Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

Generally, yes! IV furosemide for treatment of ascites in patients with cirrhosis should be avoided for couple of reasons.

First, in contrast to patients with congestive heart failure in whom the absorption of oral furosemide may be impaired due to bowel wall edema, patients with cirrhosis and ascites appear to absorb oral furosemide efficiently, similarly to that of control patients.1   Another reason for avoiding IV furosemide in this setting is the possibility of a significant drop in the GFR with its attendant rise in BUN and serum creatinine, clinically resembling a picture of hepatorenal syndrome.2

Although the mechanism of the adverse effect of IV furosemide on the renal function of patients with cirrhosis is not totally clear, furosemide-induced vasoconstriction, not intrasvascular volume depletion due to sodium wasting, seems to play an important role.3

Nevertheless, certain situations may necessitate the use of IV furosemide in patients with cirrhosis and ascites, such as in single doses to help identify patients who will be responsive to diuretics, and in patients in need of prompt diuresis such as those with concurrent pulmonary edema. In a somewhat reassuring study, a single dose of 80 mg IV furosemide reliably identified cirrhotic patients with ascites responsive to diuretics, without a significant risk of deteriorating renal function.3

 

References

  1. Sawhney VK, Gregory PB, Swezey SE, et al. Furosemide disposition in cirrhotic patients. Gastroenterology 1981; 81: 1012-16. https://www.ncbi.nlm.nih.gov/pubmed/7286579
  2. Daskalopoulos G, Laffi G, Morgan T, et al. Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascites. Gastroenterology 1987;92:1859-1863. https://www.ncbi.nlm.nih.gov/pubmed/3569760
  3. Spahr, L., Villeneuve, J., Tran, H. K., & Pomier-Layrargues, G. Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites. Hepatology 2001;33:28-31. https://www.ncbi.nlm.nih.gov/pubmed/11124817

 

Contributed by Sam Miller, MD, Mass General Hospital, Boston, MA.

 

Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

My patient with cirrhosis has a large right sided pleural effusion with only a small amount of ascites. Could this effusion still be related to his cirrhosis?

Yes! Although we often associate pleural effusions in patients with cirrhosis with the presence of large ascites, some patients present with hepatic hydrothorax even in the absence of significant ascites.1-3  

In fact, in a study involving 77 patients with hepatic hydrothorax, 49% had minimal or small and 9% had no detectable ascites!1  Interestingly, nearly three-quarters of patients in this study had right sided pleural effusion with 10% having bilateral and 17% having left sided effusion only. Hepatic hydrothorax without ascites as the first sign of liver cirrhosis has also been reported.2

Although the mechanism(s) behind hepatic hydrothorax is not fully clear, the passage of peritoneal fluid into the pleural cavity through defects in the tendinous portion of the diaphragm assisted by negative intrathoracic pressure during inspiration is commonly favored. 1-3  

Supportive evidence includes a number of studies involving intraperitoneal injection of air, dyes or technetium 99 m-sulfur colloid that have demonstrated the trans-diaphragmatic flow of ascites into the pleural cavity. 1-4  In the absence of ascites, a complete equilibrium between the amount of ascites produced and its flow into and reabsorption by the pleural cavity is assumed.1,2

Bonus Pearl: Did you know that although most patients with hepatic hydrothorax have a transudative pleural effusion according to Light’s criteria, 1 study showed that 18% of patients may meet the Light’s criteria for an exudative effusion? 5,6

