Spontaneous bacterial peritonitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Spontaneous bacterial peritonitis (SBP) is a form of peritonitis that occurs in most of the patients with advanced cirrhosis, in 10-30% of hospitalized patients with ascites and in various other clinical settings, such as nephrotic syndrome, heart failure, tuberculous infection, continuous ambulatory peritoneal dialysis for chronic renal failure.^{[1] [2]} SBP is diagnosed with a positive bacterial culture for a single organism and an AF ( ascitic fluid) : polymorphonuclear (PMN) cell count of > 250/mm3, in the absence of a surgically treatable intra-abdominal source of infection. More than 60% of SBP episodes are caused by enteric gram-negative organisms such as Escherichia coli and Kleibsella. Selective intestinal decontamination (SID) with fluorinated quinolones suppresses the gram-negative intestinal flora and is known to reduce the incidence of SBP.^[3][4] SBP results due to the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped into the blood stream. Clinical signs and symptoms are non specific and indistinguishable from secondary peritonitis. Ascitic fluid analysis is helpful in differentiating SBP from secondary peritonitis. Because of the lack of specificity and sensitivity of clinical signs and symptoms, cirrhotic patients with unexplained deterioration should undergo a diagnostic paracentesis. Once diagnosed, patients with SBP should receive prompt empiric antibiotic treatment ( Cephalosporins) without waiting for the ascitic fluid culture. Failure of prompt initiation of antibiotics results in significant and potentially fatal deterioration in the clinical status of the patient. Patients who survive an episode of SBP are at high risk of recurrence. Patients with cirrhosis and ascites developing abdominal pain and/or temperature >100F are more prone to have SBP and should receive empiric antibiotic treatment. Early detection and treatment improve outcome and prevent complications such as shock and renal failure.^[5]

To see a comprehensive video about SBP, click here.

Kerr and colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients while Harold O.Conn , M.D, a world-renowned hepatologist (1964) introduced the term “spontaneous bacterial peritonitis” for the first time in English literature. Later in the history, SBP was studied extensively by many renowned researchers and health care professionals as this condition was seen among many patients with cirrhosis, which has lead to the thorough understanding and recognition of SBP.

Spontaneous bacterial peritonitis is one of the variants of ascitic fluid infections.^[6]. Classification of ascitic fluid infections is based on neutrophil count and culture report.^[7][8]. Asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells.^[9]. SBP is also classified based on the routes of infection and the clinical setting as follows Health care-associated, Nosocomial, Community acquired, Multi-drug resistant, Recurrent.

Spontaneous bacterial peritonitis is thought to result from a combination of factors related to cirrhosis and ascites such as: altered microbial flora, hypo-motility of the intestine, intestinal bacterial overgrowth, increased intestinal mucosal permeability, bacterial translocation to lymph nodes. Presence of ascites is an important risk factor for the development of bacterial translocation. In healthy individuals, bacteria that colonize lymph nodes are killed by local immune defenses. However, in the setting of cirrhosis, an acquired state of immunodeficiency there is: malfunctioning of the reticulo-endothelial and neutrophilic system, reduced cellular and humoral bactericidal function which favor the spread of bacteria to the blood stream.^[10][11][12]

