Portal hypertension natural history, complications and prognosis: Difference between revisions

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__NOTOC__
__NOTOC__
{{Portal hypertension}}
{{Portal hypertension}}
{{CMG}}; {{AE}}
{{CMG}}; {{AE}}{{EG}}


==Overview==
==Overview==
Portal hypertension is increased [[Hepatic vein|hepatic venous]] pressure gradient (HVPG) above 5 mmHg. The symptoms of portal hypertension usually develop in the third to fourth decades of life, and generally start with symptoms such as [[esophageal varices]], [[caput medusae]], [[spider angioma]], and [[splenomegaly]]. [[Esophageal varices]] typically developes at the rate of 5-15% per year in [[cirrhosis]] patients. Most of the [[Cirrhosis|cirrhotic]] patients will develop the [[varices]], atleast once during the lifetime. Approximately 60% of patients with [[cirrhosis]] develop [[ascites]] in 10 years. 10% of hospitalized patients with [[cirrhosis]] will involve in [[Spontaneous bacterial peritonitis|spontaneous bacterial peritonitis (SBP)]]. If left untreated, 20-40% of patients with [[SBP]] may progress to death. 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.


==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
* Portal hypertension is increased hepatic venous pressure gradient (HVPG) above 5 mmHg.  
* Portal hypertension is increased [[Hepatic vein|hepatic venous]] pressure gradient (HVPG) above 5 mmHg.  
* 90% of the cases are due to hepatic cirrhosis.<ref name="Al-BusafiMcNabb-Baltar2012">{{cite journal|last1=Al-Busafi|first1=Said A.|last2=McNabb-Baltar|first2=Julia|last3=Farag|first3=Amanda|last4=Hilzenrat|first4=Nir|title=Clinical Manifestations of Portal Hypertension|journal=International Journal of Hepatology|volume=2012|year=2012|pages=1–10|issn=2090-3448|doi=10.1155/2012/203794}}</ref>
* 90% of the cases are due to [[hepatic cirrhosis]].<ref name="Al-BusafiMcNabb-Baltar2012">{{cite journal|last1=Al-Busafi|first1=Said A.|last2=McNabb-Baltar|first2=Julia|last3=Farag|first3=Amanda|last4=Hilzenrat|first4=Nir|title=Clinical Manifestations of Portal Hypertension|journal=International Journal of Hepatology|volume=2012|year=2012|pages=1–10|issn=2090-3448|doi=10.1155/2012/203794}}</ref>
* 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.
* The stage of [[cirrhosis]] severity is determined base on [[Child-Pugh score|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.
<div align="center">
<div align="center">
{| class="wikitable"
{|
! rowspan="2" |Parameter
! rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Parameter
! colspan="3" |Points
! colspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" + |Points
|-
|-
!1
! style="background:#4479BA; color: #FFFFFF;" align="center" + |1
!2
! style="background:#4479BA; color: #FFFFFF;" align="center" + |2
!3
! style="background:#4479BA; color: #FFFFFF;" align="center" + |3
|-
|-
|Ascites
| style="background:#DCDCDC;" align="center" + |[[Ascites]]
|None
| style="background:#F5F5F5;" align="center" + |None
|Mild/Moderate
| style="background:#F5F5F5;" align="center" + |Mild/Moderate
|Tense
| style="background:#F5F5F5;" align="center" + |Tense
|-
|-
|Hepatic encephalopathy
| style="background:#DCDCDC;" align="center" + |[[Hepatic encephalopathy]]
|None
| style="background:#F5F5F5;" align="center" + |None
|Grade 1-2
| style="background:#F5F5F5;" align="center" + |Grade 1-2
|Grade 3-4
| style="background:#F5F5F5;" align="center" + |Grade 3-4
|-
|-
|Bilirubin μMol/L (mg/dL)
| style="background:#DCDCDC;" align="center" + |[[Bilirubin]] μMol/L (mg/dL)
|<34.2 (<2)
| style="background:#F5F5F5;" align="center" + |<34.2 (<2)
|34.2–51.3 (2-3)
| style="background:#F5F5F5;" align="center" + |34.2–51.3 (2-3)
|>51.3 (>3)
| style="background:#F5F5F5;" align="center" + |>51.3 (>3)
|-
|-
|Albumin g/L (g/dL)
| style="background:#DCDCDC;" align="center" + |[[Albumin]] g/L (g/dL)
|>35 (>3.5)
| style="background:#F5F5F5;" align="center" + |>35 (>3.5)
|28–35 (2.8–3.5)
| style="background:#F5F5F5;" align="center" + |28–35 (2.8–3.5)
|<28 (<2.8)
| style="background:#F5F5F5;" align="center" + |<28 (<2.8)
|-
|-
| rowspan="2" |PT (Sec)  
| rowspan="2" style="background:#DCDCDC;" align="center" + |[[Prothrombin time|PT]] (Sec)<br>or<br>[[INR]]
 