References

  1. Badillo R, Rockey DC. Hepatic hydrothorax: Clinical features, management, and outcomes in 77 patients and review of the literature. Medicine 2014;93:135-142. https://www.ncbi.nlm.nih.gov/pubmed/24797168
  2. Kim JS, Kim CW, Nam HS, et al. Hepatic hydrothorax without ascites as the first sign of liver cirrhosis. Respirology Case Reports 2016;4:16-18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4722098/
  3. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88:188-91. https://www.ncbi.nlm.nih.gov/pubmed/3964765
  4. Holt KA, Oliviera E, Rohatgi PK. Hepatic hydrothorax demonstration by Tc-99 sulfur colloid ascites scan. Clin Nucl Med 1999;24:609. https://www.ncbi.nlm.nih.gov/pubmed/10439187 
  5. Light RW. New treatment for hepatic hydrothorax? Ann Am Thorac Soc 2016;13:773-74. https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.201603-223ED
  6. Bielsa S, Porcel JM, Castellote J, et al. Solving the Light’s criteria misclassification rate of cardiac and hepatic transudates. Respirology 2012;17”721-726. https://www.ncbi.nlm.nih.gov/pubmed/22372660
My patient with cirrhosis has a large right sided pleural effusion with only a small amount of ascites. Could this effusion still be related to his cirrhosis?

My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?

There is a high prevalence of extra-pyramidal or Parkinson-like (PL) clinical findings in patients with cirrhosis. In fact, over 75% of patients with cirrhosis may exhibit PL signs, such as tremor, rigidity, and akinesia, with 88% also showing hyperintensity in the globus pallidus of basal ganglia on T1-weighted brain MRI.1

What’s even more interesting is the similarity between PL clinical and MRI findings among patients with cirrhosis and those with Manganese (Mn) toxicity.2,3 More specifically, similar MRI findings involving the globus pallidus have been reported in Mn-exposed workers, patients with cirrhosis, and those undergoing total parenteral nutrition with excessive Mn replacement. 4 These observations seem more than coincidental as 67% of patients with cirrhosis have been reported to have elevated blood Mn concentrations, with significantly higher levels in patients with previous portacaval anastomoses or transjugular intrahepatic portosystemic shunt (TIPS).1

Mn-induced parkinsonism is distinguishable from classic Parkinson’s disease in several ways, including the absence of Lewy bodies, more frequent dystonia, and less resting tremor.5 Also, remember that Mn-induced PL disease does NOT respond to L-dopa, a drug used to treat early stages of PD. 5 This finding can be explained by the fact that, in contrast to Parkinson’s disease where many of the dopamine-producing cells in the substantia nigra of the brain degenerate resulting in dopamine deficiency, in Mn-induced PL disease the problem is release of dopamine into synapses not its production.5

Bonus Pearl: Did you know that due to its paramagnetic properties, manganese can be effectively seen by MRI!

References

  1. Spahr L, Butterworth RF, Fontaine S, et al. Increased blood manganese in cirrhotic patients: relationship to pallidal m agnetic resonance signal hyperintensity and neurological symptoms. Hepatology 1996;24:1116-1120. https://www.ncbi.nlm.nih.gov/pubmed/8903385
  2. Hauser RA, Zesiewicz TA, Rosemurgy AS, et al. Manganese intoxication and chronic liver failure. Ann Neurol 1994;36:871-75. https://www.ncbi.nlm.nih.gov/pubmed/7998773
  3. Krieger S, Jaub M, Jansen O, et al. Neuropsychiatric profile and hyperintense globus pallidus on T1-weighted magnetic resonance images in liver cirrhosis. Gastroenterol 1996;111:147-55. https://www.ncbi.nlm.nih.gov/pubmed/8698193
  4. Lucchini R, Albini E, Placidi D, et al. Brain magnetic resonance imaging and manganese exposure. Neurotoxicity 2000;21:769-75. https://www.ncbi.nlm.nih.gov/pubmed/11130281
  5. Kwakye GF, Paoliello MMB, Mukhopadhyay S, et al. Manganese-induced parkinsonism and Parkinson’s disease: Shared and distinguishable features. Int J Environ Res Public Health 2015;12;7519-40. https://www.ncbi.nlm.nih.gov/pubmed/26154659

Don’t forget to sign up under menu to get future pearls right into your mailbox!