• Alterations in the systemic immune response: Bacteremia in a healthy host results in rapid coating of the bacteria by IgG/complement components which help in engulfing and killing of the bacteria by circulating neutrophils. But in cirrhosis, several abnormalities have been described which lead to defective clearance of the bacteria include : decreased serum levels of complement components (C3, C4), impaired chemotaxis, poor function and phagocytic activity of neutrophils, decreased function of Fc-gamma-receptors in macrophages.
• Reticuloendothelial system phagocytic activity: The stationary macrophages, such as the Kupffer cells of the liver, assist the circulating neutrophils in the extraction and killing of particulate matter (e.g., bacteria) from the systemic circulation. In Cirrhosis, there is hepatic reticuloendothelial system (RES) dysfunction and kupffer cells are decreased in number with impaired function along with the malfunctioning of the neutrophilic system. Patients with the most severe dysfunction of RES are at highest risk of bacteremia and concomitant shortened survival, due to sepsis. The presence of intrahepatic and extra hepatic porto-systemic shunts as a consequence of portal hypertension, prevent circulating bacteria from encountering kupffer cells. The final consequence of these abnormalities is the prolongation of bacteremia and eventual seeding of other sites, including ascitic fluid. ^[13]
• Ascitic fluid defense mechanisms, decreased local AF opsonic activity: The presence of bacteria in ascitic fluid does not guarantee infection will develop, as ascitic fluid is capable of humoral self-defense due to the effectiveness of the complement system and patients with adequate activity of this vital bactericidal system do not develop AF bacterial infections. In patients with ascitic fluid C3 < 1g/dl and a protein level < 1g/dl are at an increased predisposition to SBP. The complement levels may be deficient because of increased consumption of these components or because of impaired synthesis, resulting in colonization of AF by bacteria. The decreased antimicrobial ability and can eventually lead to the development of infection bacteremia/ endotoxemia leading to activation of cytokine cascade. NO and TNF are important mediators of the further vasodilation and renal failure that often accompany SBP.

Spontaneous bacterial peritonitis is a blood-borne infection caused by Enteric organisms in 70% of cases (Mono-microbial origin in 90% of cases). Aerobic gram-negative bacteria like Escherichia coli account for half of the cases. Gram-positive cocci Streptococcus species in 20% cases with enterococcus accounting for 5% of the cases. Staphylococcus aureus and Streptococcus salivarius are less frequent causes. Poly-microbial infection is Iatrogenic (more likely associated with abdominal paracentesis) or intra-abdominal source of infection. The cause of SBP has not been established definitively but is believed to involve hematogenous spread of organisms in a patient with a diseased liver and altered portal circulation resulting in defect in the usual filtration function. In adults, spontaneous bacterial peritonitis occurs most commonly in conjunction with cirrhosis of the liver and portal hypertension (frequently as a result of alcoholism and hepatitis).

SBP has to be differentiated from other abdominal conditions presenting with fever and abdominal pain. It also has to be differentiated from secondary peritonitis, chemical peritonitis, peritoneal dialysis peritonitis, chronic tuberculous peritonitis.

Spontaneous bacterial peritonitis (SBP) is a potentially life threatening complication in patients with cirrhosis and is seen in hospitalized patients. The prevalence of SBP in cirrhotic patients with ascites admitted to the hospital ranges from 10%-30%.^[14]. Studies have demonstrated a 12% incidence of spontaneous bacterial peritonitis in patients admitted with decompensated cirrhosis. 2 studies examining asymptomatic patients presenting for a therapeutic paracentesis showed a combined 2.5% incidence of spontaneous bacterial peritonitis. Overall one-year mortality rate after a first episode of SBP is 30%-93% regardless of its recurrence. The mean age of presentation of SBP was 49 years. There is no gender difference in the incidence of SBP in patients with ascites.

Common risk factors in cirrhotic patients with ascites include: Low protein level in ascitic fluid (<1 g/dL), upper GI bleeding, low complement concentration (complement 3) in ascitic fluid, renal failure, Elevated serum bilirubin level (>4 mg/dL), use of Proton pump inhibitors (PPI) in cirrhotic patients, Child-Pugh stage C, Model For End-Stage Liver Disease MELD ≥ 22.^[15]

There is no definitive screening test for spontaneous bacterial peritonitis. According to Liver International journal, it has been demonstrated that fecal calprotectin concentrations (FCCs) are significantly elevated in cirrhotic patients and are dependent on the severity of liver disease. Assessing FCCs may help to identify cirrhotic patients with hepatic encephalopathy and SBP as a significant correlation emerged between elevated fecal calprotection and these complications.^[16] However, there is insufficient evidence to recommend routine screening for SBP.

Early diagnosis and initiating treatment is the most important factor for improving the survival and avoiding the complications of SBP. The sooner the diagnosis, the better the outcome. Mortality due to SBP remains high probably due to associated advanced liver disease.

