History
The diagnosis of peritonitis is usually clinical. History should include recent abdominal surgery, previous episodes of peritonitis, travel history, use of immunosuppressive agents, and the presence of diseases (eg, inflammatory bowel disease, diverticulitis, peptic ulcer disease) that may predispose to intra-abdominal infections.
A broad range of signs and symptoms are seen in spontaneous bacterial peritonitis (SBP). A high index of suspicion must be maintained when caring for patients with ascites, particularly those with acute clinical deterioration. As many as 30% of patients are completely asymptomatic. Manifestations of SBP may include the following:
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Fever and chills (as many as 80% of patients)
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Abdominal pain or discomfort (found in as many as 70% of patients)
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Worsening or unexplained encephalopathy
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Diarrhea
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Ascites that does not improve following administration of diuretic medication
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Worsening or new-onset renal failure
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Ileus
Abdominal pain, which may be acute or insidious, is the usual chief complaint of patients with peritonitis. Initially, the pain may be dull and poorly localized (visceral peritoneum); often, it progresses to steady, severe, and more localized pain (parietal peritoneum). Abdominal pain may be exacerbated by any movement (eg, coughing, flexing the hips) and local pressure. If the underlying process is not contained, the pain becomes diffuse. In certain disease entities (eg, gastric perforation, severe acute pancreatitis, intestinal ischemia), the abdominal pain may be generalized from the beginning.
Abdominal distention may be noted, as well as signs of dysfunction of other organs. Symptoms may be subtle in patients on corticosteroids, in diabetic patients with advanced neuropathy, and in hospitalized patients, especially the very young and the very old. In the presence of ascites, decreased friction between the visceral and parietal peritoneal surfaces may reduce the symptoms of abdominal pain, as seen in patients with SBP.
Anorexia and nausea are frequent symptoms and may precede the development of abdominal pain. Vomiting may be due to underlying visceral organ pathology (ie, obstruction) or be secondary to peritoneal irritation.
Physical Examination
On physical examination, patients with peritonitis generally appear unwell and in acute distress. Many of them have a temperature that exceeds 38° C, although patients with severe sepsis may become hypothermic. Tachycardia may be present, as a result of the release of inflammatory mediators, intravascular hypovolemia from anorexia, vomiting and fever, and third-space losses into the peritoneal cavity. With progressive dehydration, patients may become hypotensive (5-14% of patients), as well as oliguric or anuric; with severe peritonitis, they may present in overt septic shock.
When examining the abdomen of a patient with suspected peritonitis, the patient should be supine. A roll or pillows underneath the patient's knees may allow for better relaxation of the abdominal wall.
On abdominal examination, almost all patients demonstrate tenderness to palpation. In most patients—even those with generalized peritonitis and severe diffuse abdominal pain—the point of maximal tenderness or referred rebound tenderness roughly overlies the pathologic process (ie, the site of maximal peritoneal irritation).
Most patients demonstrate increased abdominal wall rigidity. The increase in abdominal wall muscular tone may be voluntary, in response to or in anticipation of the abdominal examination, or involuntary because of the 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.
Signs of hepatic failure (eg, jaundice, angiomata) may be noted.
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 cul de sac abscess.
In female patients, vaginal and bimanual examination findings may be consistent with pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarian abscess), but exam findings are often difficult to interpret in severe peritonitis.
A complete physical examination is important for excluding conditions whose presentation may resemble that of peritonitis. 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.
Remember that the presentation and the findings on clinical examination may be entirely inconclusive or unreliable in patients with significant immunosuppression (eg, severe diabetes, steroid use, posttransplant status, HIV infection), in patients with altered mental state (eg, head injury, toxic encephalopathy, septic shock, analgesic agents), in patients with paraplegia, and in patients of advanced age. With localized deep peritoneal infections, fever and/or an elevated WBC count may be the only signs present. As many as 20% of patients with spontaneous bacterial peritonitis demonstrate very subtle signs and symptoms. New onset or deterioration of existing encephalopathy may be the only sign of the infection at the initial presentation. Most patients with tuberculous peritonitis demonstrate vague symptoms and may be afebrile.
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Peritonitis and abdominal sepsis. Diagnostic and therapeutic approach to peritonitis and peritoneal abscess.
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Peritonitis and abdominal sepsis. A 48-year-old man underwent suprapubic laparotomy, right hemicolectomy, and gastroduodenal resection for right colon cancer invading the first portion of the duodenum. After surgery, the patient developed abdominal pain and distention. Computed tomography (CT) scanning was used to confirm an anastomotic dehiscence. Figure A shows a contrast-enhanced scan of the abdomen and pelvis that reveals multiple fluid collections, perihepatic ascites, and mild periportal edema. A collection of fluid containing an air-fluid level is visible anterior to the left lobe of the liver. A second collection is anterior to the splenic flexure of the colon. In figure B, a third fluid collection is present in the inferior aspect of the lesser space and in the transverse mesocolon. Figure C shows the pelvis with a collection of free fluid in the rectovesical pouch.
