Cirrhosis natural history, complications and prognosis: Difference between revisions
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===Natural History=== | ===Natural History=== | ||
*The symptoms of cirrhosis usually develop in the fourth or fifth decade of life, and start with symptoms such as [[fever]], [[anorexia]], [[fatigue]], [[weakness]], [[nausea]], [[vomiting]], [[weight loss]] and [[jaundice]].<ref name="pmid25203153">{{cite journal |vauthors=Sajja KC, Mohan DP, Rockey DC |title=Age and ethnicity in cirrhosis |journal=J. Investig. Med. |volume=62 |issue=7 |pages=920–6 |year=2014 |pmid=25203153 |pmc=4172494 |doi=10.1097/JIM.0000000000000106 |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid18328931">{{cite journal |vauthors=Schuppan D, Afdhal NH |title=Liver cirrhosis |journal=Lancet |volume=371 |issue=9615 |pages=838–51 |year=2008 |pmid=18328931 |pmc=2271178 |doi=10.1016/S0140-6736(08)60383-9 |url=}}</ref> | *The symptoms of cirrhosis usually develop in the fourth or fifth decade of life, and start with symptoms such as [[fever]], [[anorexia]], [[fatigue]], [[weakness]], [[nausea]], [[vomiting]], [[weight loss]] and [[jaundice]].<ref name="pmid25203153">{{cite journal |vauthors=Sajja KC, Mohan DP, Rockey DC |title=Age and ethnicity in cirrhosis |journal=J. Investig. Med. |volume=62 |issue=7 |pages=920–6 |year=2014 |pmid=25203153 |pmc=4172494 |doi=10.1097/JIM.0000000000000106 |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid18328931">{{cite journal |vauthors=Schuppan D, Afdhal NH |title=Liver cirrhosis |journal=Lancet |volume=371 |issue=9615 |pages=838–51 |year=2008 |pmid=18328931 |pmc=2271178 |doi=10.1016/S0140-6736(08)60383-9 |url=}}</ref> | ||
*If left untreated, patients with cirrhosis may progress to develop [[ascites]], [[esophageal varices]], [[hepatic encephalopathy]], [[spontaneous bacterial peritonitis]], [[Hepatopulmonary syndrome|hepatopulmonary]] and [[hepatorenal syndrome]].<ref name="pmid29128051">{{cite journal |vauthors=Lindenmeyer CC, McCullough AJ |title=The Natural History of Nonalcoholic Fatty Liver Disease-An Evolving View |journal=Clin Liver Dis |volume=22 |issue=1 |pages=11–21 |year=2018 |pmid=29128051 |doi=10.1016/j.cld.2017.08.003 |url=}}</ref><ref name="pmid25230084">{{cite journal |vauthors=Bloom S, Kemp W, Lubel J |title=Portal hypertension: pathophysiology, diagnosis and management |journal=Intern Med J |volume=45 |issue=1 |pages=16–26 |year=2015 |pmid=25230084 |doi=10.1111/imj.12590 |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid8550036">{{cite journal |vauthors=Arroyo V, Ginès P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Schölmerich J |title=Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club |journal=Hepatology |volume=23 |issue=1 |pages=164–76 |year=1996 |pmid=8550036 |doi=10.1002/hep.510230122 |url=}}</ref><ref name="pmid1833293">{{cite journal |vauthors=Wilkinson SP, Moore KP, Arroyo V |title=Pathogenesis of ascites and hepatorenal syndrome |journal=Gut |volume=Suppl |issue= |pages=S12–7 |year=1991 |pmid=1833293 |pmc=1405222 |doi= |url=}}</ref><ref name="pmid1435935">{{cite journal |vauthors=Epstein M |title=The hepatorenal syndrome--newer perspectives |journal=N. Engl. J. Med. |volume=327 |issue=25 |pages=1810–1 |year=1992 |pmid=1435935 |doi=10.1056/NEJM199212173272509 |url=}}</ref> | *If left untreated, patients with cirrhosis may progress to develop [[ascites]], [[esophageal varices]], [[hepatic encephalopathy]], [[spontaneous bacterial peritonitis]], [[Hepatopulmonary syndrome|hepatopulmonary]] and [[hepatorenal syndrome]].