Chapter 7 Acute peritonitis
Inflammation and infection of the peritoneal cavity are commonly encountered problems in the practice of clinical medicine today. In general, the term peritonitis refers to a constellation of signs and symptoms, which includes abdominal pain and tenderness on palpation, abdominal wall muscle rigidity, and systemic signs of inflammation.
The peritoneum is the largest and most complex serous membrane in the body. It forms a closed sac by lining the interior surfaces of the abdominal wall (anterior and lateral), by forming the boundary to the retroperitoneum (posterior), by covering the extraperitoneal structures in the pelvis (inferior), and by covering the undersurface of the diaphragm (superior). This parietal layer of the peritoneum reflects onto the abdominal visceral organs to form the visceral peritoneum. It thereby creates a potential space between the 2 layers (i.e., the peritoneal cavity).
The peritoneum consists of a signle layer of flattened mesothelial cells over loose areolar tissue. The loose connective tissue layer contains a rich network of vascular and lymphatic capillaries, nerve endings, and immune-competent cells, particularly lymphocytes and macrophages. The peritoneal surface cells are joined by junctional complexes, thus forming a dialyzing membrane that allows passage of fluid and certain small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by macrophages allow for clearance of macromolecules.
Normally, the amount of peritoneal fluid present is less than 50 mL, and only small volumes are transferred across the considerable surface region in a steady state each day.
The peritoneal fluid represents plasma ultrafiltrate, with electrolyte and solute concentrations similar to that of neighboring interstitial spaces and a protein content of less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small numbers of desquamated mesothelial cells and various numbers and morphologies of migrating immune cells (reference range is < 300 cells/mL, predominantly of mononuclear morphology).
The organs are divided into:
intraperitoneal (stomach, small bowel, colon, sigmoid colon);
mesoperitoneal (liver, ascending and descending colon);
Functions of peritoneum
1. Protection. Attachments of protection are:
greater omentum often covers wound, organ perforation, place of perforation;
peritoneal exudation has antibacterial properties.
Parietal peritoneum is innervated by intercostal nerves. After irritation of parietal peritoneum visceromotor reflex has appeared. As a result patient has local pain and muscle tenderness.
Visceral peritoneum is innervated by sympatric and parasympatic nerves. Therefore visceral pain isn’t localized. Doctors have to remember, that inflammation of pelvic peritoneum (it doesn’t have somatic innervations) isn’t accompanied by muscle tenderness.
5. Plastic function. After traumatic injury or starting of inflammation layers of fibrin have formed. They confine infection.
The first classification of peritonitis was suggested by Miculich (1886): 1) septic, 2) purulent, 3) progressive fibrinopurulent, 4) local. In 1912 Grekov defined the phases of peritonitis: early (1–2 days), late (3–5 days), final (6–21 days).
Modern classification of acute peritonitis
(Shalimov A. A., 1981)
According to origin
1. Рrimary. It occurs in the absence of an apparent intra-abdominal source of infection and is observed almost exclusively in patients with ascites formation.
2. Secondary. The common aetiologic entities of secondary peritonitis include: esophagus Boerhaave’s syndrome (spontaneous rapture), malignancy, trauma, iatrogenic, peptic ulcer perforation, cholecystitis, acute pancreatitis, bowel perforation, ischaemic bowel, strangulated hernia, bowel obstruction, diverticulitis, ulcerative colitis and Crohn’s disease, appendicitis.
According to aetiology
1. Microflora of the digestive tract (E. coli, Enterococcus, Pseudomonas, Proteus, Streptococcus, Staphylococcus, Anaerobic infection).