| style="background:#F5F5F5;" align="center" + |<4
or
| style="background:#F5F5F5;" align="center" + |4–6
 
| style="background:#F5F5F5;" align="center" + |>6
INR
|<4
|4–6
|>6
|-
|-
|<1.7
| style="background:#F5F5F5;" align="center" + |<1.7
|1.7–2.3
| style="background:#F5F5F5;" align="center" + |1.7–2.3
|>2.3
| style="background:#F5F5F5;" align="center" + |>2.3
|}
|}
</div>
</div>


===Natural History===
===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 symptoms of portal hypertension usually develop in the third to 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.<ref name="GroszmannGarcia-Tsao2005">{{cite journal|last1=Groszmann|first1=Roberto J.|last2=Garcia-Tsao|first2=Guadalupe|last3=Bosch|first3=Jaime|last4=Grace|first4=Norman D.|last5=Burroughs|first5=Andrew K.|last6=Planas|first6=Ramon|last7=Escorsell|first7=Angels|last8=Garcia-Pagan|first8=Juan Carlos|last9=Patch|first9=David|last10=Matloff|first10=Daniel S.|last11=Gao|first11=Hong|last12=Makuch|first12=Robert|title=Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis|journal=New England Journal of Medicine|volume=353|issue=21|year=2005|pages=2254–2261|issn=0028-4793|doi=10.1056/NEJMoa044456}}</ref>
*The [[hepatic vein]] [[pressure gradient]] (HVPG) threshold for portal hypertension to become clinically [[symptomatic]] is 10-12mm Hg.<ref name="GroszmannGarcia-Tsao2005">{{cite journal|last1=Groszmann|first1=Roberto J.|last2=Garcia-Tsao|first2=Guadalupe|last3=Bosch|first3=Jaime|last4=Grace|first4=Norman D.|last5=Burroughs|first5=Andrew K.|last6=Planas|first6=Ramon|last7=Escorsell|first7=Angels|last8=Garcia-Pagan|first8=Juan Carlos|last9=Patch|first9=David|last10=Matloff|first10=Daniel S.|last11=Gao|first11=Hong|last12=Makuch|first12=Robert|title=Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis|journal=New England Journal of Medicine|volume=353|issue=21|year=2005|pages=2254–2261|issn=0028-4793|doi=10.1056/NEJMoa044456}}</ref>
*Esophageal varices occur when the HVPG reaches 10 mmHg. 40% of Child A and 85% of Child C cirrhosis may progress to esophageal varices.<ref name="Garcia-TsaoGroszmann1985">{{cite journal|last1=Garcia-Tsao|first1=Guadalupe|last2=Groszmann|first2=Roberto J.|last3=Fisher|first3=Rosemarie L.|last4=Conn|first4=Harold O.|last5=Atterbury|first5=Colin E.|last6=Glickman|first6=Morton|title=Portal pressure, presence of gastroesophageal varices and variceal bleeding|journal=Hepatology|volume=5|issue=3|year=1985|pages=419–424|issn=02709139|doi=10.1002/hep.1840050313}}</ref>  
*[[Esophageal varices]] occur when the HVPG reaches 10 mmHg. 40% of Child A and 85% of Child C [[cirrhosis]] may progress to [[esophageal varices]].<ref name="Garcia-TsaoGroszmann1985">{{cite journal|last1=Garcia-Tsao|first1=Guadalupe|last2=Groszmann|first2=Roberto J.|last3=Fisher|first3=Rosemarie L.|last4=Conn|first4=Harold O.|last5=Atterbury|first5=Colin E.|last6=Glickman|first6=Morton|title=Portal pressure, presence of gastroesophageal varices and variceal bleeding|journal=Hepatology|volume=5|issue=3|year=1985|pages=419–424|issn=02709139|doi=10.1002/hep.1840050313}}</ref>  
*Esophageal varices are typically developed 5-15% per year after cirrhosis. Most of the cirrhotic patients will develop the varices during the lifetime.<ref name="Al-BusafiMcNabb-Baltar2012" />
*[[Esophageal varices]] typically developes at the rate of 5-15% per year in [[cirrhosis]] patients.Most of the [[Cirrhosis|cirrhotic]] patients will develop the [[varices]], atleast once during the lifetime.<ref name="Al-BusafiMcNabb-Baltar2012" />
*Esophageal varices enlarge and progress about 8% per year.<ref name="MerliNicolini2003">{{cite journal|last1=Merli|first1=Manuela|last2=Nicolini|first2=Giorgia|last3=Angeloni|first3=Stefania|last4=Rinaldi|first4=Vittorio|last5=De Santis|first5=Adriano|last6=Merkel|first6=Carlo|last7=Attili|first7=Adolfo Francesco|last8=Riggio|first8=Oliviero|title=Incidence and natural history of small esophageal varices in cirrhotic patients|journal=Journal of Hepatology|volume=38|issue=3|year=2003|pages=266–272|issn=01688278|doi=10.1016/S0168-8278(02)00420-8}}</ref> The varices are bleeding 5-15% per year.<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>
*[[Esophageal varices]] enlarge and progress at the rate of 8% per year.<ref name="MerliNicolini2003">{{cite journal|last1=Merli|first1=Manuela|last2=Nicolini|first2=Giorgia|last3=Angeloni|first3=Stefania|last4=Rinaldi|first4=Vittorio|last5=De Santis|first5=Adriano|last6=Merkel|first6=Carlo|last7=Attili|first7=Adolfo Francesco|last8=Riggio|first8=Oliviero|title=Incidence and natural history of small esophageal varices in cirrhotic patients|journal=Journal of Hepatology|volume=38|issue=3|year=2003|pages=266–272|issn=01688278|doi=10.1016/S0168-8278(02)00420-8}}</ref> The [[varices]] [[Bleed|bleeds]] at the rate of 5-15% per year.<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>
<br>
<br>
<div align="center">
<div align="center">
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</div>


