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{{Gastrointestinal varices}}
{{Gastrointestinal varices}}
{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{HK}}


==Overview==
==Overview==
If untreated, recurrent variceal hemorrhage occurs in 60% of patients, usually within 1-2 years of the initial [[hemorrhage]]. Gastrointestinal varices are an indication of increased [[Portal venous system|portal venous]] pressure, especially in [[Cirrhosis|cirrhotic]] patients. The progressive increase in [[portal]] pressure leads to a progressive increase in size of the varices and an increased [[vascular]] wall tension. Variceal [[hemorrhage]] resulting from rupture occurs when the expanding force exceeds the maximal wall tension. Complications include, transient [[dysphagia]], [[chest pain]], [[esophageal]] [[ulceration]], ulcerogenic bleeding, post-therapeutic [[hemorrhage]], [[esophageal]] [[strictures]], [[Pleural effusion|pleural effusions]], [[pericarditis]] and [[portal vein thrombosis]]. Factors associated with a poor [[prognosis]] of presence of [[bacterial]] infections, HVPG >20 mm Hg, [[alcohol]] intake and [[obesity]]. The AIMS65 score is the best predictor of [[mortality]] in patients with variceal [[bleeding]].


==Natural History==
==Natural History==
Gastrointestinal varices are an indication of increased portal venous pressure, especially in cirrhotic patients. The progressive increase in portal pressure leads to a progressive increase in size of the varices and an increased vascular wall tension. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. The following sequence of events typically summarizes the natural history of gastrointestinal varices:
If untreated, recurrent variceal hemorrhage occurs in 60% of patients, usually within 1-2 years of the initial [[hemorrhage]].<ref name="García-PagánBosch2003">{{cite journal|last1=García-Pagán|first1=Juan C|last2=Bosch|first2=Jaime|title=Prevention of variceal rebleeding|journal=The Lancet|volume=361|issue=9376|year=2003|pages=2245|issn=01406736|doi=10.1016/S0140-6736(03)13750-6}}</ref> Gastrointestinal varices are an indication of increased [[Portal venous system|portal venous]] pressure, especially in [[Cirrhosis|cirrhotic]] patients. The progressive increase in [[portal]] pressure leads to a progressive increase in size of the varices and an increased [[vascular]] wall tension. Variceal [[hemorrhage]] resulting from rupture occurs when the expanding force exceeds the maximal wall tension. The following sequence of events typically summarizes the [[Natural history of disease|natural history]] of gastrointestinal varices:


=== (i) No varices ===
=== (i) No varices ===
* Early stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is less than 10 mmHg (normal)
* Early stages of [[chronic liver disease]], where the hepatic venous portal pressure gradient (HPVG) is less than 10mmHg (normal)


=== (ii) Small varices - No hemorrhage ===
=== (ii) Small varices - No hemorrhage ===
* Middle to late stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is greater than equal to 10 mmHg
* Middle to late stages of [[chronic liver disease]], where the hepatic venous portal pressure gradient (HPVG) is greater than equal to 10mmHg
* Development rate is 8 % per year
* Development rate is 8 % per year


=== (iii) Large varices - No hemorrhage ===
=== (iii) Large varices - No hemorrhage ===
* The size increases with progression of cirrhosis and due to hyperdynamic circulation
* The size increases with progression of [[cirrhosis]] and due to [[hyperdynamic circulation]]
* Progression from small to large varices is 8 % per year
* Progression from small to large varices is 8 % per year<ref name="urlwww.journal-of-hepatology.eu">{{cite web |url=http://www.journal-of-hepatology.eu/article/S0168-8278(03)00011-4/pdf |title=www.journal-of-hepatology.eu |format= |work= |accessdate=}}</ref>


