods such as pastries, pies, and fried foods.

Dyspepsia syndrome. Frequent symptoms which disturb a patient, are nausea, frequent vomitting, at first by gastric maintenance, and later with a touch of bile. Afterwards feelings of swelling of stomach, delay of emptying and gases often join to them.

This is usually accompanied by a low-grade fever, diarrhea, and granulocytosis. The gallbladder may be tender and distended. More severe symptoms such as high fever, shock and jaundice indicate the development of complications such as abscess formation, perforation or ascending cholangitis. Another complication, gallstone ileus, occurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading to symptoms of intestinal obstruction.

Examination. During examination almost in all patients subicterus of sclera even at the normal passage of bile can be observed. Tongue, as a rule, assesses by stratifications of whiter-grey colour. Patients complain for dryness in mouth. In difficult cases the tongue is usually dry, assessed by white stratification with a yellow spot in the center, that depends on passing of attack of disease.

Increase of temperature of body is brief and insignificant (on the average to 37,2 0) at catarrhal cholecystitis and more proof (within the limits of 38 0 ) at its destructive forms.

Tachycardia to a certain extent testifies the degree of intoxication. At first hours of disease the pulse, usually, is relevant to the temperature, and at progress of process, especially with development of peritonitis, it becomes frequent and of weak filling.

During palpation painfulness in the place of crossing of right costal arc with the external edge of direct muscle of stomach can be observed (the Kehr's point). By superficial and deep palpation of right hypochondrium, as a rule, painfulness, increased gall-bladder is exposed, that can be important as a symptom, and sometimes determining for the diagnosis.

The row of characteristic symptoms is determined in the clinic of acute cholecystitis

Murphy's symptoms is a delay of breathing during palpation of gall-bladder on inhalation.

Kehr's symptom is strengthening of pain at pressure on the area of gall-bladder, especially on deep inhalation.

Ortner's symptom painfulness at the easy pattering on right costal arc by the edge of palm.

Mussy's symptom painfulness at palpation between the legs (above a collar-bone) of right nodding muscle.

Blumberg's signs are the increases of painfulness at the rapid taking away of fingers by which a front abdominal wall is pressed on. This symptom is not pathognomic for cholecystitis but matters very much in diagnostics of peritonitis.

It is also needed to mark the importance of gradation of expression of symptoms: acutely positive, poorly positive, doubtful, absent.

Symptoms of acute cholecystitis can grow during 23 hours, and then without some treatment, under act of hot-water bottle or only after the conservative treatment is begun, quickly go to the slump and disappear completely. It always means, that the reason which caused acute inflammation is liquidated (a spasm disappeared, concrement passes by a duct, the ball of mucus moves up and others).

Destructive cholecystitis by the demonstration is the most difficult clinical picture. Thus, gangrenous cholecystitis as a rule, runs across with the acutely expressed phenomena of intoxication and is accompanied by the clinic of bilious peritonitis. The perforation can complicate phlegmonous or gangrenous cholecystitis and then the sudden worsening of the patients condition comes on the background of the expressed clinic of destructive process. It shows up at the beginning the sudden strengthening of pain and rapid growth of the phenomena of peritonitis. But it is needed to mark that such clinical picture can develop only in case of perforated maintenance of gall-bladder in free abdominal cavity.

Laboratory information. Leukocytosis within the limits of 10x109/L and more, change of leukocytic formula to the left, lymphopenia and increased ESR. Laboratory values may be notable for an elevated alkaline phosphatase, possibly an elevated bilirubin (although this may indicate choledocholithiasis), and possibly an elevation of the WBC count. CRP (C-reactive protein) is often elevated. The degree of elevation of these laboratory values may depend on the degree of inflammation of the gallbladder. Patients with acute cholecystitis are much more likely to manifest abnormal laboratory values, while in chronic cholecystitis the laboratory values are frequently normal.

Sonographic examination of gall-bladder can expose the increase of its sizes, bulge of walls, development of perivesical abscesses, presence or absence of concrement and their sizes. Sonography is a sensitive and specific modality for diagnosis of acute cholecystitis; adjusted sensitivity and specificity for diagnosis of acute cholecystitis are 88% and 80%, respectively. The diagnostic criteria are gallbladder wall thickening greater than 3mm, pericholecystic fluid and sonographic Murphy's sign. Gallstones are not part of the diagnostic criteria as acute cholecystitis may occur with or without them.



Sonography. Acute calculous cholecystitis.


Sonography. Acute calculous phlegmonous cholecystitis.


Sonography. Acute calculous gangrenous cholecystitis


Sciagraphy survey of organs of abdominal cavity allows to establish the presence X-ray photography-positive of concrement with maintenance of calcium in the projection of gall-bladder.

CT scan. The reported sensitivity and specificity of CT scan findings are in the range of 9095%. CT is more sensitive than ultrasonography in the depiction of pericholecystic inflammatory response and in localizing pericholecystic abscesses, pericholecystic gas, and calculi outside the lumen of the gallbladder. CT cannot see noncalcified gallbladder calculi, and cannot assess for a Murphy's sign.


Variants of clinical passing and complications

Clinical passing of acute cholecystitis is various and depends on the row of reasons among which degree of violation of passage of bile by a cystic duct and choledochus, virulence of infection, presence or absence of pancreato-cystic reflux (pelting of pancreatic juice) have the most value. To this passing it is needed to add the preceding anatomic and functional changes of gall-bladder and adjoining organs, and also the state of protective and regulator mechanisms of patient.

Features of passing of acute cholecystitis in the declining and old-year patients. For them large frequency of development of destructive forms of cholecystitis and their complication by peritonitis are characteristic. Thus, it is needed to state that such changes in gall-bladder can develop already in the first hour of peritonitis as a result of perforation of bubble. Atipical passing in these patients shows up, mainly, by disparity of clinical picture of disease to the pathomorphologic changes present in gall-bladder. In clinical picture in patients with the first plan the symptoms of intoxication come often forward, while pain and signs of peritonitis can be not acutely expressed.

Hydropsy of gall-bladder is its aseptic inflammation, that arises up as a result of blockade of cystic duct by concrement or mucus. The bile from a bubble is sucked in, and on replacement transparent exudation accumulates in its formation. During palpation increased and unpainfully gall-bladder is marked in patients.

Empyema of gall-bladder is unliquidated timely hydropsy, that at repeated infection is transformed in a new form. Gall-bladder in such patients is palpated as a dense, moderately painful formation, however, the symptoms of irritation of peritoneum, as a rule, are absent. The high temperature of body, chill are periodically observed. In blood high leucocytosis with the change of formula of blood to the left is present.

Biliary pancreatitis. Worsening of the patients condition, appearance of pain, frequent vomitting, signs of cardio-vascular insufficiency, high amylasuria, presence of infiltrate in epigastric area and positive Voskresensky's and Mayo-Robson's symptoms are its basic signs.

An icterus arises up at violation of passage of bile in duodenum as a result of obturation of choledochus by concrement, by putty or through the edema of head of pancreas. Thus icterus sclera, bilirubinemia, dark urine and light unpainted excrement arise.

Cholangitis. The Sharko triad is characteristic for the patient with this pathology. Next to pain syndrome and icterus, the temperature of body rises to 3839 0, there is a fever, high leucocytosis and decline of sizes of functional tests of liver is observed.

Hepatitis shows up by icterus, growth of the phenomena of general weakness, increase in the blood of indexes of alanine aminotransferase and asparaginase and alkaline phosphatase. Liver at this pathology during palpation is painful with acute edges.

Infiltrate is a complication, that can arise on 34 days after the attack of acute cholecystitis. Dull pain presence of dense tumular formation with unclear contours in right hypochondrium, increase of temperature of body to 37,538 0 that negative symptoms of irritation of peritoneum are characteristic for it.

Abscess. Patients with this pathology complain about high temperature, pain in the right overhead quadrant of abdomen, where painful tumular formation is palpated, the fever, general weakness, absence of appetite, icterus, sometimes vomitting. Roentgenologicly in right hypochondrium the horizontal level of liquid and gas is observed above it. High leucocytosis with the change of leukocytic formula to the left is present in blood.

Hepatic-kidney insufficiency often can arise at the most difficult forms of cholecystitis. The general condition of patient is difficult, acutely expressed intoxication, excitation, hallucinations, delirium, oliguria and anuria are observed.

Gall bladder perforation (GBP) is a rare but life-threatening complication of acute cholecystitis. The early diagnosis and treatment of GBP are crucial to decrease patient morbidity and mortality.

Approaches to this complication will vary based on the condition of an individual patient, the evaluation of the treating surgeon or physician, and the facilities' capability. Perforation can happen at the neck from pressure necrosis due to the impacted calculus, or at the fundus. It can result in a local abscess, or perforation into the general peritoneal cavity. If the bile is infected, diffuse peritonitis may occur readily and rapidly and may result in death A retrospective study looked at 332 patients who received medical and/or surgical treatment with the diagnosis of acute cholecystitis. Patients were treated with analgesics and antibiotics within the first 36 hours after admission (with a mean of 9 hours), and proceeded to surgery for a cholecystectomy. Two patients died and 6 patients had further complications. The morbidity and mortality rates were 37.5% and 12.5%, respectively in the present study. The authors of this study suggests that early diagnosis and emergency surgical treatment of gallbladder perforation are of crucial importance.

Peritonitis is the most frequent complication during the perforation of gall-bladder in free abdominal cavity and shows up by tormina and repeated vomitting. Patients are covered with a death-damp, the skin is pale, arterial pressure falls, pulse is frequent and of weak filling. During the objective inspection the tension of muscles of front abdominal wall is marked, positive guardian symptom in the right half of abdomen or along it is observed.


Differential diagnostics

Perforated ulcer. For this disease the Mondor's triad (knife-like pain, tension of muscles of front abdominal wall and ulcerous anamnesis) and positive Spizharskyy's symptom are characteristic (disappearance of hepatic dullness). During roentgenoscopy survey of organs of abdominal cavity in a patient pneumoperitoneum as sickle-shaped strip under the right or left dome of diaphragm is exposed.

Kidney colic. Pain at right-side kidney colic also can be localized in right hypochondrium. However, it is always accompanied by disorders of urination, and at cholecystitis, it as a rule, is not present. Next to it, kidney pain always irradiates downward after passing of ureter, in privy parts. Except, for this pathology micro- or macrohematuria, presence of concrement in a bud, exposed at sonography and on survey urogram, absence of function of bud during chromocystoscopy can be characteristic.

Acute appendicitis. It is needed always to remember, that the subhepatic location of the pathologically changed appendix is also able to show up pain in right hypochondrium. However, for patients with acute appendicitis beginning of pain in epigastric area, absence of hepatic anamnesis, expressed dyspeptic phenomena, inflammatory changes from the side of gall-bladder at sonography are inherent.

Heart attack of myocardium. The so called cholecysto-cardial syndrome which quite often imitates stenocardia pain and suspicion on possibility of origin of heart attack of myocardium can develop. Electrocardiography examination is decisive in establishment of diagnosis. However, laparoscopy is applied in doubtful cases.

Pancreatitis. Acute pancreatitis is accompanied by the expressed pain in the epigastric area of belting character. At palpation in left costal-vertebral corner patients feel painfulness (the Mayo-Robson's symptom), and it is not at cholecystitis.




The basis of disease of pancreas is degenerative-inflammatory processes which are considered to be acute pancreatitis, the so called autolysis tissue by its own enzymes. In the structure of acute pathology of organs of abdominal cavity this disease takes the third place after acute appendicitis and cholecystitis. Women suffer from acute pancreatitis 33,5 times more frequently than men.