*Approximately 60% of patients with cirrhosis develop [[ascites]] in 10 years.<ref name="GinésQuintero1987">{{cite journal|last1=Ginés|first1=Pere|last2=Quintero|first2=Enrique|last3=Arroyo|first3=Vicente|last4=Terés|first4=Josep|last5=Bruguera|first5=Miguel|last6=Rimola|first6=Antoni|last7=Caballería|first7=Joan|last8=Rodés|first8=Joan|last9=Rozman|first9=Ciril|title=Compensated cirrhosis: Natural history and prognostic factors|journal=Hepatology|volume=7|issue=1|year=1987|pages=122–128|issn=02709139|doi=10.1002/hep.1840070124}}</ref>
*Approximately 60% of patients with [[cirrhosis]] develop [[ascites]] in 10 years.<ref name="GinésQuintero1987">{{cite journal|last1=Ginés|first1=Pere|last2=Quintero|first2=Enrique|last3=Arroyo|first3=Vicente|last4=Terés|first4=Josep|last5=Bruguera|first5=Miguel|last6=Rimola|first6=Antoni|last7=Caballería|first7=Joan|last8=Rodés|first8=Joan|last9=Rozman|first9=Ciril|title=Compensated cirrhosis: Natural history and prognostic factors|journal=Hepatology|volume=7|issue=1|year=1987|pages=122–128|issn=02709139|doi=10.1002/hep.1840070124}}</ref>
*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.<ref name="CárdenasArroyo2003">{{cite journal|last1=Cárdenas|first1=Andrés|last2=Arroyo|first2=Vicente|title=Mechanisms of water and sodium retention in cirrhosis and the pathogenesis of ascites|journal=Best Practice & Research Clinical Endocrinology & Metabolism|volume=17|issue=4|year=2003|pages=607–622|issn=1521690X|doi=10.1016/S1521-690X(03)00052-6}}</ref>
*At least 1500 cc [[ascites]] is necessary to become identifiable through [[Physical examination|physical exam]]. The severe increase in intraabdominal [[pressure]] may lead to respiratory problems and/or [[Abdominal hernia|abdominal hernias]].<ref name="CárdenasArroyo2003">{{cite journal|last1=Cárdenas|first1=Andrés|last2=Arroyo|first2=Vicente|title=Mechanisms of water and sodium retention in cirrhosis and the pathogenesis of ascites|journal=Best Practice & Research Clinical Endocrinology & Metabolism|volume=17|issue=4|year=2003|pages=607–622|issn=1521690X|doi=10.1016/S1521-690X(03)00052-6}}</ref>
*10% of hospitalized patients with cirrhosis will involve in spantanous bacterial peritonitis (SBP).<ref name="NousbaumCadranel2007">{{cite journal|last1=Nousbaum|first1=Jean-Baptiste|last2=Cadranel|first2=Jean-François|last3=Nahon|first3=Pierre|last4=Khac|first4=Eric Nguyen|last5=Moreau|first5=Richard|last6=Thévenot|first6=Thierry|last7=Silvain|first7=Christine|last8=Bureau|first8=Christophe|last9=Nouel|first9=Olivier|last10=Pilette|first10=Christophe|last11=Paupard|first11=Thierry|last12=Vanbiervliet|first12=Geoffroy|last13=Oberti|first13=Frédéric|last14=Davion|first14=Thierry|last15=Jouannaud|first15=Vincent|last16=Roche|first16=Bruno|last17=Bernard|first17=Pierre-Henri|last18=Beaulieu|first18=Sandrine|last19=Danne|first19=Odile|last20=Thabut|first20=Dominique|last21=Chagneau-Derrode|first21=Carinne|last22=de