Portal hypertension natural history, complications and prognosis

Revision as of 18:10, 1 November 2017 by Eiman (talk | contribs)
Jump to navigation Jump to search

Portal Hypertension Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Portal Hypertension 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

CT

MRI

Echocardiography and Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Portal hypertension 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 Portal hypertension 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 Portal hypertension natural history, complications and prognosis

CDC on Portal hypertension natural history, complications and prognosis

Portal hypertension natural history, complications and prognosis in the news

Blogs on Portal hypertension natural history, complications and prognosis

Directions to Hospitals Treating Portal hypertension

Risk calculators and risk factors for Portal hypertension natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Natural History, Complications, and Prognosis

  • Portal hypertension is increased hepatic venous pressure gradient (HVPG) above 5 mmHg.
  • 90% of the cases are due to hepatic cirrhosis.[1]
  • The stage of cirrhosis severity is determined base on Child-Pugh-Turcotte (CPT) scoring system, including Child A if 5-6 points, Child B if 7-9 points, and Child C if 10-15 points.
Parameter Points
1 2 3
Ascites None Mild/Moderate Tense
Hepatic encephalopathy None Grade 1-2 Grade 3-4
Bilirubin μMol/L (mg/dL) <34.2 (<2) 34.2–51.3 (2-3) >51.3 (>3)
Albumin g/L (g/dL) >35 (>3.5) 28–35 (2.8–3.5) <28 (<2.8)
PT (Sec)

or

INR

<4 4–6 >6
<1.7 1.7–2.3 >2.3

Natural History

  • The symptoms of portal hypertension usually develop in the third and fourth decades of life, and generally start with symptoms such as esophageal varices, caput medusae, spider angioma, and splenomegaly.
  • The HVPG threshold for portal hypertension to become clinically symptomatic is 10-12mm Hg.[2]
  • Esophageal varices occur when the HVPG reaches 10 mmHg. 40% of Child A and 85% of Child C cirrhosis may progress to esophageal varices.[3]
  • Esophageal varices are typically developed 5-15% per year after cirrhosis. Most of the cirrhotic patients will develop the varices during the lifetime.[1]
  • Esophageal varices enlarge and progress about 8% per year.[4] The varices are bleeding 5-15% per year.[5]


 
 
 
Gastroesophageal varices type 1, via Wikipedia.org
 
 
 
 
Gastroesophageal varices type 2, via Wikipedia.org
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Gastroesophageal varices type 1
Extend along the lesser curvature
 
 
 
 
Gastroesophageal varices type 2
Extend along the fundus
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Isolated gastric varices type 1, via Wikipedia.org
 
 
 
 
Isolated gastric varices type 2, via Wikipedia.org
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Isolated gastric varices type 1
Located in the fundus and tend to be tortuous and complex
 
 
 
 
Isolated gastric varices
Located in the body, antrum, or around the pylorus
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  • Approximately 60% of patients with cirrhosis develop ascites in 10 years.[6]
  • At least 1500 cc ascites is necessary to become identifiable through physical exam. The severe increase in intra-abdominal pressure may lead to respiratory problems or abdominal hernias.[7]
  • 10% of hospitalized patients with cirrhosis will involve in spantanous bacterial peritonitis (SBP).[8]
  • If left untreated, 20-40% of patients with SBP may progress to death.[9]
  • Hepatorenal syndrome incidence rate in cirrhotic patients is 20% in 1 year and 40% in 5 years period.[10]
  • If left untreated, 100% of patients with type 1 hepatorenal syndrome may progress to death.[11]
  • If left untreated, most of the patients with portal hypertension and cirrhosis may progress to hepatic encephalopathy.

Complications

Prognosis

  • The presence of variceal bleeding, spontaneous bacterial peritonitis, and hepatorenal syndrome are associated with a particularly poor prognosis among patients with portal hypertension. They are the leading causes of death among patients with portal hypertension.
  • When esophageal varices bleed the average rate of 6-week mortality become ≥ 20%, despite improved therapies.[12]
  • When ascites occurs the 2-year mortality rate become 50%, without liver transplantation.[13]
  • When SBP occurs the mortality rate of 20-40% is expected.[9]
  • Prognosis is generally very poor in type 1 hepatorenal syndrome, all of them would die despite appropriate treatments.[11]