=== (iv) Variceal hemorrhage ===
=== (iv) Variceal hemorrhage ===
* Intravascular pressure in varices greater than the variceal wall tension leads to variceal rupture
* [[Intravascular]] pressure in varices greater than the variceal wall tension leads to variceal rupture
* Rate of rupture of esophageal varices is 5 - 15 % per year
* Rate of rupture of esophageal varices is 5 - 15 % per year
* Rate of rupture of gastric varices is 25 % (greater in IGV1 and GOV2)
* Rate of rupture of gastric varices is 25 % (greater in IGV1 and GOV2)<ref name="pmid24078893">{{cite journal |vauthors=Menasherian-Yaccobe L, Jaqua NT, Kenny P |title=Successful treatment of bleeding gastric varices with splenectomy in a patient with splenic, portal, and mesenteric thromboses |journal=Case Rep Surg |volume=2013 |issue= |pages=273531 |year=2013 |pmid=24078893 |pmc=3776550 |doi=10.1155/2013/273531 |url=}}</ref>


=== (v) Recurrent hemorrhage ===
=== (v) Recurrent hemorrhage ===
* Persistent increase in portal pressure leads to recurrence after treatement if the underlying cause is not addressed
* Persistent increase in [[portal]] pressure leads to recurrence after treatment if the underlying cause is not addressed
 
=== Correlation between severity of cirrhosis and progression of varices ===
The following factors are associated with progression from small to large varices, at the time of baseline endoscopy:<ref name="pmid12586291">{{cite journal |vauthors=Merli M, Nicolini G, Angeloni S, Rinaldi V, De Santis A, Merkel C, Attili AF, Riggio O |title=Incidence and natural history of small esophageal varices in cirrhotic patients |journal=J. Hepatol. |volume=38 |issue=3 |pages=266–72 |year=2003 |pmid=12586291 |doi= |url=}}</ref><ref>{{cite journal|title=Prediction of the First Variceal Hemorrhage in Patients with Cirrhosis of the Liver and Esophageal Varices|journal=New England Journal of Medicine|volume=319|issue=15|year=1988|pages=983–989|issn=0028-4793|doi=10.1056/NEJM198810133191505}}</ref>
 
* Severe [[cirrhosis]] (Child-Pugh class B and C)
* [[Alcoholic cirrhosis]]
* Presence of red wale marks (defined as longitudinal dilated [[venules]] resembling whip marks on the variceal surface)
{| class="wikitable"
|+Child-Pugh Classification of the Severity of Cirrhosis
! rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Clinical feature/laboratory finding
! colspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" + |Points*
|-
! style="background:#4479BA; color: #FFFFFF;" align="center" + |1
! style="background:#4479BA; color: #FFFFFF;" align="center" + |2
! style="background:#4479BA; color: #FFFFFF;" align="center" + |3
|-
|'''[[Encephalopathy]]'''
|None
|Grade 1–2
   (or precipitant-induced)
|Grade 3–4
   (chronic)
|-
|'''[[Ascites]]'''
|None
|Mild/Moderate
   ([[diuretic]]-responsive)
|Tense
   ([[diuretic]]-refractory)
|-
|'''[[Bilirubin]] (mg/dL)'''
|<2
|2–3
|>3
|-
|'''[[Albumin]] (g/dL)'''
|>3.5
|2.3–3.5
|<2.8
|-
|[[Prothrombin time]] or [[international normalized ratio]] ([[INR]])
|<4
|4–6
|>6
|-
| 
|<1.7
|1.7–2.3
|>2.3
|}
'''Interpretation of [[Child-Pugh score]]'''
 