<ref name="pmid29128051">{{cite journal |vauthors=Lindenmeyer CC, McCullough AJ |title=The Natural History of Nonalcoholic Fatty Liver Disease-An Evolving View |journal=Clin Liver Dis |volume=22 |issue=1 |pages=11–21 |year=2018 |pmid=29128051 |doi=10.1016/j.cld.2017.08.003 |url=}}</ref><ref name="pmid25230084">{{cite journal |vauthors=Bloom S, Kemp W, Lubel J |title=Portal hypertension: pathophysiology, diagnosis and management |journal=Intern Med J |volume=45 |issue=1 |pages=16–26 |year=2015 |pmid=25230084 |doi=10.1111/imj.12590 |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid8550036">{{cite journal |vauthors=Arroyo V, Ginès P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Schölmerich J |title=Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club |journal=Hepatology |volume=23 |issue=1 |pages=164–76 |year=1996 |pmid=8550036 |doi=10.1002/hep.510230122 |url=}}</ref><ref name="pmid1833293">{{cite journal |vauthors=Wilkinson SP, Moore KP, Arroyo V |title=Pathogenesis of ascites and hepatorenal syndrome |journal=Gut |volume=Suppl |issue= |pages=S12–7 |year=1991 |pmid=1833293 |pmc=1405222 |doi= |url=}}</ref><ref name="pmid1435935">{{cite journal |vauthors=Epstein M |title=The hepatorenal syndrome--newer perspectives |journal=N. Engl. J. Med. |volume=327 |issue=25 |pages=1810–1 |year=1992 |pmid=1435935 |doi=10.1056/NEJM199212173272509 |url=}}</ref><ref name="pmid14654322">{{cite journal |vauthors=Ginès P, Guevara M, Arroyo V, Rodés J |title=Hepatorenal syndrome |journal=Lancet |volume=362 |issue=9398 |pages=1819–27 |year=2003 |pmid=14654322 |doi=10.1016/S0140-6736(03)14903-3 |url=}}</ref> | ||
*The general course of cirrhosis is characterized by a long stage of compensation, which may be followed by deterioration and development of specific complications. | *The general course of cirrhosis is characterized by a long stage of compensation, which may be followed by deterioration and development of specific complications. | ||
*Life threatening complications may develop in almost any patient. Once the first complication in a patient with cirrhosis is seen, it is soon followed by numerous other complications that significantly decrease [[life expectancy]]. | *Life threatening complications may develop in almost any patient. Once the first complication in a patient with cirrhosis is seen, it is soon followed by numerous other complications that significantly decrease [[life expectancy]]. | ||
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**[[Etiology]] of cirrhosis | **[[Etiology]] of cirrhosis | ||
**Disease progression | **Disease progression | ||
**Development of [[hepatocellular carcinoma]] | **Development of [[hepatocellular carcinoma]]<ref name="pmid14667750">{{cite journal |vauthors=Llovet JM, Burroughs A, Bruix J |title=Hepatocellular carcinoma |journal=Lancet |volume=362 |issue=9399 |pages=1907–17 |year=2003 |pmid=14667750 |doi=10.1016/S0140-6736(03)14964-1 |url=}}</ref> | ||
**Ability of the patient to withstand a chosen therapeutic intervention | **Ability of the patient to withstand a chosen therapeutic intervention | ||
**Ability of the intervention to significantly improve the outcome | **Ability of the intervention to significantly improve the outcome | ||
| Line 42: | Line 42: | ||
