Peritonitis
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.
Etiology and pathogenesis
The main causes of peritonitis are the acute inflammation of abdominal viscera, discontinuity and disturbed permeability of their walls, open and closed traumas of the abdomen with the damage of viscera with following microbial contamination of peritoneal space.
Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation. The infectious agents are represented by Escherichia colli, Staphylococcus and Enterococcus, Proteus, Streptococcus and also nonclostridial anaerobes. At least in 30 % of cases association of two or more agents occur.
Primary peritonites occur very rarely and result from pneumococcal, streptococcal and staphylococcal infection.
Besides microbial peritonites, caused by peritoneal contamination, distinguished also aseptic peritoneal inflammation, which result from entering of different chemical noninfectious agents into peritoneal cavity (blood, urine, bile, pancreatic juice, etc.). It’s so called toxico-chemical peritonitis. But with the development of aseptic inflammation bacteria penetrate into peritoneal space with transformation of peritonitis into bacterial.
Chronic peritonitis is mainly caused by tuberculosis, which agents are usually located extraperitoneally (lungs, mediastinal lymph nodes) or in mesenteric lymph nodes and by hematogenous way enter the peritoneum.
Intestinal obstruction is a complete or partial violation of passing of maintenance by the intestinal tract.
Etiology and pathogenesis
The principal reasons of intestinal obstruction can be:
1) commissures of abdominal cavity after traumas, wounds, previous operations and inflammatory diseases of organs of abdominal cavity and pelvis;
2) long mesentery of small intestine or colon, that predetermines considerable mobility of their loops;
3) tumours of abdominal cavity and retroperitoneal space.
Such principal reasons can cause violation of passing of intestinal maintenance, disorder of suction from the intestine and loss of plenty of electrolytes both from vomiting and in the intestine cavity as a result of disorders of bloodflow in its wall.
Pathomorphology
The morphological signs of dynamic intestinal obstruction are: small thickening of wall (at considerable paresis is thinning), friability of tissue (the bowel breaks easily) and presence of liquid maintenance and gases in cavity of bowel. At mechanical obstruction it is always possible to expose the obstacle: strang, commissures, tumours, jammings of hernia, cicatricial strictures, wrong entered drainages, tampons and others like that. In place of compression strangulation is exposed. The bowel loop higher strangulation is extended, and distally — collapsed. In case of released invagination on small distance two strangulation furrows are observed, and distally from the second ring cylinder expansion of bowel lumen is observed.
Classification
(by D.P.Chuhrienko, 1958)
Acute intestinal obstruction is divided:
I. According to morphofunctional signs.
1. Dynamic intestinal obstruction:
а) paralytic;
б) spastic;
в) hemostatic (embolic, thrombophlebitic).
2. Mechanical intestinal obstruction(Fig.1):
а) strangulated, volvulus, jamming;(Fig. 2)
б) obturation (closing of bowel lumen, squeezing from outside);
в) mixed (invagination, spike intestinal obstruction).
II. According to clinical passing.
1. Acute.
2. Chronic.
III. According to the level of obstruction.
1. Small intestinal.
2. Large intestinal:
а) high;
б) low.
IV. According to the passing of intestinal maintenance.
1. Complete.
2. Partial.
V. According to the origin.
1. Innate.
2. Acquired.
VI. According to development of pathological process.
1. Stage of acute violation of intestinal passage.
2. Stage of hemodynamic disorders of bowel wall and its mesentery.
3. Stage of peritonitis.
Fig.1. Types of mechanical intestinal obstruction. Obstacle reason of obturation: 1-Obturation; 2-Constriction; 3- Compression; 4- Angulation
Fig.2. Mechanical intestinal obstruction. The disorders of blood circulation:
1-Strangulation; 2- Jamming; 3- Volvulus; 4- Invagination
Clinical management
Beginning of clinical signs of intestinal obstruction is sudden — in 1–2 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 75–80 % 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 85–90% 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.
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 Mondor’s symptom, “noise of beginning, quietness of end”).
There are other symptoms pathognomic for intestinal obstruction.
The Vala’s symptom is the limited elastic sausage-shaped formation.
The Sklarov’s 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 Klojber’s bowl. (Fig.3; Fig.4)
Fig. 3. Intestinal obstruction.
X-ray examination of abdominal cavity –
presence of the Klojber’s 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.
Irrigogram
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 1–2 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.
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.
Differential diagnostics
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.
Tactics and choice of treatment method
During the first 1,5–2 hours after hospitalization of patient complex conservative therapy which has the differential-diagnostic value and can be preoperative preparation is conducted.