Lédinghen|first22=Victor|last23=Mathurin|first23=Philippe|last24=Pauwels|first24=Arnaud|last25=Bronowicki|first25=Jean-Pierre|last26=Habersetzer|first26=François|last27=Abergel|first27=Armand|last28=Audigier|first28=Jean-Christian|last29=Sapey|first29=Thierry|last30=Grangé|first30=Jean-Didier|last31=Tran|first31=Albert|title=Diagnostic accuracy of the Multistix 8 SG reagent strip in diagnosis of spontaneous bacterial peritonitis|journal=Hepatology|volume=45|issue=5|year=2007|pages=1275–1281|issn=02709139|doi=10.1002/hep.21588}}</ref>
*Based on grade of [[cirrhosis]], international [[ascites]] club presented a grading system.<ref name="pmid12830009">{{cite journal |vauthors=Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R, Arroyo V |title=The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club |journal=Hepatology |volume=38 |issue=1 |pages=258–66 |year=2003 |pmid=12830009 |doi=10.1053/jhep.2003.50315 |url=}}</ref>
*If left untreated, 20-40% of patients with SBP may progress to death.<ref name="pmid18293275">{{cite journal |vauthors=Tandon P, Garcia-Tsao G |title=Bacterial infections, sepsis, and multiorgan failure in cirrhosis |journal=Semin. Liver Dis. |volume=28 |issue=1 |pages=26–42 |year=2008 |pmid=18293275 |doi=10.1055/s-2008-1040319 |url=}}</ref>
<br>
*Hepatorenal syndrome incidence rate in cirrhotic patients is 20% in 1 year and 40% in 5 years period.<ref name="pmid8514039">{{cite journal |vauthors=Ginès A, Escorsell A, Ginès P, Saló J, Jiménez W, Inglada L, Navasa M, Clària J, Rimola A, Arroyo V |title=Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites |journal=Gastroenterology |volume=105 |issue=1 |pages=229–36 |year=1993 |pmid=8514039 |doi= |url=}}</ref>
{| align="center"
*If left untreated, 100% of patients with type 1 hepatorenal syndrome may progress to death.<ref name="SalernoGerbes2008">{{cite journal|last1=Salerno|first1=F.|last2=Gerbes|first2=A.|last3=Gines|first3=P.|last4=Wong|first4=F.|last5=Arroyo|first5=V.|title=Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis|journal=Postgraduate Medical Journal|volume=84|issue=998|year=2008|pages=662–670|issn=0032-5473|doi=10.1136/gut.2006.107789}}</ref>
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Grade
*If left untreated, most of the patients with portal hypertension and cirrhosis may progress to hepatic encephalopathy.
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Definition
|-
| style="background:#DCDCDC;" align="center" + |Grade 1
| style="background:#F5F5F5;" + |Mild [[ascites]] only detectable by [[ultrasound]]
|-
| style="background:#DCDCDC;" align="center" + |Grade 2
| style="background:#F5F5F5;" + |Moderate [[ascites]] evident by moderate symmetrical distension of [[abdomen]]
|-
| style="background:#DCDCDC;" align="center" + |Grade 3
| style="background:#F5F5F5;" + |Large or gross [[ascites]] with marked [[abdominal distension]]
|}
 