****Due to increased pressure, [[fluid]] leaks through the [[Circulatory system|vasculature]] into the [[abdominal cavity]] | ****Due to increased pressure, [[fluid]] leaks through the [[Circulatory system|vasculature]] into the [[abdominal cavity]] | ||
***[[Esophageal varices]]: Increased pressure in the [[portal vein]] leads to collateral portal blood flow through [[Blood vessel|vessels]] in the [[stomach]] and [[esophagus]] | ***[[Esophageal varices]]: Increased pressure in the [[portal vein]] leads to collateral portal blood flow through [[Blood vessel|vessels]] in the [[stomach]] and [[esophagus]] | ||
***[[Portal vein thrombosis]] | ***[[Portal vein thrombosis]]<ref name="pmid7737629">{{cite journal |vauthors=Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G |title=Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension |journal=Hepatology |volume=21 |issue=5 |pages=1238–47 |year=1995 |pmid=7737629 |doi= |url=}}</ref> | ||
***Easy [[bruising]] and [[hemorrhage|bleeding]] - due to the decreased production of [[coagulation]] factors | ***Easy [[bruising]] and [[hemorrhage|bleeding]] - due to the decreased production of [[coagulation]] factors | ||
***[[Jaundice]] | ***[[Jaundice]] | ||
***[[Itch]]ing ([[pruritus]]) | ***[[Itch]]ing ([[pruritus]]) | ||
***[[Hepatic encephalopathy]] : due to inability of the [[liver]] to clear [[ammonia]] and related nitrogenous substances from the blood, which are carried to the [[brain]] | ***[[Hepatic encephalopathy]] : due to inability of the [[liver]] to clear [[ammonia]] and related nitrogenous substances from the blood, which are carried to the [[brain]]<ref name="pmid10728803">{{cite journal |vauthors=Butterworth RF |title=Complications of cirrhosis III. Hepatic encephalopathy |journal=J. Hepatol. |volume=32 |issue=1 Suppl |pages=171–80 |year=2000 |pmid=10728803 |doi= |url=}}</ref> | ||
****The features of [[hepatic encephalopathy]] are as follows: | ****The features of [[hepatic encephalopathy]] are as follows: | ||
*****Changes in [[sleep]] pattern ([[insomnia]] and [[hypersomnia]]) | *****Changes in [[sleep]] pattern ([[insomnia]] and [[hypersomnia]]) | ||
| Line 61: | Line 61: | ||
**[[Infection]]: due to [[immune system]] dysfunction | **[[Infection]]: due to [[immune system]] dysfunction | ||
***Non specific [[Medical sign|signs]] and [[Symptom|symptoms]] | ***Non specific [[Medical sign|signs]] and [[Symptom|symptoms]] | ||
**[[Spontaneous bacterial peritonitis]]: | **[[Spontaneous bacterial peritonitis]]:<ref name="pmid16979776">{{cite journal |vauthors=Riordan SM, Williams R |title=The intestinal flora and bacterial infection in cirrhosis |journal=J. Hepatol. |volume=45 |issue=5 |pages=744–57 |year=2006 |pmid=16979776 |doi=10.1016/j.jhep.2006.08.001 |url=}}</ref><ref name="pmid10094951">{{cite journal |vauthors=Papatheodoridis GV, Patch D, Webster GJ, Brooker J, Barnes E, Burroughs AK |title=Infection and hemostasis in decompensated cirrhosis: a prospective study using thrombelastography |journal=Hepatology |volume=29 |issue=4 |pages=1085–90 |year=1999 |pmid=10094951 |doi=10.1002/hep.510290437 |url=}}</ref> | ||
***[[Infection]] of the [[fluid]] in the [[abdomen]] due to [[ascites]] with intestinal [[bacteria]] | ***[[Infection]] of the [[fluid]] in the [[abdomen]] due to [[ascites]] with intestinal [[bacteria]] | ||
***[[Symptom|Symptoms]] and [[Medical sign|signs]] include [[pain]], [[tenderness]] and [[altered mental status]] | ***[[Symptom|Symptoms]] and [[Medical sign|signs]] include [[pain]], [[tenderness]] and [[altered mental status]] | ||
***[[Patient]] may be asymptomatic in early stages | ***[[Patient]] may be asymptomatic in early stages | ||
***Findings on diagnostic [[paracentesis]] such as a positive culture and/or [[absolute neutrophil count]] >250/mm3 are confirmatory | ***Findings on diagnostic [[paracentesis]] such as a positive culture and/or [[absolute neutrophil