Internet Book of Critical Care (IBCC)

Online Medical Education on Emergency Department (ED) Critical Care, Trauma, and Resuscitation

You are here: Home / IBCC / Spontaneous Bacterial Peritonitis (SBP)


Spontaneous Bacterial Peritonitis (SBP)

by

CONTENTS

presenting clinical features

(back to contents)

presenting signs & symptoms
  • SBP is often subtle (for example, 13% of patients are asymptomatic).(19266595)
    • SBP is present in ~10% of patients admitted to the hospital with cirrhotic ascites, so it should be suspected in any cirrhotic patient who is admitted to the hospital even in the absence of symptoms.(29653741)
  • Fever or hypothermia.
  • Nausea/vomiting, diarrhea, or ileus.
  • Abdominal pain occurs in about half of patients.  However, SBP usually doesn't cause frank peritoneal signs or focal pain (if these are present, then secondary bacterial peritonitis should be suspected).
SBP can cause dysfunction of other organs
  • SBP can trigger failure of other organs.  In many cases, these other organ failures are more obvious than SBP itself.  Consequently, presenting symptoms may center around the failure of other organs:
    • Hepatorenal syndrome.
    • Hepatic encephalopathy may be a presenting feature.
    • Gastrointestinal hemorrhage or other foci of bleeding may also be the most obvious clinical finding. (SBP itself may lead to a coagulopathy, causing patients with smoldering underlying SBP to present with gastrointestinal hemorrhage).
    • Septic shock can occur (although this may be difficult to sort out from the chronic hyperdynamic circulation often seen in cirrhosis).
  • Acute-on-chronic liver failure (ACLF)
    • SBP can lead to full-blown acute-on-chronic liver failure (ACLF), a condition marked by multiple organ failures (e.g., encephalopathy, shock, and renal failure).  ACLF has many parallels to septic shock and may be grossly conceptualized as a form of inflammation-induced multiorgan failure which occurs in the context of cirrhosis (more on ACLF here).

paracentesis

(back to contents)

indications for diagnostic paracentesis
  • (1) Clinical suspicion for spontaneous bacterial peritonitis.
  • -or-
  • (2) Any patient with cirrhosis and ascites who is admitted to the hospital for clinical deterioration.
    • This includes admission for GI bleed.  (SBP may cause disseminated intravascular coagulation, which may precipitate a GI bleed.  So there can actually be a causal relationship between infection and bleeding.)
  • ⚠️ SBP usually occurs in the context of large-volume ascites which should be easily accessible via paracentesis.  If the patient has a small volume of ascites which isn't easily sampled, then high-risk paracentesis is not beneficial.  Serial ultrasonography may be performed to determine if the ascites expands over time, at which point paracentesis may be reconsidered.

tips on diagnostic paracentesis in the cirrhotic patient
  • There is no need to correct the INR (in cirrhosis, the INR doesn't predict bleeding).
    • Further discussion of pre-procedure hematology considerations for cirrhotic patients here.
  • Consider using a very thin lumbar puncture needle (e.g., a 24-gague needle).
    • Throw away the stylet and simply attach the needle to a 60-ml syringe.
    • Using a smaller bore needle decreases the risk of ascites leakage and pain.
  • Before needle insertion, look with ultrasonography:
    • (a) Confirm that there is a sizable pocket of fluid.
    • (b) Measure the thickness of the abdominal wall.
    • (c) Use Doppler to exclude the presence of any arteries running through the abdominal wall.
    • You don't necessarily have to use real-time imaging while you insert the needle, especially if the pocket is sizable.
labs to obtain 
  • General labs
    • 💉 Blood cultures
  • Analysis of ascitic fluid
    • Cell count & differential
    • Gram stain
    • Bacterial cultures (Ideally, culture bottles should be inoculated at the bedside:  10 ml each into an anaerobic bottle and an aerobic bottle.)
    • Total protein, albumin
    • Glucose
    • Lactate dehydrogenase

differentiating spontaneous versus secondary bacterial peritonitis

(back to contents)

what is the difference between spontaneous bacterial peritonitis vs. secondary bacterial peritonitis?
  • Spontaneous bacterial peritonitis involves a single bacterium translocating into the ascites and growing.  It is more common and should generally respond to medical therapy.
  • Secondary bacterial peritonitis is the presence of perforation or inflammation of an intra-abdominal organ (e.g., cholecystitis) in the presence of ascites.  This is much less common than spontaneous bacterial peritonitis.  Secondary bacterial peritonitis may often fail to respond to antibiotics alone, so it's essential to recognize this as a separate entity.