It is directed on warning of the complications related to pain shock, correction of homeostasis and, simultaneously, is the attempt of liquidation of intestinal obstruction by unoperative methods.
1. The measures directed for the fight against abdominal pain shock include conducting of neuroleptanalgesia, procaine paranephric block and introduction of spasmolytics. Patients with the expressed pain syndrome and spastic intestinal obstruction positive effect can be attained by epidural anaesthesia also.
2. Liquidation of hypovolemia with correction of electrolyte, carbohydrate and albuminous exchanges is achieved by introduction of salt blood substitutes, 5–10 % solution of glucose, gelatinol, albumen and plasma of blood. There are a few methods suitable for use in the urgent surgery of calculation of amount of liquid necessary for liquidation of hypovolemia. Most simple and accessible is a calculation by the values of hematocrit. If to consider 40 % for the high bound of hematocrit norm, on each 5 % above this size it is needed to pour 1000 ml of liquids.
3. Correction of hemodynamic indexes, microcirculation and disintoxication therapy is achieved by intravenous infusion of Reopolyhlukine and Neohemodes.
4. Decompression of intestine truct is achieved by conducting of nasogastric drainage and washing of stomach, and also conducting of siphon enema. It is needed to underline that technically the correct conducting of siphon enema has the important value for the attempt of liquidation of intestinal obstruction by conservative facilities, therefore this manipulation must be conducted in presence of a doctor. For such enema the special device is used with the rectal tip, by a PVC pipe by a diameter of 1,5–2,0 cm and watering-can of very thin material. A liquid into the colon is brought to appearance of the pain feeling, then drop the watering-can below the level of patient who lies. The passage of gases and excrement is looked after. As a rule, this manipulation is to repeat repeatedly with the use of plenty of warm water (to 15–20 and more litres).
Liquidating of the intestinal obstruction by such conservative facilities is succeeded in 50–60 % patients with mechanical intestinal
obstruction.
Patients with dynamic paralytic intestinal obstruction are expedient to stimulation of peristalsis of intestine to be conducted, besides, necessarily after infusion therapy and correction of hypovolemia. A lot of kinds of stimulation of intestine peristalsis are offered. Most common of them are:
1) hypodermic introduction of 1,0 ml of 0,05 % solution of proserin; 2) through 10 min — 60 ml intravenously stream of 10 % solution of chlorous sodium; 3) hypertensive enema.
Surgical treatment of intestinal obstruction must include such important moments:
1. According to middle laparotomy executed the novocaine blockade of mesentery of small and large intestine and operative exploration of abdominal cavity organs during which the reason of intestinal obstruction and expose viability of intestine is set.(Fig.9)
Fig.9.Intestinal obstruction.
Overblowning of small intestine
The revision at small intestine obstruction begins from the Treitz’ ligament to iliocecal corner. At large intestine obstruction the hepatic, splenic and rectosigmoid parts are observed intently. Absence of pathological processes after revisioeeds the examination of places of cavity and jamming of internal hernia: internal inguinal and femoral rings, obturator openings, pockets of the Treitz’ ligament, Winslow’s opening, diaphragm and periesophageal opening.
2. Liquidation of reasons of obstruction (scission of connection, that squeezes a bowel, violence of volvulus and node formation of loops, desinvagination, deleting of obturative tumours and others like that).
It is needed to mark that the unique method of liquidation of acute intestinal obstruction does not exist. At the lack of viability of bowel the resection of nonviable area is executed with 30–40 cm of afferent and 15–20 cm of efferent part with imposition of “side-to-side”(Fig. 10; Fig. 11) anastomosis or “end-to-end”(Fig.12).
Fig 10.The resection of the small intestine with imposition of
anastomosis”side – to side”
-mobilization of segment of the small intestine
–peritonization of the stump of bowel
Fig.11. Enteroenteroanastomosis “side-to-side” is formed.
A B C
Fig 12. The resection of the small intestine
with imposition of “end-to-end” anastomosis
A- mobilization and removing of the changed loop of the bowel
B- formation of the back lip of anastomosis
C- Final view of enteroenteronastomosis
3. Intubation. (Fig.13) Decompression of intestine foresees conducting in the small intestine of elastic probe by thickness of 8–9 mm and length of 3–3,5 м with the plural openings by a diameter 2–2,5 mm along all probe, except for part, that will be in the oesophagus, pharynx and outwardly. A few methods of conducting of probe are offered in a bowel (nasogastric, through gastrostomy, ceco- or appendicostoma). Taking it into account, such procedure needs to be executed individually and according to indications.