count]] >250/mm3 are confirmatory | ||
**[[Hepatorenal syndrome]]: | **[[Hepatorenal syndrome]]:<ref name="pmid22173162">{{cite journal |vauthors=Fede G, D'Amico G, Arvaniti V, Tsochatzis E, Germani G, Georgiadis D, Morabito A, Burroughs AK |title=Renal failure and cirrhosis: a systematic review of mortality and prognosis |journal=J. Hepatol. |volume=56 |issue=4 |pages=810–8 |year=2012 |pmid=22173162 |doi=10.1016/j.jhep.2011.10.016 |url=}}</ref> | ||
***has a very high mortality of over 50% | ***has a very high mortality of over 50% | ||
***arises due to decreased [[perfusion]] to the kidneys, leading to [[acute renal failure]] | ***arises due to decreased [[perfusion]] to the kidneys, leading to [[acute renal failure]] | ||
| Line 73: | Line 73: | ||
***bears poor [[patient]] prognosis | ***bears poor [[patient]] prognosis | ||
**[[Lung|Pulmonary]] diseases associated with cirrhosis include: | **[[Lung|Pulmonary]] diseases associated with cirrhosis include: | ||
***[[Hepatopulmonary syndrome]]: | ***[[Hepatopulmonary syndrome]]:<ref name="pmid12500204">{{cite journal |vauthors=Arguedas MR, Abrams GA, Krowka MJ, Fallon MB |title=Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation |journal=Hepatology |volume=37 |issue=1 |pages=192–7 |year=2003 |pmid=12500204 |doi=10.1053/jhep.2003.50023 |url=}}</ref><ref name="pmid15758649">{{cite journal |vauthors=Fallon MB |title=Mechanisms of pulmonary vascular complications of liver disease: hepatopulmonary syndrome |journal=J. Clin. Gastroenterol. |volume=39 |issue=4 Suppl 2 |pages=S138–42 |year=2005 |pmid=15758649 |doi= |url=}}</ref> | ||
****presents as a triad comprising of the following: | ****presents as a triad comprising of the following: | ||
*****existing [[liver]] disease | *****existing [[liver]] disease | ||
| Line 81: | Line 81: | ||
*** [[Liver|Hepatic]] [[hydrothorax]]: | *** [[Liver|Hepatic]] [[hydrothorax]]: | ||
**** intra-[[Abdomen|abdominal]] fluid may seep in through the [[Thoracic diaphragm|diaphragm]] into the [[pleural space]] leading to a [[pleural effusion]] | **** intra-[[Abdomen|abdominal]] fluid may seep in through the [[Thoracic diaphragm|diaphragm]] into the [[pleural space]] leading to a [[pleural effusion]] | ||
*** [[Portopulmonary hypertension]]: | *** [[Portopulmonary hypertension]]:<ref name="pmid12891571">{{cite journal |vauthors=Blendis L, Wong F |title=Portopulmonary hypertension: an increasingly important complication of cirrhosis |journal=Gastroenterology |volume=125 |issue=2 |pages=622–4 |year=2003 |pmid=12891571 |doi= |url=}}</ref> | ||
**** due to increased [[blood pressure]] over the [[Lung|lungs]] as a consequence of [[portal hypertension]]<ref name="PHD" /> | **** due to increased [[blood pressure]] over the [[Lung|lungs]] as a consequence of [[portal hypertension]]<ref name="PHD" /> | ||
** [[Cardiomyopathy]]: | ** [[Cardiomyopathy]]:<ref name="pmid16741552">{{cite journal |vauthors=Gaskari SA, Honar H, Lee SS |title=Therapy insight: Cirrhotic cardiomyopathy |journal=Nat Clin Pract Gastroenterol Hepatol |volume=3 |issue=6 |pages=329–37 |year=2006 |pmid=16741552 |doi=10.1038/ncpgasthep0498 |url=}}</ref> | ||
*** presents with normal or increased [[cardiac output]] at rest but notably decreases in [[stress]] conditions | *** presents with normal or increased [[cardiac output]] at rest but notably decreases in [[stress]] conditions | ||
** [[Muscle cramps]]: | ** [[Muscle cramps]]: | ||
| Line 89: | Line 89: | ||
===Prognosis=== | ===Prognosis=== | ||