Right lower quadrant abdominal ultrasound showing features concerning for secondary bacterial peritonitis:  (1) Septations (2) Debris visible within the fluid.  This patient had a bowel perforation, not spontaneous bacterial peritonitis.  
🚩 red flags for secondary bacterial peritonitis
  • Frank peritoneal signs on exam or localizing abdominal pain.
  • Ultrasonography showing complex, loculated fluid (video above).
  • Gram stain or culture of ascitic fluid showing multiple different organisms.
  • At least two of the following criteria are present:(2293571)
    • Total protein >1 g/dL
    • Glucose <50 mg/dL (2.8 mM)
    • Lactate dehydrogenase above the upper limit of normal for serum
  • A patient who is treated for “spontaneous bacterial peritonitis” fails to improve.
evaluation for suspected secondary bacterial peritonitis
  • The key test is a CT scan of the abdomen/pelvis, to exclude any focus of infection requiring source control.
  • If biliary pathology is suspected, right upper quadrant ultrasonography may also be helpful.

diagnosis of SBP

(back to contents)

diagnostic criteria for SBP
  • This depends essentially on two findings within the context of ascites caused by cirrhosis:
    • (1) Ascites neutrophil count >250/mm3.
    • (2) Exclusion of secondary bacterial peritonitis (section above)
  • (Some criteria require the presence of a positive culture.  However, a positive culture is often absent, and this doesn't pragmatically affect management.)

treatment

(back to contents)

antibiotics 
  • Coverage is needed for gram-negative bacilli and also for selected gram-positive organisms (mostly pneumococcus, staphylococcus, and streptococcus).
  • The usual therapy for community-acquired SBP is a third-generation cephalosporin (e.g., ceftriaxone two grams IV daily), started before culture results are available.
  • About half of spontaneous bacterial peritonitis is acquired in the hospital (nosocomial SBP), which may involve more resistant organisms.  Broader coverage may be appropriate for such patients (e.g., piperacillin-tazobactam or a carbapenem).  Precise regimens will vary depending on the hospital's antibiogram and whether the patient has recently been colonized or infected with any drug-resistant organisms (e.g., MRSA).
  • Antibiotics should be narrowed appropriately if ascitic fluid cultures are positive.
  • A five-day course of antibiotics is generally adequate, although longer courses may be considered with certain pathogens (e.g., pseudomonas).
avoid hepatorenal syndrome & decompensated cirrhosis
  • Spontaneous bacterial peritonitis may push patients into a state of decompensated cirrhosis, marked by hypotension, malperfusion, and hepatorenal syndrome.  In severe cases, this may evolve into acute-on-chronic liver failure (ACLF, more on this here).  The following treatments should be implemented preemptively, to avoid this.
  • (1) Albumin has been proven to reduce the incidence of hepatorenal syndrome and mortality.(10432325)  The treatment regimen is 1.5 gram/kg of 20% albumin at the time of diagnosis, followed by 1 gram/kg albumin 48 hours later.
    • (There is some debate regarding whether albumin may be omitted among patients at low risk for hepatorenal syndrome, based on retrospective subgroup analysis.  However, omission of albumin hasn't been adequately validated in this subgroup.  Furthermore, a meta-analysis concluded that albumin caused improvements, regardless of disease severity.)(32533951)
  • (2) Discontinue beta-blockers, as these may increase the risk of hypotension and hepatorenal syndrome.(24631577)  Consider holding other antihypertensives or vasodilators as well (especially ACE inhibitors or ARBs).
  • (3) Discontinue or avoid any nephrotoxins.
large-volume paracentesis ??
  • Since spontaneous bacterial peritonitis is purely an infection of ascitic fluid, drainage of the fluid theoretically could be used as a method of eliminating the infected material (“source control”).
  • There is currently only one very small study on this.  Large-volume paracentesis didn't affect hard endpoints.(16048569)
  • Large-volume paracentesis may be performed, but only if indicated for another reason (e.g., resolution of symptoms due to tense ascites).
if the patient doesn't improve:
  • Consider the possibility of secondary bacterial peritonitis and the need for a CT scan to exclude underlying pathology.
  • A repeat paracentesis with reculturing of the ascitic fluid may be considered after 48 hours.  If the neutrophil count isn't decreasing to <25% of the pretreatment value, this carries a substantial likelihood of treatment failure.(29653741)  Some ascitic fluid should be inoculated into blood culture bottles at the bedside, to optimize the likelihood of culturing any drug-resistant organisms.  Escalation to broader antibiotics may be considered, if no surgical focus of infection is detected.

