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| __NOTOC__
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| {{CMG}}; {{AE}} {{SH}} | | {{CMG}}; {{AE}} {{SH}} |
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| ==Overview==
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| Extracorporeal liver support has been a much studied topic throughout the last 50 years. Albumin dialysis as a therapeutic option for patients with acute liver failure or acute decompensation of chronic liver disease was introduced in the mid-nineties. The Molecular Adsorbent Recirculating System (MARS) is based on the concept of albumin dialysis and allows for the removal of protein-bound as well as water-soluble toxins. Besides its role as a sufficient volume expander human serum albumin is an important scavenger for molecules with pathophysiological relevance in liver failure. Albumin dialysis enables the selective regeneration of patient's albumin resulting in an increase of albumin binding capacity. Clinically, an improvement of central and local hemodynamics as well as liver-, brain-, and kidney-functions were observed. Thus, the treatment can contribute to liver regeneration and stabilization of vital organ functions and thus help to bridge patients to liver transplantation or to recovery of native liver function. Proper patient selection is critical for clinical success. Aggressive treatment of infections and sepsis seems to be a decisive pre-requisite for its safe and efficient use. Cautious anticoagulation with heparin is the common standard. Citrate use is recommended for patients prone to bleeding. Today, albumin dialysis MARS is among the best studied liver support methods. It appears as a valuable therapeutic tool for the treatment of various complications of of liver failure, especially hemodynamic instability and hepatic encephalopathy. Further studies will need to help defining the optimal patient selection and technical process parameters such as session length and frequency of treatment.
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| he aim of extracorporeal albumin dialysis (ECAD) is to reduce endogenous toxins accumulating in liver failure. To date, ECAD is conducted mainly with the Molecular Adsorbents Recirculating System (MARS). However, single-pass albumin dialysis (SPAD) has been proposed as an alternative.
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| http://www.webaisf.org/media/12203/09_angeli.pdf
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| https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699252/
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| survival 28 days
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| '''Indication'''
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| acute liver ailure
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| acute on chronic liver ailure
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| fulminant hepatic failure
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| sub fulminant hepatic failure
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| hepatic encaphalopathy gade 2 or above
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| acutely decmpensated liver cirrhosis
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| hyperbilirubinemia >5
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| hrs
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| progssive hperbilrubinemia
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| '''contraindications'''
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| platelets count<50,000
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| DIC
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| INR.2.3
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| uncontrolled infection
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| https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128463/
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| Liver dialysis
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| 20% albumin sol,
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| ammonia, aromatic amino acids
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| merceptans
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| bilirubin
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| bile acids
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| cytokines
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| nitricoxide
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| **The first circuit consists of [[human serum albumin]], is in contact with the patient's blood through a semipermeable membrane and has two special filters to clean the albumin after it has absorbed toxins from the patient's blood.
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| *The second circuit consists of a hemodialysis machine and is used to clean the albumin in the first circuit, before it is recirculated to the semipermeable membrane in contact with the patient's blood.
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| The MARS system can remove a number of toxins, including [[ammonia]], [[bile acids]], [[bilirubin]], [[copper]], [[iron]] and [[phenols]].
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| MARS development started at the University of [[Rostock]] in [[Germany]]. It has 510 (k) approval from the [[Food and Drug Administration]] (FDA) for drug overdoses and poisoning as of June [[2005]] and is available in the [[USA]] since the end of 2005.[http://www.gambro.com/upload/Press%20Releases/2005/MARS_510k.pdf] Canada's first MARS unit arrived at the [[Toronto General Hospital]] in 2005.
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| The Molecular Adsorbents Recirculation System (MARS), is the best known extracorporal liver dialysis system and has existed for approximately ten years. It consists of two separate dialysis circuits. The first circuit consists of human serum albumin, is in contact with the patient's blood through a semipermeable membrane and has two filters to clean the albumin after it has absorbed toxins from the patient's blood. The second circuit consists of a hemodialysis machine and is used to clean the albumin in the first circuit, before it is recirculated to the semipermeable membrane in contact with the patient's blood.
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| ==Classification==
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| ==Historical Perspective==
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| ==Pathophysiology==
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| ==Causes==
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| ===Common casuses===
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| The most common Cause of the splenic rupture remains blunt trauma to the abdomen.The other common causes of splenic rupture includes.<ref name="pmid19787754">{{cite journal |vauthors=Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D |title=Systematic review of atraumatic splenic rupture |journal=Br J Surg |volume=96 |issue=10 |pages=1114–21 |year=2009 |pmid=19787754 |doi=10.1002/bjs.6737 |url=}}</ref>
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| * Neoplasms
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| * Infections
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| * Non Infectious
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| * Therapy related
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| * Mechanical Causes
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| ===Less common causes===
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| The less common causes of splenic rupture are difficult to diagnose and can be threatening.