Symptoms and clinical passing

The diagnosis of gallstone pancreatitis should be suspected if the patient has a prior history of biliary colic. Although gallstone pancreatitis is the most common cause of pancreatitis, other etiologies must be considered, prior to initiating treatment, like moderate to heavy alcohol consumption over a period of years. Other causes include medication, genetic diseases, infectious agents, postoperative states, endoscopic procedure involving pancreatic and bile ducts and other types of injury to pancreas. It goes without saying that a detailed history and careful physical examination are the first step towards making the diagnosis. Laboratory and radiological investigations are critical for diagnosis as well as prediction of prognosis when a patient presents with gallstone pancreatitis. Documenting an elevated serum amylase and/or lipase is helpful in diagnosing pancreatitis. Serum amylase is elevated in at least 75% of cases of acute pancreatitis and remains elevated for 5-10 days in most patients. However, amylase lacks specificity for pancreatitis because it can be elevated in other disorders. Lipase is more specific for pancreatitis, but both enzymes may be increased in renal failure and various abdominal conditions (e.g., perforated ulcer, mesenteric vascular occlusion and intestinal obstruction). Other causes of increased serum amylase include salivary gland dysfunction, macro amylasemia, and tumors that secrete amylase.  Serum lipase has a longer half life than amylase and therefore tends to remain elevated for longer. Using a cut-off of three times the upper limit of normal, the sensitivity of serum lipase for pancreatitis approaches 90% in patients presenting with abdominal pain. A urine dipstick for trypsinogen-2 has sensitivity and specificity of more than 90% for acute pancreatitis. 

The disease begins suddenly, after the surplus reception of rich spicy food and use of alcohol. Pain, vomiting and phenomena of dynamic intestinal obstruction are considered the most characteristic signs of acute pancreatitis.

A stomach-ache is permanent and so strong, that can result in shock, localized in an epigastric area and left hypochondrium. Some patients feel pain in right hypochondrium with irradiation in the back, loin or breastbone.

Pain irradiation on acute pancreatitis

In a short period of time after appearance of pain there is a repeated strong vomiting, that does not facilitate the state of patient.

In general vomiting is considered a frequent and characteristic symptom. It is repeated or continuous and never brings facilitation. Vomit masses contain bile, as admixture, and at the difficult form of acute pancreatitis remind coffee-grounds.

Nausea, hiccup, belch and dryness in a mouth are attributed as less characteristic symptoms of this pathology.

During the examination the skin is pale, often subicterus. Some patients have cyanosys with a marble picture as a result of violation of microcirculation. Later the component of respiratory insufficiency can join it. At progressive general condition the patient quickly gets worse to passing of acute pancreatitis, intoxication grows. The skin takes shelter with sticky sweat.

The temperature of body of patients at the beginning of disease can be normal. It rises at resorption of products of autolysis tissue and development of inflammatory process in bilious ways.

The pulse in most cases is at first slow, then becomes frequent, notedly passing ahead the increase of temperature of body.

Arterial pressure goes down.

The tongue in the first hour of disease is moist, assessed by white and grey raid. At vomiting by bile the raid has yellow or greenish tint.

The abdominal is blown away, peristaltic noises are loosened. The signs of paresis of stomach and intestine demonstrate early. They need to be included in the pathological process of mesentery root of bowel. At palpation painfulness in an epigastric area and in right, and sometimes and in left, hypochondrium is marked. However, in spite of great pain in stomach, it remains soft for a long time. A little later there is moderate tension or resistance of muscles of front abdominal wall.

Poor local symptoms during heavy intoxication are characteristic for the early period of acute pancreatitis. Later there are symptoms of irritation of peritoneum, and at percussion dulling is marked in lateral parts of abdominal as a result of accumulation of liquid, and also the sign of aseptic phlegmon of retroperitoneal cellulose as slurred or edema of lumbar area is seen. For diagnostics of acute pancreatitis there is the row of characteristic symptoms which have different clinical value.

The Mondors symptom is violet spots on face and trunk.

The Lagermph's symptom is acute cyanosys of person.

The Halsted's Symptom is cyanosys of abdominal skin.

The Gray's symptom is cyanosys of lateral walls of abdomen.



The Kullen's symptom is the yellow colouring of skin near a belly-button.

The Korte's symptom is painful resistance as a lumbar bar in a epigastric area on 67 cm higher belly-button.

The Voskresynskyy's symptom is absence of pulsation of abdominal aorta in an epigastric area.

The Mayo-Robson's symptom is feeling of pain at pressure by fingers in the left costal-vertebral corner.

The Rozdolskyy's symptom painfulness at percussion above pancreas.

The Blumberg's symptom in patients with acute pancreatitis more frequently is low-grade. Such feature of this sign of irritation of peritoneum needs to be explained by character of localization of pathological process, mainly in retroperitoneal spacious.

In clinical passing of pancreatonecrosis it is possible to select three periods (V.S. Saveljev, 1978).

The I period (hemodynamic violations and pancreatogenic shock) lasts during 23 days. Violation of central hemodynamics, diminishment of volume of circulatory blood and disorders of microcirculation, which at first arise as a result of angiospasm, are considered the most characteristic signs, and later as a result of joining of the intravascular rolling up and laying of elements of blood.

The II period (insufficiency of parenchymatous organs) lasts from 3rd to the 7th day of disease. Violation of functions of basic organs and systems, sign of cardio-vascular, hepatic and kidney insufficiency and growth of violations of breathing are thus observed. In this period there is possible damaging of the central nervous system, which is erected mainly to disorders of psyche, appearances of delirium and commas which in the eventual result are the main reasons of patients death.

The III period (postnecrosis dystrophic and festering complications) comes in 12 weeks after the beginning of disease. During it, on the background of progress of necrosis processes in pancreas, the regenerative changes develop, there are parapancreatic infiltrate and cysts, cystic fibrosis of pancreas. Aseptic retroperitoneal phlegmon which strengthens intoxication can also develop. There is festering pancreatitis at joining of infection. During this period such complications, as erosive bleeding, internal or external fistula, retroperitoneal phlegmon, can develop in patients.

From laboratory information leucocytosis which at the necrosis and hemorrhagic forms of pancreatitis sometimes arrives at 25-30 109, lymphopenia, change of leukocytic formula to the left and the increased ESR are characteristic. Growth of activity of amylase of blood and urine is very often marked, and is the important sign of pancreatitis. For estimation of the state of other organs maintenance of general albumen and its factions, glucose of blood, bilirubin, urea, electrolytes, acid-base equilibrium (ABE), and also the state of blood coagulation are determined. It is necessary to mark that the exposure of hypocalcemia is considered a bad predictive sign of heavy passing of acute pancreatitis.

Several tests can help differentiate biliary pancreatitis from other causes of pancreatitis. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase and serum bilirubin are the so-called liver function tests; they should be reviewed before making a confident diagnosis. 

In a recent study, the specificity of a serum ALT level of more than 150 IU/L for diagnosing gallstone pancreatitis was 96%.  Unfortunately, the sensitivity was only 48%. This means that if the patient has a serum high ALT in the appropriate setting one can be fairly sure that the etiology of pancreatitis is biliary, but a normal AL T does not exclude gallstones as a cause. Experimental biochemical markers that may hold promise for assessing the severity of disease include trypsinogen activation peptide, interleukin-6, interleukin-10, procalcitonin, phospholipase A2 and C-reactive protein levels. Currently, these markers have limited clinical availability, but there is significant interest in better understanding markers of immune response and pancreatic injury because these could be valuable tools for reliably predicting the severity of acute pancreatitis and supplementing imaging modalities.

Ultrasonic examination of gall-bladder and pancreas often specifies the increase of their sizes, bulge of walls and presence or absence of concrement of gall-bladder and general bilious duct.

The finding of gallstones and dilatation of the extra hepatic biliary tree on cross-sectional abdominal imaging lends further support to the diagnosis of gallstone pancreatitis. However, the sensitivity for detection of dilated bile ducts from biliary obstruction ranges in various studies from 55 to 91% . Trans abdominal ultrasonography seldom visualizes the pancreas in patients with acute pancreatitis due to air in the distended loops of the small bowel.

Pic. Sonography.


Computer tomography enables to describe in details the changes in pancreas and surrounding organs.



Pic. Computer tomography

Helical computerized tomography (CT) is one choice for accurate imaging diagnosis and staging of pancreatitis. A CT allows identification of pancreatic edema, fluid or cysts, and the severity of pancreatitis to be graded, detects complications including development of pseudocysts, abscess, necrosis, hemorrhage, and vascular occlusion. 

The CT criteria for diagnosis of pancreatic necrosis are dependent on the detection of areas which lack glandular enhancement, which may be focal or more diffuse. Balthazar et al.  showed that there was close correlation between the presence and extent of necrosis and course of hospitalization including morbidity and mortality. Based on this work a CT severity index was developed which attempted to use CT as a numeric grading system for the radiological grading of pancreatitis. The system provides a score between 0 and 10 with higher morbidity and mortality found with higher scores. A severity score of 7-10 had 92% complication rate and 17% mortality rate while a score of 0-1 had nil morbidity or mortality. 

Caution in defining pancreatic necrosis is important as areas of peri pancreatic fluid can simulate areas of necrosis. Pancreatic necrosis is ideally detected on scans performed 48-72 hours after the onset of an attack of acute pancreatitis. Scans done within the first 24 hours may be falsely negative or equivocal. Although scans are commonly done at time of admission, the need for a second study should be kept in mind for patients without rapid improvement initially.

The CT finding of CBD stones may have sensitivity as high as 80%, as noted by Baron et al, . who reviewed 69 patients with biliary obstruction, 12 of whom subsequently proved to have CBD stones (10 identified by the CT scan). However, according to experiences of many gastroenterologists, CT is often less sensitive than trans abdominal ultrasound. Contrast-enhanced CT scans are more valuable than noncontrasted ones for assessing the severity of acute pancreatitis. CT scans can be normal in 15-20% of patients with mild pancreatitis. Not all patients with acute pancreatitis require a CT scan. This can be reserved when the diagnosis is in doubt, severe pancreatitis is suspected or conservative management fails.

At sciagraphy survey of organs of abdominal cavity gives a possibility to expose the unfolded horseshoe of duodenum, pneumatization, expansion of transverse colon (the Gobia's symptom). On the 1st stage of diagnostics in the plan of differential diagnosis of acute destructive pancreatitis with other diseases of abdominal cavity, diagnostics of distribution of destructive damaging of different parts of pancreas and estimation of distribution of parapancreatitis is possible only by the method of computer tomography which depending on clinico-laboratory signs and weight of passing is needed to apply in a different period, and sometimes a few times in dynamics with interval of 45 days.

Laparoscopy and laparocentesis are often used for a doubtful diagnosis or necessity of taking away the exudation of abdominal cavity for biochemical or bacteriological examination.

Retrograde endoscopic cholangiopancreatography is used in case of mechanical icterus and suspicion of choledocholithiasis. The last methods are invasive and can if it is necessary transform from diagnostic to manipulation treatments: laparoscopic draining of abdominal cavity at pancreatogenic peritonitis and endoscopic papillotomy at choledocholithiasis and biliary pancreatitis.


Variants of clinical passing and complications

Clinical passing of disease can be abortive, slowly or quickly progressive. At abortive passing the process is limited to acute edema of pancreas with convalescence in 710 days.

Rapid progress is characteristic for pancreatonecrosis. In patients expressed toxemia, impregnation by exudation of retroperitoneal cellulose and development of fermentative hemorrhagic peritonitis can be seen. Strengthening of stomachache, continuous vomiting, proof paresis of intestine, positive symptoms of irritation of peritoneum and growth of hemodynamic violations are the clinical signs of necrosis of pancreas.

There is a formation of parapancreatic infiltrate at slow progress.