My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?

Should my patient with suspected alcoholic hepatitis undergo liver biopsy?

Although a characteristic clinical history and biochemical pattern of liver injury can strongly suggest the diagnosis of alcoholic hepatitis (AH), a definitive diagnosis is confirmed with liver biopsy only. In fact, in 30% of patients clinically diagnosed as having AH, a liver biopsy may lead to an alternative diagnosis.1Understandably, many physicians are reluctant to proceed with biopsy in this fragile patient population given the associated risks, notably bleeding. For this reason, most patients with AH are clinically diagnosed without a liver biopsy. However, there are certain instances in which a biopsy can be helpful, including when:2

  • Diagnosis of AH is in doubt
  • Suspicion for another disease process that may be contributing in parallel to AH is high
  • Obtaining prognostic data or identification of advanced hepatic fibrosis or cirrhosis in AH is desired

Thus, liver biopsy findings may influence short- and long-term management in AH. For these reasons, the European Association for the Study of the Liver recommends consideration of a liver biopsy in patients with AH.3 To minimize the bleeding risk, the transjugular approach is preferred.

References

  1. Mookerjee RP, Lackner C, Stauber R, et al. The role of liver biopsy in the diagnosis and prognosis of patients with acute deterioration of alcoholic cirrhosis. J Hepatol 2011; 55:1103-1111 Link
  2. Altamirano J, Miquel R, Katoonizadeh A, et al. A histologic scoring system for prognosis of patients with alcoholic hepatitis. Gastroenterology 2014;146: 1231-1239. PDF
  3. European Association for the Study of Liver. EASL clinical practical guidelines: management of alcoholic liver disease. J Hepatol 2012; 57:399-420. PDF

Contributed by Jay Luther, MD, Gastrointestinal Unit, Mass General Hospital, Boston, MA.

Should my patient with suspected alcoholic hepatitis undergo liver biopsy?

What is the significance of Terry’s nails in my hospitalized patient?

Terry’s nails were first described in 1954 in patients with hepatic cirrhosis (prevalence 82%, majority related to alcohol abuse) (1). Since then, they have been reported in a variety of other conditions, including adult-onset diabetes mellitus (AODM), chronic congestive heart failure, chronic renal failure, pulmonary tuberculosis, and Reiter’s syndrome (2).

A 1984 study found Terry’s nails in 25% of hospitalized patients (3).  In this study, cirrhosis, chronic congestive heart failure, and AODM were significantly associated with Terry’s nails, while pulmonary tuberculosis, rheumatoid arthritis and cancer were not. The presence of Terry’s nails may be particularly concerning in patients 50 y of age or younger as it increases the relative risk of cirrhosis, chronic congestive heart failure or AODM by 5-fold (18-fold for cirrhosis alone) in this age group (3).

Terry’s nails should be distinguished from Lindsay’s nails or “half and half” nails. Although both nail abnormalities are characterized by an opaque white proximal portion, Terry’s nails have a thinner distal pink to brown transverse band no more than 3 mm wide (3) (Fig 1), while the same anomaly is wider and occupies 20%-60% of the nail bed in Lindsay’s nails (Fig 2). Of interest, Lindsay’s nails have been reported in up to 40% of patients with chronic kidney disease (4,5).

References

1. Terry R. White nails in hepatic cirrhosis. Lancet 1954;266:757-59. https://www.ncbi.nlm.nih.gov/pubmed/13153107 
2. Nia AM, Ederer S, Dahlem K, et al. Terry’s nails: a window to systemic diseases. Am J Med 2011;124:603-604. https://www.ncbi.nlm.nih.gov/pubmed/21683827 
3. Holzberg M, Walker HK. Terry’s nails: revised definitions and new correlations. Lancet 1984;1(8382):896-99. https://www.ncbi.nlm.nih.gov/pubmed/6143196 
4. Pitukweerakul S, Pilla S. Terry’s nails and Lindsay’s nails: Two nail abnormalities in chronic systemic diseases. J Gen Intern Med 31;970.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945547/ 
5. Gagnon AL, Desai T. Dermatological diseases in patients with chronic kidney disease 2013;2:104-109.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891143/