 5–6 points: Child A
 
7–9 points: Child B
 
10–15 points: Child C


==Complications==
==Complications==
Gastrointestinal varices may be complicated by the following:
* Variceal [[hemorrhage]]
* Post-[[sclerotherapy]] complications:<ref name="pmid7564871">{{cite journal |vauthors=Jaspersen D, Schwacha H, Sauer B, Wzatek J, Schorr W, Graf zu Dohna P, Hammar CH |title=[Complications of endoscopic sclerotherapy of esophageal varices] |language=German |journal=Leber Magen Darm |volume=25 |issue=4 |pages=171–4 |year=1995 |pmid=7564871 |doi= |url=}}</ref><ref name="pmid2219326">{{cite journal |vauthors=Pillay P, Starzl TE, Van Thiel DH |title=Complications of sclerotherapy for esophageal varices in liver transplant candidates |journal=Transplant. Proc. |volume=22 |issue=5 |pages=2149–51 |year=1990 |pmid=2219326 |pmc=2952499 |doi= |url=}}</ref><ref name="pmid3264465">{{cite journal |vauthors=Hunter GC, Steinkirchner T, Burbige EJ, Guernsey JM, Putnam CW |title=Venous complications of sclerotherapy for esophageal varices |journal=Am. J. Surg. |volume=156 |issue=6 |pages=497–501 |year=1988 |pmid=3264465 |doi= |url=}}</ref>
** Transient [[dysphagia]]
** [[Chest pain]]
** [[Esophageal]] [[ulceration]]
** Ulcerogenic [[bleeding]]
** Post-therapeutic [[hemorrhage]]
** [[Esophageal]] strictures
** [[Pleural effusion|Pleural effusions]]
** [[Pericarditis]]
** [[Portal vein thrombosis]]


==Prognosis==
==Prognosis==
The AIMS65 score is best predictor of mortality in patients with variceal bleeding. The score is calculated as follows:
Six-week [[mortality]] is used as a predictor of [[prognosis]] for variceal [[hemorrhage]]<ref name="pmid26047908">{{cite journal |vauthors=de Franchis R |title=Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension |journal=J. Hepatol. |volume=63 |issue=3 |pages=743–52 |year=2015 |pmid=26047908 |doi=10.1016/j.jhep.2015.05.022 |url=}}</ref> The six-week [[mortality]] for variceal [[hemorrhage]] ranges from a low of 15% to a high of 25%<ref name="pmid24148622">{{cite journal |vauthors=Reverter E, Tandon P, Augustin S, Turon F, Casu S, Bastiampillai R, Keough A, Llop E, González A, Seijo S, Berzigotti A, Ma M, Genescà J, Bosch J, García-Pagán JC, Abraldes JG |title=A MELD-based model to determine risk of mortality among patients with acute variceal bleeding |journal=Gastroenterology |volume=146 |issue=2 |pages=412–19.e3 |year=2014 |pmid=24148622 |doi=10.1053/j.gastro.2013.10.018 |url=}}</ref><ref name="pmid23007003">{{cite journal |vauthors=Amitrano L, Guardascione MA, Manguso F, Bennato R, Bove A, DeNucci C, Lombardi G, Martino R, Menchise A, Orsini L, Picascia S, Riccio E |title=The effectiveness of current acute variceal bleed treatments in unselected cirrhotic patients: refining short-term prognosis and risk factors |journal=Am. J. Gastroenterol. |volume=107 |issue=12 |pages=1872–8 |year=2012 |pmid=23007003 |doi=10.1038/ajg.2012.313 |url=}}</ref>
* Factors associated with a poor [[prognosis]] include:<ref name="pmid25460564">{{cite journal |vauthors=Tandon P, Abraldes JG, Keough A, Bastiampillai R, Jayakumar S, Carbonneau M, Wong E, Kao D, Bain VG, Ma M |title=Risk of Bacterial Infection in Patients With Cirrhosis and Acute Variceal Hemorrhage, Based on Child-Pugh Class, and Effects of Antibiotics |journal=Clin. Gastroenterol. Hepatol. |volume=13 |issue=6 |pages=1189–96.e2 |year=2015 |pmid=25460564 |doi=10.1016/j.cgh.2014.11.019 |url=}}</ref><ref name="pmid18093686">{{cite journal |vauthors=Abraldes JG, Villanueva C, Bañares R, Aracil C, Catalina MV, Garci A-Pagán JC, Bosch J |title=Hepatic venous pressure gradient and prognosis in patients with acute variceal bleeding treated with pharmacologic and endoscopic therapy |journal=J. Hepatol. |volume=48 |issue=2 |pages=229–36 |year=2008 |pmid=18093686 |doi=10.1016/j.jhep.2007.10.008 |url=}}</ref><ref name="pmid19445938">{{cite journal |vauthors=Everhart JE, Lok AS, Kim HY, Morgan TR, Lindsay KL, Chung RT, Bonkovsky HL, Ghany MG |title=Weight-related effects on disease progression in the hepatitis C antiviral long-term treatment against cirrhosis trial |journal=Gastroenterology |volume=137 |issue=2 |pages=549–57 |year=2009 |pmid=19445938 |pmc=3148692 |doi=10.1053/j.gastro.2009.05.007 |url=}}</ref><ref name="pmid21567436">{{cite journal |vauthors=Berzigotti A, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Morillas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Groszmann RJ |title=Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis |journal=Hepatology |volume=54 |issue=2 |pages=555–61 |year=2011 |pmid=21567436 |pmc=3144991 |doi=10.1002/hep.24418 |url=}}</ref><ref name="pmid23234725">{{cite journal |vauthors=Marcellin P, Gane E, Buti M, Afdhal N, Sievert W, Jacobson IM, Washington MK, Germanidis G, Flaherty JF, Aguilar Schall R, Bornstein JD, Kitrinos KM, Subramanian GM, McHutchison JG, Heathcote EJ |title=Regression of cirrhosis during treatment with tenofovir disoproxil fumarate for chronic hepatitis B: a 5-year open-label follow-up study |journal=Lancet |volume=381 |issue=9865 |pages=468–75 |year=2013 |pmid=23234725 |doi=10.1016/S0140-6736(12)61425-1 |url=}}</ref><ref name="pmid14999703">{{cite journal |vauthors=Monto A, Patel K, Bostrom A, Pianko S, Pockros P, McHutchison JG, Wright TL |title=Risks of a range of alcohol intake on hepatitis C-related fibrosis |journal=Hepatology |volume=39 |issue=3 |pages=826–34 |year=2004 |pmid=14999703 |doi=10.1002/hep.20127 |url=}}</ref>
** Presence of [[bacterial]] infections
**HVPG >20 mm Hg
**[[Alcohol]] intake
**[[Obesity]]