References

  1. 1.0 1.1 Al-Busafi, Said A.; McNabb-Baltar, Julia; Farag, Amanda; Hilzenrat, Nir (2012). "Clinical Manifestations of Portal Hypertension". International Journal of Hepatology. 2012: 1–10. doi:10.1155/2012/203794. ISSN 2090-3448.
  2. Groszmann, Roberto J.; Garcia-Tsao, Guadalupe; Bosch, Jaime; Grace, Norman D.; Burroughs, Andrew K.; Planas, Ramon; Escorsell, Angels; Garcia-Pagan, Juan Carlos; Patch, David; Matloff, Daniel S.; Gao, Hong; Makuch, Robert (2005). "Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis". New England Journal of Medicine. 353 (21): 2254–2261. doi:10.1056/NEJMoa044456. ISSN 0028-4793.
  3. Garcia-Tsao, Guadalupe; Groszmann, Roberto J.; Fisher, Rosemarie L.; Conn, Harold O.; Atterbury, Colin E.; Glickman, Morton (1985). "Portal pressure, presence of gastroesophageal varices and variceal bleeding". Hepatology. 5 (3): 419–424. doi:10.1002/hep.1840050313. ISSN 0270-9139.
  4. Merli, Manuela; Nicolini, Giorgia; Angeloni, Stefania; Rinaldi, Vittorio; De Santis, Adriano; Merkel, Carlo; Attili, Adolfo Francesco; Riggio, Oliviero (2003). "Incidence and natural history of small esophageal varices in cirrhotic patients". Journal of Hepatology. 38 (3): 266–272. doi:10.1016/S0168-8278(02)00420-8. ISSN 0168-8278.
  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. Ginés, Pere; Quintero, Enrique; Arroyo, Vicente; Terés, Josep; Bruguera, Miguel; Rimola, Antoni; Caballería, Joan; Rodés, Joan; Rozman, Ciril (1987). "Compensated cirrhosis: Natural history and prognostic factors". Hepatology. 7 (1): 122–128. doi:10.1002/hep.1840070124. ISSN 0270-9139.
  7. Cárdenas, Andrés; Arroyo, Vicente (2003). "Mechanisms of water and sodium retention in cirrhosis and the pathogenesis of ascites". Best Practice & Research Clinical Endocrinology & Metabolism. 17 (4): 607–622. doi:10.1016/S1521-690X(03)00052-6. ISSN 1521-690X.
  8. Nousbaum, Jean-Baptiste; Cadranel, Jean-François; Nahon, Pierre; Khac, Eric Nguyen; Moreau, Richard; Thévenot, Thierry; Silvain, Christine; Bureau, Christophe; Nouel, Olivier; Pilette, Christophe; Paupard, Thierry; Vanbiervliet, Geoffroy; Oberti, Frédéric; Davion, Thierry; Jouannaud, Vincent; Roche, Bruno; Bernard, Pierre-Henri; Beaulieu, Sandrine; Danne, Odile; Thabut, Dominique; Chagneau-Derrode, Carinne; de Lédinghen, Victor; Mathurin, Philippe; Pauwels, Arnaud; Bronowicki, Jean-Pierre; Habersetzer, François; Abergel, Armand; Audigier, Jean-Christian; Sapey, Thierry; Grangé, Jean-Didier; Tran, Albert (2007). "Diagnostic accuracy of the Multistix 8 SG reagent strip in diagnosis of spontaneous bacterial peritonitis". Hepatology. 45 (5): 1275–1281. doi:10.1002/hep.21588. ISSN 0270-9139.
  9. 9.0 9.1 Tandon P, Garcia-Tsao G (2008). "Bacterial infections, sepsis, and multiorgan failure in cirrhosis". Semin. Liver Dis. 28 (1): 26–42. doi:10.1055/s-2008-1040319. PMID 18293275.
  10. Ginès A, Escorsell A, Ginès P, Saló J, Jiménez W, Inglada L, Navasa M, Clària J, Rimola A, Arroyo V (1993). "Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites". Gastroenterology. 105 (1): 229–36. PMID 8514039.
  11. 11.0 11.1 Salerno, F.; Gerbes, A.; Gines, P.; Wong, F.; Arroyo, V. (2008). "Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis". Postgraduate Medical Journal. 84 (998): 662–670. doi:10.1136/gut.2006.107789. ISSN 0032-5473.
  12. D'Amico, G (2003). "Upper digestive bleeding in cirrhosis. Post-therapeutic outcome and prognostic indicators". Hepatology. 38 (3): 599–612. doi:10.1053/jhep.2003.50385. ISSN 0270-9139.
  13. D'amico, Gennaro; Morabito, Alberto; Pagliaro, Luigi; Marubini, Ettore (1986). "Survival and prognostic indicators in compensated and decompensated cirrhosis". Digestive Diseases and Sciences. 31 (5): 468–475. doi:10.1007/BF01320309. ISSN 0163-2116.

Template:WS Template:WH