Spontaneous bacterial peritonitis pathophysiology: Difference between revisions

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:Escape of enteric bacteria to systemic circulation through:<ref name="pmid15723320">{{cite journal| author=Wiest R, Garcia-Tsao G| title=Bacterial translocation (BT) in cirrhosis. | journal=Hepatology | year= 2005 | volume= 41 | issue= 3 | pages= 422-33 | pmid=15723320 | doi=10.1002/hep.20632 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15723320  }} </ref>
:Escape of enteric bacteria to systemic circulation through:<ref name="pmid15723320">{{cite journal| author=Wiest R, Garcia-Tsao G| title=Bacterial translocation (BT) in cirrhosis. | journal=Hepatology | year= 2005 | volume= 41 | issue= 3 | pages= 422-33 | pmid=15723320 | doi=10.1002/hep.20632 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15723320  }} </ref>
:❑ Bacterial translocation<ref name="pmid11211904">{{cite journal| author=Cirera I, Bauer TM, Navasa M, Vila J, Grande L, Taurá P et al.| title=Bacterial translocation of enteric organisms in patients with cirrhosis. | journal=J Hepatol | year= 2001 | volume= 34 | issue= 1 | pages= 32-7 | pmid=11211904 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11211904  }} </ref>
:❑ Bacterial translocation<ref name="pmid11211904">{{cite journal| author=Cirera I, Bauer TM, Navasa M, Vila J, Grande L, Taurá P et al.| title=Bacterial translocation of enteric organisms in patients with cirrhosis. | journal=J Hepatol | year= 2001 | volume= 34 | issue= 1 | pages= 32-7 | pmid=11211904 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11211904  }} </ref>
::• Luminal bacteria within colonize mesenteric [[lymph nodes]]
::• Luminal bacteria within colonize mesenteric [[lymph nodes]].<ref name="pmid7890896">{{cite journal| author=Runyon BA, Squier S, Borzio M| title=Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis. | journal=J Hepatol | year= 1994 | volume= 21 | issue= 5 | pages= 792-6 | pmid=7890896 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7890896  }} </ref>
::• Organisms from the mesenteric [[lymph nodes]] → Systemic circulation through thoracic duct lymph → percolates through the liver and weep across Glisson's capsule → Ascitic fluid  
::• Organisms from the mesenteric [[lymph nodes]] → Systemic circulation through thoracic duct lymph → percolates through the liver and weep across Glisson's capsule → Ascitic fluid.
::• Transient [[bacteremia]] → Prolonged bacteremia ( due to ↓ Reticulo endothelial system activity ) → Ascites Colonization ( due to ↓ ascitic fluid bactericidal activity ) → Spontaneous bacterial [[peritonitis]] )
::• Transient [[bacteremia]] → Prolonged bacteremia ( due to ↓ Reticulo endothelial system activity ) → Ascites Colonization ( due to ↓ ascitic fluid bactericidal activity ) → Spontaneous bacterial [[peritonitis]] )
:❑ Portal Vein
:❑ Portal Vein
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::• The extent and rate of intraperitoneal spread of contamination depend on the volume and nature of the [[exudate]] and on the effectiveness of the localizing processes
::• The extent and rate of intraperitoneal spread of contamination depend on the volume and nature of the [[exudate]] and on the effectiveness of the localizing processes
::• If peritoneal defenses aided by the appropriate supportive measures control the [[inflammatory]] process, the disease may resolve spontaneously ('''Sterile ascites''')<ref name="pmid4018735">{{cite journal| author=Runyon BA, Morrissey RL, Hoefs JC, Wyle FA| title=Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. | journal=Hepatology | year= 1985 | volume= 5 | issue= 4 | pages= 634-7 | pmid=4018735 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4018735  }} </ref><ref name="pmid4018735">{{cite journal| author=Runyon BA, Morrissey RL, Hoefs JC, Wyle FA| title=Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. | journal=Hepatology | year= 1985 | volume= 5 | issue= 4 | pages= 634-7 | pmid=4018735 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4018735  }} </ref><ref name="pmid8677940">{{cite journal| author=Ho H, Zuckerman MJ, Ho TK, Guerra LG, Verghese A, Casner PR| title=Prevalence of associated infections in community-acquired spontaneous bacterial peritonitis. | journal=Am J Gastroenterol | year= 1996 | volume= 91 | issue= 4 | pages= 735-42 | pmid=8677940 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8677940  }} </ref> → Consumption of humoral bactericidal factors due to frequent colonization → Increased susceptibility to '''SBP'''<ref name="pmid3257456">{{cite journal| author=Titó L, Rimola A, Ginès P, Llach J, Arroyo V, Rodés J| title=Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors. | journal=Hepatology | year= 1988 | volume= 8 | issue= 1 | pages= 27-31 | pmid=3257456 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3257456  }} </ref>