Figure 1. Terry’s nails in a patient with end-stage liver disease

Figure 2. Lindsay’s nails in a patient with chronic kidney disease

If you liked this post, SELRES_9060f380-b0ce-41bb-b812-fe2595cb3460SELRES_4b9ffe76-4732-435c-a61e-cb3aba28fef9SELRES_055e8f9c-d15f-4b5c-8ddc-c9eb04539366sign upSELRES_055e8f9c-d15f-4b5c-8ddc-c9eb04539366SELRES_4b9ffe76-4732-435c-a61e-cb3aba28fef9SELRES_9060f380-b0ce-41bb-b812-fe2595cb3460 on the P4P home page and receive future pearls delivered directly into your mailbox!

What is the significance of Terry’s nails in my hospitalized patient?

Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

Although umbilical hernia in patients with cirrhosis and ascites is common and often “expected” (a rate of 20% during the course of their disease), it can be associated with significant risk of complications such as incarceration, ascites drainage, peritonitis, and spontaneous rupture or evisceration from necrosis of overlying skin.1,2

A 2007 retrospective study involving patients with cirrhosis and umbilical hernia reported a complication rate of 77% and related mortality of 15% among those managed conservatively (mean period of observation ~ 5 years); MELD score could not predict failure of conservative management (median 22 in complicated vs 24 in uncomplicated).3

Because the risk of death with hernia repair in urgent settings is 7x higher than for elective hernia repair in cirrhotic patients, there has been increasing interest in elective repair in patients with well-compensated cirrhosis.3 Interestingly, the reported surgical complication rates among patients with well-compensated cirrhosis appear similar to those in noncirrhotic patients.3 If the patient is expected to undergo liver transplantation in the near future, elective hernia repair can be postponed and managed concomitantly.

Bonus pearl: Did you know that spontaneous umbilical hernia rupture is also known as “Flood syndrome” (should be easy to remember!), first described by Frank B Flood, a surgical resident back in 1961? 4

References

  1. Marsman HA, Heisterkamp J, Halm JA, et al. Management in patients with liver cirrhosis and an umbilical hernia. Surgery 2007;142:372-5. https://www.ncbi.nlm.nih.gov/pubmed/17723889
  2. Coelho, JCU, Claus CMP, Campos ACL, et al. Umbilical hernia in patients with liver cirrhosis: a surgical challenge. World J Gastrointest Surg 2016;8:476-82. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942747/
  3. Martens P, Laleman W. Umbilical hernia in a patient with cirrhosis. Cleveland Clin J Med 2015;82: 404-5. https://www.mdedge.com/ccjm/article/100682/hepatology/umbilical-hernia-patient-cirrhosis
  4. Nguyen ET, Tudtud-Hans LA. Flood syndrome: spontaneous umbilical hernia rupture leaking ascitic fluid-a case report. Perm J 2017;21:16-152. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5499604/ 

If you liked this pearl, subscribe to P4P and have future pearls delivered right into your mailbox!

Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

Why isn’t my patient with congestive heart failure or end-stage liver disease losing weight despite being on diuretic therapy? Is the diuretic dose too low, or is the salt intake too high?

When a patient with congestive heart failure (CHF) or end-stage liver disease (ESLD) doesn’t respond as expected to diuretic therapy, measurement of urinary sodium (Na) can be helpful.

In low effective arterial blood volume states (eg, CHF and ESLD) aldosterone secretion is high, resulting in high urine potassium (K) and low urine Na concentrations. However, in the presence of diuretics, urinary Na excretion should rise.