*The prognosis of patients varies with existing function of the [[liver]], etiology of cirrhosis, progression of the disease, development of [[Hepatocellular carcinoma|HCC]] and ability to withstand therapy. | *The prognosis of patients varies with existing function of the [[liver]], etiology of cirrhosis, progression of the disease, development of [[Hepatocellular carcinoma|HCC]] and ability to withstand therapy.<ref name="pmid7895544">{{cite journal |vauthors=Chu CM, Chang KY, Liaw YF |title=Prevalence and prognostic significance of bacterascites in cirrhosis with ascites |journal=Dig. Dis. Sci. |volume=40 |issue=3 |pages=561–5 |year=1995 |pmid=7895544 |doi= |url=}}</ref> | ||
{| | {| | ||
| Line 109: | Line 109: | ||
===Scoring Systems=== | ===Scoring Systems=== | ||
* [[Model for End-Stage Liver Disease]] | * [[Model for End-Stage Liver Disease]]<ref name="pmid12512033">{{cite journal |vauthors=Wiesner R, Edwards E, Freeman R, Harper A, Kim R, Kamath P, Kremers W, Lake J, Howard T, Merion RM, Wolfe RA, Krom R |title=Model for end-stage liver disease (MELD) and allocation of donor livers |journal=Gastroenterology |volume=124 |issue=1 |pages=91–6 |year=2003 |pmid=12512033 |doi=10.1053/gast.2003.50016 |url=}}</ref><ref name="pmid15719393">{{cite journal |vauthors=Wiesner RH |title=Evidence-based evolution of the MELD/PELD liver allocation policy |journal=Liver Transpl. |volume=11 |issue=3 |pages=261–3 |year=2005 |pmid=15719393 |doi=10.1002/lt.20362 |url=}}</ref><ref name="pmid15885353">{{cite journal |vauthors=Huo TI, Wu JC, Lin HC, Lee FY, Hou MC, Lee PC, Chang FY, Lee SD |title=Evaluation of the increase in model for end-stage liver disease (DeltaMELD) score over time as a prognostic predictor in patients with advanced cirrhosis: risk factor analysis and comparison with initial MELD and Child-Turcotte-Pugh score |journal=J. Hepatol. |volume=42 |issue=6 |pages=826–32 |year=2005 |pmid=15885353 |doi=10.1016/j.jhep.2005.01.019 |url=}}</ref> | ||
* [[Pediatric end-stage liver disease|Pediatric End-Stage Liver Disease]] | * [[Pediatric end-stage liver disease|Pediatric End-Stage Liver Disease]] | ||
* [[Child-Pugh score]] | * [[Child-Pugh score]] | ||
Revision as of 21:22, 15 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]
Overview
Cirrhosis is an irreversible process, the course of which is highly variable in patients. The natural history progresses in such a way that there is a lengthy stage of compensation, followed by the development of complications and sequelae as a result of the cirrhosis. The devastating complications include complete liver failure or the development of hepatocellular carcinoma. Other complications include portal hypertension, ascites, jaundice, itching, esophageal varices, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome and cardiomyopathy. Prognosis depends on the causes, existing complications and a variety of factors which make the prediction of life expectancy questionable. There are scores which classify disease severity and to determine suitability for liver transplantation in patients.
Natural History
- The symptoms of cirrhosis usually develop in the fourth or fifth decade of life, and start with symptoms such as fever, anorexia, fatigue, weakness, nausea, vomiting, weight loss and jaundice.[1][2][3]
- If left untreated, patients with cirrhosis may progress to develop ascites, esophageal varices, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatopulmonary and hepatorenal syndrome.[4][5][2][6][7][8][9]
- The general course of cirrhosis is characterized by a long stage of compensation, which may be followed by deterioration and development of specific complications.