2. Microflora non-connected with the digestive tract (tuberculous infection, gonococcal infection).
3. Aseptic (pancreatogenic, bilious).
According to cause
According to character of exudate
According to spreading of infection
1. Local (inflammatory process is localized only in 1 anatomy region).
2. Diffuse (inflammatory process is localized in 2–5 anatomy regions).
3. Total (inflammatory process is localized in 6–9 anatomy regions).
Phases of peritonitis
1. Reactive (< 24 hours).
2. Toxic (24–72 hours).
3. Terminal (>72 hours).
Peritonitis is a serious manifestation of the surgical infection. The leading parts are: a) pathogenic microflora; b) intoxication; c) hypovolemia; d) deep metabolic disturbances.
The first phase – reactive phase
1. From the moment the aggressive factor has gotten into abdominal cavity, the signs of inflammation (oedema, hyperemia, and exudation) start.
10 minutes – appearance of exudate into abdominal cavity.
2 hours – formation of adhesions between peritoneum, bowels and large omentum starts.
18 hours – formation of friable mass has been completed.
2. Activation of function of hypothalamo-pituitary-adrenal axis.
3. Activation of biologically active substances: kinins, biogenic amines. They control blood circulation and intestinal motor function.
4. Activation of immune response.
5. Onset of microcirculation disturbances.
6. Development of adynamic ileus. But barrier function of bowel wall is survived.
The second phase – toxic phase
1. The leading factor at this stage is intoxication. Exactly intoxication usually determines the result of treatment. The constituents of intoxication are:
peritoneal exudate which is absorbed;
microflora (exo- end endotoxins);
proteolytic enzymes, which are released after destruction of leucocytes (cathepsins);
toxic substances, which are produced and absorbed into paretic bowels (phenols, skatoles).
2. Adynamic ileus. Distended bowel wall loses barrier function and translocation of microorganisms starts. Free liquid is collected into intestinal lumen – “sequestration of liquid into the third space” (transudate, digestive juice).
3. The organism can’t limit the infection and inflammatory process spreads into all abdominal cavity.
4. Immune response is depressed.
The third phase – terminal phase
This is a stage of septic shock and multiple organ failure. The changes are irreversible. Intoxication, disturbances of metabolism and haemodynamic are fatal.
Toxic hepatitis. Liver is the first organ which gets toxic substances per portal vein system. Liver metabolic disorders start: protein and pigmental metabolism, function of disintoxication is decreasing .
Toxic nephropathy: proteinuria, microhaematuria, azotemia.
Toxic myocardiodystrophy: hollowness of tones, tachycardia, extrasystole, ST segment depression.
Toxic alteration of lungs: respiratory distress syndrome (“shock lung”).
Clinical diagnostic of acute peritonitis
Clinical manifestations of acute peritonitis depend on:
disease which causes the peritonitis;
stage of peritonitis;
spreading of peritonitis;
characteristics of microflora;
activity of immune response.
The diagnosis of peritonitis is usually clinical. Essentially, all patients present with some degree of abdominal pain. This pain may be acute or more insidious in onset. Initially, the pain is often dull and poorly localized (visceral peritoneum) and then progresses to steady, severe, and more localized pain (parietal peritoneum).
If the infectious process is not contained, the pain becomes diffuse. In certain disease entities (e.g., gastric perforation, severe acute pancreatitis, intestinal ischaemia), the abdominal pain may be generalized from the beginning.
Anorexia and nausea are frequently present. Vomiting may occur because of the underlying visceral organ pathology or secondary to the peritoneal irritation.
On physical examination, patients with peritonitis most often appear unwell and in acute distress. Fever with temperatures that can exceed 38 C is usually present, but patients with severe sepsis may present with hypothermia.
Tachycardia is caused by the release of inflammatory mediators and intravascular hypovolemia caused by anorexia and vomiting, fever, and third-space losses into the peritoneal cavity and bowels.
With progressive dehydration, patients may become hypotensive, they may demonstrate decreased urine output, and, with severe peritonitis, they may present septic shock.
On abdominal examination, essentially all patients demonstrate tenderness to palpation. In most patients (even with generalized peritonitis and severe diffuse abdominal pain), the point of maximal tenderness roughly overlies the pathologic process (i.e., the site of maximal peritoneal irritation).