*10% of hospitalized patients with [[cirrhosis]] will involve in [[Spontaneous bacterial peritonitis|spontaneous bacterial peritonitis (SBP)]].<ref name="NousbaumCadranel2007">{{cite journal|last1=Nousbaum|first1=Jean-Baptiste|last2=Cadranel|first2=Jean-François|last3=Nahon|first3=Pierre|last4=Khac|first4=Eric Nguyen|last5=Moreau|first5=Richard|last6=Thévenot|first6=Thierry|last7=Silvain|first7=Christine|last8=Bureau|first8=Christophe|last9=Nouel|first9=Olivier|last10=Pilette|first10=Christophe|last11=Paupard|first11=Thierry|last12=Vanbiervliet|first12=Geoffroy|last13=Oberti|first13=Frédéric|last14=Davion|first14=Thierry|last15=Jouannaud|first15=Vincent|last16=Roche|first16=Bruno|last17=Bernard|first17=Pierre-Henri|last18=Beaulieu|first18=Sandrine|last19=Danne|first19=Odile|last20=Thabut|first20=Dominique|last21=Chagneau-Derrode|first21=Carinne|last22=de Lédinghen|first22=Victor|last23=Mathurin|first23=Philippe|last24=Pauwels|first24=Arnaud|last25=Bronowicki|first25=Jean-Pierre|last26=Habersetzer|first26=François|last27=Abergel|first27=Armand|last28=Audigier|first28=Jean-Christian|last29=Sapey|first29=Thierry|last30=Grangé|first30=Jean-Didier|last31=Tran|first31=Albert|title=Diagnostic accuracy of the Multistix 8 SG reagent strip in diagnosis of spontaneous bacterial peritonitis|journal=Hepatology|volume=45|issue=5|year=2007|pages=1275–1281|issn=02709139|doi=10.1002/hep.21588}}</ref>
*If left untreated, 20-40% of patients with [[SBP]] may progress to death.<ref name="pmid18293275">{{cite journal |vauthors=Tandon P, Garcia-Tsao G |title=Bacterial infections, sepsis, and multiorgan failure in cirrhosis |journal=Semin. Liver Dis. |volume=28 |issue=1 |pages=26–42 |year=2008 |pmid=18293275 |doi=10.1055/s-2008-1040319 |url=}}</ref>
*[[Incidence]] of [[hepatorenal syndrome]] in [[Cirrhosis|cirrhotic]] patients is 20% in 1 year and 40% in 5 years period.<ref name="pmid8514039">{{cite journal |vauthors=Ginès A, Escorsell A, Ginès P, Saló J, Jiménez W, Inglada L, Navasa M, Clària J, Rimola A, Arroyo V |title=Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites |journal=Gastroenterology |volume=105 |issue=1 |pages=229–36 |year=1993 |pmid=8514039 |doi= |url=}}</ref>
*If left untreated, 100% of patients with type 1 [[hepatorenal syndrome]] may progress to death.<ref name="SalernoGerbes2008">{{cite journal|last1=Salerno|first1=F.|last2=Gerbes|first2=A.|last3=Gines|first3=P.|last4=Wong|first4=F.|last5=Arroyo|first5=V.|title=Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis|journal=Postgraduate Medical Journal|volume=84|issue=998|year=2008|pages=662–670|issn=0032-5473|doi=10.1136/gut.2006.107789}}</ref>
*If left untreated, most of the patients with portal hypertension and [[cirrhosis]] may progress to [[hepatic encephalopathy]].
<br>
<div align="center">'''Grading for different stages of [[hepatic encephalopathy]], called West Haven Criteria'''<ref name="pmid11870389">{{cite journal |vauthors=Ferenci P, Lockwood A, Mullen K, Tarter R, Weissenborn K, Blei AT |title=Hepatic encephalopathy--definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1998 |journal=Hepatology |volume=35 |issue=3 |pages=716–21 |year=2002 |pmid=11870389 |doi=10.1053/jhep.2002.31250 |url=}}</ref></div>
{{family tree/start}}
{{family tree| | | | | | | | B01 | | | | | | | |B01='''West Haven Criteria'''<br>hepatic encephalopathy grading}}
{{family tree| | |,|-|-|-|v|-|^|-|v|-|-|-|.| | |}}
{{family tree| | C01 | | C02 | | C03 | | C04 | |C01='''''Grade 1'''''|C02='''''Grade 2'''''|C03='''''Grade 3'''''|C04='''''Grade 4'''''}}
{{family tree| | |!| | | |!| | | |!| | | |!| | |}}
{{family tree| boxstyle=text-align: left;| | D01 | | D02 | | D03 | | D04 | |D01=•Mild loss of consciousness<br>•[[Euphoria]] or [[anxiety]] <br>• Lowered attention span<br>•Impaired performance of addition|D02=•[[Lethargy]] or [[apathy]]<br>•Minimal [[disorientation]] to time and place<br>•Subtle [[personality]] change<br>•Inappropriate behavior<br>•Impaired performance of subtraction|D03=•[[Somnolence]] to semi-[[stupor]], but<br>responsive to verbal stimuli<br>•[[Confusion]]<br>•Gross [[disorientation]]|D04=•[[Coma]] (unresponsive to verbal<br>or noxious stimuli)
}}
{{family tree/end}}
 