- Life threatening complications may develop in almost any patient. Once the first complication in a patient with cirrhosis is seen, it is soon followed by numerous other complications that significantly decrease life expectancy.
- Prediction of the exact course of the disease and generalization to the entire population is difficult.
- Several factors play a key role in determining the course of the disease:
- Existing hepatic function
- Etiology of cirrhosis
- Disease progression
- Development of hepatocellular carcinoma[10]
- Ability of the patient to withstand a chosen therapeutic intervention
- Ability of the intervention to significantly improve the outcome
Decompensated Cirrhosis
- In patients with stable cirrhosis, decompensation may occur due to various causes:
- constipation
- infection
- Increased alcohol intake
- Medications
- Bleeding from esophageal varices or dehydration
- Patients with decompensated cirrhosis generally require:
- Admission to the hospital
- Close monitoring of the fluid balance, mental status
- Emphasis on adequate nutrition
- Medical treatment - with diuretics, antibiotics, laxatives or enemas, thiamine, steroids, acetylcysteine and pentoxifylline.
- Administration of saline is generally avoided as it would add to the already high total body sodium content that typically occurs in cirrhosis
Complications
- The high mortality rate associated with cirrhosis is primarily due to complications.
- Common complications of cirrhosis include:[4][11]
- Complications due to portal hypertension include:
- Ascites : Ascites is the most common complication of cirrhosis
- Due to increased pressure, fluid leaks through the vasculature into the abdominal cavity
- Esophageal varices: Increased pressure in the portal vein leads to collateral portal blood flow through vessels in the stomach and esophagus
- Portal vein thrombosis[12]
- Easy bruising and bleeding - due to the decreased production of coagulation factors
- Jaundice
- Itching (pruritus)
- Hepatic encephalopathy : due to inability of the liver to clear ammonia and related nitrogenous substances from the blood, which are carried to the brain[13]
- The features of hepatic encephalopathy are as follows:
- Changes in sleep pattern (insomnia and hypersomnia)
- Unresponsiveness
- Forgetfulness
- Poor concentration
- asterixis
- Coma
- The features of hepatic encephalopathy are as follows:
- Sensitivity to drugs due to decreased metabolism in the liver
- Ascites : Ascites is the most common complication of cirrhosis
- Hepatocellular carcinoma is primary liver cancer and is most commonly seen in cirrhotic patients with:
- Infection: due to immune system dysfunction
- Spontaneous bacterial peritonitis:[14][15]
- Infection of the fluid in the abdomen due to ascites with intestinal bacteria
- Symptoms and signs include pain, tenderness and altered mental status
- Patient may be asymptomatic in early stages
- Findings on diagnostic paracentesis such as a positive culture and/or absolute neutrophil count >250/mm3 are confirmatory
- Hepatorenal syndrome:[16]
- has a very high mortality of over 50%
- arises due to decreased perfusion to the kidneys, leading to acute renal failure
- may be masked clinically due to decreased muscle mass and hepatic urea synthesis in cirrhotic patients leading to only a small elevation of BUN and creatinine
- diagnosis of exclusion as causes of renal dysfunction need to be excluded first
- bears poor patient prognosis
- Pulmonary diseases associated with cirrhosis include:
- Hepatopulmonary syndrome:[17][18]
- Hepatic hydrothorax:
- intra-abdominal fluid may seep in through the diaphragm into the pleural space leading to a pleural effusion
- Portopulmonary hypertension:[20]
- due to increased blood pressure over the lungs as a consequence of portal hypertension[19]
- Cardiomyopathy:[21]
- presents with normal or increased cardiac output at rest but notably decreases in stress conditions
- Muscle cramps:
- occur due to reduction in circulating plasma volume
- Complications due to portal hypertension include:
Prognosis
- The prognosis of patients varies with existing function of the liver, etiology of cirrhosis, progression of the disease, development of HCC and ability to withstand therapy.[22]
| Well-Compensated, no alcohol | 35% mortality at 2 years |
| Onset of Ascites | 50% mortality at 2 years |
| Variceal bleeding | 65% mortality at 1 year (35% short-term mortality) |
Poor Prognostic Factors
- Prolonged prothrombin time
- Serum Bilirubin >10 mg/dL
- Hepatic encephalopathy
- Azotemia
- Leukocytosis
- Unresponsive to steroid treatment
- Reversal portal flow on doppler USG
Scoring Systems
- Model for End-Stage Liver Disease[23][24][25]
- Pediatric End-Stage Liver Disease
- Child-Pugh score
- Child-Turcotte classification
- The severity of cirrhosis is commonly classified with the Child-Turcotte and Child-Pugh scores. It was devised in 1964 by Child and Turcotte and modified in 1973 by Pugh et al.[26]
- The Child-Pugh score uses bilirubin, albumin, INR, presence and severity of ascites and encephalopathy to classify patients in class A, B or C types.