According to the 2010 European Association for the Study of the Liver clinical practice guidelines the diagnosis of SBP is based on:^[17]

• Diagnostic paracentesis:
  • A diagnostic paracentesis should be carried out in all patients with cirrhosis and ascites at hospital admission to rule out SBP.^[18][19]
  • A diagnostic paracentesis should also be performed in patients with gastrointestinal bleeding, shock, fever, or other signs of systemic inflammation, gastrointestinal symptoms, as well as in patients with worsening liver and/or renal function, and hepatic encephalopathy.
• Ascitic fluid cell analysis
  • The diagnosis of SBP is based on neutrophil count in ascitic fluid of >250/mm³ as determined by microscopy.
  • At present there are insufficient data to recommend the use of automated cell counters or reagent strips for the rapid diagnosis of SBP.
• Ascitic fluid culture
  • Ascitic fluid culture is frequently negative even if performed in blood culture bottles and is not necessary for the diagnosis of SBP, but it is important to guide antibiotic therapy.
  • Blood cultures should be performed in all patients with suspected SBP before starting antibiotic treatment.
  • Some patients may have an ascitic neutrophil count less than 250/mm³ but with a positive ascitic fluid culture. This condition is known as bacterascites.
  • If the patient exhibits signs of systemic inflammation or infection, the patient should be treated with antibiotics.
  • Otherwise, the patient should undergo a second paracentesis when culture results come back positive.
  • Patients in whom the repeat ascitic neutrophil count is >250/mm3 should be treated for SBP, and the remaining patients (i.e., neutrophils <250/mm3) should be followed up .

The diagnosis of SBP is based on two of the following criteria from guidelines:^[20]

• Abdominal pain and/or hyperthermia, and/or abdominal and rebound tenderness (excluding secondary peritonitis);
  
• Ascitic fluid PMN count 250 cells/mm³
  
• Positive ascitic fluid bacterial culture.
  
• In the case of a traumatic paracentesis, with the entry of blood into the ascitic fluid (typically ascitic red cells greater than 10,000 cells/mm3) the PMN count should be corrected by subtracting one PMN for every 250 red cells/mm³ from the absolute PMN count.

80-90% of patients with spontaneous bacterial peritonitis are symptomatic, in many cases the presentation is subtle. Spontaneous bacterial peritonitis may be present in 10–20% of patients hospitalized with chronic liver disease, sometimes in the absence of any suggestive symptoms or signs. Patients with SBP most often present with: abdominal pain, fever, altered mental status (hepatic encphalopathy).^[21][22]

The clinical examination findings in spontaneous bacterial peritonitis are usually unpredictable, so there should be a low threshold to consider SBP in any patient with cirrhosis. Fever, acute abdominal and altered mental status are the physical findings. Physical examination typically demonstrates signs of chronic liver disease with ascites. Abdominal tenderness is present in less than 50% of patients, and its presence suggests other processes.

Early Diagnostic paracentesis (< 72hrs) is recommended in all cirrhotic patients with ascites. Paracentesis reveals an ascitic fluid with a total white cell count of up to 500 cells/mcL with a high polymorphonuclear (PMN) cell count (250/mm³ more). Ascitic fluid analysis and culture should be performed before initiating antibiotic therapy by bedside inoculation of ascitIc fluid ≥ 10 mL into blood culture bottles. Ascitic fluid analysis is the gold standard for the confirmation of the diagnosis of spontaneous bacterial peritonitis.^[23][18]

• Ceftriaxone 1 g IV Q12H started as soon as possible after suspecting SBP.^[24]
• Severe pencillin allergy:
  • Moxifloxacin 400 mg IV/PO Q24H.
• Renal dysfunction:
  • Patients with serum.creatinine > 1 mg/dl, BUN >30 mg/dl or total bilirubin >4 mg/dl should receive albumin(infusion25%) 1.5 g/kg on day 1 and 1 g/kg on day 3. including the standard antibiotic therapy.^[25][26]