===Complications===
===Complications===
*Common complications of portal hypertension include:
*Common complications of portal hypertension include:<ref name="pmid17414843">{{cite journal |vauthors=Blei AT |title=Portal hypertension and its complications |journal=Curr. Opin. Gastroenterol. |volume=23 |issue=3 |pages=275–82 |year=2007 |pmid=17414843 |doi=10.1097/MOG.0b013e3280b0841f |url=}}</ref>
**[[Spontaneous bacterial peritonitis]]
**[[Spontaneous bacterial peritonitis]]
** [[Hepatorenal syndrome]]
** [[Hepatorenal syndrome]]
** [[Hepatic encephalopathy]]
** [[Hepatic encephalopathy]]
** [[Congestive gastropathy]]
** Congestive gastropathy
** [[Hypersplenism]]
** [[Hypersplenism]]
** [[Ascites]]
** [[Ascites]]
** [[Variceal bleeding]]
** [[Variceal bleeding]]
** [[Renal failure]]
** [[Renal failure]]
** Hepatic hydrothorax
** [[Liver|Hepatic]] [[hydrothorax]]
** Hepatopulmonary syndrome
** [[Hepatopulmonary syndrome]]
** Portopulmonary hypertension
** [[Portopulmonary hypertension]]
** Cirrhotic cardiomyopathy
** [[Cirrhosis|Cirrhotic]] [[cardiomyopathy]]
===Prognosis===
===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.
*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.<ref name="D'Amico2003">{{cite journal|last1=D'Amico|first1=G|title=Upper digestive bleeding in cirrhosis. Post-therapeutic outcome and prognostic indicators|journal=Hepatology|volume=38|issue=3|year=2003|pages=599–612|issn=02709139|doi=10.1053/jhep.2003.50385}}</ref>
*When [[esophageal varices]] bleed the average rate of 6-week [[Mortality rate|mortality]] become ≥ 20%, despite improved therapies.<ref name="D'Amico2003">{{cite journal|last1=D'Amico|first1=G|title=Upper digestive bleeding in cirrhosis. Post-therapeutic outcome and prognostic indicators|journal=Hepatology|volume=38|issue=3|year=2003|pages=599–612|issn=02709139|doi=10.1053/jhep.2003.50385}}</ref>
*When ascites occurs the 2-year mortality rate become 50%, without liver transplantation.<ref name="D'amicoMorabito19862">{{cite journal|last1=D'amico|first1=Gennaro|last2=Morabito|first2=Alberto|last3=Pagliaro|first3=Luigi|last4=Marubini|first4=Ettore|title=Survival and prognostic indicators in compensated and decompensated cirrhosis|journal=Digestive Diseases and Sciences|volume=31|issue=5|year=1986|pages=468–475|issn=0163-2116|doi=10.1007/BF01320309}}</ref>
*When [[ascites]] occurs the 2-year [[mortality]] rate become 50%, without [[liver transplantation]].<ref name="D'amicoMorabito19862">{{cite journal|last1=D'amico|first1=Gennaro|last2=Morabito|first2=Alberto|last3=Pagliaro|first3=Luigi|last4=Marubini|first4=Ettore|title=Survival and prognostic indicators in compensated and decompensated cirrhosis|journal=Digestive Diseases and Sciences|volume=31|issue=5|year=1986|pages=468–475|issn=0163-2116|doi=10.1007/BF01320309}}</ref>