Among early complications of acute pancreatitis shock, peritonitis and acute cardiac, pulmonary, hepatic and kidney insufficiency can be distinguished.

Before later complications it is needed to deliver the abscesses of pancreas, subdiaphragmatic, interintestinal abscesses, pyogenic abscess omentum bag, phlegmons of retroperitoneal space and erosive bleeding.

In future formations of pseudocysts, fistula of pancreas, intestinal fistula and development of saccharine diabetes are possible.


Diagnosis program

1. Anamnesis and physical methods of inspection.

2. General analysis of blood and urine.

3. Biochemical blood test (amylase, bilirubin, sugar).

4. Analysis of urine on diastase.

5. Sonography.

6. Computer tomography.

7. Cholecystocholangiography.

8. Endoscopic retrograde cholangiopancreatography.

9. Laparoscopy.

10. Laparocentesis.


Differential diagnostics

Acute pancreatitis needs to be differentiated with the row of acute diseases of organs of abdominal cavity.

Acute mechanical intestinal obstruction. In patients with this pathology pain is of the alternated character and is accompanied by nausea, vomiting, delay of gases and emptying. It is possible to see the Klojber bowls on the sciagram survey of organs of abdominal cavity.

Acute cholecystitis runs with characteristic localization of pain and muscular defense, with presence of increased, painful gall-bladder or infiltrate in right hypochondrium. Often acute (especially lately) pancreatitis develops on the background of gallstone disease (biliary pancreatitis).

Thrombosis or embolism of mesenteric vessels. Both for pancreatitis and for the thrombosis of mesenteric vessels great pain at soft abdomen (absence of defense muscles of front abdominal wall), that precedes to development of peritonitis, is inherent. Yet from the beginning the disease gains heavy character of passing. In anamnesis in such patients a heart disease or heart attack of myocardium rheumatic is met. As a result of gangrene of intestine, the symptoms of peritonitis appear very quickly and intoxication grows. The fragments of mucus shell are found in flushing waters of intestine at the detailed examination, which have the appearance of meat flushing.

A perforated gastric and duodenum ulcer is distinguished by the presence of dagger pain, defense of abdominal wall, ulcerous anamnesis.


Tactics and choice of treatment method

The conservative method is considered the basic one for treatment of acute pancreatitis, but in connection with that unsuccessful conservative treatment of patients with acute pancreatitis can often put a question about the necessity of operation, therefore patients must be in permanent surgical establishment. Thus acute pancreatitis with heavy passing is necessary to be treated under the conditions of separation of intensive therapy.

Before conservative treatment hunger, bed rest, fight against pain and enzymic toxemia, conducting of acid-base state, prophylaxis of festering infection and acute ulcers of digestive duct are to be entered .



Patients stomach is washed by cold soda solution and a cold on an epigastric area and left hypochondrium is used. Medicinal therapy is prescribed also: spasmolytics (papaverine, platyphyllin, no-shparum, baralgine, atropine); inhibitor of protease (contrical, trasilol, gordox, antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive action of inhibitor of protease is marked only in the first days of disease which are subject to conditioned application of large doses. Antibiotics of wide spectrum of action: a) tienam, which most effective in the prophylaxis of festering pancreatitis, as is selected by pancreatic juice; b) cephalosporins (kefzol, cefazoline); c) cefamizine (mefoxine).

Disintoxication therapy is conducted also (5 % but 10 % solutions of glucose, hemodes, reopolyhlukine, polyhlukine, plasma of blood, only from 3 to 5 liters on days, in accordance with a necessity).

For the improvement of rheological properties of blood heparine is prescribed (5 000 ODES every 4 hours).

If patients have the expressed pain syndrome and phenomena of general intoxication during all pain period plus 48 hours (by Bakulev), hunger is used. Such mode lasts on the average of 24 days. The parenteral feed of albuminous hydrolyzate is thus conducted, by the mixtures of amino acid and fatty emulsion. Alkaline water of to 12 l. and albuminous-carbohydrate diet are also appointed. Infusion therapy is complemented by plasma, by albumen, hemodes, reopolyhlukine. The improvements of microcirculation in pancreas are achieved due to introduction of reopolyhlukine, komplamine, trental and heparin 5000 ODES 6 times per days under the control the indexes of the coagulation system of blood. Anticholinergic drug (sulfate of atropine, methacin, platyphyllin), 2-histamin blocker (cimetidine, ranisan, ranitidine, famotidine, omeprazol) are also applied. For the removal of pain: 1) sulfate of the atropine 0,1 % 1 ml + promedol 2 % 1 ml + papaverine 2 % 2 ml + analgin 50 % 2 ml; 2) isotonic solution of chloride of sodium 500 ml + baralgine 5 ml + diphenhydramine hydrochloride 1 % 1 ml + papaverine 2 % 2 ml + magnesium the sulfate 25 % 5 ml + ascorbic acid 5 ml + lipoic acid 0,5 % 2 ml + novocaine 0,5 % 10 ml. are used. From the first days by a nasogastral probe the permanent aspiration of gastric maintenance is conducted also. The Motility function of gastro-intestinal highway gets better at application of cerucal or primperane. With the same purpose forced diuresis (maninil, furosemide, aminophylline) is used on the background of intravenous introduction of plenty of liquid.

At uneffective conservative treatment of patients with acute pancreatitis of middle weight and heavy form it is expedient to apply surgical treatment.

Surgical treatment is carried out for patients with biliary pancreatitis (for a day long from the beginning of disease) in combination with the destructive forms of cholecystitis, at complications of acute pancreatitis by peritonitis, abscess of omentum bag or phlegmon of retroperitoneal cellulose.

Overhead-middle laparotomy, which allows to estimate the state of pancreas, bilious ways and other organs of abdominal cavity, is the best access in this situation. In case of destructive pancreatitis the possible use of lumbar laparotomy from left to right hypochondrium through a mesogastric area is useful.

Cholecystectomy is executed at calculous cholecystitis, phlegmonous inflammation of walls of gall-bladder and biliary pancreatitis. If there are more than 0,9 cm at expansion of choledochus, presence of concrement, ointment-like bile in it, increase of concentration of bilirubin in the whey of blood over 21 mmol/L, choledochuslithotomy is complemented by external draining of choledochus. Information of lithiasis of general bilious duct is absent, cholecystectomy in patients with acute pancreatitis is complemented by external draining of choledochus, better by Pikovskyy method (through stump of cystic duct).

Transduodenal sphincteroplasty is shown at fixed concrement of large duodenal papilla, if they are diagnosed intraoperative, and also in the cases of papillotomy with extraction of concrement when there is no possibility to execute endoscopic operation .

Omentopancreatopexy. After laparotomy and cutting of gastro-colon and gastro-pancreatic ligament mobile part of large omentum through opening in gastro-colon ligament is conducted and fixed by separate stitches to the peritoneum along the overhead and lower edges of pancreas. Such operation needs to be considered rational at the expressed edema of pancreas and presence of necrosis in it.

Abdominisation of pancreas. A cellulose round pancreas (along the lower and overhead edges of body and tail) is infiltrated by solution of novocaine, after it parietal peritoneum is cut. Under the body and tail glands free end of omentum is conducted and is bundled by a gland. This operation is able to warn the hit of enzymes and products of disintegration in retroperitoneal space.

Sequestrectomy is deleting of necrosis part of gland within the limits of nonviable tissue. Operation is executed in a dull way.

Necrectomy (deleting of necrosis part of gland within the limits of healthy tissue) is executed by an acute way: tissue of gland is cut on verge of necrosis and bleeding vessels are carefully bandaged.

The resection of pancreas is deleting the part of organ with its transversal cutting within the limits of the unchanged (ad ulus) tissue of gland. The resections of tail and body of pancreas are distinguished.

Pancreatectomy is a complete deleting of pancreas. Operative treatment is applied infrequently. After the resection of pancreas adequate draining of its bed is very responsible.

The prognosis of disease depends on character of morphological changes of parapancreatic to the cellulose in pancreas. The more difficult destructive changes, the worst the prognosis.



The typical perforation of gastric or duodenum ulcer is strengthening of necrosis process in the area of ulcerous crater with subsequent disturbance of integrity of wall, that result to the permanent effluence of gastroduodenal content and air in a free abdominal cavity.


Diagnosis program

1. Anamnesis and physical examination.

2. Global analysis of blood and urine, biochemical blood test,


3. X-Ray examination of abdominal cavity organs for presence of free gas (pneumoperitoneum).

4. Pneumogastrography, contrasting pneumogastrography.

5. Fiber-gastroduodenoscopy.

6. Sonography of abdominal cavity organs.

7. Laparocentesis with the Neymark diagnostic test (to the 23 ml of abdominal cavity exudate adds 45 drops of the 10 % solution of iodine. If the admixtures of gastric content appear in exudate, then under action of iodine gastric content gets a dirtily-dark blue color).

8. Laparoscopy.



Intestinal obstruction is a complete or partial violation of passing of maintenance by the intestinal tract.

Ileus is commonly defined simply as bowel obstruction. However, authoritative sources define it as decreased motor activity of the GI tract due to non-mechanical causes. In such sense, this does not include motility disorders that result from structural abnormalities, and, therefore, some mechanical obstructions are misnomers, such as gallstone ileus and meconium ileus, and are not true examples of ileus.


Clinical management

Main symptoms:

          moderate, diffuse abdominal discomfort


          abdominal distension

          nausea/vomiting, especially after meals

          lack of bowel movement and/or flatulence

          excessive belching

Beginning of clinical signs of intestinal obstruction is sudden in 12 hours after taking the meal. The pain in the abdomen has the intermittent character and is met in all forms of mechanical intestinal obstruction. However, some types of strangulated intestinal obstruction (node formation, volvulus of thin and colons) can be accompanied by permanent pain. It is needed to mark that at spike intestinal obstruction, invagination and obturation cramp-like pain can be considered as pathognomic sign of disease. For paralytic intestinal obstruction more frequent is inherent permanent pain which is accompanied by the progressive swelling of abdomen. At spastic obstruction of intestine the pain is mainly acute, the abdomen is not blown away, sometimes pulled in.

Nausea and vomiting are met in 7580 % patients with the heaviest forms of high level of intestinal obstruction (node formation, volvulus of small intestine, spike obstruction). At obturation obstruction and invagination they are observed not so often.

There is a characteristic thirst which can be considered as an early symptom. Besides, the higher intestinal obstruction, the greater the thirst.

Swelling of abdomen, the delay of emptying and gases are observed in 8590% patients, mainly, with the high forms of obstruction (volvulus of small intestine, spike intestinal obstruction).

Together with that, for invagination emptying by liquid excrement with the admixtures of mucus and blood are more characteristic.

The abdomen may be distended and tympanic, depending on the degree of abdominal and bowel distention, and may be tender. A distinguishing feature is absent or hypoactive bowel sounds, in contrast to the high-pitched sound of obstruction. The silent abdomen of ileus reveals no discernible peristalsis or succussion splash.

In patients during palpation the soft abdomen is observed, sometimes with easy resistance of front abdominal wall, and at percussion high tympanitis. At auscultation at the beginning of disease increased peristaltic noises are present, then gradual fading of peristalsis is positive (the Mondors symptom, noise of beginning, quietness of end).

There are other symptoms pathognomic for intestinal obstruction.

The Valas symptom is the limited elastic sausage-shaped formation.

The Sklarovs symptom is the noise of intestinal splash.

The Kywul's symptom is the clang above the exaggerated bowel.

The Schlange's symptom is the peristalsis of bowel, that arises after palpation of abdomen.

The Spasokukotsky's symptom is noise of falling drop.

The Hochenegg's symptom incompletely closed anus in combination with balloon expansion of ampoule of rectum.