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| Some less common causes of splenic rupture are as follows:
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| * Autologus stem cell transplantation in AL Amyloidosis patients<ref name="pmid29093392">{{cite journal| author=Sato S, Tamai Y, Okada S, Kannbe E, Takeda K, Tanaka E| title=Atraumatic Splenic Rupture due to Ectopic Extramedullary Hematopoiesis after Autologous Stem Cell Transplantation in a Patient with AL Amyloidosis. | journal=Intern Med | year= 2017 | volume= | issue= | pages= | pmid=29093392 | doi=10.2169/internalmedicine.9018-17 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29093392 }} </ref>
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| *
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| *
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| *
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| ==Differentiating Splenic Rupture from Other Diseases==
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| ==Epidemiology and Demographics==
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| ==Risk Factors==
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| ==Screening==
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| ==Natural History, Complications and Prognosis==
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| ==Diagnosis==
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| ==Diagnostic Study of Choice==
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| == History and Symptoms==
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| ==Physical Examination==
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| == Laboratory Findings==
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| ==Electrocardiogram==
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| ==X-Ray==
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| ==MRI==
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| ==Other Imaging Findings==
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| ==Other Diagnostic Studies==
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| == Algorithms ==
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| {{familytree/start}}
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| {{familytree | | | | | | | | | | | | | | | | | | | | | | | A01 |A01='''Major molecular events in the pathogenesis of HCC'''}}
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| {{familytree | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|+|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|.| | | }}
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| {{familytree | | | | B01 | | | | | | | | | | | | | | | | | B02 | | | | | | | | | | | | | | | B03 |B01='''Genomic alterations'''|B02='''Epigenetic modifications'''|B03='''Growthfactor pathway alterations'''}}
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| {{familytree | | |,|-|^|-|.| | | | | | | | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|-|.| | | | | | | | |!| | |}}
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| {{familytree | | C01 | | C02 | | | | | | | | C03 | | | | | C04 | | | | | | C05 | | | | | | | C06 |C01=Gene Mutations|C02=Gene Amplification|C03=DNA methylation micro RNA|C04=Micro RNA|C05=LNC RNA|C06=Major Signaling pathways}}
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| {{familytree | | |!| | | |!| | | | | | | | | |!| | | | | | |!| | | | | | | |!| | | | | | | | |!| |}}
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| {{familytree |boxstyle=text-align: left; | | D01 | | D02 | | | | | | | | D03 | | | | | D04 | | | | | | D05 | | | | | | | D06 |D01=•TERT promoter<br>•TP53<br>•CTNNB1<br>•AXIN1<br>•AXIN2<br>•ATM<br>•RPS6KA3<br>•JAK1<br>•IL6R<br>•IL6ST<br>•ARID1<br>•ARID2
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| |D02=•CCND1<br>•FGF19<br>•CDKNA2A<br>•CDKNA2B<br>•AXIN1<br>•IRF2<br>•MET|D03=GSTP1<br>•E-Cadherin<br>•CDKNA2<br>•RASSF1A<br>•SOCS-3<br>•MIGMT|D04=•MiR-155<br>•Mir-122<br>•Mir-224<br>•Mir-21|D05=•HULC<br>•HEIH<br>•Dreh<br>•MVIH<br>•HOTAIR<br>•MDIG<br>•LINE1|D06=•Wnt/β –catenin<br>•Tyrosine kinase pathways<br>EGF<br>HGF/c-MET<br>FGF<br>VEGF<br>•IGF<br>•HIF<br>•TGF β <br>•Hedgehog}}
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| {{familytree/end}}
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| [[image:512px-Jaundice08.jpg|thumb|350px|center| Elderly Male with jaundice from pancreatic cancer, By James Heilman, MD (Own work) [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons <ref name="urlFile:Jaundice08.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AJaundice08.jpg |title=File:Jaundice08.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
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| The incidence of HCC has almost tripled since the early 1980s in the United States where it is the fastest rising cause of cancer-related deaths1. According to population based Surveillance Epidemiology and End Results registry data, the overall HCC age adjusted incidence rates for liver and intrahepatic ducts cancer is as high as 8 per 100,000 underling population in 2010 (Fig. 1) of which at least 6 per 100,000 related to HCC. Men are at approximately three times higher risk than women. Asian men (i.e., Chinese, Korean, Filipino, and Japanese) have the highest age-adjusted incidence rates. However, the largest proportional increases have occurred among Hispanics followed by blacks and non-Hispanic whites, whereas the lowest proportional increases have occurred among Asians. In contrast to Asians/Pacific Islanders, HCC incidence rates are reported to be higher among Hispanics born in the United States than among foreign-born Hispanics2. HCC incidence rates have increased in each successive birth cohort born between 1900 and 19593 (Fig. 2). In addition, the age distribution of HCC patients has shifted to younger ages, with the greatest proportional increases among individuals 45–60 years old (Fig. 2). There is a south to north gradient in the incidence and mortality of HCC; Southern states including Texas, Louisiana, and Mississippi have some of the highest HCC incidence rates in the nation (Fig. 3). In one study, Texas Latino and especially South Texas Latinos had the highest age-adjusted HCC incidence rates (as high as 10.6/100,000)4.
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| ==References==
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| {{Reflist|2}}
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