Fig. 13. Nasogastrointestinal probe
Each of them has the advantages and failings. In connection with the threat of origin of pneumonia, entering an intubation probe to the patients of old ages is better by means of gastrostomy. Most surgeons avoid the method of introduction of probe through ceco- or appendicostoma because of technical difficulties of passing in a small intestine through a Bauhin’s valve.(Fig.14)
Fig.14. Types of decompression of digestive tract
Today the most wide clinical application has intubation of intestine extracted by the nasogastric method with the use of other thick probe as explorer of the first (by L.J. Kovalchuk, 1981)(Fig.15). Such method not only simplifies procedure of intubation but also facilitates penetration through the piloric sphincter and duodenojejunal bend, and also warns passing of intestinal maintenance in a mouth cavity and trachea. Thus probe is tried to be conducted in the small intestine as possible farther and deleted the next day after appearance of peristalsis and passage of gases, however not later than on 7th days, because more protracted sign of probe carries the real threat of formation of bedsores in the wall of bowel.
1. Gastric probe-guide is placed 2. Beginning of intubation 3. Intubation till caecum
through the gastric probe-guide
distally to pylorus per os
4. Removing of gastric probe 5. Fixation of proximal part
of intestinal probe to the nasal cathether
6. Removing of proximal part of intestinal 7. Proximal part is removed
through the nose
probe from the oral cavity through the nose
8. Final view of nasogastrointestinal intubation
Fig.15. Principles of nasogastrointestinal intubation
4. Sanation and draining of abdominal cavity is executed by the generally accepted methods of washing of antiseptic. Draining of the abdominal cavity it is needed from four places: in both iliac areas and both hypochondrium, better by the coupled synthetic drain pipes.
Classification
Peritonites are classified:
1. According to the character of microbial contamination:
A: primary
B: secondary.
2. According to clinical course:
A: acute
B: chronic.
3. According to the etiological agents:
A: peritonites, which caused by bacteria of digestive tract (E. colli, staphylococci, streptococci, proteus, anaerobes, etc.)
B: which caused by bacteria, which exist out of gastrointestinal tube (gonococci, pneumococci, streptococcus haemolyticus, etc.).
C: distinguished aseptic (nonbacterial peritonites), resulting from irritation by blood, bile, pancreatic juice or urine.
4. According to the character of exudate:
A: serous;
B: fibrinous;
C: fibrinopurulent;
D: purulent;
E: hemorrhagic;
F: “peritonitus sicca”.
5. According to the extension of inflammatory process:
A: local;
B: diffuse;
C: generalized.
Dependent on duration of the disease and degree of pathological alterations in the clinical course of peritonitis distinguished three stages:
· reactive (first 24 hours) maximal manifestation of local signs of the disease;
· toxic (24-72 hours) – gradual reducing of local signs and increasing of general intoxication.
· terminal (after 72 hours) – severe, often unreversable intoxication on the background of sharply expressed local manifestations of peritoneal inflammation.
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.
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 unknowature and whose symptoms, signs, and laboratory findings are suggestive of a threat of life, exploratory laparotomy remains the most prudent diagnostic procedure.
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 (
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 localizatioear 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
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.
A B
C
Fig. 6. Diagnotic and management of
A – Digital rectal examination
B – Diagnostic puncture through anterior rectal wall
C – The drainage is placed through anterior rectal wall
The diagnostic program
1. Complaints and history of the disease.
2. Physical findings.
3. General blood and urine analyses.
4. Biochemical blood analysis (protein and its fractions).
5. Examination of the exudate (bacteriological, cytological).
6. Laparoscopy. (Fig.7)
7. Plain film of the abdomen.
8. Laparocentesis.
Fig.7. Purulent peritonitis(Laparoscopic picture)
Differential diagnostics
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.
Tactics and choice of treatment
The treatment of acute peritonitis should be always carried out with appreciation of clinical form and stage of the disease, causative factor, extension of inflammatory process, degree of metabolic disturbances and dysfunction of vital organs of the patient.
The complex of treatment of peritonitis should include:
1) early operative approach in order to liquidate the source of peritonitis;
2) sanation of peritoneal cavity by means of lavage, adequate drainage and antibiotic therapy;
3) intubation and decompression of gastrointestinal tract and liquidation of paralytic ileus;(Fig.8)
4) metabolic correction (acid-base balance, blood electrolytes, protein metabolism, energetic metabolism);
5) restore and support of visceral function (kidney, liver, heart, lung) and prevention of complications.