=== AIMS65 score ===
The AIMS65 score is best predictor of [[mortality]] in patients with variceal [[bleeding]]. The score is calculated as follows:
{| class="wikitable"
{| class="wikitable"
!Variable
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Variable
!Score
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Score
|-
|-
|Albumin
|[[Albumin]]
|1
|1
|-
|-
|INR
|[[INR]]
|1
|1
|-
|-
|Systolic blood pressure
|[[Blood pressure|Systolic blood pressure]]
|1
|1
|-
|-
|Altered mental status
|[[Altered mental status]]
|1
|1
|-
|-

Latest revision as of 13:30, 26 January 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

If untreated, recurrent variceal hemorrhage occurs in 60% of patients, usually within 1-2 years of the initial hemorrhage. Gastrointestinal varices are an indication of increased portal venous pressure, especially in cirrhotic patients. The progressive increase in portal pressure leads to a progressive increase in size of the varices and an increased vascular wall tension. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. Complications include, transient dysphagia, chest pain, esophageal ulceration, ulcerogenic bleeding, post-therapeutic hemorrhage, esophageal strictures, pleural effusions, pericarditis and portal vein thrombosis. Factors associated with a poor prognosis of presence of bacterial infections, HVPG >20 mm Hg, alcohol intake and obesity. The AIMS65 score is the best predictor of mortality in patients with variceal bleeding.