Patients undergoing active diuresis are often restricted to a 2 g (88 mEq) Na intake/day, with ~10 mEq excreted via non-urinary sources (primarily stool), and ~ 78 mEq excreted in the urine to “break even” — that is, to maintain the same weight.

Although historically measured 1, a 24-hour urine Na and K collection is tedious, making spot urine Na/K ratio more attractive as a potential proxy.  Approximately 90% of patients who achieve a urinary Na/K ratio ≥1 will have a urinary Na excretion ≥78 mEq/day — that is to say, they are sensitive to the diuretic and will have a stable or decreasing weight at the current dose. 2,3

Urine Na/K may be interpreted as follows:

  • ≥1 and losing weight suggests effective diuretic dose, adherent to low Na diet
  • ≥1 and rising weight suggests effective diuretic dose, non-adherent to low Na diet
  • <1 and rising weight suggests ineffective diuretic dose

The “ideal” Na/K ratio as relates to responsiveness to diuretics has ranged from 1.0 to 2.5.4 In acutely decompensated heart failure patients on spironolactone, a K-sparing diuretic, Na/K ratio >2 at day 3 of hospitalization may be associated with improved outcome at 180 days. 5

Remember also that if the patient’s clinical syndrome is not correlating well with the ratio, it’s always a good idea to proceed to a 24-hour urine collection.

 

References

  1. Runyon B. Refractory Ascites. Semin Liver Dis. Semin Liver Dis. 1993 Nov;13(4):343-51. https://www.ncbi.nlm.nih.gov/pubmed/8303315
  2. Stiehm AJ, Mendler MH, Runyon BA. Detection of diuretic-resistance or diuretic-sensitivity by spot urine Na/K ratios in 729 specimens from cirrhotics with ascites: approximately 90 percent accuracy as compared to 24-hr urine Na excretion (abstract). Hepatology 2002; 36: 222A.
  3. da Silva OM, Thiele GB, Fayad L. et al. Comparative study of spot urine Na/K ratio and 24-hour urine sodium in natriuresis evaluation of cirrhotic patients with ascites. GE J Port Gastroenterol 2014;21:15-20 https://pdfs.semanticscholar.org/4dc3/4d18d202c6fa2b30a1f6563baab80d877921.pdf
  4. El-Bokl M, Senousy, B, El-Karmouty K, Mohammed I, Mohammed S, Shabana S, Shelby H. Spot urinary sodium for assessing dietary sodium restriction in cirrhotic ascites. World J Gastroenterol 2009; 15:3631. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721236/
  5. Ferreira JP, Girerd N, Medeiros PB, et al. Spot urine sodium excretion as prognostic marker in acutely decompensated heart failure: the spironolactone effect. Clin Res Cardiol 2016;105:489-507. https://www.ncbi.nlm.nih.gov/pubmed/26615605

 

Contributed by Alyssa Castillo, MD, with valuable input from Sawalla Guseh, MD, both from Mass General Hospital, Boston, MA.

Why isn’t my patient with congestive heart failure or end-stage liver disease losing weight despite being on diuretic therapy? Is the diuretic dose too low, or is the salt intake too high?

Does my patient about to undergo immunosuppressive therapy need antiviral prophylaxis even if she tests positive for hepatitis B surface antibody?

The presence of hepatitis B surface antibody (HBsab) in patients who also test positive for core antibody does not necessarily confer full protection against hepatitis B virus (HBV) reactivation during immunosuppression (incidence 4.3%). 1 This is because despite having HBsab and no HB surface antigen,  a small portion of patients continue to have detectable HBV DNA in the serum and are therefore at risk of reactivation during severe immunosuppression. 2

In fact, the American Gastroenterological Association recommends against using anti-HBs status to guide antiviral prophylaxis in anti-HBc-positive patients. 1

Overall, antiviral prophylaxis may reduce the risk of HBV reactivation by 87% (C.I. 70%-94%). Antiviral drugs with a high barrier to resistance (eg, entecavir) are preferred over lamivudine.