The AASLD guidelines suggest using long term antibiotic prophylaxis in patients with: Ascitic fluid total protein less than 1.5 g/dL and with at least one of the following: Serum creatinine greater than or equal to 1.2 mg/dL, Blood urea nitrogen greater than or equal to 25 mg/dL, serum sodium less than or equal to 130 mEq/L, or Child-Turcotte-Pugh greater than or equal to 9 points (with bilirubin greater than or equal to 3 mg/dL). Daily oral norfloxacin in patients with more advanced liver disease has shown to prevent the development of spontaneous bacterial peritonitis and hepatorenal syndrome and improved survival rates at 3 months. Norfloxacin also reduced SBP recurrence rates from 68% to 20%.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Kerr and his colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients while Harold O.Conn , M.D, a world-renowned hepatologist (1964) introduced the term “spontaneous bacterial peritonitis” for the first time in English literature.Later in the history, SBP was studied extensively by many renowned researchers and health care professionals as this condition was seen among many patients with cirrhosis, which has lead to the thorough understanding and recognition of SBP.

Spontaneous bacterial peritonitis was known to emerge from different stages as follows:

• A few case reports have appeared in the French and American literature but the condition attracted little attention until 1958.
• In 1958, Caroli and Platteborse described 20 patients with cirrhosis developing coliform septicemia and peritonitis, in whom Gram-negative organisms were cultured from blood, ascitic fluid, or both.
• Kerr and colleagues in 1963 published two papers on the ascitic fluid infection as a complication of cirrhosis.^[1]
• Prof Harold O. Conn was the first to use term “spontaneous bacterial peritonitis” in English literature in 1964.
• Krencker 1907; Brule et al 1939; Cachin 1955; Navasa et al 1999 described that ascitic fluid infections were most common in patients with cirrhosis.
• Spontaneous bacterial peritonitis (SBP), reported by Caroli and Platteborse (1958) has had its importance increased since Kerr and colleagues (1963) and Conn (1964) published two papers about this cirrhosis complication almost simultaneously.^[2]
• Kerr and colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients while Harold O.Conn , M.D, a world-renowned hepatologist (1964) introduced the term “spontaneous bacterial peritonitis” for the first time in English literature.
• Later in the history, SBP was studied extensively by many renowned researchers and health care professionals as this condition was seen among many patients with cirrhosis, which has lead to the thorough understanding and recognition of SBP.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2] Shivani Chaparala M.B.B.S [3] Ahmed Younes M.B.B.CH [4]

Spontaneous bacterial peritonitis is one variant of ascitic fluid infections.^[1] Classification of ascitic fluid infections is based on neutrophil count and culture report.^[2][3] Asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells.^[4] SBP is also classified based on the routes of infection and the clinical setting as follows health care-associated, nosocomial, community acquired, multi-drug resistant and recurrent.

• Spontaneous bacterial peritonitis is one of the variants of ascitic fluid infections.^[1]
• Classification of ascitic fluid infections is based on neutrophil count and culture report.^[2][3]
• Asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells.^[4]

Based on the route of infection SBP is classified as follows:^[2][10]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Intestinal bacterial overgrowth in cirrhotic patients, defective intestinal barrier and defective host immune response are the 3 determinant factors for bacterial translocation explaining SBP.

Three factors play a role in the pathogenesis of SBP:

• Bacterial overgrowth in cirrhotic patients: secondary to decreased intestinal motility and frequent use of PPIs in this population of patients.

• Defective intestinal barrier: secretory and physical barriers (which normally prevent bacteria from moving from the intestinal lumen) are defective in cirrhotic patients ^[1]

• Decreased immunity: both local and systemic immunity are decreased in cirrhotic patients.

• Intestinal motility decreases with cirrhosis. Increased sympathetic drive and oxidant stress are believed to be the reasons for the reduced mobility.
• Also, cirrhotic patients administer PPIs more frequently than other patient populations.
• The diminished intestinal motility makes the intestinal contents more stagnant and allows the bacterial contents to overgrow and thus predisposes to SBP.^[2]

Normally, the intestinal mucosa is impermeable to bacteria because of two lines of defense^[2];the secretory component and physical component. Both are affected by the development of cirrhosis.