Natural History

If untreated, recurrent variceal hemorrhage occurs in 60% of patients, usually within 1-2 years of the initial hemorrhage.[1] Gastrointestinal varices are an indication of increased portal venous pressure, especially in cirrhotic patients. The progressive increase in portal pressure leads to a progressive increase in size of the varices and an increased vascular wall tension. Variceal hemorrhage resulting from rupture occurs when the expanding force exceeds the maximal wall tension. The following sequence of events typically summarizes the natural history of gastrointestinal varices:

(i) No varices

  • Early stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is less than 10mmHg (normal)

(ii) Small varices - No hemorrhage

  • Middle to late stages of chronic liver disease, where the hepatic venous portal pressure gradient (HPVG) is greater than equal to 10mmHg
  • Development rate is 8 % per year

(iii) Large varices - No hemorrhage

(iv) Variceal hemorrhage

  • Intravascular pressure in varices greater than the variceal wall tension leads to variceal rupture
  • Rate of rupture of esophageal varices is 5 - 15 % per year
  • Rate of rupture of gastric varices is 25 % (greater in IGV1 and GOV2)[3]

(v) Recurrent hemorrhage

  • Persistent increase in portal pressure leads to recurrence after treatment if the underlying cause is not addressed

Correlation between severity of cirrhosis and progression of varices

The following factors are associated with progression from small to large varices, at the time of baseline endoscopy:[4][5]

  • Severe cirrhosis (Child-Pugh class B and C)
  • Alcoholic cirrhosis
  • Presence of red wale marks (defined as longitudinal dilated venules resembling whip marks on the variceal surface)
Child-Pugh Classification of the Severity of Cirrhosis
Clinical feature/laboratory finding Points*
1 2 3
Encephalopathy None Grade 1–2

   (or precipitant-induced)

Grade 3–4

   (chronic)

Ascites None Mild/Moderate

   (diuretic-responsive)

Tense

   (diuretic-refractory)

Bilirubin (mg/dL) <2 2–3 >3
Albumin (g/dL) >3.5 2.3–3.5 <2.8
Prothrombin time or international normalized ratio (INR) <4 4–6 >6
  <1.7 1.7–2.3 >2.3

Interpretation of Child-Pugh score

 5–6 points: Child A

7–9 points: Child B

10–15 points: Child C

Complications

Gastrointestinal varices may be complicated by the following:

Prognosis

Six-week mortality is used as a predictor of prognosis for variceal hemorrhage[9] The six-week mortality for variceal hemorrhage ranges from a low of 15% to a high of 25%[10][11]

AIMS65 score

The AIMS65 score is best predictor of mortality in patients with variceal bleeding. The score is calculated as follows:

Variable Score
Albumin 1
INR 1
Systolic blood pressure 1
Altered mental status 1
Age > 65 years 1