Immunosuppressants often requiring HBV prophylaxis include: 1-3

  • B cell-depleting agents (eg, rituximab, ofatumumab)
  • Anthracycline derivatives (eg, doxorubicin, epirubicin)
  • Prednisone (4 weeks or more)
  • Tumor necrosis factor inhibitors (eg, etanercept, adalimumab, certolizumab, infliximab)
  • Other cytokine or integrin inhibitors (eg, abatacept, ustekinumab, natalizumab, vedolizumab)

Traditional immunosuppressive agents such as azathioprine, 6-mercaptopurine and methotrexate are often considered “low-risk” and do not generally require prophylaxis. 1

Fun Fact: Did you know that hepatitis B virus is very old and probably originated in birds when dinosaurs roamed the earth? 4

References

  1. Reddy KR, Beavers KL, Hammond SP, et al. American Gastroenterological Association Institute Guideline on the prevention and treatment of hepatitis B virus reactivation during immunosuppressive drug therapy. Gastroenterology 2015;148:215-19. https://www.ncbi.nlm.nih.gov/pubmed/25447850
  2. Gigi E, Georgiou T, Mougiou D, et al. Hepatitis B reactivation in a patient with rheumatoid arthritis with antibodies to hepatitis B surface antigen treated with rituximab. HIPPOKATRIA 2013;17:91-93. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738290/
  3. Kim EB, Kim DS, Park SJ, et al. Hepatitis B virus reactivation in a surface antigen-negative and antibody-positive patient after rituximab plus CHOP chemotherapy. Cancer Res Treat 2008;40:36-38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699087/
  4. Suh A, Brosius J, Schmitz J, et al. The genome of a Mesozoic paleovirus reveals the evolution of hepatitis B virus. Nature Communications 2013; Article no. 1791. http://www.nature.com/articles/ncomms2798
Does my patient about to undergo immunosuppressive therapy need antiviral prophylaxis even if she tests positive for hepatitis B surface antibody?

What could be causing low serum haptoglobin in my patient with no evidence of hemolysis?

 

There are many causes of low serum haptoglobin besides hemolysis, including1-4:

  • Cirrhosis of the liver
  • Disseminated ovarian carcinomatosis
  • Pulmonary sarcoidosis
  • Elevated estrogen states
  • Repetitive physical exercise
  • Hemodilution
  • Blood transfusions
  • Drugs (eg, oral contraceptives, chlorpromazine, indomethacin, isoniazid, nitrofurantoin, quinidine, and streptomycin)
  • Iron deficiency anemia
  • Megaloblastic anemia (by destruction of megaloblastic RBC precursors in the bone marrow)
  • Congenital causes

Less well-known is that congenital haptoglobin deficiency (“anhaptoglobinemia”) may not be so rare in the general population at a prevalence of 1% among whites and 4% among African-Americans (>30% in blacks of West African origin)3. Measurement of serum hemopexin, another plasma protein that binds heme, may help distinguish between this condition and acquired hypohaptoglobinemia— in the absence of hemolysis, hemopexin levels should remain unchanged3,5.

Final Fun Fact: Did you know that serum haptoglobin is often low during the first 6 months of life?

References

  1. Shih AWY, McFarane A, Verhovsek M. Haptoglobin testing in hemolysis: measurement and interpretation. Am J Hematol 2014;89: 443-47. https://www.ncbi.nlm.nih.gov/pubmed/24809098
  2. Sritharan V, Bharadwaj VP, Venkatesan K, et al. Dapsone induced hypohaptoglobinemia in lepromatous leprosy patients. Internat J Leprosy 1981;307-310. https://www.ncbi.nlm.nih.gov/pubmed/7198620
  3. Delanghe J, Langlois M, De Buyzere M, et al. Congenital anhaptoglobinemia versus acquired hypohaptoglobinemia. Blood 1998;9: 3524. http://www.bloodjournal.org/content/bloodjournal/91/9/3524.full.pdf
  4. Haptoglobin blood test. https://medlineplus.gov/ency/article/003634.htm. Accessed August 6, 2017.
  5. Smith A, McCulloh RJ. Hemopexin and haptoglobin: allies against heme toxicity from hemoglobin not contenders. Front. Physiol 2015;6:187. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485156/pdf/fphys-06-00187.pdf