::• If peritoneal defenses aided by the appropriate supportive measures control the [[inflammatory]] process, the disease may resolve spontaneously ('''Sterile ascites''')<ref name="pmid4018735">{{cite journal| author=Runyon BA, Morrissey RL, Hoefs JC, Wyle FA| title=Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. | journal=Hepatology | year= 1985 | volume= 5 | issue= 4 | pages= 634-7 | pmid=4018735 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4018735  }} </ref><ref name="pmid4018735">{{cite journal| author=Runyon BA, Morrissey RL, Hoefs JC, Wyle FA| title=Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. | journal=Hepatology | year= 1985 | volume= 5 | issue= 4 | pages= 634-7 | pmid=4018735 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4018735  }} </ref><ref name="pmid8677940">{{cite journal| author=Ho H, Zuckerman MJ, Ho TK, Guerra LG, Verghese A, Casner PR| title=Prevalence of associated infections in community-acquired spontaneous bacterial peritonitis. | journal=Am J Gastroenterol | year= 1996 | volume= 91 | issue= 4 | pages= 735-42 | pmid=8677940 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8677940  }} </ref> → Consumption of humoral bactericidal factors due to frequent colonization → Increased susceptibility to '''SBP'''<ref name="pmid3257456">{{cite journal| author=Titó L, Rimola A, Ginès P, Llach J, Arroyo V, Rodés J| title=Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors. | journal=Hepatology | year= 1988 | volume= 8 | issue= 1 | pages= 27-31 | pmid=3257456 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3257456  }} </ref>
::• If the ascitic fluid bactericidal activity is poor-moderate → '''Culture negative neutrocytic ascites''' (CNNA) or '''SBP''' → delay / inappropriate treatment → ''death'' due to [[sepsis]] and multi organ failure.
::• If the ascitic fluid bactericidal activity is poor-moderate → '''Culture negative neutrocytic ascites''' (CNNA) or '''SBP''' → delay / inappropriate treatment → ''death'' due to [[sepsis]] and multi organ failure.<ref name="pmid3371881">{{cite journal| author=Runyon BA| title=Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. | journal=Hepatology | year= 1988 | volume= 8 | issue= 3 | pages= 632-5 | pmid=3371881 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3371881  }} </ref><ref name="pmid6500513">{{cite journal | author = Runyon BA, Hoefs JC | title = Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis | journal = Hepatology | volume = 4 | issue = 6 | pages = 1209–11 | year = 1984 | pmid = 6500513 | doi = 10.1002/hep.1840040619| url = | issn = }}</ref>
::• Second possible outcome is a confined '''[[abscess]]'''
::• Second possible outcome is a confined '''[[abscess]]'''
::• A third possible outcome results when the peritoneal and systemic defense mechanisms are unable to localize the inflammation, which progresses to '''spreading diffuse [[peritonitis]]''' due to increased [[virulence]] of bacteria, greater extent and duration of contamination, and impaired host defenses.
::• A third possible outcome results when the peritoneal and systemic defense mechanisms are unable to localize the inflammation, which progresses to '''spreading diffuse [[peritonitis]]''' due to increased [[virulence]] of bacteria, greater extent and duration of contamination, and impaired host defenses.
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====Routes of infection====
* Hematogenous
* Lymphogenous
* Transmural migration through an intact bowel wall from the intestinal lumen
* Bacterial translocation: Enteric bacteria from the bowel lumen → Mesenteric [[lymph nodes]] → Systemic circulation (via the [[thoracic duct]])
* Enteric bacteria → [[Portal vein]] → liver / portosystemic shunts ( in [[portal hypertension]]) → [[Systemic circulation]].
* Conn and Fessel postulated that organisms removed from the [[systemic circulation]] by the liver contaminate hepatic lymph and pass through the permeable lymphatic walls into the ascitic fluid
* Enteric bacteria may also gain access to the [[peritoneal cavity]] by traversing directly the intact intestinal wall.
====Hypo-motility====
* Distal propulsion of luminal contents by intestinal [[peristalsis]] is a critical factor in the inhibition of bacterial colonization and replication in the proximal gastro-intestinal tract, which leads to bacterial overgrowth.