Patients with severe peritonitis often avoid all motion and keep their hips flexed to relieve the abdominal wall tension.
The abdomen is often distended, with hypoactive-to-absent bowel sounds. This finding reflects a generalized ileus and may not be present if the infection is well localized.
Occasionally, the abdominal examination reveals an inflammatory mass. Examining the abdomen of a patient with peritonitis and mass, the patient should be supine to left lateral position for better relaxation of the abdominal wall.
Rectal examination often elicits increased abdominal pain, particularly with inflammation of the pelvic organs but rarely indicates a specific diagnosis. A tender inflammatory mass toward the right may indicate appendicitis, and anterior fullness and fluctuation may indicate a pelvic abscess. In female patients, vaginal and bimanual examination may lead to the differential diagnosis of pelvic inflammatory disease.
A complete physical examination is important. Thoracic processes with diaphragmatic irritation (e.g., empyema), extraperitoneal processes (e.g., pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (e.g., infection, rectus haematoma) may mimic certain signs and symptoms of peritonitis.
Always examine the patient carefully for the presence of external hernias to rule out intestinal incarceration.
Remember that the presentation and the findings on clinical examination may be entirely inconclusive or unreliable in patients with significant immunosuppression (e.g., severe diabetes, steroid use, posttransplaint status, HIV), in patients with altered mental state (e.g., head injury, toxic encephalopathy, septic shock, analgesic agents), in patients with paraplegia, and in patients of advanced age.
CBC with differential, serum electrolytes with renal function. Most patients with intra-abdominal infections demonstrate leukocytosis (>11,000 cells/mL) with a shift to the immature forms on the differential cell count. Patients in severe sepsis, patients who are immunocompromised, and patients with certain types of infections (e.g., fungal, cytomegaloviral) may demonstrate absence of leukocytosis or leucopenia.
Blood chemistry may reveal dehydration and acidosis.
Liver function tests, if clinically indicated.
Amylase and lipase, if pancreatitis is suspected.
Urinalysis is essential to rule out urinary tract diseases (e.g., pyelonephritis, renal stone disease); however, patients with lower abdominal and pelvic infections often demonstrate WBC in the urine and microhaematuria.
In patients with diarrhoea, evaluate a stool for specific culture (i.e., Salmonella, Shigella, cytomegalovirus), if the patient’s history suggests infectious enterocolitis.
Aerobic and anaerobic blood cultures.
Peritoneal fluid evaluation (i.e., paracentesis, aspiration of abdominal fluid collections, intraoperative peritoneal fluid cultures).
When assessign a peritoneal fluid sample for peritoneal infection, evaluate the sample for pH, glucose, protein, lactate dehydrogenase, cell count, Gram stain, and aerobic and anaerobic cultures, a peritoneal fluid amylase.
Radiographs. Plain films of the abdomen (e.g., 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.
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. 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.
Ultrasonic. Abdominal Ultrasonic may be helpful in the evaluation of right upper quadrant (e.g., perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvic pathology (e.g., appendicitis, tubo-ovarian abscess, Douglas pouch abscess), but the examination is sometimes limited because of patient discomfort, abdominal distension, and bowel gas interference.
Ultrasonography may detect increased amounts of peritoneal fluid, 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 of 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.
Over the past several years, Ultrasonic-guided aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of abdominal fluid collections.
Computed tomography scans of the abdomen and pelvis remain the diagnostic study of choice for peritoneal abscess and the related visceral pathology. CT scan is indicated in all cases where the diagnosis cannot be established on clinical grounds and findings on abdominal plain films. Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans can detect small quantities of fluid, regions of inflammation and other GI tract pathology, with sensitivities that approach 100%.
Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and drained under CT guidance.