spontaneous bacterial empyema

(back to contents)

hepatic hydrothorax & spontaneous bacterial empyema
  • Hepatic hydrothorax:
    • In some patients with cirrhosis, ascitic fluid tracks into the pleural space, leading to a pleural effusion (commonly termed “hepatic hydrothorax”).  This may result from tiny holes in the diaphragm and the negative pressure of the thorax, causing ascitic fluid to be drawn into the chest.
    • The overall pathophysiology of hepatic hydrothorax is largely identical to that of ascites (e.g., treatment may involve diuretics and TIPS to reduce the portal pressure).
  • Spontaneous bacterial empyema is the thoracic version of spontaneous bacterial peritonitis.  Essentially, a bacterium translocates into the hepatic hydrothorax and replicates, leading to an infection in the pleural space.  Spontaneous bacterial empyema may coexist with spontaneous bacterial peritonitis, or it may occur on its own.
clinical features of spontaneous bacterial empyema may include:  
  • Localizing symptoms, such as chest discomfort or respiratory failure.
  • Fever and chills (although, similar to SBP, systemic inflammatory symptoms may be muted in cirrhosis).
  • Systemic manifestations of infection, similar to SBP (e.g., encephalopathy, hypotension, hepatorenal syndrome, acute-on-chronic liver failure).
diagnosis
  • The diagnosis of spontaneous bacterial empyema is largely identical to that of spontaneous bacterial peritonitis, with the following main differences:
    • Unlike spontaneous bacterial peritonitis, not all patients with pleural effusion necessarily require thoracentesis upon hospital admission.
    • Indications to perform thoracentesis may include:  therapeutic relief from respiratory failure, or clinical suspicion of infection.
  • 💡 Whenever a patient with cirrhosis receives a thoracentesis for any reason, pleural fluid should be analyzed for cell count and microbiology to exclude spontaneous bacterial empyema.
  • The diagnostic criteria for spontaneous bacterial empyema are:
    • One of the following
      • >250 neutrophils/mm3 in pleural fluid plus a positive bacterial culture.
      • >500 neutrophils/mm3 in the pleural fluid with a negative pleural culture.
      • (Note:  The overall pattern of pleural fluid labs doesn't usually resemble a typical empyema; for example, glucose may be normal)
    • Lack of another cause of empyema (e.g., absence of underlying pneumonia).
    • If bacteria are cultured from the pleura, then only one species should be present (monomicrobial infection).  If multiple species are present, this suggests secondary empyema (e.g., due to bronchopleural fistula or mediastinitis).
treatment 
  • The treatment of spontaneous bacterial empyema is similar to that of spontaneous bacterial peritonitis.
  • The same antibiotics may be utilized, along with albumin (see above discussion on treatment).
  • Although this is an “empyema,” placement of a chest tube is typically not indicated.
    • Chest tubes are relatively contraindicated in cirrhosis, due to concerns regarding excessive fluid shifts.
    • Indications for tube drainage may include frank purulence (which is uncommon) or failure to respond to medical management.

podcast

(back to contents)

Follow us on iTunes

 

questions & discussion

(back to contents)

To keep this page small and fast, questions & discussion about this post can be found on another page here.

  • Failure to consider and test for spontaneous bacterial peritonitis among patients admitted to the hospital with cirrhosis and ascites.
  • Misdiagnosing a surgical abdominal emergency as spontaneous bacterial peritonitis.
  • Failure to take adequate interventions to prevent hepatorenal syndrome (e.g., albumin administration, avoidance of nephrotoxins, and avoidance of beta-blockers).
Going further:

references

  • 02293571  Akriviadis EA, Runyon BA. Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology. 1990 Jan;98(1):127-33. doi: 10.1016/0016-5085(90)91300-u  [PubMed]
  • 10432325  Sort P, Navasa M, Arroyo V, et al.  Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999 Aug 5;341(6):403-9. doi: 10.1056/NEJM199908053410603  [PubMed]
  • 16048569  Choi CH, Ahn SH, Kim DY, et al. Long-term clinical outcome of large volume paracentesis with intravenous albumin in patients with spontaneous bacterial peritonitis: a randomized prospective study. J Gastroenterol Hepatol. 2005 Aug;20(8):1215-22. doi: 10.1111/j.1440-1746.2005.03861.x  [PubMed]
  • 19266595  Koulaouzidis A, Bhat S, Saeed AA. Spontaneous bacterial peritonitis. World J Gastroenterol. 2009 Mar 7;15(9):1042-9. doi: 10.3748/wjg.15.1042  [PubMed]
  • 24631577  Mandorfer M, Bota S, Schwabl P, et al. Nonselective β blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology. 2014 Jun;146(7):1680-90.e1. doi: 10.1053/j.gastro.2014.03.005  [PubMed]
  • 29653741  European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018 Aug;69(2):406-460. doi: 10.1016/j.jhep.2018.03.024  [PubMed]
  • 32533951  Mattos AA, Wiltgen D, Jotz RF, et al.  Spontaneous bacterial peritonitis and extraperitoneal infections in patients with cirrhosis. Ann Hepatol. 2020 Sep-Oct;19(5):451-457. doi: 10.1016/j.aohep.2020.04.010  [PubMed]

The Internet Book of Critical Care is an online textbook written by Josh Farkas (@PulmCrit), an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont.


Who We Are

We are the EMCrit Project, a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

EDECMO and RLA

Subscribe by Email

0:00
0:00