At survey roentgenoscopy or -graphy of the abdominal cavity in the loops of bowels liquids and gas are observed the Klojbers bowl. (Fig.3; Fig.4)

Fig. 3. Intestinal obstruction.

X-ray examination of abdominal cavity presence of the Klojbers bowels



Fig. 4. Intestinal obstruction.

Mechanism of Klojbers bowels

Presence of liquid levels and air in the intestines


Variants of clinical passing and complications

Strangulated obstruction. The ischemic component is the characteristic feature of this form of intestinal obstruction, that is investigation of squeezing of mesentery vessels, which determines the dynamics of pathomorphologic changes and clinical signs of disease, and the basic place among them belongs to the pain syndrome. Consequently, sudden appearance of disease, acuteness of pain syndrome and ischemic disorders in the wall of bowel cause necrosis changes of area of bowel pulling in a process. It is accompanied by the making progress worsening of the patient condition and origin of endotoxicosis.

Obturation intestinal obstruction(Fig. 5), unlike strangulated, pass not so quickly.

Fig. 5. Obturation mechanical obstruction by tumor.



In its clinical picture on the first place there are the symptoms of violation of passage on the intestine (protracted intermittent pain, flatulence), instead of symptoms of bowel destruction and peritonitis.

For high, especially strangulated, intestinal obstruction progressive growth of clinical signs of disease and violation of secretory function of intestine is inherent. Thus the volume of circulatory blood diminishes, the level of haematocritis rises and leukocytosis grows. There are also deep violations of homeostasis (hypoproteinemia, hypokalemia, hyponatremia, hypoxia and others like that). In patients with low intestinal obstruction above-named signs are less expressed, and their growth is related to more protracted passing of disease. Invagination of bowel which can be characterized by the triad of characteristic signs is the special type of intestinal obstruction with the signs of both obturation and strangulation: 1) periodicity of appearance of the intermittent attacks of pain in the abdomen; 2) presence of elastic, insignificantly painful, mobile formation in an abdominal cavity; 3) appearance of blood in the excrement or its tracks (at rectal examination).(Fig.6.)

Fig. 6. Invagination of small intestine

The special forms of obturation intestinal obstruction is the obstruction caused by gall-stones. The last are got in the small intestine as a result of bedsore in the walls of gall-bladder and bowel, that adjoins to it. It is needed to mention that intestinal obstruction can be caused by concrement with considerably more small diameter than bowel lumen. The mechanism of such phenomenon is related to irritating action of bilious acids on the bowel wall. The last answers this action by a spasm with the dense wedging of stone in the bowel lumen.

Development of intestinal obstruction caused by gall-stones the attack of colic and clinic of acute cholecystitis precede always. Characteristically, that in the process of development of disease the pain caused by acute cholecystitis calms down, whereupon the new pain characteristic of other pathology intestinal obstruction appears.

Dynamic intestinal obstruction is divided into paralytic and spastic(Fig.7). Paralytic obstruction often arises after different abdominal operations, inflammatory diseases of organs of abdominal cavity, traumas and poisonings.


Fig.7. Spastic dynamic intestinal obstrucnion

The reason of spastic intestinal obstruction can be the lead poisonings, low-quality meal, neuroses, hysterias, helminthiasis and others like that. Clinic of dynamic intestinal obstruction is always variable in signs and depends on a reason, that caused it. Disease is characterized by pain in the abdomen, delay of gases and emptying. During palpation the abdomen is blown away, painful, however soft. To diagnose this form of intestinal obstruction is not difficult, especially, if its etiology is known.

Hemostatic intestinal obstruction (Fig.8) develops after embolism or thromboses of mesenteric arteries and thromboses of veins, there can be mixed forms. Embolism of mesenteric arteries arises in patients with heart diseases (mitral and aortic failings, heart attack of myocardium, warty endocarditis) and declared by damaging, mainly, upper mesentery arteries. Beginning of disease, certainly, is acute, with nausea, sometimes vomiting. At first there is a picture of acute abdominal ischemic syndrome, that is often accompanied by shock (frequent pulse, decline of arterial and pulse pressure, death-damp, cyanosys of mucus membranes and acrocyanosis). Patients become excitative, uneasy, occupy the forced knee-elbow position or lie on the side with bound legs.

Fig.8. Hemostatic intestinal obstruction. Embolism of upper mesenteric arteries. Necrosis of small intestines.


During the examination the abdomen keeps symmetry, abdominal wall is soft, the increased peristalsis is heard from the first minutes during 12 hours (hypoxic stimulation of peristalsis), which later goes out gradually (grave quiet). According to the phenomena of intoxication peritonitis grow quickly. At the beginning of disease the delay of gases and emptying is observed, later there is diarrhea with the admixtures of blood in an excrement. When the last is heavy to set macroscopically, it is needed to explore scourage of intestine.

Small-bowel obstruction (SBO). The most common cause of small-bowel obstruction (SBO) is postsurgical adhesions. Postoperative adhesions can be the cause of acute obstruction within 4 weeks of surgery or of chronic obstruction decades later. The incidence of SBO parallels the increasing number of laparotomies performed in developing countries. Another commonly identified cause of SBO is an incarcerated groin hernia. Other etiologies include malignant tumor (20%), hernia (10%), inflammatory bowel disease (5%), volvulus (3%), and miscellaneous causes (2%). The causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and intussusception.

History. Obstruction can be characterized as either partial or complete versus simple or strangulated. No accurate clinical picture exists to detect early strangulation of obstruction.

Abdominal pain, often described as crampy and intermittent, is more prevalent in simple obstruction. Often, the presentation may provide clues to the approximate location and nature of the obstruction. Usually, pain that occurs for a shorter duration of time and is colicky and accompanied by bilious vomiting may be more proximal. Pain that lasts as long as several days, is progressive in nature, and is accompanied by abdominal distention may be typical of a more distal obstruction.

Changes in the character of the pain may indicate the development of a more serious complication (ie, constant pain of a strangulated or ischemic bowel).

Patients also report the following:


            Vomiting - Associated more with proximal obstructions

            Diarrhea - An early finding

            Constipation - A late finding, as evidenced by the absence of flatus or bowel movements

            Fever and tachycardia - Occur late and may be associated with strangulation

            Previous abdominal or pelvic surgery, previous radiation therapy, or both - May be part of the patient's medical history

            History of malignancy - Particularly ovarian and colonic malignancy


Physical Examination

Abdominal distention is present. The duodenal or proximal small bowel has less distention when obstructed than the distal bowel has when obstructed. Hyperactive bowel sounds occur early as GI contents attempt to overcome the obstruction; hypoactive bowel sounds occur late.

Exclude incarcerated hernias of the groin, femoral triangle, and obturator foramina. Proper genitourinary and pelvic examinations are essential. Look for the following during rectal examination:

            Gross or occult blood, which suggests late strangulation or malignancy

            Masses, which suggest obturator hernia

Check for symptoms commonly believed to be more diagnostic of intestinal ischemia, including the following:

            Fever (temperature >100F)

            Tachycardia (>100 beats/min)

            Peritoneal signs

No reliable way exists to differentiate simple from early strangulated obstruction on physical examination. Serial abdominal examinations are important and may detect changes early.

Complications of SBO include the following:


            Intra-abdominal abscess

            Wound dehiscence


            Short-bowel syndrome (as a result of multiple surgeries)

            Death (secondary to delayed treatment)

Large-bowel obstruction (LBO) is an emergency condition that requires early identification and intervention. Approximately 60% of mechanical large-bowel obstructions (LBOs) are caused by malignancies, 20% are caused by diverticular disease, and 5% are the result of colonic volvulus. The most common causes of adult large-bowel obstruction are as follows:

            Neoplasm (benign or malignant)

            Stricture (diverticular or ischemic)

            Volvulus (eg, colonic, sigmoid, cecal)

            Incarcerated hernia

            Intussusception, usually with an identifiable anatomic abnormality in adults but not in children

            Impaction or obstipation

            Gallstone ileus


Neoplasms and diverticular disease

Obstructions caused by tumors tend to have a gradual onset and result from tumor growth narrowing the colonic lumen.

Diverticulitis is associated with muscular hypertrophy of the colonic wall. Repetitive episodes of inflammation cause the colonic wall to become fibrotic and thickened, leading to luminal narrowing.



A colonic volvulus results when the colon twists on its mesentery, which impairs the venous drainage and arterial inflow. Symptoms of this condition are usually abrupt.

A sigmoid volvulus typically occurs in older, debilitated individuals with a history of chronic constipation, or those living in an institutionalized setting.

A cecal volvulus is caused by a congenital defect in the peritoneum, which results in inadequate fixation of the cecum, and increased cecal mobility. Patients usually present with this disorder in the sixth decade of life.


Intussusception is primarily a pediatric disease; however, it is estimated that between 5% and 16% of all intussusceptions in the Western world occur in adults, of which approximately two thirds of adult intussusception cases are caused by tumors. Two main types of intussusception affect the large bowel: enterocolic and colocolic.

Enterocolic intussusceptions involve both the small bowel and the large bowel. These are composed of either ileocolic intussusceptions or ileocecal intussusceptions, depending on where the lead point is located.

Colocolic intussusceptions involve only the colon. They are classified as either colocolic or sigmoidorectal intussusceptions.


Acute colonic pseudo-obstruction/Ogilvie syndrome

Acute colonic pseudo-obstruction (ACPO), or Ogilvie syndrome, has many etiologies. This disorder is typically seen in elderly patients who are hospitalized with a severe illness. In a retrospective review of more than 1400 cases of acute colonic pseudo-obstruction, the most common predisposing conditions were operative and nonoperative trauma (11%), infections (10%), and cardiac disease (10-18%).

History. Obtain the patient's history of bowel movements, flatus, obstipation (ie, no gas or bowel movement), and symptoms. Attempt to distinguish complete bowel obstruction from partial obstruction, which is associated with passage of some gas or stool, and from ileus. Also inquire about the patient's current and past history in an attempt to determine the most likely cause.

Major complaints in patients with large-bowel obstruction (LBO) include abdominal distention, nausea, vomiting, and crampy abdominal pain. An abrupt onset of symptoms makes an acute obstructive event (eg, cecal or sigmoid volvulus) a more likely diagnosis. A history of chronic constipation, long-term cathartic use, and straining at stools implies diverticulitis or carcinoma.

Changes in the patient's caliber of stools (eg, passage of melanotic bloody stools) strongly suggest carcinoma. When associated with weight loss, the likelihood of neoplastic obstruction increases.

A history of recurrent left lower quadrant abdominal pain over several years is more consistent with diverticulitis, a diverticular stricture, or similar problems.

A history of aortic surgery suggests the possibility of an ischemic stricture.


Diagnostic program

1. Anamnesis and physical methods of examination (auscultation of abdomen, percussion and others like that).

2. General analysis of blood, urines and biochemical blood test.

3. Survey sciagraphy of organs of abdominal cavity.

4. Coagulogramm.

5. Electrocardiography.

6. Irrigography.


Small-Bowel Obstruction Workup Approach Considerations

If the diagnosis is unclear, admission and observation are warranted to detect early obstructions. Essential laboratory tests are needed; these include the following:

            Serum chemistries - Results are usually normal or mildly elevated

            Blood urea nitrogen (BUN) level - If the BUN level is increased, this may indicate decreased volume state (eg, dehydration)

            Creatinine level - Creatinine level elevations may indicate dehydration

            Complete blood count (CBC) - The white blood cell (WBC) count may be elevated with a left shift in simple or strangulated obstructions; increased hematocrit is an indicator of volume state (ie, dehydration)

            Lactate dehydrogenase tests


            Type and crossmatch - The patient may require surgical intervention

            Laboratory tests to exclude biliary or hepatic disease are also needed; they include the following:

            Phosphate level

            Creatine kinase level

            Liver panels

Studies have been performed to evaluate the use of water-soluble oral contrast as a tool in the management of SBO and as a predictive tool for nonoperative resolution of adhesive SBO. It does not cause resolution of the SBO, but it may reduce the hospital stay in patients not requiring surgery.


