Liver transplant might help keep infection at bay
Published on: Tuesday, December 17, 2019
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The presence of these signs in a patient is sometimes referred to as peritonism. The localisation of these manifestations depends on whether peritonitis is localised (eg appendicitis or diverticulitis before perforation) or generalised abdominal pain (with involvement of poorly localising intervention of visceral peritoneal layer) and may become localised later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.
Primary peritonitis is an acute febrile illness often confused with appendicitis in children. Fever abdominal pain nausea and vomiting, and diarrhea usually are present with diffuse abdominal tenderness and rebound tenderness and bowel sounds are hypoactive or absent. In cirrhotic patients with primary peritonitis, pre-existing ascites is present. In some patients, the clinical manifestations are typical.
The onset may be insidious and findings of peritoneal irritation may be absent in an abdomen distended with ascites. Fever (temperature >37 Celsius [> 100 Fahrenheit]) is the most common presenting sign, occurring in 50-80 per cent of cases and may present without abdominal signs or symptoms or the process may be clinically silent. Primary peritonitis in cirrhotic patients is generally associated with other features of end-stage liver disease (hepatorenal syndrome, progressive encephalopathy, and variceal bleeding). Primary peritonitis always should be considered in the differential diagnosis of decompensation of previously stable chronic liver disease.
It is important to recognise spontaneous bacterial peritonitis early in the course of infection because there is frequently a very short window of opportunity during which to intervene to ensure a good outcome.
If the opportunity is missed, shock ensues, followed rapidly multiorgan failure. Survival is unlikely in patients who develop shock prior to initiation of empiric antibiotics. One report estimated that survival decreased by approximately 8 per cent for each hour of delay in starting antibiotics in patients with septic shock.
Diagnosis
Primary peritonitis is diagnosed by ruling-out a primary intra-abdominal source of infection. Computed tomography (CT) with oral and intravenous contrast material has greatly enhanced the detection of intra-abdominal sources of peritonitis.
Surgery often can be directed towards a potential source of infection identified on the basis of CT findings, rather than by the approach of a full exploratory laparotomy, which was used more commonly in this setting before the availability of CT and was associated with high rates of mortality in this setting before the availability of CT and was associated with high rates of mortality in certain groups of patients, such as cirrhotic patients. Patients with primary peritonitis usually respond within 48 – 72 hours to appropriate antimicrobial therapy.
The observation of an exceptional rate of decline in the ascetic fluid leukocytes after initiation of antimicrobial therapy for primary peritonitis also has been found to be helpful differentiate primary from secondary bacterial peritonitis. The finding of pneumococci in peritoneal fluid may not indicate primary peritonitis, as illustrated by a case report of appendicitis and secondary peritonitis caused by pneumococci.
Secondary bacterial peritonitis (SBP) should be suspected in patients with cirrhosis who develop signs and symptoms of fever, abdominal pain, altered mental status, abdominal tenderness or hypertension. In addition, patients with ascites admitted to the hospital for other reasons should also undergo paracentesis to look for evidence of SBP. The importance of paracentesis was demonstrated in a review of a disease of 17, 711 patients with cirrhosis ascites who were admitted to the hospital with primary diagnosis of ascites or encephalopathy.
Treatment
Patients with primary SBP, empiric therapy should be initiated with as soon as possible to maximise with patient’s chance of survival. However, antibiotics to be given until ascetic fluid has been obtained for culture. Most cases of primary peritonitis are due to gut bacteria such as Escherichia coli and Klebsiella, though Streptococcal and Staphylococcal infections can also occur. As a result broad-spectrum therapy is warranted until the results of susceptibility testing is available.
Runyon and associates recommend cefotaxime 2g intravenously every eight hours because it has been shown to produce excellent ascetic fluid levels. In addition, to antibiotic therapy, patients with SBP who are taking a non-selective beta blocker should have the medication discontinued and initiation of supportive measures such as vigorous rehydration and correction of electrolyte disturbances.
Disease outcome
The treatment of primary peritonitis has been reported to be successful in more than half of cirrhotic patients but because of the frequency of accompanying end-stage cirrhosis, the overall mortality rate in cirrhotic adults has been 95 per cent. Subsequent studies, however, reported lower mortality rates of 70 per cent and 57 per cent and 28 percent and 47 per cent, respectively, died from the primary peritonitis. Patients with poorest prognosis were found to have renal insufficiency, hypothermia, hyperbilirubinemia and hypoalbuminemia. The lower mortality rates in these later series can perhaps be explained by the less frequent of less frequency of hepatic encephalopathy. The lowest hospitalisation and infection-related mortality rates (37.8 per cent and 2.2 per cent), reported later were attributed to early diagnosis and treatment. However, patients suffering severe liver disease to develop SBP have poor long-term prognosis; 1 and 2 year mortality rates are 70 per cent and 80 per cent respectively.
Prevention
A patient who has survived one episode of primary peritonitis has an increased 1-year probability of another episode. A combined meta-analysis of 13 trials in which antibiotic prophylaxis was given to hospitalised patients with cirrhosis, who had various risk factors for infection, showed an overall decrease in mortality and decrease in bacterial infection.
One concern with prolonged antibiotic prophylaxis is the potential selection of resistant gut bacterial flora, which can cause spontaneous infection. In randomised trials researches have studied both intermittent and continuous prophylaxis.
These include selective decontamination of the bowel and oral norfloxacin (400mg daily), trimethoprimsulfamethoxzole (double-strength dose given once daily for 5 days each week) and ciprofloxacin (a single weekly dose of 750mg or 500mg daily). Most who have had one or more episodes of spontaneous bacterial peritonitis. A similar approach to prevent infection in patients awaiting liver transplantation is often undertaken, although randomised trials supporting this practice are lacking. Guidelines for the use of preoperative antimicrobial prophylaxis recommendations include the use of prophylactic cefazolin in esophageal gastroduodenal surgery, high risk individuals those with morbid obesity and those undergoing biliary tract surgery and for those individuals older than 70 years of age.
Peritonitis is an inflammation of the peritoneum usually occurs in patients with underlying causes frequently cirrhosis, ascites, nephrotic syndrome, patients on continuous dialysis, rupture of viscus, ulcerated lesions of colon and pelvic inflammatory disease. Early diagnosis and empiric antibiotic therapy is important. Survival is decreased if delay in starting antibiotics in patients with septic shock.
Summary
Intra-abdominal infection can be caused by various sources. Primary peritonitis or SBP is an ascetic infection. Peritonitis has been categorised as primary, secondary, tertiary or in patients with continuous dialysis. Frequent symptoms of ascites should undergo paracentesis to confirm SBP. Frequently isolated bacterial pathogens include gut flora, coagulase negative staphylococci and nosocomial multidrug resistant organisms in tertiary peritonitis. Cefotaxime 2g intravenously every eight hours produce excellent ascetic fluid levels, with supported measures to correct electrolyte imbalance. It is important to diagnose SBP early; delay in diagnosis may result in septic shock. High mortality and decreased survival by approximately 8 per cent of each hour of delay in starting antibiotics in patients with septic shock.
* This is the third and final part of this series on peritonitis. The second instalment was carried on November 26.
* Scientific information provided here is intended for readers only and is not medical advice.
About the author
Murtaza Mustafa is a former Associate Professor at the Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, with interest in infectious diseases, multi-drug resistant bacteria, tuberculosis, Heliobacter pylori, MRSA, CA-MRSA and Melioidosis. He has three book-research monographs and 133 national and international publications to his credit.