• The secretory defense mechanism is composed of mucins, immunoglobulins and bile salts. Bile salts are protective through preventing adherence and internalization of bacteria. Bile acids are decreased in cirrhosis partly due to reduced secretion from diseased liver and partly from increased conjugation by the flourishing intestinal flora. This gives bacteria easier access through the mucosa especially that E.coli (which is the most common strain isolated from SBP patients) has high ability to adhere to the intestinal mucosa and evade the host immune defenses.
• The physical component is the intestinal epithelium itself. Intestinal mucosa is more permeable as a result of increased oxidant stress,NO proinflammatory cytokines & increased intercellular spaces as a result of vasodilation, edema from portal hypertension.

• Kupffer cells (local macrophages of the liver) normally contribute in eradicating infection with neutrophils. But as a result of the extrahepatic portosystemic shunts, bacteria in the circulation do not come in contact with these cells.
• As a result of defective liver synthetic functions, complement levels decrease (both in serum and ascitic fluid).
• The neutrophils seem to have declined granulocyte functions as adherence, chemotaxis, and bacterial killing.

Bacteria that translocate are carried through lymphatics. It can reach the ascitic fluid either through the circulation then through the liver. It can have access to the peritoneal cavity. Another way is through rupture of the lymphatic vessel carrying the contaminated lymph under pressure from portal hypertension and the increased lymph content.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Spontaneous bacterial peritonitis is a blood-borne infection caused by enteric organisms in 70% of cases (mono-microbial origin in 90% of cases). Aerobic gram-negative bacteria like Escherichia coli account for half of the cases. Gram-positive cocci Streptococcus species in 20% cases and enterococcus accounting for 5% of the cases. Staphylococcus aureus and Streptococcus salivarius are less frequent causes. Poly-microbial infection is mostly iatrogenic (more likely associated with abdominal paracentesis) or intra-abdominal source of infection. The cause of SBP is not definitively established, but is believed to involve hematogenous spread of organisms in patients with liver disease and altered portal circulation in adults, spontaneous bacterial peritonitis occurs in conjunction with cirrhosis of the liver and portal hypertension.

• Spontaneous bacterial peritonitis is often a blood-borne infection caused by enteric organisms in 70% of the cases (mono-microbial in 90%).
• Aerobic gram-negative bacteria like Escherichia coli account for half of the cases.
• Gram-positive cocci Streptococcus species account for 20% cases and enterococcus accounts for 5% of the cases.

• Staphylococcus aureus and Streptococcus salivarius are less frequent causes.
• Poly-microbial infection is mostly iatrogenic (associated with abdominal paracentesis) or intra-abdominal source of infection.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2];Ahmed Younes M.B.B.CH [3]

SBP must be differentiated from other abdominal conditions presenting with fever and abdominal pain. It also has to be differentiated from secondary peritonitis, chemical peritonitis, peritoneal dialysis peritonitis, chronic tuberculous peritonitis.

Spontaneous bacterial peritonitis presents with fever and abdominal pain. Diseases presenting with similar features include:

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Spontaneous bacterial peritonitis (SBP) is a potentially life threatening complication in patients with cirrhosis and has typically been described in hospitalized patients.The prevalence of SBP in cirrhotic patients with ascites admitted to the hospital ranges from 10%-30%.^[1].Studies have demonstrated a 12% incidence of spontaneous bacterial peritonitis in patients admitted with decompensated cirrhosis. 2 studies examining asymptomatic patients presenting for a therapeutic paracentesis showed a combined 2.5% incidence of spontaneous bacterial peritonitis.Overall one-year mortality rate after a first episode of SBP is 30%-93% regardless of its recurrence.The mean age of presentation of SBP was 49 years.In patients with ascites both sexes are affected equally.

• The prevalence of SBP in cirrhotic patients with ascites admitted to the hospital ranges from 10%-30%.^[2]
• About 50% of cases are present at the time of hospitalization and 50% develop during the hospitalization.

• The reported incidence of SBP in patients with decompensated cirrhosis is 12%.

