Peritonitis secondary

Peritonitis may be classified as primary, secondary, or tertiary. Primary peritonitis, also called spontaneous bacterial peritonitis, is an infection of the peritoneal cavity without an evident source of bacteria from the abdomen.1,2 In secondary peritonitis, a focal disease process is evident within the abdomen. Secondary peritonitis may involve perforation of the gastrointestinal (GI) tract (possibly because of ulceration, ischemia, or obstruction), postoperative peritonitis, or posttraumatic peritonitis (e.g., blunt or penetrating trauma). Tertiary peritonitis occurs in critically ill patients and is infection that persists or recurs at least 48 hours after apparently adequate management of primary or secondary peritonitis. 

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... 

Intraabdominal infections have a wide spectrum of clinical features. Peritonitis usually is easily recognized, but intraabdominal abscess often may continue for long periods of time. Patients with primary and secondary peritonitis present quite differently. 

The treatment of intraabdominal infection most often requires the coordinated use of three major modalities (1) prompt drainage, (2) support of vital functions, and (3) appropriate antimicrobial therapy to treat infection not eradicated by surgery. Antimicrobials are an important adjunct to drainage procedures in the treatment of secondary intraabdominal infections however, the use of antimicrobial agents without surgical intervention usually is inadequate. For most cases of primary peritonitis, drainage procedures may not be required, and antimicrobial agents become the mainstay of therapy. 

Primary peritonitis is treated with antimicrobials and rarely requires drainage. Secondary peritonitis requires surgical removal of the inflamed or gangrenous tissue to prevent further bacterial contamination. If the surgical procedure is sub-optimal, attempts are made to provide drainage of the infected or gangrenous structures. 

Whether diagnosed with primary or secondary peritonitis, monitor the patient for relief of symptoms. Once antimicrobials are initiated and the other important therapies described earlier are used, most patients should show improvement within 2 to 3 days. Successful antimicrobial therapy with resolution of infection will result in decreased pain, manifested as resolution of abdominal guarding and decreased use of pain medications over time. The patient should not appear in distress, with the exception of recognized discomfort and pain from incisions, drains, and a nasogastric tube. 

For patients with primary peritonitis, if peritoneal dialysate cultures were positive initially, repeat cultures should be negative. For patients with secondary peritonitis, monitor the amount of fluid draining if a drain was placed. The volume of drainage should lessen as the infection resolves. Repeat abdominal radiographs should return to normal. 

Dougherty SH. Antimicrobial culture and susceptibility testing has little value for routine management of secondary bacterial peritonitis. Clin Infect Dis 1997 25(suppl 2) S258-261. 

Peritonitis is defined as the acute, inflammatory response of peritoneal lining to microorganisms, chemicals, irradiation, or foreign body injury. Peritonitis may be classified as either primary or secondary. With primary peritonitis, an intraabdominal focus of disease may not be evident. In secondary peritonitis, a focal disease process is evident within the abdomen. 

In secondary peritonitis, bacteria most often enter the peritoneum or retroperitoneum as a result of disruption of the integrity of the GI tract caused by diseases or traumatic injuries. 

Peritoneal dialysis Cirrhosis with ascites Nephrotic syndrome Secondary bacterial peritonitis... 

Pathogens Isolated from Patients with Secondary Peritonitis ... 

Secondary peritonitis is treated surgically, and this is called source control, which refers to the physical measures undertaken to eradicate the... 

Although inhalation is usually of secondary importance, the effects from the dust or mist will vary ftom mild irritation to severe pneumonitis, depending on the severity of exposure. Ingestion produces severe abdominal pain, corrosion of the lips, mouth, tongue, and pharynx, and the vomiting of large pieces of mucosa. In severe cases, circulatory failure, esophageal perforation, and peritonitis may occur. 

Intraabdominal infections have a wide spectrum of clinical features often depending on the specific disease process, the location and the magnitude of bacterial contamination, and concurrent host factors. Patients with primary and secondary peritonitis present quite differently (Table 42-3). If peritonitis continues untreated, the patient may experience hypovolemic shock from fluid loss into the peritoneum, bowel wall, and lumen. This may be accompanied by generalized sepsis. Intraabdominal abscess may pose a diagnostic challenge as the symptoms are neither specific nor dramatic. 

Each of these 3 forms of SBP has to be delimited from secondary bacterial peritonitis. In bacterial ascites, several types of microorganisms, including fungi, can usually be identified after subculturing. As a rule, the cell count exceeds 10,000/mm, the LDH value is elevated (> 225 U/1), and the glucose concentration is < 50 mg/dl. 

Akriviadis, A., Runyon, B.A. Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology 1990 98 127-133... 

A 58-year-old woman with end-stage renal insufficiency secondary to diabetic nephropathy developed abdominal wall cellulitis 4 days after insertion of a peritoneal dialysis catheter. She was given vancomycin, cefepime, and metronidazole in reduced doses (doses not stated) and 2 days later developed dysarthria, an intention tremor, dysmetria, and dysdiadochokinesia. Routine biochemical tests were unchanged and a CT scan of the brain was unremarkable, but an MRI scan showed cerebral and cerebellar atrophy with multifocal ischemic glial lesions. Metronidazole was withdrawn and 2 days later her symptoms and signs had completely resolved. 

There is increased sensitivity to vitamin D in patients who are undergoing renal dialysis and who have an abnormal calcium/phosphorus ratio. Patients on continuous ambulatory peritoneal dialysis (CAPD) who develop secondary hyperparathyroidism may already have low bone turnover or adynamic bone lesions, and if treated indiscriminately with calcitriol their low bone turnover can get worse (62). 

Delmez JA. Calcitriol and secondary hyperparathyroidism in continuous ambulatory peritoneal dialysis patients. Perit Dial Int 1993 13(2) 95-7. 

Nitrate and nitrites can combine with secondarys amines to form dimethylnitrosamines, which are acutely toxic and cause centrilobular necrosis, fibrous occlusion of central veins, and pleural and peritoneal hemorrhages in animals. In the body nitrates are converted to nitrites, which can oxidize hemoglobin to methemoglobin and lead to cyanosis. 

Biliary tract diseases, such as cholecystitis, cause up to fourfold elevations of the serum AMY activity as a result of either primary or secondary pancreatic involvement. Various intraabdominal events can lead to a significant increase in serum AMY activities up to a fourfold elevation and sometimes beyond. Such increases may be due to leakage of the P-AMY from the intestine into the peritoneal cavity and then into the circulation. Peritonitis and acute appendicitis have been reported to produce a slight elevation (up to twofold and threefold) of serum AMY activity. Serum AMY is normal in most patients with ectopic pregnancies, but increases have been seen in advanced cases of ruptured ectopic pregnancy. 

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