- Class A type has a favorable prognosis, while class C is at a high risk of death.
- Modern scores, used in the allocation of liver transplants are the Model for End-Stage Liver Disease (MELD) score and its pediatric counterpart, the Pediatric End-Stage Liver Disease (PELD) score.
References
- ↑ Sajja KC, Mohan DP, Rockey DC (2014). "Age and ethnicity in cirrhosis". J. Investig. Med. 62 (7): 920–6. doi:10.1097/JIM.0000000000000106. PMC 4172494. PMID 25203153.
- ↑ 2.0 2.1 Williams EJ, Iredale JP (1998). "Liver cirrhosis". Postgrad Med J. 74 (870): 193–202. PMC 2360862. PMID 9683971.
- ↑ Schuppan D, Afdhal NH (2008). "Liver cirrhosis". Lancet. 371 (9615): 838–51. doi:10.1016/S0140-6736(08)60383-9. PMC 2271178. PMID 18328931.
- ↑ 4.0 4.1 Lindenmeyer CC, McCullough AJ (2018). "The Natural History of Nonalcoholic Fatty Liver Disease-An Evolving View". Clin Liver Dis. 22 (1): 11–21. doi:10.1016/j.cld.2017.08.003. PMID 29128051.
- ↑ Bloom S, Kemp W, Lubel J (2015). "Portal hypertension: pathophysiology, diagnosis and management". Intern Med J. 45 (1): 16–26. doi:10.1111/imj.12590. PMID 25230084.
- ↑ Arroyo V, Ginès P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Schölmerich J (1996). "Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club". Hepatology. 23 (1): 164–76. doi:10.1002/hep.510230122. PMID 8550036.
- ↑ Wilkinson SP, Moore KP, Arroyo V (1991). "Pathogenesis of ascites and hepatorenal syndrome". Gut. Suppl: S12–7. PMC 1405222. PMID 1833293.
- ↑ Epstein M (1992). "The hepatorenal syndrome--newer perspectives". N. Engl. J. Med. 327 (25): 1810–1. doi:10.1056/NEJM199212173272509. PMID 1435935.
- ↑ Ginès P, Guevara M, Arroyo V, Rodés J (2003). "Hepatorenal syndrome". Lancet. 362 (9398): 1819–27. doi:10.1016/S0140-6736(03)14903-3. PMID 14654322.
- ↑ Llovet JM, Burroughs A, Bruix J (2003). "Hepatocellular carcinoma". Lancet. 362 (9399): 1907–17. doi:10.1016/S0140-6736(03)14964-1. PMID 14667750.
- ↑ García-Criado A, Castellón D (2017). "Presentation of the series "Cirrhosis of the liver and its complications"". Radiologia. doi:10.1016/j.rx.2017.10.003. PMID 29169606.
- ↑ Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G (1995). "Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension". Hepatology. 21 (5): 1238–47. PMID 7737629.
- ↑ Butterworth RF (2000). "Complications of cirrhosis III. Hepatic encephalopathy". J. Hepatol. 32 (1 Suppl): 171–80. PMID 10728803.
- ↑ Riordan SM, Williams R (2006). "The intestinal flora and bacterial infection in cirrhosis". J. Hepatol. 45 (5): 744–57. doi:10.1016/j.jhep.2006.08.001. PMID 16979776.
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