Plain Radiography

Obtain plain radiographs first for patients in whom small-bowel obstruction (SBO) is suspected. At least 2 views, supine or flat and upright, are required. Plain radiographs are diagnostically more accurate in cases of simple obstruction. However, diagnostic failure rates of as much as 30% have been reported.

In one small study, the sensitivity of plain radiography was reported to be 75%, and specificity was reported to be 53%; similar findings were reported in a second study. In another study, plain films were more accurate in the detection of acute SBO and the accuracy was higher if interpreted by more-experienced radiologists.

Plain radiography is of little assistance in differentiating strangulation from simple obstruction. Some have used abdominal radiography to distinguish between complete obstruction and partial or no SBO.

A study by Lappas et al proposed that 2 findings were more predictive of a higher grade or complete SBO: (1) the presence of an air-fluid differential height in the same small-bowel loop and (2) the presence of a mean level width greater than 25 mm.The study found that when the 2 findings are present, the obstruction is most likely high grade or complete. When both are absent, the authors proposed, a low-grade (partial) SBO is likely or nonexistent.

Dilated small-bowel loops with air-fluid levels indicate SBO, as does absent or minimal colonic gas. SBO is demonstrated in the radiographs below.


CT scanning

Computed tomography (CT) scanning is the study of choice if the patient has fever, tachycardia, localized abdominal pain, and/or leukocytosis.

CT scanning is useful in making an early diagnosis of strangulated obstruction and in delineating the myriad other causes of acute abdominal pain, particularly when clinical and radiographic findings are inconclusive. It also has proved useful in distinguishing the etiologies of small-bowel obstruction (SBO), that is, in distinguishing extrinsic causes (such as adhesions and hernia) from intrinsic causes (such as neoplasms and Crohn disease). In addition, CT scanning differentiates the above from intraluminal causes, such as bezoars. The modality may be less useful in the evaluation of small bowel ischemia associated with obstruction.

CT scanning is capable of revealing abscess, inflammatory process, extraluminal pathology resulting in obstruction, and mesenteric ischemia and enables the clinician to distinguish between ileus and mechanical small bowel obstruction in postoperative patients.

The modality does not require oral contrast for the diagnosis of SBO, because the retained intraluminal fluid serves as a natural contrast agent.

Obstruction is present if the small-bowel loop is greater than 2.5 cm in diameter dilated proximal to a distinct transition zone of collapsed bowel less than 1 cm in diameter. A smooth beak indicates simple obstruction without vascular compromise; a serrated beak may indicate strangulation. Bowel wall thickening, portal venous gas, or pneumatosis indicates early strangulation.

One small series reported a sensitivity of 93%, a specificity of 100%, and an accuracy of 94% for CT scanning in the detection of obstructions. Another series reported a sensitivity of 92% and specificity of 71% in the correct identification of partial or complete SBO.


Ultrasonography is less costly and invasive than CT scanning and may reliably exclude SBO in as many as 89% of patients; specificity is reportedly 100%.

In a small study by Jang et al in which the use of bedside ultrasonography by emergency physicians was compared with radiography for the detection of small-bowel obstruction (SBO), emergency physician ̶ performed ultrasonography compared favorably with radiography. Dilated bowel on ultrasonography had a sensitivity of 91% and a specificity of 84% for SBO, while radiography had a sensitivity of 46% and a specificity of 66%.


Large-Bowel Obstruction Workup.

Approach Considerations

Laboratory studies are directed at evaluating the dehydration and electrolyte imbalance that may occur as a consequence of large-bowel obstruction (LBO) and at ruling out ileus as a diagnosis.

Routine complete blood cell count (CBC), serum chemistries, and urine specific gravity should be evaluated. A decreased hematocrit level, particularly with evidence of chronic iron-deficiency anemia, may suggest chronic lower gastrointestinal (GI) bleeding, particularly due to colon cancer. A stool guaiac test also should be performed, for similar reasons.

Obtain a prothrombin time (PT) as well as a type and crossmatch.

Although bowel obstruction, or even constipation, may mildly elevate the white blood cell (WBC) count, substantial leukocytosis should prompt reconsideration of the diagnosis. Ileus, secondary to an intra-abdominal or extra-abdominal infection or another process, is a possibility.

The suggestion of an abnormal anion gap (see the Anion Gap calculator) also should prompt an arterial blood gas (ABG) measurement and/or a serum lactate level measurement.


Plain Radiography

Obtain an upright chest radiograph to determine whether free air is present, which would suggest perforation of a hollow viscus and ileus rather than organic obstruction, as well as flat and upright abdominal radiographs, which may demonstrate dilatation of the small and/or large bowel and air-fluid levels.

Chest radiographs will demonstrate free air if perforation has occurred (see the first image below); abdominal radiographs may be diagnostic of sigmoid or cecal volvulus (ie, kidney bean appearance on the radiograph) (see the second and third images below, respectively). Intramural air is an ominous sign that suggests colonic ischemia. The absence of free air does not exclude perforation (this finding may be absent in half of all perforations).

Tracing colonic air around the colon, into the left gutter, and down into the rectum or demonstrating an abrupt cut-off in colonic air suggests the anatomic location of the obstruction.

A dilated colon without air in the rectum is more consistent with obstruction. The presence of air in the rectum is consistent with obstipation, ileus, or partial obstruction. However, this finding can be misleading, particularly if the patient has undergone rectal examinations or enemas.


Radiocontrast Radiography

Contrast studies include an enema with water-soluble contrast (ie, Gastrografin) (see the following images) or computed tomography (CT) scanning with intravenous (IV) and oral (PO) or rectal (PR) contrast. Contrast studies that reveal a column of contrast ending in a "bird's beak" are suggestive of colonic volvulus.

Indications for imaging with contrast

Radiopaque contrast material may be administered and imaging of the colon may be performed under the following circumstances:

            Perform it if the diagnosis of large bowel obstruction is suspected but not proven

            If differentiation between obstipation and obstruction is required

            If localization is required for surgical intervention


Water-soluble contrast vs barium

Water-soluble Gastrografin has important advantages over barium as a contrast agent and generally should be used first. Gastrografin usually does not cause chemical peritonitis if the patient has colonic perforation, and it has an osmotic laxative effect that may actually wash out an obstipated colon.

If large-bowel perforation is ruled out using a Gastrografin study but a more detailed anatomic definition is required (particularly of the right colon), a barium enema may be performed.


Computed Tomography Scanning

Although computed tomography (CT) scanning is useful to help rule out intra-abdominal abscess or other causes of ileus, this imaging modality is generally not used initially in patients with large-bowel obstruction (LBO), unless the diagnosis is still in question.

CT scanning, particularly with rectal contrast, may demonstrate a mass or evidence of metastatic disease. Generally, the findings do not alter management, because these patients will be explored and operatively decompressed, regardless of the CT scan findings.

CT colography may be useful in evaluating these patients, not only to delineate the source of the obstruction but also to rule out synchronous proximal lesions, which may occur in about 1% of patients and which might motivate a more extended resection if identified and if the patient's condition will tolerate the more extensive procedure.


Flexible Endoscopy

Flexible endoscopy preceded by rectal enema may be useful in evaluating left-sided colonic obstruction, including the anatomic location and pathology of the lesion. Because the cecum is not reached in such cases, the endoscopist must be alert to the possibility of incorrectly identifying anatomic landmarks and the location of the obstruction.

An abdominal radiograph with the tip of the endoscope at the site of the obstruction may be extraordinarily helpful in identifying and documenting the location of the large-bowel obstruction (LBO).

Although flexible endoscopy is relatively comfortable for the patient and provides a better view than rigid sigmoidoscopy, rigid sigmoidoscopy may also be used, depending on the availability of resources and training of personnel.

Right-sided colonic obstruction is more difficult to evaluate without first administering an oral bowel preparation, which is contraindicated in the setting of bowel obstruction.


Differential diagnostics

            Abortion, Threatened

            Alcoholic Ketoacidosis


            Cholecystitis and Biliary Colic in Emergency Medicine



            Diverticular Disease



            Inflammatory Bowel Disease

            Mesenteric Ischemia

Intestinal obstruction must be differentiated with the acute diseases of organs of abdominal cavity.

The perforation of gastroduodenal ulcer, as well as intestinal obstruction, passes acutely with inherent to it by sudden intensive pain and tension of muscles of abdomen. However, in patients with this pathology, unlike intestinal obstruction, the abdomen is not exaggerated, and pulled in with wooden belly tension of muscles of front abdominal wall. There is also characteristic ulcerous anamnesis. Roentgenologic and by percussion pneumoperitoneum is observed. Certain difficulties in conducting of differential diagnostics of intestinal obstruction can arise at atipical passing and in case of the covered perforations.

Acute pancreatitis almost always passes with the phenomena of dynamic intestinal obstruction and symptoms of intoxication and repeated vomiting, with rapid growth. During the examination in such patients, unlike intestinal obstruction, rigidity of abdominal wall and painfulness is observed in the projections of pancreas and positive Korte's symptom and Mayo-Robson's. The examination of diastase of urine and amylase of blood have important value in establishment of diagnosis.

Acute cholecystitis. Unlike intestinal obstruction, patients with this pathology complain for pain in right hypochondrium, that irradiate in the right shoulder-blade, shoulder and right subclavian area. Difficulties can arise, when the symptoms of dynamic intestinal obstruction appear on the basis of peritonitis.

The clinic of kidney colic in the signs and character of passing are similar to intestinal obstruction, however, attacks of pain in the lumbar area with characteristic irradiation in genital parts, the thigh and dysuric disorders help to set the correct diagnosis. Certain difficulties in conducting of differential diagnostics also can arise in difficult patients, at frequent vomiting which sometimes can be observed in patients with kidney colic.


Table. Characteristics of Ileus, Pseudo-obstruction, and Mechanical Obstruction




Mechanical Obstruction (Simple)


Mild abdominal pain, bloating, nausea, vomiting, obstipation, constipation

Crampy abdominal pain, constipation, obstipation, nausea, vomiting, anorexia

Crampy abdominal pain, constipation, obstipation, nausea, vomiting, anorexia

Physical Examination Findings

Silent abdomen, distention, tympanic

Borborygmi, tympanic, peristaltic waves, hypoactive or hyperactive bowel sounds, distention, localized tenderness

Borborygmi, peristaltic waves, high-pitched bowel sounds, rushes, distention, localized tenderness

Plain Radiographs

Large and small bowel dilatation, diaphragm elevated

Isolated large bowel dilatation, diaphragm elevated

Bow-shaped loops in ladder pattern, paucity of colonic gas distal to lesion, diaphragm mildly elevated, air-fluid levels




Peritonitis is the acute or chronic peritoneal inflammation with characteristic local and general changes in the organism and severe dysfunction of organs and vital systems of the organism. Peritonitis is an inflammation of the peritoneum, the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs. Peritonitis may be localized or generalised, and may result from infection (often due to rupture of a hollow organ as may occur in abdominal trauma or appendicitis) or from a non-infectious process.