*When SBP occurs the mortality rate of 20-40% is expected.<ref name="pmid18293275" />
*When [[SBP]] occurs the [[mortality rate]] of 20-40% is expected.<ref name="pmid18293275" />
*Prognosis is generally very poor in type 1 hepatorenal syndrome, all of them would die despite appropriate treatments.<ref name="SalernoGerbes2008" />
*[[Prognosis]] is generally very poor in type 1 [[hepatorenal syndrome]], all of them would die despite appropriate treatments.<ref name="SalernoGerbes2008" />
*General [[prognosis]] in cirrhotic patients is as follows:
{{family tree/start}}
{{family tree|boxstyle=text-align: left; | | | | | | | | | | |,| A01 |-| A02 | |A01=HVPG of 10 mmHg|A02=• Gastroesophageal [[varices]]<br>• [[Hepatocellular carcinoma]]<br>• Decompensation after [[hepatocellular carcinoma]] resection}}
{{family tree| | | | | | | | | | |!| | | | | | | | |}}
{{family tree|boxstyle=text-align: left; | | | | | | |,| B01 |+| B02 |-| B03 | |B01='''''Compensated [[cirrhosis]]'''''|B02=HVPG of 12 mmHg|B03=• [[varices|Variceal]] [[bleeding]]}}
{{family tree| | | | | | |!| | | |!| | | | | | | | |}}
{{family tree|boxstyle=text-align: left; | | | | | | |!| | | |`| C01 |-| C02 | |C01=HVPG of 16 mmHg|C02=• First decompensation after [[varices]]<br>• [[Mortality]]}}
{{family tree| | | | | | |!| | | | | | | | | | | | |}}
{{family tree| | | | D01 |(| | | | | | | | | | | | |D01='''Prognostic significance of <br>HVPG in cirrhotic patients'''}}
{{family tree|boxstyle=text-align: left; | | | | | | |!| | | |,| D02 |-| D03 | |D02=HVPG of 16 mmHg|D03=• [[varices|Variceal]] rebleeding<br>• [[Mortality]]}}
{{family tree| | | | | | |!| | | |!| | | | | | | | |}}
{{family tree|boxstyle=text-align: left; | | | | | | |!| | | |)| E01 |-| E02 | |E01=HVPG of 20 mmHg|E02=• Uncontrollable active [[varices|variceal]] [[bleeding]]<br>• Low 1-year survival}}
{{family tree| | | | | | |`| F01 |(| | | | | | | | |F01='''''Decompensated [[cirrhosis]]'''''}}
{{family tree|boxstyle=text-align: left; | | | | | | | | | | |)| F01 |-| F02 | |F01=HVPG of 22 mmHg|F02=• [[Mortality]] in [[alcoholic cirrhosis]] and acute [[alcoholic hepatitis]]}}
{{family tree| | | | | | | | | | |!| | | | | | | | |}}
{{family tree|boxstyle=text-align: left; | | | | | | | | | | |`| G01 |-| G02 | |G01=HVPG of 30 mmHg|G02=• [[Spontaneous bacterial peritonitis|Spontaneous bacterial peritonitis (SBP)]]}}
 