* Probably due to disturbances in the intestinal peristalsis, gastric acid and mucosal immunity in cirrhotic patients.
<ref name="pmid6500513">{{cite journal | author = Runyon BA, Hoefs JC | title = Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis | journal = Hepatology | volume = 4 | issue = 6 | pages = 1209–11 | year = 1984 | pmid = 6500513 | doi = 10.1002/hep.1840040619| url = | issn = }}</ref> Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.<ref name="pmid3371881">{{cite journal| author=Runyon BA| title=Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. | journal=Hepatology | year= 1988 | volume= 8 | issue= 3 | pages= 632-5 | pmid=3371881 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3371881  }} </ref><ref name="pmid15920324">{{cite journal| author=Sheer TA, Runyon BA| title=Spontaneous bacterial peritonitis. | journal=Dig Dis | year= 2005 | volume= 23 | issue= 1 | pages= 39-46 | pmid=15920324 | doi=10.1159/000084724 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15920324  }} </ref>
* Studies have shown that the incidenceof bacterial overgrowth in the small intestine was significantly higher in liver cirrhotic patients with history of SBP than in those without SBP (70% vs. 20%).
* Once bacteria reach a critical concentration in the gut lumen, they “spill over”, and escape the gut, “translocating” to mesenteric lymph nodes.Then they enter lymph, blood, and eventually ascitic fluid.<ref name="pmid7890896">{{cite journal| author=Runyon BA, Squier S, Borzio M| title=Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis. | journal=J Hepatol | year= 1994 | volume= 21 | issue= 5 | pages= 792-6 | pmid=7890896 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7890896  }} </ref>
** Prolonged [[bacteremia]] secondary to compromised host defenses
** Intrahepatic shunting of colonized [[blood]] and
** Defective bactericidal activity within the ascitic fluid.<ref name="pmid6500513">{{cite journal | author = Runyon BA, Hoefs JC | title = Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis | journal = Hepatology | volume = 4 | issue = 6 | pages = 1209–11 | year = 1984 | pmid = 6500513 | doi = 10.1002/hep.1840040619| url = | issn = }}</ref> Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.<ref name="pmid3371881">{{cite journal| author=Runyon BA| title=Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. | journal=Hepatology | year= 1988 | volume= 8 | issue= 3 | pages= 632-5 | pmid=3371881 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3371881  }} </ref><ref name="pmid15920324">{{cite journal| author=Sheer TA, Runyon BA| title=Spontaneous bacterial peritonitis. | journal=Dig Dis | year= 2005 | volume= 23 | issue= 1 | pages= 39-46 | pmid=15920324 | doi=10.1159/000084724 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15920324  }} </ref>


With respect to compromised [[immune system|host defenses]], patients with severe acute or chronic liver disease are often deficient in [[Complement system|complement]] and may also have malfunctioning of the [[neutrophil]]ic and [[reticuloendothelial systems]].<ref name="pmid19561863">Alaniz C, Regal RE (2009) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19561863 Spontaneous bacterial peritonitis: a review of treatment options.] ''P T'' 34 (4):204-10. PMID: [https://pubmed.gov/19561863 19561863]</ref>
With respect to compromised [[immune system|host defenses]], patients with severe acute or chronic liver disease are often deficient in [[Complement system|complement]] and may also have malfunctioning of the [[neutrophil]]ic and [[reticuloendothelial systems]].<ref name="pmid19561863">Alaniz C, Regal RE (2009) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19561863 Spontaneous bacterial peritonitis: a review of treatment options.] ''P T'' 34 (4):204-10. PMID: [https://pubmed.gov/19561863 19561863]</ref>