Interpretation of AIMS65 score

Score 0 = No risk

Score 1-2 = Moderate risk

Score > 2 = High risk

References

  1. ↑ García-Pagán, Juan C; Bosch, Jaime (2003). "Prevention of variceal rebleeding". The Lancet. 361 (9376): 2245. doi:10.1016/S0140-6736(03)13750-6. ISSN 0140-6736.
  2. ↑ "www.journal-of-hepatology.eu".
  3. ↑ Menasherian-Yaccobe L, Jaqua NT, Kenny P (2013). "Successful treatment of bleeding gastric varices with splenectomy in a patient with splenic, portal, and mesenteric thromboses". Case Rep Surg. 2013: 273531. doi:10.1155/2013/273531. PMC 3776550. PMID 24078893.
  4. ↑ Merli M, Nicolini G, Angeloni S, Rinaldi V, De Santis A, Merkel C, Attili AF, Riggio O (2003). "Incidence and natural history of small esophageal varices in cirrhotic patients". J. Hepatol. 38 (3): 266–72. PMID 12586291.
  5. ↑ "Prediction of the First Variceal Hemorrhage in Patients with Cirrhosis of the Liver and Esophageal Varices". New England Journal of Medicine. 319 (15): 983–989. 1988. doi:10.1056/NEJM198810133191505. ISSN 0028-4793.
  6. ↑ Jaspersen D, Schwacha H, Sauer B, Wzatek J, Schorr W, Graf zu Dohna P, Hammar CH (1995). "[Complications of endoscopic sclerotherapy of esophageal varices]". Leber Magen Darm (in German). 25 (4): 171–4. PMID 7564871.
  7. ↑ Pillay P, Starzl TE, Van Thiel DH (1990). "Complications of sclerotherapy for esophageal varices in liver transplant candidates". Transplant. Proc. 22 (5): 2149–51. PMC 2952499. PMID 2219326.
  8. ↑ Hunter GC, Steinkirchner T, Burbige EJ, Guernsey JM, Putnam CW (1988). "Venous complications of sclerotherapy for esophageal varices". Am. J. Surg. 156 (6): 497–501. PMID 3264465.
  9. ↑ de Franchis R (2015). "Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension". J. Hepatol. 63 (3): 743–52. doi:10.1016/j.jhep.2015.05.022. PMID 26047908.
  10. ↑ Reverter E, Tandon P, Augustin S, Turon F, Casu S, Bastiampillai R, Keough A, Llop E, González A, Seijo S, Berzigotti A, Ma M, Genescà J, Bosch J, García-Pagán JC, Abraldes JG (2014). "A MELD-based model to determine risk of mortality among patients with acute variceal bleeding". Gastroenterology. 146 (2): 412–19.e3. doi:10.1053/j.gastro.2013.10.018. PMID 24148622.
  11. ↑ Amitrano L, Guardascione MA, Manguso F, Bennato R, Bove A, DeNucci C, Lombardi G, Martino R, Menchise A, Orsini L, Picascia S, Riccio E (2012). "The effectiveness of current acute variceal bleed treatments in unselected cirrhotic patients: refining short-term prognosis and risk factors". Am. J. Gastroenterol. 107 (12): 1872–8. doi:10.1038/ajg.2012.313. PMID 23007003.
  12. ↑ Tandon P, Abraldes JG, Keough A, Bastiampillai R, Jayakumar S, Carbonneau M, Wong E, Kao D, Bain VG, Ma M (2015). "Risk of Bacterial Infection in Patients With Cirrhosis and Acute Variceal Hemorrhage, Based on Child-Pugh Class, and Effects of Antibiotics". Clin. Gastroenterol. Hepatol. 13 (6): 1189–96.e2. doi:10.1016/j.cgh.2014.11.019. PMID 25460564.
  13. ↑ Abraldes JG, Villanueva C, Bañares R, Aracil C, Catalina MV, Garci A-Pagán JC, Bosch J (2008). "Hepatic venous pressure gradient and prognosis in patients with acute variceal bleeding treated with pharmacologic and endoscopic therapy". J. Hepatol. 48 (2): 229–36. doi:10.1016/j.jhep.2007.10.008. PMID 18093686.
  14. ↑ Everhart JE, Lok AS, Kim HY, Morgan TR, Lindsay KL, Chung RT, Bonkovsky HL, Ghany MG (2009). "Weight-related effects on disease progression in the hepatitis C antiviral long-term treatment against cirrhosis trial". Gastroenterology. 137 (2): 549–57. doi:10.1053/j.gastro.2009.05.007. PMC 3148692. PMID 19445938.
  15. ↑ Berzigotti A, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Morillas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Groszmann RJ (2011). "Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis". Hepatology. 54 (2): 555–61. doi:10.1002/hep.24418. PMC 3144991. PMID 21567436.
  16. ↑ Marcellin P, Gane E, Buti M, Afdhal N, Sievert W, Jacobson IM, Washington MK, Germanidis G, Flaherty JF, Aguilar Schall R, Bornstein JD, Kitrinos KM, Subramanian GM, McHutchison JG, Heathcote EJ (2013). "Regression of cirrhosis during treatment with tenofovir disoproxil fumarate for chronic hepatitis B: a 5-year open-label follow-up study". Lancet. 381 (9865): 468–75. doi:10.1016/S0140-6736(12)61425-1. PMID 23234725.
  17. ↑ Monto A, Patel K, Bostrom A, Pianko S, Pockros P, McHutchison JG, Wright TL (2004). "Risks of a range of alcohol intake on hepatitis C-related fibrosis". Hepatology. 39 (3): 826–34. doi:10.1002/hep.20127. PMID 14999703.
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