Nuclear medicine scans have little use in the initial evaluation of patients with suspected peritonitis or intra-abdominal sepsis. They are most frequently used in the evaluation of fever of unknown origin or in patients with persistent fever despite adequate antibiotic treatment and negative CT scan findings.
Magnetic resonance imaging is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses.
Contrast studies. Conventional contrast studies (i.e., upper gastrointestinal tract and colorectal contrast enema, fistulogram, contrast studies of drains and stents) are reserved for specific indications in the setting of suspected peritonitis or peritoneal abscess.
The general principles guiding the treatment of intra-abdominal infections are 4-fold:
1) to control the infectious source;
2) to eliminate bacteria and toxins;
3) to maintain organ system function;
4) to control the inflammatory process.
Medical, nonoperative interventional, and operative treatment options are complimentary, not competitive, in the treatment of peritoneal infections.
Medical support includes:
1) systemic antibiotic therapy;
2) intensive care with haemodynamic, pulmonary, and renal replacement support;
3) nutrition and metabolic support;
4) inflammatory response modulation therapy.
Treatment of peritonitis and intra-abdominal sepsis always begins with volume resuscitation, correction of potential electrolyte and coagulation abnormalities, and empiric broad-spectrum parenteral antibiotic coverage.
Antibiotic therapy. It is based on culture results.
Gram-negative E. coli.
Second-generation cephalosporin, penicillins with anaerobic activity, quinolones with anaerobic activity, quinolone and metronidazole, aminoglycoside and metronidazole:
Gram-positive Streptococcus species.
Anaerobic Bacteroides fragiles.
Other Bacteroides species.
Anaerobic Streptococcus species.
Tertiary Gram-negative Enterobacter species.
Enterococcus speciez second-generation cephalosporin.
Triazoles or amphotericin (considered in fungal aetiology).
Several studies suggest that antibiotic therapy is not as effective in later stages of the infection and that early (preoperative) systemic antibiotic therapy can result in significant reduction of concentration and growth rates of viable bacteria in the peritoneal fluid. Therefore, begin empiric therapy as soon as the diagnosis of peritoneal infection is suspected. The initial therapy for acute peritonitis must be mainly active against gram-negative organisms (E. coli, Enterobacteriaceae species) and anaerobes (e.g., B. fragilis).
In severe and hospital-acquired intra-abdominal infections, imipenem, piperacillin/tazobactam, and a combination of aminoglycosides and metronidazole are often effective.
Carbapenem is effective compared to piperacillin or tazobactam in the treatment of complicated intra-abdominal infection and was well tolerated.
Additional clinical antimicrobial studies are underway investigating the efficacy of new quinolones in the treatment of intra-abdominal infection.
The optimal duration of antibiotic therapy must be individualized and depends on the underlying pathology, severity of infection, speed and effectiveness of source control, and the patient response to therapy.
In uncomplicated peritonitis with early adequate source control, a course of 5–7 days is adequate in most cases. Complicated persistent infections and infections in patients who are immunocompromised may warrant a prolonged course of antibiotic therapy.
Some patients demonstrate persistent signs of inflammation without a defined infectious focus. In these patients, continued broad-spectrum antibiotic therapy may be more useful.
Nonoperative drainage. Today, abundant literature documents the safety and efficacy of Ultrasonic- and CT-guided percutaneous drainage of abdominal and extraperitoneal abscesses.
Common reasons for failure of primary nonoperative management include enteric fistula (e.g., anastomotic dehiscence), pancreatic involvement, infected clot, and multiple or multilocated abscesses.
In peritoneal abscess formation caused by subacute bowel perforation (e.g., diverticulitis, Crohn’s disease, appendicitis), primary percutaneous management with percutaneous drainage was successful in most patients.
Surgery remains an important therapeutic modality for all cases of peritoneal infection. Any operation should address the first 2 principles of the treatment of intra-peritoneal infections: early and definitive source control and elimination of bacteria and toxins from the abdominal cavity.
