a) How would you diagnose Spontaneous Bacterial Peritonitis (SBP)? (30% marks)
b) List four common organisms causing SBP. (20% marks)
c) Other than SBP, list six common causes of decompensation of chronic liver disease.
d) In a patient with suspected SBP, microscopy of ascitic fluid is reported as showing gram positive cocci, gram negative bacilli and fungal elements. What is the likely diagnosis? (20% marks)
a) How would you diagnose Spontaneous Bacterial Peritonitis (SBP)? (3 marks)
Occurs in patients with cirrhosis and ascites
Signs and symptoms of fever, abdominal pain, abdominal tenderness, altered mental status, hypotension. May be relatively asymptomatic and requires high degree of suspicion.
Diagnosis confirmed by paracentesis:
Neutrophil count > 250 cells/mm3
Other tests that may be used in diagnosis include: Albumin, Total protein, glucose, and LDH
Other causes of peritonitis should be excluded.
b) List 4 common organisms causing SBP (2 marks)
c) Other than SBP List 6 common causes of decompensation of chronic liver disease (3 marks)
Upper GI Bleeding
Alcohol consumption / alcoholic hepatitis
Dehydration / over diuresis
Portal vein thrombosis
d) In a patient with suspected SBP microscopy of ascitic fluid is reported as showing gram positive cocci, gram negative bacilli and fungal elements. What is the likely diagnosis? (2 marks)
Overall answered well – candidates should be careful to read the question and just give the number of answers that are required: extra answers do not gain marks.
a) The question "how'd you diagnose that" could be interpreted two ways. One might try to give the laboratory diagnostic criteria for spontaneous bacterial peritonitis:
- Ascitic fluid neutrophil count must be > 250/mm3
- Positive ascitic bacterial culture (for one organism only)
- No other obvious (eg. surgical) source for these bacteria
Alternatively, one might respond that the diagnosis of SBP is made by performing paracentesis, which results from having a clinical suspicion in any patient who manifests the following features, on the background of the following risk factors:
- Risk factors
- Child-Pugh Grade C cirrhosis
- Ascitic fluid protein level less than 10g/L
- Gastrointestinal bleeding
- Urinary tract infection
- Intestinal bacterial overgrowth
- Invasive devices: central lines, peripheral cannulae, IDCs
- Previous SBP episodes
- Clinical features
- Fever: 68%
- Abdominal pain 49%
- Tenderness on abdominal palpation 39%
- Rebound tenderness 10%
- Decreased level of consciousness 54%
b) According to Koulaouzidis et al (2009), here is a list of organisms most usually responsible for the classic monomicrobial SBP:
- E. coli 37%
- K. pneumoniae 17%
- Misc gram-positives 14%
- S. pneumoniae 12%
- Misc. gram-negatives 10%
- S. viridans 9%%
c) Apart from SBP, the following causes of acute decompensation are listed in Kim et al (2013)
- Reactivation of a hepatitis virus (eg. hep B, C)
- Drug-induced toxicity
- Gastrointestinal haemorrhage
- Portal vein thrombosis
- Ischaemic insult of any sort (eg. shock)
- Autoimmune hepatitis
- Wilson disease
Would a TIPS procedure be one of the causes of acute decompensation of liver disease? Would that earn any marks? It is difficult to say. It certainly would cause a worsening of hepatic encephalopathy (usually), but portal hypertension and ascites should be improved. These consensus recommendations describe decompensation as " variceal haemorrhage, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy, hepatopulmonary syndrome and jaundice. ". Of the official college answers, a couple of the answers (UGI bleeding, portal load) would also mainly give you encephalopathy by itself. Furthermore, people who discuss complications of TIPS describe hepatic decompensation as one of the rare but well-documented possibilities (Suhocki et al, 2015) - where the shunt either reverses portal flow or causes ischaemia by squishing the major vessels accidentally.
d) If the patient's ascitic fluid has multiple organisms, there are two possible explanations:
- The needle punctured the gut and some gut content was aspirated inadvertently into the culture bottles
- The patient has a perforated gut and has secondary bacterial peritonitis
In the latter case, mortality without surgery is essentially 100%. Some sort of urgent abdominal imaging would then be called for, to exclude this differential. If there is no evidence of surgical pathology, the zoo can be managed with the aforementioned broad-spectrum drugs without fear of complications: Runyon, the world guru on SBP, in his UpToDate article writes "we have never encountered an episode of this variant in which surgical intervention was required."
Such, Jose, and Bruce A. Runyon. "Spontaneous bacterial peritonitis." Clinical infectious diseases (1998): 669-674.
Foris, Lisa A., and Melanie T. Stapleton. "Spontaneous Bacterial Peritonitis." (2017).
Koulaouzidis, Anastasios, Shivaram Bhat, and Athar A. Saeed. "Spontaneous bacterial peritonitis." World Journal of Gastroenterology: WJG 15.9 (2009): 1042.
Runyon, Bruce A. "Chapter 91. Ascites and Spontaneous Bacterial Peritonitis." (2002).
Kim, Tae Yeob, and Dong Joon Kim. "Acute-on-chronic liver failure." Clinical and molecular hepatology 19.4 (2013): 349.
Suhocki, Paul V., et al. "Transjugular intrahepatic portosystemic shunt complications: prevention and management." Seminars in interventional radiology. Vol. 32. No. 2. Thieme Medical Publishers, 2015.