Spontaneous bacterial peritonitis

As a spontaneous bacterial peritonitis is called a bacterial infection within the peritoneal cavity of the abdominal cavity without the perforation in the abdomen of a lying hollow organ as a source of bacterial infection. The spontaneous bacterial peritonitis is usually based on a pre-existing accumulation of fluid ( ascites ) within the peritoneal cavity, which can often occur with liver cirrhosis or kidney diseases. The diagnosis of the disease is made by obtaining and analyzing the ascites. Treatment is given by giving antibiotics .

distribution

Spontaneous bacterial peritonitis is the most common bacterial infection in cirrhotic patients. It is responsible for around 10-30% of infectious diseases in hospital patients. Risk factors for the occurrence of SBP are simultaneous bleeding in the digestive tract and low protein content (less than 1.5 g / dl) in the ascites. Medication with proton pump inhibitors can increase the risk of SBP by blocking acid in the stomach.

Cause and development of the disease

The SBP requires the presence of fluid in the peritoneal space, as it can occur with liver cirrhosis, with other liver diseases with increased pressure in the portal vein circulation or with kidney diseases. The ascites itself is considered to be the location of the significantly reduced immune defense. It is assumed that the bacteria colonize the ascites through translocation from the intestine. Disturbances in the barrier function of the intestine and a chronic change in the intestinal microbiome due to immunosuppression, as postulated in liver diseases, should favor the occurrence of bacterial colonization.

Investigation methods

Ascites can be detected very easily and with the highest sensitivity through an ultrasound examination of the abdomen. The extraction of the fluid through the puncture with a hollow needle ( paracentesis ) is mandatory for diagnosis or to rule out SBP and is advisable for therapeutic reasons in the case of high amounts of ascites. The determination of more than 500 cells per mm ³ or more than 250 segmented granulocytes per mm ³ in the ascites aspirate is decisive for the diagnosis of SBP . If one of these cell numbers is exceeded, an SBP can be assumed. The establishment of a bacterial culture from the ascites is advisable, but only in 60% of cases leads to the detection of the bacterium causing the infection. Gram- negative pathogens are mostly found in outpatient settings , while infections occurring in hospitals are mostly gram-positive bacteria. However, SBP is also possible with a lower number of cells, which often occurs with gram-positive pathogens.

The differentiation from secondary peritonitis, which occurs on the basis of a hollow organ perforation, can also be made by further examinations of the removed ascites. A very high cell count, a high LDH (> 225 mU / ml), a reduced glucose content (<50 mg / dl) or an increased protein content (> 1 g / dl) can be indicative of secondary peritonitis. However, due to the sensitivity of 68% of these laboratory parameters, they cannot replace the exclusion of secondary peritonitis by imaging .

pathology

The microscopic examination showed a granulocytic cell picture. A pathologist should examine the removed ascites to rule out neoplasia , which can also cause cell-rich ascites.

treatment

A calculated antibiotic treatment should be started immediately after the laboratory diagnosis has been confirmed. The standard therapy in the occurrence of severe symptoms is intravenous administration of a third-generation cephalosporin antibiotic , e.g. B. Ceftriaxone . Circulatory instability, the presence of a gastric ulcer or gastrointestinal bleeding, the development of hepatic encephalopathy or acute kidney failure are regarded as serious symptoms . Carbapenems are considered reserve antibiotics . Due to the different spectrum of pathogens, nosocomially acquired SBP can also be treated primarily with a carbapenem. Uncomplicated SBP can be treated orally with fluoroquinolones . The maximum duration of therapy should be five days. The success of the therapy can be monitored by the return of the laboratory-chemical inflammation parameters. Monitoring with a renewed examination of the ascites is also possible, here a decrease of at least 25% is expected after 48 hours of treatment. If there is a special local resistance situation, other antibiotics can also be used.

The administration of albumin can support the recovery of kidney function , especially when large amounts of ascites are punctured .

prevention

After SBP has taken place, prophylaxis should be carried out using orally administered fluoroquinolone or trimethoprim / sulfamethoxazole . Patients with a low protein content in the ascites (<1.5 g / dl) can receive prophylaxis. Prophylaxis should also be used in advanced liver disease. The prerequisite for this is 9 points in the Child-Pugh Score , hyponatremia or the onset of renal insufficiency .

Prospect of healing

The risk of dying from SBP is between 10 and 50%, depending on the patient group. Since SBP is often a sign of worsening liver disease , the 1-year survival rate after surviving SBP is 7 to 69%.

Individual evidence

1. ↑ ^{a b c d} R. Wiest, A. Krag, A. Gerbes: Spontaneous bacterial peritonitis: recent guidelines and beyond. In: Gut 2012; 61: 297-310
2. ↑ S3 guideline ascites. Retrieved July 6, 2017 . 
3. ↑ ^{a b c d e f g} A. L. Gerbes, V. Gülberg, T. Sauerbruch, R. Wiest, B. Appenrodt, MJ Bahr, MM Dollinger, M. Rössle, M. Schepke: S3 guideline “Ascites, spontaneous bacterial peritonitis , Hepatorenal Syndrome " . In: Journal of Gastroenterology 2011; 49: 749-779

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