Gastrointestinal varices natural history, complications and prognosis

Jump to navigation Jump to search

Gastrointestinal varices Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Gastrointestinal varices from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Guidelines for Management

Case Studies

Case #1

Gastrointestinal varices natural history, complications and prognosis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Gastrointestinal varices natural history, complications and prognosis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Gastrointestinal varices natural history, complications and prognosis

CDC on Gastrointestinal varices natural history, complications and prognosis

Gastrointestinal varices natural history, complications and prognosis in the news

Blogs on Gastrointestinal varices natural history, complications and prognosis

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Gastrointestinal varices natural history, complications and prognosis

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.