Symptomatology and clinical course


The clinical picture of acute peritonitis is determined by the character of primary causative lesion, duration of inflammatory process, its extension and also the stage of the disease. Predominant clinical sign is the abdominal pain, which gradually increases. Firstly it is localized in the region of the source of peritonitis and then extends all over the abdomen. Elderly patients may experience lacking pain and even pay no attention on it, but general malaise, loss of appetite, and weakness are evident. This course is also characteristic for postoperative peritonitis, which results from parting of sutures (of anastomosis or site of perforation) or leaking colon carcinoma. Simultaneously with the increase of pain also change the general appearance. The patient looks anxious, with drawn features, hollowed-eyed. Further this is accompanied by nausea and vomiting: on initial stages vomit is of gastric contents, later duodenal and thereafter is of intestinal contents. With progression of the disease vomiting becomes constant, effortless and overcomes into frequent regurgitation by brown fluid with foul-smelling. Patient's lips and tongue are dry, with brown fur. Respiration is of thoracic type and is shallow and rapid. In order to prevent pain the patient speaks very quite. Every change of position results in increase of pain, thus the patient lies with the knee drawn up to relax the abdominal wall.

Often the vomiting is accompanied by hiccup, which results from irritation of diaphragmatic peritoneum. This is considered to be an unfavorable prognostic sign. The patient tries to retain distended abdomen by his hands during hiccup and thus provokes increase of pain.

During examination observed restricted movements of abdominal wall, which is mainly expressed over the inflammatory focus. Abdominal percussion reveals the region of maximal painfulness, which response the site of lesion, high tympanic sound as a result of intestinal gaseous dilatation, but sometimes dullness, caused by cumulation of great amount of exudate. On palpation revealed muscular tension of abdominal wall. Especially expressed the muscular rigidity in case of perforation of hollow organs ("board-like abdomen"). Pelvic location of peritonitis usually causes less clinical manifestations. In such cases a diagnostic value has digital examination of the rectum and bimanual palpation of the pelvis and lower abdomen, which reveals overhanging and painfulness of anterior rectal wall or posterior vaginal vault owing to accumulation of the exudate.

The clinical manifestation of peritonitis is various and individual. It depends on the character of primary lesion, extension of inflammatory process, and defensive properties of the organism. The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, and abdominal guarding, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). The presence of these signs in a patient is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may become localized later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

Collateral manifestations: diffuse abdominal rigidity ("washboard abdomen") is often present, especially in generalized peritonitis, Fever, Sinus tachycardia, Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating.


In reactive stage of the disease the most common are the pain, muscular rigidity and positive Shchotkin-Blumberg's symptom. The general state changed a little the patient is active, sometimes excite. A moderate tachycardia and hypertension commonly observed.(Fig.1)




Fig.1. Shchotkin-Blumberg's symptom.


In toxic stage of the disease the pain and muscular defense tend to diminish, but on palpation the muscular tenderness and Shchotkin-Blumberg's symptom retain on the same level. More evident the signs of intestinal paresis (abdominal distension, absence of peristalsis). The general state is worsened. The patient is apathetic, the skin is blanched or cyanotic. Observed progressing of tachycardia, decreasing of blood pressure and rising of temperature. In blood analysis revealed leukocytosis and deviation of the differential count to the left.

In terminal stage of the disease the feeling of pain disappears, but the patient suffer from the uncontrollable vomiting by congested fecal contents. The patient is adynamic, with drawn features and blanched or cyanotic skin. The pulse becomes increasingly rapid small and thready. The arterial pressure tends to diminish. No peristalsis is evident and no bowel sounds are heard on auscultation. Shchotkin-Blumberg's symptom is slightly expressed. The respiration is rapid, with congested rales, and oliguria develops. This clinical pattern resembles a septic shock. The prognosis in this stage is serious and the patient will die if the urgent treatment is not be applied.

Plain films of the chest and abdomen with the patient in both supine and the erect position are essential. The chest x-ray examination assists in identifying thoracic causes of the acute abdomen and sometimes reveals specific x-ray findings of intraabdominal catastrophes (e.g. free air under the diaphragm associated with perforation of the gastrointestinal tract).

Laparoscopy is a rapid, direct, and often definitive method of identifying the cause of peritonitis in difficult cases. Finally, for patients who have acute intraabdominal problem of unknown nature and whose symptoms, signs, and laboratory findings are suggestive of a threat of life, exploratory laparotomy remains the most prudent diagnostic procedure.


Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute renal failure.

A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum

Sepsis may develop, so blood cultures should be obtained.


Variants of clinical course and complications

Postoperative peritonitis is characterized by atypical and even asymptomatic course. This results from administering of analgesics, antibiotics and anesthetics. The general state of the patient after the operation is gradually worsens.

The most earliest and frequent sign of postoperative peritonitis is the increase of abdominal pain on the background of the previous satisfactory condition, tachycardia, high temperature, leukocytosis, deviation of the differential count to the left, elevation of erythrocyte sedimentation rate. The pain and muscular rigidity usually expressed slightly or absent at all. Later (on the 5-6th day) the general state continues to be worsened, which manifest by dry tongue, lack of peristalsis, expressed nausea, vomiting, tachycardia and shallow breathing. General weakness, adynamia, general intoxication and rebound tenderness symptoms progress. The outcomes of postoperative peritonitis are usually unfavorable, and they prevented by early repeated operation.

The specific complications of acute peritonitis include inflammatory infiltrates and abscesses of abdominal cavity (Fig.2) (subphrenic, subhepatic, interintestinal and pelvic), dynamic ileus, intestinal fistula, suppuration of postoperative wound, eventration, peritoneal adhesions, etc.

Fig.2.Localizations of abscesses of abdominal cavity

1, 2 Right and left subdiafragmatic abscesses

3 - Subhepatic abscess

4 Interintestinal abcesses

5, 6, 7 Right iliac abscesses

8 Left iliac abscess

9 Abscess of the small pelvis (Douglas space abscess)

The patients with subphrenic abscess (Fig.3) as a rule complain of the pain in epigastrium and lower chest, which irradiates into the shoulder and increases during cough and deep breathing. Sometimes revealed painfulness during digital pressing and swelling of soft tissues in the region of 7-10th Intercostals space. The patients are suffering from nausea, hiccup, and high temperature. Sometimes they must stay in forced position: supine or semisedentary. The tongue is dry, the abdomen is slightly bloated, and rebound tenderness symptoms are usually absent. In blood revealed leukocytosis, deviation of the differential count to the left. The abscess requires a surgical treatment. If the abscess is located near anterior abdominal wall, it is drained by means of oblique access under the costal arch. The abscesses, which located in posterior subphrenic space, are drained after the previous puncture through the access after resection of X rib. (Fig.4)

Fig.3. Subphrenic abscess


Fig.4. Dranaige of subdiafragmatic abscess


Subhepatic abscess is characterized by the pain and presence of infiltrate below right costal arch, positive Shchotkin-Blumberg symptom. The abscess is drained through the incision along right costal arch.

The clinical pattern of interintestinal abscess is vague. It is formed mostly on the 12-14th day after appearance of peritonitis. The patients complain of the high temperature and dull pain in the site of its location. The abdomen is soft, but during palpation revealed dense, painful infiltrate. In case of localization near to abdominal wall one can observe muscular tension and positive Shchotkin-Blumberg symptom. The roentgenological or ultrasound investigation often reveals focal shadow with air-fluid level. The abscess is drained over the site of its localization, dividing the bowel loops.

Abscesses of small pelvis mostly occur as a result of appendicitis(Fig.5) or accumulation of the exudates in Douglas space in diffuse peritonitis.


Fig.5. The localization of appendiceal abscess

depending the appendix location


Such patients complain of constant pain in the lower abdomen, high temperature, painful urinary excretion and tenesmus. The palpation of the abdomen usually reveals no pathology. But the digital rectal examination finds out a painful infiltrate that drawn into the rectum. (Fig.6) The mucosa over the infiltrate is edematous and immovable. The vaginal examination of the female patients reveals overhanging of posterior vaginal vault and painfulness of cervical shift. Often on the background of solid consistency of the infiltrate the softened regions are palpated, which respond to accumulation of pus. The purulent sites of small pelvis in males are drained through the anterior wall of the rectum and in females through the posterior vaginal vault. For this purpose the infiltrate is punctured by thick needle and under its check the abscess is drained by means of scalpel incision. Then the incision is expanded by clamp, the pus is aspirated and the abscess cavity is drained by rubber strap, which is fixed to perineum.







Fig. 6. Diagnotic and management of Douglas space abscess

A - Digital rectal examination

B Diagnostic puncture through anterior rectal wall

C The drainage is placed through anterior rectal wall


The diagnostic program

Complaints and history of the disease.

Physical findings.

General blood and urine analyses.

Biochemical blood analysis (protein and its fractions).

Examination of the exudate (bacteriological, cytological).

Laparoscopy. (Fig.7)

Plain film of the abdomen.



Fig.7. Purulent peritonitis(Laparoscopic picture)


Tests and diagnosis


To diagnose peritonitis, your doctor will talk with you about your medical history and perform a physical exam. When peritonitis is associated with peritoneal dialysis, your signs and symptoms, particularly cloudy dialysis fluid, may be enough for your doctor to diagnose the condition.

In cases of peritonitis in which the infection may be a result of other medical conditions (secondary peritonitis) or in which the infection arises from fluid buildup in your abdominal cavity (spontaneous peritonitis), your doctor may recommend the following tests to confirm a diagnosis:

Peritoneal fluid analysis. Using a thin needle, your doctor may take a sample of the fluid in your peritoneum (paracentesis). If you have peritonitis, examination of this fluid may show an increased white blood cell count, which typically indicates an infection or inflammation. A culture of the fluid may also reveal the presence of bacteria.

Diagnostic paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP. In peritoneal dialysis patients with a peritoneal catheter, fluid should be withdrawn using sterile technique. Ultrasonography may aid paracentesis if ascites is minimally detectable or questionable.

The results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, prove the most useful in guiding therapy for those with SBP. With regard to ascitic fluid culture, direct inoculation of routine blood culture bottles at the bedside with 10 mL of ascitic fluid has been reported to significantly increase the sensitivity of microbiologic studies.

The single best predictor of SBP is an ascitic fluid neutrophil count of greater than 500 cells/L, which carries a sensitivity of 86% and a specificity of 98%. By lowering the ascitic fluid neutrophil count threshold to 250 cells/μ L, the sensitivity increases to 93% with only a minimal decrease in specificity to 94%.

The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cell count, Gram stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreatic leak is suspected, amylase analysis should be added to the panel. Bilirubin and creatinine levels can be analyzed as well, if a biliary or urinary leak is suspected as a possible etiology. The peritoneal/ascitic fluid characteristics or levels are then compared with their respective serum values.

The fluid in bacterial peritonitis generally demonstrates a low pH and low glucose levels with elevated protein and LDH levels. Traditionally, ascitic fluid pH of less that 7.34 was consistent with a diagnosis of SBP; however, ascitic pH is less commonly measured because it is unreliable and lacks specificity for the condition.

SBP is established when the polymorphonuclear neutrophil (PMN) count is 250 cells/L or greater in conjunction with a positive bacterial culture result. In most of these cases, as mentioned previously, cultures are positive for a single organism. Obviously, these patients should receive antibiotic therapy. Although up to 30% of cultures remain negative, most of these patients are presumed to have bacterial peritonitis; they should be treated. A significantly decreased peritoneal fluid glucose level (< 50 mg/dL), a peritoneal fluid LDH level much greater than the serum LDH, a peritoneal fluid WBC count greater than 10,000 cells/L, a pH lower than 7.0, high amylase levels, multiple organisms on Gram stain, or recovery of anaerobes from the culture raises the suspicion of SP in these patients. Some authors recommend repeating the paracentesis in 48-72 hours to monitor treatment success (decrease in neutrophil count to < 50% of the original value).