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Peritonitis and abdominal sepsis. A 78-year-old man was admitted with a history of prior surgery for small bowel obstruction and worsening abdominal pain, distended abdomen, nausea, and obstipation. In figure A, a marked amount of portal venous gas within the liver, mesenteric venous gas, and pneumatosis intestinalis are consistent with ischemic small intestine. The superior mesenteric artery appears patent. The liver has a nodular contour consistent with cirrhosis. In figures B and C, markedly distended loops of small intestine containing fluid and air-fluid levels are consistent with a small bowel obstruction. No focal fluid collections are identified.
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Peritonitis and abdominal sepsis. A 35-year-old man with a history of Crohn disease presented with pain and swelling in the right abdomen. In figure A, a thickened loop of terminal ileum is evident adherent to the right anterior abdominal wall. In figure B, the right anterior abdominal wall is markedly thickened and edematous, with adjacent inflamed terminal ileum. In figure C, a right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall.
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Peritonitis and abdominal sepsis. Gram-negative Escherichia coli.
Tables
Source Regions |
Causes |
Esophagus |
Boerhaave syndrome Malignancy Trauma (mostly penetrating) Iatrogenic* |
Stomach |
Peptic ulcer perforation Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor) Trauma (mostly penetrating) Iatrogenic* |
Duodenum |
Peptic ulcer perforation Trauma (blunt and penetrating) Iatrogenic* |
Biliary tract |
Cholecystitis Stone perforation from gallbladder (ie, gallstone ileus) or common duct Malignancy Choledochal cyst (rare) Trauma (mostly penetrating) Iatrogenic* |
Pancreas |
Pancreatitis (eg, alcohol, drugs, gallstones) Trauma (blunt and penetrating) Iatrogenic* |
Small bowel |
Ischemic bowel Incarcerated hernia (internal and external) Closed loop obstruction Crohn disease Malignancy (rare) Meckel diverticulum Trauma (mostly penetrating) |
Large bowel and appendix |
Ischemic bowel Diverticulitis Malignancy Ulcerative colitis and Crohn disease Appendicitis Colonic volvulus Trauma (mostly penetrating) Iatrogenic |
Uterus, salpinx, and ovaries |
Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst) Malignancy (rare) Trauma (uncommon) |
*Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon, often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel injury (eg, mechanical, thermal) are common causes of leak in the postoperative period. |
|
Type |
Organism |
Percentage |
Aerobic |
|
|
Gram negative |
Escherichia coli |
60% |
|
Enterobacter/Klebsiella |
26% |
|
Proteus |
22% |
|
Pseudomonas |
8% |
Gram positive |
Streptococci |
28% |
|
Enterococci |
17% |
|
Staphylococci |
7% |
Anaerobic |
Bacteroides |
72% |
|
Eubacteria |
24% |
|
Clostridia |
17% |
|
Peptostreptococci |
14% |
|
Peptococci |
11% |
Fungi |
Candida |
2% |
Peritonitis (Type) |
Etiologic Organisms |
Antibiotic Therapy (Suggested) |
|
Class |
Type of Organism |
||
Primary |
Gram-negative |
E coli (40%) K pneumoniae (7%) Pseudomonas species (5%) Proteus species (5%) Streptococcus species (15%) Staphylococcus species (3%) Anaerobic species (< 5%) |
Third-generation cephalosporin |
Secondary |
Gram-negative |
E coli Enterobacter species Klebsiella species Proteus species |
Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole |
Gram-positive |
Streptococcus species Enterococcus species |
||
Anaerobic |
Bacteroides fragilis Other Bacteroides species Eubacterium species Clostridium species Anaerobic Streptococcus species |
||
Tertiary |
Gram-negative |
Enterobacter species Pseudomonas species Enterococcus species |
Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole Carbapenems Triazoles or amphotericin (considered in fungal etiology) (Alter therapy based on culture results.) |
Gram-positive |
Staphylococcus species |
||
Fungal |
Candida species |
||
Routine |
Optional |
Unusual |
Less Helpful |
Cell count |
Obtain culture in blood culture (BC) bottles. |
Tuberculosis (TB) smear and culture |
pH |
Albumin |
Glucose |
Cytology |
Lactate |
Total protein |
Lactate dehydrogenase (LDH) |
Triglyceride |
Cholesterol |
|
Amylase |
Bilirubin |
Fibronectin |
|
Gram stain |
|
Alpha 1-antitrypsin |
|
|
|
Glycosaminoglycans |