Revision as of 05:02, 29 January 2017

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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]

Overview

SBP is a result of culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped.[1][2][3]

Pathophysiology

 
 
Patients with decompensated cirrhosis leading to portal Hypertension[4][5]
 
 
 
 
 
 
 
 
 
Intestinal hypo-motility and local pro-inflammatory phenomenon[6]
 
 
 
 
 
 
 
 
 
Bacterial overgrowth:
Increased intestinal permeability and decreased local and systemic immune system in cirrhosis and its relation to bacterial infections and prognosis. [6][7][8]
 
 
 
 
 
 
 
 
 
Routes of entry of pathogens into the ascitic fluid
Escape of enteric bacteria to systemic circulation through:[9]
❑ Bacterial translocation[5]
• Luminal bacteria within colonize mesenteric lymph nodes.[10]
• Organisms from the mesenteric lymph nodes → Systemic circulation through thoracic duct lymph → percolates through the liver and weep across Glisson's capsule → Ascitic fluid.
• Transient bacteremia → Prolonged bacteremia ( due to ↓ Reticulo endothelial system activity ) → Ascites Colonization ( due to ↓ ascitic fluid bactericidal activity ) → Spontaneous bacterial peritonitis )
❑ Portal Vein
• Porto-systemic shunt
• ↓RES function in the liver
❑ Lymphatic rupture
• Contaminated lymph carried by lymphatics
• Ruptured Lymphatics due to high flow and high pressure associated with portal hypertension ( BACTERASCITES )[11]
❑ Other source of organisms
• IV catheters, skin, urinary, and respiratory tract
 
 
 
 
 
 
 
 
 
Endotoxemia and Cytokine response
❑ Endotoxemia → release of pro-inflammatory cytokines produced by macrophages and other host cells in response to bacteria in the serum and peritoneal exudate
• Tumor necrosis factor-α (TNF-α)
• Interleukin (IL)-1,6
• Interferon-γ (IFN-γ)
• Soluble adhesion molecules
❑ Systemic and Abdominal manifestations of peritonitis mediated by cytokines[12][2]
• The effector molecules (Nitric oxide) and cytokines,Tumour necrosis factor (TNF) that help kill the bacteria have undesired side effects as they cause vasodilation and renal failure that accompany SBP.[13][12][14]
• Studies have shown that the presence of whole bacteria or DNA, in serum and ascitic fluid leads to stimulation of immune defences, effector molecules, and cytokines which in turn impact on hemodynamics, renal function and survival.[13]
 
 
 
 
 
 
 
 
 
Host response
❑ Local response

Outpouring of fluid into the peritoneal cavity at sites of irritation with:

• High protein content (>3 g/dL)
• Many cells, primarily polymorphonuclear leukocytes, that phagocytose and kill organisms
• Formation of Fibrinous exudate on the inflamed peritoneal surfaces → Adhesion formation between adjacent bowel, mesentery, and omentum
• Localization of the inflammatory process is aided further by inhibition of motility in the involved intestinal loops
• The extent and rate of intraperitoneal spread of contamination depend on the volume and nature of the exudate and on the effectiveness of the localizing processes
• If peritoneal defenses aided by the appropriate supportive measures control the inflammatory process, the disease may resolve spontaneously (Sterile ascites)[1][1][11] → Consumption of humoral bactericidal factors due to frequent colonization → Increased susceptibility to SBP[15]
• If the ascitic fluid bactericidal activity is poor-moderate → Culture negative neutrocytic ascites (CNNA) or SBP → delay / inappropriate treatment → death due to sepsis and multi organ failure.[16][17]
• Second possible outcome is a confined abscess
• A third possible outcome results when the peritoneal and systemic defense mechanisms are unable to localize the inflammation, which progresses to spreading diffuse peritonitis due to increased virulence of bacteria, greater extent and duration of contamination, and impaired host defenses.
❑ Systemic response