1. Gastric probe-guide is placed 2. Beginning of intubation 3. Intubation till caecum
through the gastric probe-guide
distally to pylorus per os
4. Removing of gastric probe 5. Fixation of proximal part
of intestinal probe to the nasal cathether
6. Removing of proximal part of intestinal 7. Proximal part is removed
through the nose
probe from the oral cavity through the nose
8. Final view of nasogastrointestinal intubation
Fig.8. Principles of nasogastrointestinal intubation
The preoperative preparation in patients with peritonitis should be individual and lasted at least 2-3 hours. In extremely advanced cases, which associated with toxic shock and low arterial pressure it can last to 4-6 hours and must include nasogastric decompression of the stomach with active aspiration, catheterization of two veins, one of which is central, catheterization of bladder for diuresis control, infusion therapy.
The infusion therapy includes 5 % solution of glucose, solution of albumins, plasma, rheopolyglucin, vitamins of B and C group, solution of sodium hydrocarbonatis. The volume of fluid infusion should be at least 1.5-
The most common access in diffuse peritonitis is a median laparotomy, which is the most suitable for abdominal revision. In case of localized peritonitis (acute appendicitis) oblique incision may be used. The main goal of surgery must be elimination of infectious focus (appendectomy, cholecystectomy) or closure of stomach opening (perforating ulcer) or disrupture of hollow viscera. The exudate must be maximum removed and peritoneal cavity washed up by antiseptic solutions and thereafter the intestinal decompression and draining of peritoneal space is performed.
Fig.9. Scheme of the draining abdominal cavity
at extensive purulent peritonitis
In diffuse peritonitis the peritoneal cavity is drained in right and left hypochondrium and both left and right inguinal regions. It is better to use double or multiple polyethylene tubes, which are the most suitable for peritoneal dialysis. ( Fig.9);( Fig.10);( Fig.11)
Fig.9. Localization of the drainages at peritoneal dialysis
Fig.10. Scheme of localization of the drainages
at peritoneal dialysis(Lateral view)
Fig.11. The position of the patient at peritoneal dialysis
Thus the infectious exudate and toxic substances are eliminated and antibiotics and antiseptic solutions are flown into the abdomen through these tubes. In 1.5-2 hours after the operation before the dialysis the patient takes a semisedentary position. Then the solutions flow in through the upper tubes and flow out through the lower. This procedure is performed as far as the solution from the lower tubes becomes clear, using for this purpose 10-
In recent years instead of dialysis applied peritoneal lavage. Controllable peritoneostomy(Fig.12) in association with lavage, epidural anesthesia and intestinal intubation allow to rather promptly carry out sanation of peritoneal cavity and liquidation of inflammatory process. These procedures are repeated in 1-2 days up to complete elimination of pus, fibrin and necrotic tissues. After the last sanation the abdominal wall is closed.
Fig.12. Wide plane drainage of abdominal cavity(begining):
1- bottom of operative wound
2- gauze(matrix)
3- tube for irrigation
4- gauze drainages
5- laparotomy wound margins
Fig.12. Wide plane drainage of abdominal cavity(finishing):
1- laparotomy wound margins
2- sutures on the skin
3- gauze(matrix), which covers drainages
4- tube for irrigation
5- intestines
Fig.13. Reconstruction of anterior abdominal wall
1- laparotomy wound margins
2- rubber-line dranaige
3- primary delayed suture
Antibacterial therapy is performed by means of intraabdominal and parenteral (intramuscular, intravenous, endolymphatic) administering of antibiotics. It is desirable to use broad-spectrum antibiotics and after results of antibioticogram possible to apply direct correction. The antibiotics are advisable to use in combination with sulfanilamides, metrogyl, immunostimulators.
A struggle against paralytic ileus is a very important in the complex of treatment of peritonitis. It should begin during operation by means of intestinal decompression, mesenteric blockade, gastric lavage, and detoxycation therapy. For restitution of peristalsis used proserin, 10 % solution of sodium chloride, hypertonic enema. One of the most important factors in the treatment of peritonitis is the complete restore of the volume of circulating blood, correction of acid-base balance, blood electrolytes, protein metabolism. The total amount of fluid is calculated with account of its loss during vomiting, urinary excretion, drainage discharges and also respiration. For energetic compensation infused concentrated solution of glucose, sorbitol and lipid emulsion. Also plasma, erythrocyte and blood transfusions are used. In order to prevent hypoxia oxygenotherapy or hyperbaric oxygenation are applied.