 

In collaboration with Kris Olson, MD, MPH, Mass General Hospital, Boston, MA

What could be causing low serum haptoglobin in my patient with no evidence of hemolysis?

Why are patients with cirrhosis and upper gastrointestinal bleed routinely treated with antibiotics?

Cirrhotic patients with upper gastrointestinal bleed (UGIB) are at high risk of bacterial infections: 22% during the first 48 h after admission, 35-66% within 2 weeks of initial bleeding1. Antibiotic prophylaxis has been shown to reduce short term mortality, bacterial infections, early rebleeding and volume of blood transfused1-4.

But what is the exact connection between UGIB and bacterial infections in cirrhosis? One hypothesis is that UGIB sets up the host for bacterial infection via translocation (eg, due to hypovolemia), procedures necessary in the management of bleeding (eg endoscopy, sclerotherapy, IV access), and aspiration pneumonia. More intriguing is the reverse hypothesis—that is the bacterial infection serves as a trigger for UGIB.  Several lines of evidence support this view1,2.

  • Cirrhotic patients admitted for non-UGIB-related conditions may be 4x more likely to develop UGIB during their hospitalization in the presence of bacterial infection on admission4
  • Infections predispose to early variceal rebleeding
  • Infection/endotoxemia increase portal pressure, and impair liver function and coagulation
  • Commonly cited risk factors for variceal bleeding (eg, hepatic venous pressure gradient, liver function, size of varices) do not readily explain why bleeding occurs unpredictably and why despite daily increases in portal pressure (eg, following daily meals and exercises), UGIB is relatively infrequent.

 

References

  1. Thalheimer U, Triantos CK, Samonakis DN, et al. Infection, coagulation, and variceal bleeding in cirrhosis. Gut 2005;54:556-63. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774431
  2. Goulis J. Bacterial infection in the pathogenesis of variceal bleeding. Is there any role for antibiotic prophylaxis in the cirrhotic patient. Ann Gastroenterol 2001;14:205-11. http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=4&ved=0ahUKEwjNh-rhlpLVAhXGdD4KHSurANcQFgg4MAM&url=http%3A%2F%2Fwww.annalsgastro.gr%2Findex.php%2Fannalsgastro%2Farticle%2Fdownload%2F80%2F71&usg=AFQjCNHJfAyYAjuNXpwsWGrVuyuxxgJYKg
  3. Soares-Weiser K, Brezis, Tur-Kaspa R, et al. Antibiotic prophylaxis of bacterial infections in cirrhotic inpatients: a meta-analysis of randomized controlled trials. Scand J Gastroenterol 2003;38:193-200. http://www.tandfonline.com/doi/abs/10.1080/00365520310000690
  4. Anastasioua J, Williams R. When to use antibiotics in the cirrhotic patient? The evidence base. Ann Gastroenterol. 2013; 26(2): 128–131. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959942
  5. Benavides J, Fernandez N, Colombato L, et al. Further evidence linking bacterial infection and upper G.I. bleeding in cirrhosis. Results from a large multicentric prospective survey in Argentina. J Hepatol 2003;38 (suppl 2):A176. http://www.journal-of-hepatology.eu/article/S0168-8278(03)80592-5/abstract

 

Don’t forget to sign up under menu to get future pearls right into your mailbox!

Why are patients with cirrhosis and upper gastrointestinal bleed routinely treated with antibiotics?