The operative approach is directed by the underlying disease process and the type and severity of the intra-abdominal infection. The surgeon should always strive to arrive at a specific diagnosis and delineate the intra-abdominal anatomy as accurately as possible prior to the operation.
However, in severe abdominal sepsis, a delay of operative management may lead to a significantly higher need for reoperations and overall worse outcomes; early exploration may be indicated.
Open-abdomen technique and scheduled reoperation
In certain situations, staging the operative approach to intraperitoneal infections is appropriate. Staging may be performed as a scheduled second-look operation or through open management, with or without temporary closure (laparostomy).
Second-look operations may be used in a “damage control” manner. In these cases, the patient at initial operation is severely ill and unstable from septic shock or coagulopathy (e.g., mediator liberation, disseminated intravascular coagulation). The goal of the initial operation is to provide preliminary drainage and to remove obviously necrotic tissue.
Then, the patient is resuscitated and stabilized for 24–36 hours and returned to the operating room for a more definitive drainage and source control.
In conditions related to bowel ischaemia, the initial operation aims to remove all frankly devitalized bowel. The second-look operation serves to reevaluate for further demarcation and decision-making regarding reanastomosis or diversion.
In severe peritonitis, particularly with extensive retroperitoneal involvement (e.g., necrotizing pancreatitis), open treatment with repeat reexploration, debridement and intraperitoneal lavage has been shown to be effective.
Temporary closure of the abdomen to prevent herniation and contamination from the outside of the abdominal contents can be achieved using gauze and large, impermeable, self-adhesive membrane dressings, mesh (e.g., Vicryl, Dexon), nonabsorbable mesh (GORE-TEX, polypropylene) with or without zipper or Velcrolike closure devices, and vacuum-assisted closure (VAC) devices. Advantages of this management strategy include avoidance of abdominal compartment syndrome (ACS) and easy access for reexploration. The disadvantages include significant disruption of respiratory mechanics and potential contamination of the abdomen with nosocomial pathogens.
Gastrointestinal decompression. It is indicated in patients with severe peritonitis and ileus. It is achieved by transnasal, transstomal or transanal small or/and large bowel tube. The aims of procedure are:
removing of toxic bowel content;
stabilization of bowel motor function;
enteral nutritional supporting;
prevention of postoperative adhesion bowel obstruction.
Laparoscopy is gaining wider acceptance in the diagnosis and treatment of abdominal infections. Initial laparoscopic examination of the abdomen can assist in determination of the aetiology of peritonitis. Laparoscopic diagnosis and peritoneal lavage in patients with peritonitis secondary to diverticulitis without faecal peritoneal contamination has helped to avoid operation in most patients in small clinical trials.
Successful laparoscopic repair of perforated gastric and duodenal ulcers has also been reported.
The treatment of perihepatic infections via laparoscopic approach has been well established in acute cholecystitis, where laparoscopic cholecystectomy has become the mainstay of therapy. More recently, primary treatment of subphrenic abscesses and laparoscopic Ultrasonic-assisted drainage of pyogenic liver abscesses have been performed successfully.
Individual reports also describe successful drainage of peripancreatic fluid collections and complicated intra-abdominal abscesses that are not amenable to CT scan – or Ultrasonic-guided percutaneous drainage.
As minimally invasive procedures continue to advance technologically, use of these approaches is likely to increase, reducing the need for the open surgical approach for peritoneal abscess drainage.
Volume resuscitation and prevention of secondary organ system dysfunction are of utmost importance in the treatment of patients with intra-abdominal infections. Depending on the severity of the disease, these patients should have Foley catheters placed to monitor urine output. Use invasive haemodynamic monitoring in severely ill patients to guide volume resuscitation and inotropic support. Correct existing serum electrolyte disturbances and coagulation abnormalities as best as possible before any intervention.