• The incidence of SBP in asymptomatic patients presenting for a therapeutic paracentesis is 2.5%.^[3][4]
• In patients with ascites who underwent routine paracentesis, the incidence of active spontaneous bacterial peritonitis ranged from 10% to 27% at the time of hospital admission.^[5]
• There is an increase in prevalence of spontaneous bacterial peritonitisin patients admitted to hospital.

• The in-hospital mortality for SBP ranges from 10%-50% depending on many factors.
• Mortality is 20% even in treated SBP patients.
• Overall one-year mortality rate after a first episode of SBP is 30%-93% regardless of its recurrence.
• The effect of SBP on the mortality of cirrhotic patients with ascites is low in those surviving more than 90 days after the first SBP event.^[6]

• SBP is common in age group of 41–50 years and the mean age of presentation was 49 years.^[7]

• In patients with ascites both sexes are affected equally.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Common risk factors in cirrhotic patients with ascites include: low protein level in ascitic fluid (<1 g/dL), upper GI bleeding, low complement concentration (complement 3) in ascitic fluid, renal failure, elevated serum bilirubin level (>4 mg/dL), use of proton pump inhibitors (PPI) in cirrhotic patients have an increased risk, Child-Pugh stage C, Model For End-Stage Liver Disease (MELD) ≥ 22.

Risk factors include:^[1]

• All cirrhotic patients with ascites
• Severe liver disease (Cirrhosis)^[2]
• Low protein level in ascitic fluid ^[3]
• Upper GI bleeding poses a risk of bacteremia and SBP in a cirrhotic patient with rates of infection ranging from 17 to 21%
• Ischemia- reperfusion of the gut during variceal hemorrhage has also been proposed to interfere with the normal function of the reticuloendothelial system and to increase permeability of the intestinal mucosa
• Survivors of a prior episode of SBP are at an increased risk of recurrence with a one-year probability of almost 70%
• Minimally invasive procedures such as intravenous and urinary bladder catheterization likely predisposes to bacteremia and SBP in the cirrhotics
• Low complement concentration (complement 3) in ascitic fluid ^[3][2]
• Renal failure
• Urinary tract infections
• Intestinal bacterial overgrowth ^[4]
• The use of non-selective beta blockers in cirrhotic patients with SBP should be discouraged since it is associated with an increased risk for hemodynamic compromise, prolonged hospitalization, hepatorenal syndrome, and acute kidney injury^[5]

Factors contributing to the infection include:

• GI bleeding
• Increased colonization of the small bowel with prominent bacterial translocation
• Decreased opsonic activity in blood and ascitic fluid
• Impaired complement
• Leukocyte dysfunction
• Reduced antibodies
• Increased immunosuppressive cytokines, endotoxin, TNF

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

There is no specific screening studies for spontaneous bacterial peritonitis.

There is no specific screening studies for spontaneous bacterial peritonitis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]

Early diagnosis and initiating treatment is the most important factor for improving the survival and avoiding the complications of SBP. The sooner the diagnosis, the better the outcome.

• SBP is treatable with antibiotics but early diagnosis and intiation of empiric antibiotic therapy is the most important factor for survival.
• In a study performed in 2006, Each hour of delay of administration of empiric antibiotics was associated with increased mortality by 7.6% while administration of antibiotics at the first hour of hypotension increased overall survival to 79%.^[1]

The physician should have a high index of suspicion to diagnose SBP early and start empiric antibiotic therapy. The earlier the stage of diagnosis, the better the survival.

• With the progression of infection, septicaemia ensues with its classic symptoms and signs. Septicaemia and shock are associated with very bad prognosis.

• Hepatic decompensation in association with the progression of infection make altered mental status more likely to happen. Ammonia levels can be within normal limits or slightly elevated as hepatic decompensation is not the only element leading to the altered mental status.

• Peritoneal inflammation can be complicated with paralytic ileus. Paralytic ileus is a very poor prognostic sign with increased mortality rate.

• Diarrhea is common due to associated intestinal bacterial overgrowth.^[2]

• Mortality of SBP remains high. 1-year mortality rate is 30-90% ^[3], probably due to the advanced liver disease present in the first place.
• Early admission and prophylactic cephalosporins might have a role in decreasing mortality rate.^[4]