Culture-negative neutrocytic ascites (probable SBP) is established when the ascitic fluid culture results are negative but the PMN count is 250 cells/L or greater. This may happen in as many as 50% of patients with SBP and may not actually represent a distinctly different disease entity. Rather, it may be the result of poor culturing techniques or late-stage resolving infection. Nonetheless, these patients should be treated just as aggressively as those with positive culture results.

Monomicrobial nonneutrocytic bacterascites exists when a positive culture result coexists with a PMN count 250 cells/L or greater. Although this may often be the result of contamination of bacterial cultures, 38% of these patients develop SBP. Therefore, monomicrobial nonneutrocytic bacterascites may represent an early form of SBP. All study patients described who eventually developed SBP were symptomatic. For this reason, any patient suspected clinically of having SBP in this setting must be treated.

Tuberculous peritonitis is identified by ascites with high protein content, a low glucose and low SAAG, elevated ascitic fluid WBC count, and lymphocyte predominance. In TP, the fluid Gram stain and acid-fast stain results are rarely positive, and routine culture results are falsely negative in as many as 80% of cases. A peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL, and predominantly mononuclear cell count of more than 500 cells/L should raise the suspicion of TP, but specificity for the diagnosis is limited. Laparoscopy with visualization of granulomas on peritoneal biopsy and specific culture (which requires 4-6 wk) may be needed for definitive diagnosis.

Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) is indicated by contamination of the dialysis catheter; cloudy effluent, total fluid WBC count of greater than 100 neutrophils/L, or presence of organisms on Gram stain.

Routine intraoperative peritoneal fluid cultures in defined acute disease entities (ie, gastric or duodenal ulcer perforation, appendicitis, diverticulitis or perforation of the colon caused by obstruction or ischemia) are controversial. Several studies found no significant difference in patients with appendicitis, diverticulitis, and other common etiologies for bacterial peritonitis with regard to postoperative complication rates or overall outcomes. The antibiotic regimen was altered only 8-10% of the time based on operative culture data. In patients who had previous abdominal operations or instrumentation (eg, peritoneal dialysis catheter, percutaneous stents) and patients with prolonged antibiotic therapy, critical illness, and/or hospitalization, these cultures may reveal resistant or unusual organisms that should prompt alteration of the antibiotic strategy.

For a summary of ascitic fluid analysis, see table, below.

Table. Ascitic Fluid Analysis Summary




Less Helpful

Cell count

Obtain culture in blood culture (BC) bottles.

Tuberculosis (TB) smear and culture






Total protein

Lactate dehydrogenase (LDH)








Gram stain


Alpha 1-antitrypsin






Blood tests. A sample of your blood may be drawn and sent to a lab to check for a high white blood cell count. A blood culture also may be performed to determine if there are bacteria in your blood.

Most patients will have leukocytosis (>11,000 cells/μ L), with a shift to the immature forms on the differential cell count. Patients who have severe sepsis, are immunocompromised, or have certain types of infections (eg, fungal, cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspected SBP, hypersplenism may reduce the polymorphonuclear leukocyte count.

Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR are indicated. Liver function tests may be indicated. Amylase and lipase levels should be obtained if pancreatitis is suspected. Blood culture results are positive for the offending agent in as many as 33% of patients with SBP and may help guide antibiotic therapy. Measurement of serum albumin allows calculation of the serum-to-ascites albumin gradient (SAAG). A SAAG of more than 1.1 is noted in SBP.

Imaging tests. Your doctor may want to use an X-ray to check for holes or other perforations in your gastrointestinal tract. Ultrasound may also be used. In some cases, your doctor may use a computerized tomography (CT) scan instead of an X-ray.

Radiography.Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are often the first imaging studies obtained in patients presenting with peritonitis. Their value in reaching a specific diagnosis is limited.

Ultrasonography. Abdominal ultrasonography may be helpful in the evaluation of pathology in the right upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvis (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess). However, the examination is sometimes limited because of patient discomfort, abdominal distention, and bowel gas interference. Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its ability to detect quantities of less than 100 mL is limited. The central (perimesenteric) peritoneal cavity is not visualized well with transabdominal ultrasonography. Examination from the flank or back may improve the diagnostic yield, and providing the ultrasonographer with specific information about the patient's condition and the suspected diagnosis before the examination is important. With an experienced ultrasonographer, a diagnostic accuracy of greater than 85% has been reported in several series. Ultrasonographically guided aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of abdominal fluid collections. Advantages of ultrasound include low cost, portability, and availability. Disadvantages are that the test is operator dependent, and there is reduced visualization in the presence of overlying bowel gas and abdominal dressings.

CT scanning. If the diagnosis of peritonitis is made clinically, a CT scan is not necessary and generally delays surgical intervention without offering clinical advantage. However, CT scanning is indicated in all cases in which the diagnosis cannot be established on clinical grounds and findings on abdominal plain films. CT scans of the abdomen and pelvis remain the diagnostic study of choice for peritoneal abscess and related visceral pathology.

Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that approach 100%. (See the image below.) CT scanning can be used to evaluate for ischemia, as well as to determine bowel obstruction. An abscess is suggested by the presence of fluid density that is not bound by the bowel or other known structures. Gas within an abdominal mass or the presence of an enhancing wall and adjacent inflammatory changes are also highly suggestive of an abscess. Ischemia can be demonstrated by a clot in a large vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal vein may also suggest ischemia.

Free air is present in most cases of anterior gastric and duodenal perforation but is much less frequent with perforations of the small bowel and colon and is unusual with appendiceal perforation. Upright films are useful for identifying free air under the diaphragm (most often on the right) as an indication of a perforated viscus. Remember that the presence of free air is not mandatory with visceral perforation and that small amounts of free air are missed easily on plain films.

In abscess formation subsequent to secondary peritonitis (SP), approximately half of patients have a simple abscess without loculation, and the other half have complex abscesses secondary to fibrinous septation and organization of the abscess material. Abscess formation occurs most frequently in the subhepatic area, the pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the lesser sac, and between small bowel loops and their mesentery.

Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and drained under CT guidance; this technique has become a mainstay of therapy.

MRI. MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses. Abdominal abscesses demonstrate decreased signal intensity on T1-weighted images and homogeneous or heterogeneous increased signal intensity on T2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rim enhancement.

Limited availability and high cost, as well as the need for MRI-compatible patient support equipment and the length of the examination, currently limit its usefulness as a diagnostic tool in acute peritoneal infections, particularly for patients who are critically ill.


The above tests may also be necessary if you're receiving peritoneal dialysis and a diagnosis of peritonitis is uncertain after a physical exam and an examination of the dialysis fluid.\


Differential diagnostics


Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the presence of external hernias to rule out intestinal incarceration.

According to Adler and Gasbarra, the following should be considered in the differential diagnosis:

Aneurysm, Abdominal


Appendicitis, Acute

Mesenteric Ischemia

Urinary Tract Infection in Females

Whipple Disease

Chemical irritants (eg, bile, blood, gastric juice, barium, enema or douche contents)

Chronic peritoneal dialysis

Chylous peritonitis

Eosinophilic peritonitis

Familial Mediterranean fever

Fungal infections (eg, histoplasmosis, cryptococcosis, coccidioidomycosis)

Granulomatous peritonitis (eg, parasitic infestations, sarcoidosis, tumors, Crohn disease, starch granules)

Gynecologic disorders (Chlamydia peritonitis, salpingitis, endometriosis, teratoma, leiomyomatosis, dermoid cyst)

HIV-associated peritonitis (from opportunistic organisms)

Mesothelial hyperplasia and metaplasia

Neoplasms (eg, primary mesothelioma, secondary carcinomatosis, Pseudomyxoma peritonei)

Parasitic infections (eg, schistosomiasis, ascariasis, enterobiasis, amebiasis, strongyloidiasis)

Perforated viscus

Peritoneal encapsulation

Peritoneal loose bodies and peritoneal cysts

Peritoneal lymphangiectasis


Sclerosing peritonitis


Vascular conditions (eg, mesenteric embolus, mesenteric nonocclusive ischemia, ischemic colitis, portal vein thrombosis, mesenteric vein thrombosis)

Vasculitis (eg, systemic lupus erythematosus, allergic vasculitis [Henoch-Schönlein purpura], Kohlmeier-Degos disease, polyarteritis nodosa)


The differential diagnostics in toxic and terminal stage of peritonitis when the typical signs of the disease are present commonly makes no difficulties. But in initial (reactive) stage the sings are similar to manifestation of causative disease appendicitis, cholecystitis, pancreatitis, etc.). But there are variety of disorders, which according to their manifestation resemble peritonitis, renal colic for instance. A sharp pain, nausea, vomiting, intestinal paralysis, and false Shchotkin-Blumberg symptom (peritonism) frequently lead to misdiagnostics. A periodical pain attack with typical irradiation in thigh, perineum, dysuria, positive Pasternatsky's symptom, lack of inflammatory changes in blood analysis, presence of erythrocytes in urine help to make correct diagnosis. For its improvement applied x-ray film of the abdomen, urography and chromocystoscopy.

A diffuse abdominal pain, muscular tension of abdominal wall and peritonism often accompany hemorrhagic diatheses (Schonlein-Henoch's disease). This disorder mostly occurs in young people and manifests by multiple small hemorrhages on skin (forearm, chest, and thigh), mucous membranes of cheeks, tongue and peritoneum as well. The rectal examination reveals tarry stool or melena. In blood thrombocytopenia is observed.

Myocardial infarction especially in its location on posterior wall (abdominal form) usually accompanied by epigastric pain, nausea and vomiting. Also revealed abdominal wall tension with phenomena of peritonism. But ischemic heart disease in history and characteristic ECG changes can favor correct diagnostics.

Basal pleurisy and acute lower lobe pneumonia, causing the pain and muscular guard in epigastrium, also resemble peritonitis. Only thorough clinical examination leads to correct diagnostics.



1.     Runyon BA. Treatment and prophylaxis of spontaneous bacterial peritonitis. 

2.     "Biology Online's definition of peritonism". Retrieved 2008-08-14.

3.     Prasad AG, et al. Peritonitis, secondary. In: Ferri FF. Ferri's Clinical Advisor 2011: Instant Diagnosis and Treatment. Philadelphia, Pa.: Mosby Elsevier; 2011. 

4.     "Peritonitis: Emergencies: Merck Manual Home Edition". Retrieved 2007-11-25.

5.     Acute abdominal pain. The Merck Manuals: The Merck Manual for Healthcare Professionals.

6.     Fort GG, et al. Peritonitis, spontaneous bacterial. In: Ferri FF. Ferri's Clinical Advisor 2011: Instant Diagnosis and Treatment. Philadelphia, Pa.: Mosby Elsevier; 2011. 

7.     Picco MF (expert opinion). Mayo Clinic, Rochester, Minn. June 13, 2011.

8.     Badgwell B, Turnage RH. Abdominal Wall, umbilicus, peritoneum,mesenteries, omentum, and retroperitoneum. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery.19th ed. Philadelphia, Pa: Saunders Elsevier; 2012:chap 45.

9.     Prather C. Inflammatory and anatomic diseases of the intestine, peritoneum, mesentery, and omentum. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 144.

10.           Pavlidis TE. Cellular changes in association with defense mechanisms in intra-abdominal sepsis. Minerva Chir. Dec 2003;58(6):777-81. 

11.           Appenrodt B, Grünhage F, Gentemann MG, Thyssen L, Sauerbruch T, Lammert F. Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis. Hepatology. Apr 2010;51(4):1327-33. 

12.           Barretti P, Montelli AC, Batalha JE, Caramori JC, Cunha Mde L. The role of virulence factors in the outcome of staphylococcal peritonitis in CAPD patients. BMC Infect Dis. Dec 22 2009;9:212. 