Begin empiric broad-spectrum systemic antibiotic therapy as soon as the diagnosis of intra-abdominal infection is suspected. Remember that patients with peritonitis often have severe abdominal pain. Provide adequate analgesia with parenteral narcotic agents as soon as possible. In the setting of significant nausea, vomiting, or abdominal distension caused by obstruction or ileus, institute nasogastric decompression as soon as possible. Consider intubation and ventilator support early in patients with evidence of septic shock or altered mental status to prevent further decompensation.
In patients with severe infections and certain disease processes (e.g., necrotizing pancreatitis, bowel ischaemia), informed consent should include the potential need for several reoperations and enteric diversion. The involved physicians and surgeon should not downplay the significant morbidities associated with abdominal sepsis when discussign these issues with the patient and/or family.
A vertical midline incision is the incision of choice in most patients with generalized peritonitis because it allows access to the entire peritoneal cavity. In patients with localized peritonitis (e.g., acute appendicitis, cholecystitis), an incision directly over the site of pathology (e.g., right lower quadrant, right subcostal) is usually adequate.
In patients with an unclear aetiology of the peritonitis, initial diagnostic laparoscopy may be useful.
The intra-abdominal anatomy may be significantly distorted because of inflammatory masses and adhesions. The inflamed organs are often very friable, and the surgeon must exercise great caution when exploring the patient with peritoneal infection.
Haemodynamic instability may occur at any time during treatment because of bacteremia and cytokine release. Patients often demonstrate significant fluid shifts with third spacing. Swelling of the bowel, retroperitoneum, and abdominal wall may preclude safe abdominal closure after prolonged cases in patients who are severely ill.
Inflammation causes regional hyperemia, and sepsis may cause coagulation deficits and platelet dysfunction, leading to increased bleeding. Careful dissection and meticulous haemostasis are of utmost importance.
One of the critical decisions in the surgical treatment of patients with severe peritonitis is regarding whether to use a closed-abdomen or open-abdomen technique. The goal of the closed-abdomen technique is to provide definitive surgical treatment at the initial operation; perform primary fascial closure and perform repeat laparotomy only when clinically indicated. The goal of the open-abdomen technique is to provide easy direct access to the affected region. Source control is achieved through repeated reoperations or open packing of the abdomen. This technique may be well suited for initial damage control in extensive peritonitis. Also consider patients who are at high risk for development of abdominal compartment syndrome (e.g., intestinal distension, extensive abdominal wall and intra-abdominal organ oedema) for this technique because attempts to perform primary fascial closure under significant tension in these circumstances are associated with an increased incidence of multiorgan faluation (e.g., renal, respiratory), necrotizing abdominal wall infections, and mortality.
Postoperatively, monitor all patients closely in the appropriate clinical setting for adequacy of volume resuscitation, resolution or persistence of sepsis, and the development of organ system failure. Appropriate systemic broad-spectrum antibiotic coverage must be continued without interruption for the appropriate time.
The patient’s overall condition should improve significantly and progressively within 24–72 hours of the initial treatment (i.e., resolution of the signs and symptoms of infection, mobilization of interstitial fluid). This time course may be prolonged in patients who are critically ill with significant multiple organ system dysfunction. A lack of improvement should prompt an aggressive search for a persistent or recurrent intraperitoneal or new extraperitoneal infectious focus.
Patients requiring surgical intervention for peritonitis demonstrate a significantly increased risk for surgical site infections and wound healing failure.
All patients who are critically ill and patients receiving prolonged antibiotic therapy are at increased risk for developing secondary opportunistic infections (e.g., fungal infections, central venous catheter infections, ventilator-associated pneumonia).
Nutrition. In general, patients with peritonitis develop some degree of gut dysfunction (ileus) after exploration. If enteral feeding is contraindicated or not tolerated, parenteral nutrition should be instituted.
After resolution of peritonitis and peritoneal abscesses, follow-up care is directed mostly by specifics of the underlying disease process and the presence or absence of chronic complications (e.g., enterocutaneous fistulae).