Gastrointestinal

• Paralysis of the bowel due to local inflammation
• Progressive accumulation of fluid and electrolytes in the lumen of the adynamic bowel → distention of the bowel → inhibition of the capillary inflow and secretions
• GI bleeding because of excessive inflammation and tissue damage → ↑ vasodilatation and ↓organ perfusion

Cardiovascular

• Shift of fluid into the peritoneal cavity and bowel lumen → ↓ Effective circulating blood volume → ↑ Hematocrit and
• ↑Fluid and electrolyte loss by coexistent fever, vomiting, diarrhea → decreased venous return to the right side of the heart → decrease in cardiac output → hypotension → activation of the sympathetic nervous system and manifestations such as sweating, tachycardia, and cutaneous vasoconstriction (i.e., cold, moist skin and mottled, cyanotic extremities).
• If the blood volume replaced is sufficient enough as so to increase the cardiac output 2-3 times normal ( to satisfy the increased metabolic needs of the body in the presence of infection) a halt in the progression of the disease is seen.
• Failure to sustain increased cardiac output results in progressive lactic acidosis, oliguria, hypotension, and ultimately death if the infection cannot be controlled.

Respiratory

• Intra-peritoneal inflammation → high and fixed diaphragm → pain on respiration → basilar atelectasis with intrapulmonary shunting of blood
• Decompensation of respiratory function due to delay in the intervention → hypoxemia + hypo-capnia (respiratory alkalosis) followed by hypercapnia (respiratory acidosis)
• Pulmonary edema results because of increased pulmonary capillary leakage as a consequence of hypo-albuminemia or direct effects of bacterial toxins (adult respiratory distress syndrome) → progressive hypoxemia with decreasing pulmonary compliance which needs a ventilator assistance with increasingly higher concentrations of inspired oxygen and positive end-expiratory pressure.

Renal

• SBP → Splanchnic arterial vasodilation and systemic vascular resistance → ↓ Effective arterial blood volume → stimulation of systemic vasoconstrictors (RAAS, Sympathetic Nervous System, Arginine vasopressin) → renal vasoconstriction
• Advanced cirrhosis → ↓ production of local vasodilators and ↑ production of local vasoconstrictors[12] → Hepatorenal syndrome and death.[2]
• ↓ Organ perfusion → Ischemic and Toxic Acute Tubular Necrosis → Acute Renal Failure → Death in (30-40%) of patients.

Metabolic

• Infection → ↓body stores of Glycogen → catabolism of protein (muscle) and →extreme wasting and rapid weight loss of severely infected patients
• Infection → ↓Body heat production → exhaustion and death

Central nervous system

• Hepatic Encephalopathy may occur due to inflammation, Oxidative stress and Intestinal ammonia production on crossing the blood-brain barrier → altered mentation.

Hematological

• Sepsis → DIC
 



Diagramatic representation of pathological bacterial translocation and the associated host response



[17] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[16][3]

With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.[18]

As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[19] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[1] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[18]