13.           Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. Mar 2004;39(3):841-56.

14.           Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis.World J Gastroenterol. Nov 28 2009;15(44):5505-10.

15.           Bert F, Noussair L, Lambert-Zechovsky N, Valla D. Viridans group streptococci: an underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Eur J Gastroenterol Hepatol. Sep 2005;17(9):929-33. 

16.           Cholongitas E, Papatheodoridis GV, Lahanas A, Xanthaki A, Kontou-Kastellanou C, Archimandritis AJ. Increasing frequency of Gram-positive bacteria in spontaneous bacterial peritonitis. Liver Int. Feb 2005;25(1):57-61. 

17.           Adler SN, Gasbarra DB. A Pocket Manual of Differential Diagnosis. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005.

18.           Nouri-Majalan N, Najafi I, Sanadgol H, Ganji MR, Atabak S, Hakemi M, et al. Description of an outbreak of acute sterile peritonitis in Iran. Perit Dial Int. Jan-Feb 2010;30(1):19-22. 

19.           Evans LT, Kim WR, Poterucha JJ, Kamath PS. Spontaneous bacterial peritonitis in asymptomatic outpatients with cirrhotic ascites. Hepatology. Apr 2003;37(4):897-901. 

20.           Cheruvattath R, Balan V. Infections in Patients With End-stage Liver Disease. J Clin Gastroenterol. Apr 2007;41(4):403-11. 

21.           Soriano G, Castellote J, Alvarez C, et al. Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical and analytical characteristics, diagnosis and management. J Hepatol. Jan 2010;52(1):39-44.

22.           Marshall JC. Intra-abdominal infections. Microbes Infect. Sep 2004;6(11):1015-25. 

23.           Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous bacterial peritonitis. World J Gastroenterol. Aug 21 2009;15(31):3845-50.

24.           Gaya DR, David B Lyon T, Clarke J, Jamdar S, Inverarity D, Forrest EH, et al. Bedside leucocyte esterase reagent strips with spectrophotometric analysis to rapidly exclude spontaneous bacterial peritonitis: a pilot study. Eur J Gastroenterol Hepatol. Apr 2007;19(4):289-95. 

25.           Blot S, De Waele JJ. Critical issues in the clinical management of complicated intra-abdominal infections.Drugs. 2005;65(12):1611-20. 

26.           Hawker FH. How to feed patients with sepsis. Curr Opin Crit Care. Aug 2000;6(4):247-252. 

27.           Runyon B. Ascites and spontaneous bacterial peritonitis. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. Vol 2. 8th ed. Philadelphia, Pa: Saunders; 2006:1935-64.

28.           Colizza S, Rossi S. Antibiotic prophylaxis and treatment of surgical abdominal sepsis. J Chemother. Nov 2001;13 Spec No 1(1):193-201. 

29.           Ginés P, Rimola A, Planas R, Vargas V, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology. Oct. 1990;12(4 Pt 1):716-24.

30.           Soares-Weiser K, Brezis M, Leibovici L. Antibiotics for spontaneous bacterial peritonitis in cirrhotics.Cochrane Database Syst Rev. 2001;CD002232.

31.           Tubau F, Liñares J, Rodríguez MD, Cercenado E, Aldea MJ, González-Romo F, et al. Susceptibility to tigecycline of isolates from samples collected in hospitalized patients with secondary peritonitis undergoing surgery. Diagn Microbiol Infect Dis. Mar 2010;66(3):308-13. 

32.           Wiggins KJ, Craig JC, Johnson DW, Strippoli GF. Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database Syst Rev. Jan 23 2008;CD005284.

33.           Livingston EH, Passaro EP Jr. Postoperative ileus. Dig Dis Sci. Jan 1990;35(1):121-32.

34.           Shibata Y, Toyoda S, Nimura Y, Miyati M. Patterns of intestinal motility recovery during the early stage following abdominal surgery: clinical and manometric study. World J Surg. Oct 1997;21(8):806-9; discussion 809-10.

35.           Holte K, Kehlet H. Postoperative ileus: a preventable event. Br J Surg. Nov 2000;87(11):1480-93.

36.           Vasquez W, Hernandez AV, Garcia-Sabrido JL. Is gum chewing useful for ileus after elective colorectal surgery? A systematic review and meta-analysis of randomized clinical trials. J Gastrointest Surg. Apr 2009;13(4):649-56.

37.           Resnick J, Greenwald DA, Brandt LJ. Delayed gastric emptying and postoperative ileus after nongastric abdominal surgery: part I. Am J Gastroenterol. May 1997;92(5):751-62.

38.           Resnick J, Greenwald DA, Brandt LJ. Delayed gastric emptying and postoperative ileus after nongastric abdominal surgery: part II. Am J Gastroenterol. Jun 1997;92(6):934-40.

39.           Kalff JC, Schraut WH, Simmons RL, Bauer AJ. Surgical manipulation of the gut elicits an intestinal muscularis inflammatory response resulting in postsurgical ileus. Ann Surg. Nov 1998;228(5):652-63.

40.           Boeckxstaens GE, de Jonge WJ. Neuroimmune mechanisms in post-operative ileus. Gut. Sept 2009;58(9):1300-11.

41.           Espat NJ, Cheng G, Kelley MC, Vogel SB, Sninsky CA, Hocking MP. Vasoactive intestinal peptide and substance P receptor antagonists improve postoperative ileus. J Surg Res. Jun 1995;58(6):719-23.

42.           Kalff JC, Schraut WH, Billiar TR, Simmons RL, Bauer AJ. Role of inducible nitric oxide synthase in postoperative intestinal smooth muscle dysfunction in rodents. Gastroenterology. Feb 2000;118(2):316-27.

43.           Senagore AJ. Pathogenesis and clinical and economic consequences of postoperative ileus. Am J Health Syst Pharm. Oct 15 2007;64(20 Suppl 13):S3-7.

44.           Cameron JL, ed. Current Surgical Therapy. 7th ed. Chicago: Mosby; 2001.

45.           Tollesson PO, Cassuto J, Rimbäck G. Patterns of propulsive motility in the human colon after abdominal operations. Eur J Surg. Apr 1992;158(4):233-6.

46.           Loftus CG, Harewood GC, Baron TH. Assessment of predictors of response to neostigmine for acute colonic pseudo-obstruction. Am J Gastroenterol. Dec 2002;97(12):3118-22.

47.           Schwartz SI, ed. Principles of Surgery. 7th ed. New York, NY: McGraw-Hill; 1999.

48.           Cali RL, Meade PG, Swanson MS, Freeman C. Effect of Morphine and incision length on bowel function after colectomy. Dis Colon Rectum. Feb 2000;43(2):163-8.

49.           Ferraz AA, Cowles VE, Condon RE, Carilli S, Ezberci F, Frantzides CT, et al. Nonopioid analgesics shorten the duration of postoperative ileus. Am Surg. Dec 1995;61(12):1079-83.

50.           Purkayastha S, Tilney HS, Darzi AW, Tekkis PP. Meta-analysis of randomized studies evaluating chewing gum to enhance postoperative recovery following colectomy. Arch Surg. Aug 2008;143(8):788-93.

51.           Shang H, Yang Y, Tong X, et al. Gum chewing slightly enhances early recovery from postoperative ileus after cesarean section: results of a prospective, randomized, controlled trial. Am J Perinatol. Dec 11 2009;epub ahead of print.

52.           Waldhausen JH, Schirmer BD. The effect of ambulation on recovery from postoperative ileus. Ann Surg. Dec 1990;212(6):671-7.

53.           Zingg U, Miskovic D, Hamel CT, Erni L, Oertli D, Metzger U. Influence of thoracic epidural analgesia on postoperative pain relief and ileus after laparoscopic colorectal resection : Benefit with epidural analgesia. Surg Endosc. Feb 2009;23(2):276-82.

54.           Liu SS, Carpenter RL, Mackey DC, Thirlby RC, Rupp SM, Shine TS, et al. Effects of perioperative analgesic technique on rate of recovery after colon surgery. Anesthesiology. Oct 1995;83(4):757-65.

55.           Mann C, Pouzeratte Y, Boccara G, Peccoux C, Vergne C, Brunat G, et al. Comparison of intravenous or epidural patient-controlled analgesia in the elderly after major abdominal surgery. Anesthesiology. Feb 2000;92(2):433-41.

56.           [Best Evidence] Marret E, Rolin M, Beaussier M, Bonnet F. Meta-analysis of intravenous lidocaine and postoperative recovery after abdominal surgery. Br J Surg. Nov 2008;95(11):1331-8.

57.           Becker G, Blum HE. Novel opioid antagonists for opioid-induced bowel dysfunction and postoperative ileus. Lancet. Apr 4 2009;373(9670):1198-206.

58.           Maron DJ, Fry RD. New therapies in the treatment of postoperative ileus after gastrointestinal surgery. Am J Ther. Jan-Feb 2008;15(1):59-65.

59.           Yuan CS, Foss JF, Osinski J, Toledano A, Roizen MF, Moss J. The safety and efficacy of oral methylnaltrexone in preventing morphine-induced delay in oral-cecal transit time. Clin Pharmacol Ther. Apr 1997;61(4):467-75.

60.           Candy B, Jones L, Goodman ML, Drake R, Tookman A. Laxatives or methylnaltrexone for the management of constipation in palliative care patients. Cochrane Database Syst Rev. Jan 19 2011;CD003448.

61.           Taguchi A, Sharma N, Saleem RM, Sessler DI, Carpenter RL, Seyedsadr M, et al. Selective postoperative inhibition of gastrointestinal opioid receptors. N Engl J Med. Sep 27 2001;345(13):935-40.

62.           Tan EK, Cornish J, Darzi AW, Tekkis PP. Meta-analysis: Alvimopan vs. placebo in the treatment of post-operative ileus. Aliment Pharmacol Ther. Jan 1 2007;25(1):47-57.

63.           Senagore AJ, Bauer JJ, Du W, Techner L. Alvimopan accelerates gastrointestinal recovery after bowel resection regardless of age, gender, race, or concomitant medication use. Surgery. Oct 2007;142(4):478-86. [Medline].

64.           Zingg U, Miskovic D, Pasternak I, Meyer P, Hamel CT, Metzger U. Effect of bisacodyl on postoperative bowel motility in elective colorectal surgery: a prospective, randomized trial. Int J Colorectal Dis. Dec 2008;23(12):1175-83.

65.           Wiriyakosol S, Kongdan Y, Euanorasetr C, Wacharachaisurapol N, Lertsithichai P. Randomized controlled trial of bisacodyl suppository versus placebo for postoperative ileus after elective colectomy for colon cancer. Asian J Surg. Jul 2007;30(3):167-72.

66.           Traut U, Brügger L, Kunz R, Pauli-Magnus C, Haug K, Bucher HC, et al. Systemic prokinetic pharmacologic treatment for postoperative adynamic ileus following abdominal surgery in adults. Cochrane Database Syst Rev. Jan 23 2008;CD004930.

67.           Wattchow DA, De Fontgalland D, Bampton PA, et al. Clinical trial: the impact of cyclooxygenase inhibitors on gastrointestinal recovery after major surgery - a randomized double blind controlled trial of celecoxib or diclofenac vs. placebo. Aliment Pharmacol Ther. Nov 15 2009;30(10):987-98.

68.           Yeh YC, Klinger EV, Reddy P. Pharmacologic options to prevent postoperative ileus. Ann Pharmacother. Sep 2009;43(9):1474-85.

69.           Abd-El-Maeboud KH, Ibrahim MI, Shalaby DA, Fikry MF. Gum chewing stimulates early return of bowel motility after caesarean section. BJOG. Sep 2009;116(10):1334-9.


Prepared ass. Romaniuk T.