{{family tree/end}}
 
==References==
==References==
{{reflist|2}}
{{reflist|2}}


[[Category:Gastroenterology]]
[[Category:Gastroenterology]]
[[Category:Hepatology]]
[[Category:Hepatology]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:needs content]]
[[Category:Emergency medicine]]
[[Category:Needs overview]]
[[Category:Up-To-Date]]


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Latest revision as of 14:11, 7 December 2017

Portal Hypertension Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Overview

Portal hypertension is increased hepatic venous pressure gradient (HVPG) above 5 mmHg. The symptoms of portal hypertension usually develop in the third to fourth decades of life, and generally start with symptoms such as esophageal varices, caput medusae, spider angioma, and splenomegaly. Esophageal varices typically developes at the rate of 5-15% per year in cirrhosis patients. Most of the cirrhotic patients will develop the varices, atleast once during the lifetime. Approximately 60% of patients with cirrhosis develop ascites in 10 years. 10% of hospitalized patients with cirrhosis will involve in spontaneous bacterial peritonitis (SBP). If left untreated, 20-40% of patients with SBP may progress to death. 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.

Natural History, Complications, and Prognosis

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


 
 
 
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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 


Grade Definition
Grade 1 Mild ascites only detectable by ultrasound
Grade 2 Moderate ascites evident by moderate symmetrical distension of abdomen
Grade 3 Large or gross ascites with marked abdominal distension


Grading for different stages of hepatic encephalopathy, called West Haven Criteria[13]
 
 
 
 
 
 
 
West Haven Criteria
hepatic encephalopathy grading
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Grade 1
 
Grade 2
 
Grade 3
 
Grade 4
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
•Mild loss of consciousness
•Euphoria or anxiety
• Lowered attention span
•Impaired performance of addition
 
•Lethargy or apathy
•Minimal disorientation to time and place
•Subtle personality change
•Inappropriate behavior
•Impaired performance of subtraction
 
•Somnolence to semi-stupor, but
responsive to verbal stimuli
•Confusion
•Gross disorientation
 
•Coma (unresponsive to verbal
or noxious stimuli)
 

Complications

Prognosis

 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 10 mmHg
 
• Gastroesophageal varices
• Hepatocellular carcinoma
• Decompensation after hepatocellular carcinoma resection
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Compensated cirrhosis
 
 
HVPG of 12 mmHg
 
• Variceal bleeding
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 16 mmHg
 
• First decompensation after varices
• Mortality
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Prognostic significance of
HVPG in cirrhotic patients
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 16 mmHg
 
• Variceal rebleeding
• Mortality
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 20 mmHg
 
• Uncontrollable active variceal bleeding
• Low 1-year survival
 
 
 
 
 
 
 
 
 
 
 
Decompensated cirrhosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 22 mmHg
 
• Mortality in alcoholic cirrhosis and acute alcoholic hepatitis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HVPG of 30 mmHg
 
• Spontaneous bacterial peritonitis (SBP)
 
 
 

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. ↑ Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R, Arroyo V (2003). "The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club". Hepatology. 38 (1): 258–66. doi:10.1053/jhep.2003.50315. PMID 12830009.
  9. ↑ 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.
  10. ↑ 10.0 10.1 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.
  11. ↑ 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.
  12. ↑ 12.0 12.1 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.
  13. ↑ Ferenci P, Lockwood A, Mullen K, Tarter R, Weissenborn K, Blei AT (2002). "Hepatic encephalopathy--definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1998". Hepatology. 35 (3): 716–21. doi:10.1053/jhep.2002.31250. PMID 11870389.
  14. ↑ Blei AT (2007). "Portal hypertension and its complications". Curr. Opin. Gastroenterol. 23 (3): 275–82. doi:10.1097/MOG.0b013e3280b0841f. PMID 17414843.
  15. ↑ 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.
  16. ↑ 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.

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