References

  1. ↑ 1.0 1.1 1.2 1.3 Runyon BA, Morrissey RL, Hoefs JC, Wyle FA (1985). "Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis". Hepatology. 5 (4): 634–7. PMID 4018735.
  2. ↑ 2.0 2.1 2.2 Runyon BA (2004). "Early events in spontaneous bacterial peritonitis". Gut. 53 (6): 782–4. PMC 1774068. PMID 15138202.
  3. ↑ 3.0 3.1 Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
  4. ↑ Llach J, Rimola A, Navasa M, Ginès P, Salmerón JM, Ginès A; et al. (1992). "Incidence and predictive factors of first episode of spontaneous bacterial peritonitis in cirrhosis with ascites: relevance of ascitic fluid protein concentration". Hepatology. 16 (3): 724–7. PMID 1505916.
  5. ↑ 5.0 5.1 Cirera I, Bauer TM, Navasa M, Vila J, Grande L, Taurá P; et al. (2001). "Bacterial translocation of enteric organisms in patients with cirrhosis". J Hepatol. 34 (1): 32–7. PMID 11211904.
  6. ↑ 6.0 6.1 Chang CS, Chen GH, Lien HC, Yeh HZ (1998). "Small intestine dysmotility and bacterial overgrowth in cirrhotic patients with spontaneous bacterial peritonitis". Hepatology. 28 (5): 1187–90. doi:10.1002/hep.510280504. PMID 9794900.
  7. ↑ {{cite journal| author=Bauer TM, Steinbrückner B, Brinkmann FE, Ditzen AK, Schwacha H, Aponte JJ et al.| title=Small intestinal bacterial overgrowth in patients with cirrhosis: prevalence and relation with spontaneous bacterial peritonitis. | journal=Am J Gastroenterol | year= 2001 | volume= 96 | issue= 10 | pages= 2962-7 | pmid=11693333 | doi=10.1111/j.1572-0241.2001.04668.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11693333
  8. ↑ Rimola A, Soto R, Bory F, Arroyo V, Piera C, Rodes J (1984). "Reticuloendothelial system phagocytic activity in cirrhosis and its relation to bacterial infections and prognosis". Hepatology. 4 (1): 53–8. PMID 6693068.
  9. ↑ Wiest R, Garcia-Tsao G (2005). "Bacterial translocation (BT) in cirrhosis". Hepatology. 41 (3): 422–33. doi:10.1002/hep.20632. PMID 15723320.
  10. ↑ Runyon BA, Squier S, Borzio M (1994). "Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis". J Hepatol. 21 (5): 792–6. PMID 7890896.
  11. ↑ 11.0 11.1 Ho H, Zuckerman MJ, Ho TK, Guerra LG, Verghese A, Casner PR (1996). "Prevalence of associated infections in community-acquired spontaneous bacterial peritonitis". Am J Gastroenterol. 91 (4): 735–42. PMID 8677940.
  12. ↑ 12.0 12.1 12.2 Such J, Hillebrand DJ, Guarner C, Berk L, Zapater P, Westengard J; et al. (2001). "Tumor necrosis factor-alpha, interleukin-6, and nitric oxide in sterile ascitic fluid and serum from patients with cirrhosis who subsequently develop ascitic fluid infection". Dig Dis Sci. 46 (11): 2360–6. PMID 11713936.
  13. ↑ 13.0 13.1 Dunn DL, Barke RA, Knight NB, Humphrey EW, Simmons RL (1985). "Role of resident macrophages, peripheral neutrophils, and translymphatic absorption in bacterial clearance from the peritoneal cavity". Infect Immun. 49 (2): 257–64. PMC 262007. PMID 3894229.
  14. ↑ Navasa, Miguel; Follo, Antonio; Filella, Xavier; Jiménez, Wladimiro; Francitorra, Anna; Planas, Ramón; Rimola, Antoni; Arroyo, Vicente; Rodés, Joan (1998). "Tumor necrosis factor and interleukin-6 in spontaneous bacterial peritonitis in cirrhosis: Relationship with the development of renal impairment and mortality". Hepatology. 27 (5): 1227–1232. doi:10.1002/hep.510270507. ISSN 0270-9139.
  15. ↑ Titó L, Rimola A, Ginès P, Llach J, Arroyo V, Rodés J (1988). "Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors". Hepatology. 8 (1): 27–31. PMID 3257456.
  16. ↑ 16.0 16.1 Runyon BA (1988). "Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis". Hepatology. 8 (3): 632–5. PMID 3371881.
  17. ↑ 17.0 17.1 Runyon BA, Hoefs JC (1984). "Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis". Hepatology. 4 (6): 1209–11. doi:10.1002/hep.1840040619. PMID 6500513.
  18. ↑ 18.0 18.1 Alaniz C, Regal RE (2009) Spontaneous bacterial peritonitis: a review of treatment options. P T 34 (4):204-10. PMID: 19561863
  19. ↑ Runyon BA (1986) Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology 91 (6):1343-6. PMID: 3770358

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