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Liver — Transcript

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0:06the objectives for this lecture are as
0:09follows
0:09describe the anatomy and physiology of
0:12the liver describe an aesthetic
0:14management of the patient with advanced
0:15liver disease describe the anesthetic
0:18management of the patient presenting for
0:20a liver transplant despite advances in
0:24the perioperative care of high-risk
0:26surgical patients patients with acute or
0:28chronic liver failure continue to
0:29experience an increase incidence of
0:31post-operative complications and excess
0:33mortality identifying and addressing
0:36risk factors preoperatively may prevent
0:38post-operative morbidity and reduce
0:39mortality this lecture reviews the
0:42fundamentals of hepatic anatomy
0:43physiology and biochemistry and presents
0:46an overview of many and diverse liver
0:48diseases to provide a foundation to
0:49identify risk factors and improve
0:51preoperative conditions for anesthesia
0:53and surgery the liver is the largest
0:57solid organ in the body normally
0:59weighing between 1,200 and 1,500 grams
1:02unlike most organs the liver is able to
1:04regenerate itself following injury with
1:07repeated injury however regeneration is
1:09limited by surrounding fibrous scar
1:11tissue early in the course of many
1:13hepatic diseases the liver becomes
1:14enlarged as a consequence of fatty
1:16infiltration cellular infiltration and
1:19fibrin nodular regeneration with
1:22continued injury it decreases in size as
1:24bridging fibrosis leads to cirrhosis the
1:29functional anatomy follows the vascular
1:31supply and biliary drainage this is
1:34important because the anatomy forms of
1:35boundaries for hepatic resection of
1:37tumors and segments ectomy for a living
1:39donor liver donation the branches of the
1:42vasculature and bile ducts describe the
1:44boundaries of the eight liver segments
1:46the hepatic asanas is a microscopic unit
1:49of the liver the acid s is hexagonal in
1:52shape with the hepatic venule and bile
1:54Knik ulis at the center and the hepatic
1:56arterioles and venules at the corners
1:59fibrosis leads to portal hypertension
2:00from compression of these blood vessels
2:05hepatocyte SAR described as being in
2:07zone 1 2 or 3 based on their distance
2:09from blood flow with oxygen supply and
2:11available nutrients those in zone 3 are
2:14at greatest risk of ischemic viral and
2:16toxic injury as they are the more remote
2:18from their source of oxy
2:19and nutrients zone 3 is the area via
2:22hepatic SNS we're bridging fibrosis
2:24first occurs following ischemic or
2:26metabolic injury hepatocellular function
2:30includes the synthesis of proteins
2:32production of bile clearance of drugs
2:34and metabolites glycogenesis
2:36glycogenolysis and cholesterol and fatty
2:39acid metabolism reticulo-endothelial
2:42function includes phagocytosis via the
2:44cooper cells hematopoiesis for both red
2:47and white blood cells the production of
2:49immunoglobulins via the lymphoid tissue
2:51and lipid metabolism by lipo sites all
2:54of these functions can be impaired with
2:56liver disease
2:59this slide further describes the
3:01synthetic and excretory function this
3:06slide goes into a little bit more detail
3:08on the metabolic function the results of
3:12liver function tests provide information
3:14about hepatocyte integrity cholestasis
3:16and liver function other tests are
3:19valuable in establishing the extent of
3:21hepatocellular injury as well as
3:22morphologic and histologic effects of
3:24diseases hepatic synthetic function is
3:27easily assessed by the measurement of
3:29plasma albumin fibrinogen and the
3:31determination of the PT or the INR serum
3:35albumin and prothrombin time are the
3:37standardized tests of synthetic function
3:38and are used in the algorithm
3:40establishing the child puke score an SI
3:43a plasma cholinesterase activity can be
3:45used to measure synthetic function but
3:47this test should not be confused with
3:48the determination of the wk number the
3:51wk number can remain normal in patients
3:53with decreased levels of the normal ISO
3:55form of pseudo cholinesterase the best
3:59laboratory tests of hepatic excretion
4:01are serum levels of indirect and direct
4:03bilirubin
4:04although most forms of liver disease
4:06will eventually produce an elevation of
4:08bilirubin it is most common with biliary
4:10obstruction or secondary autoimmune
4:12biliary disease the pattern of enzyme
4:15elevation helps distinguish between
4:16hepatocellular injury biliary
4:18obstruction and alcohol abuse beyond
4:21that they are relatively nonspecific and
4:23do not provide sufficient information to
4:25discriminate amongst different liver
4:26diseases with any form of bile duct
4:29obstruction alkaline phosphatase which
4:31is normally excreted in the bile leaks
4:33into the systemic circulation patients
4:36with bile duct obstruction will develop
4:38elevated plasma levels of alkaline
4:40phosphatase before hyperbilirubinemia
4:42bile duct obstruction at the level of
4:45the Knik UI can occur with
4:46granulomatosis disease amyloidosis and
4:49infections as well as with infiltrated
4:51diseases such as leukemia and metastatic
4:53malignancies kalila thesis is a most
4:56common cause of extra hepatic bile duct
4:58obstruction but other causes include
5:00tumors strictures infection inflammation
5:03or extrinsic compression
5:08serum ast and alt are hepatic
5:11mitochondrial enzymes elevated levels
5:14indicate hepatocellular injury from a
5:16variety of causes including viral
5:18infection alcohol abuse and obesity the
5:21highest elevations of the transaminases
5:23occur with ischemic or toxic liver
5:25injury and acute viral hepatitis
5:27the serum liver enzyme response to a
5:29Patou cellular injury can be confusing
5:31because elevations occur in the early
5:33phase of injury decreasing enzyme levels
5:36may indicate either recovery or
5:38worsening to severe irretrievable injury
5:40a good example is a fulminant hepatic
5:43failure seen with acetaminophen overdose
5:45following enzyme levels can lead to a
5:47false sense of security and lower the
5:49sense of urgency for a liver
5:50transplantation in this situation factor
5:547 levels can be helpful a closed liver
5:56biopsy guided by imaging can be
5:58performed percutaneously or trans vini
6:00ously percutaneous liver biopsy is
6:03simple and safe as long as established
6:05guidelines are followed it is usually
6:07contraindicated in patients with a
6:08coagulopathy thrombocytopenia
6:11encephalopathy or tense ascites the risk
6:15include hemorrhage from penetration of a
6:16major intrahepatic vessel bio liquid
6:19peritonitis and pneumothorax or a
6:21hemothorax transvenous liver biopsy via
6:26a catheter passed from the internal
6:27jugular vein and wedged into a branch of
6:29the hepatic vein allows the measurement
6:31of the inter hepatic capillary wedge
6:33pressure a surrogate for portal venous
6:35pressure as well as the opportunity to
6:37obtain a transcatheter needle biopsy of
6:39liver parenchyma transjugular biopsy may
6:42be indicated in patients with a very
6:44small liver coagulopathy patients or
6:47patients who are uncooperative chronic
6:49hepatitis is the most common indication
6:51for liver biopsy serial liver biopsies
6:54are helpful in following the progression
6:55or resolution of a disease as well as
6:58gauging the effects of treatment
6:59percutaneous imaging and a guided biopsy
7:02can establish the diagnosis of
7:04hepatocellular carcinoma metastatic
7:06malignancy or other invasive diseases of
7:08the liver needle biopsy helps establish
7:11the severity of cirrhosis of the liver
7:13by grading the extent of fibrosis and
7:15areas of vibro nodular hyperplasia
7:18high-resolution ultrasound and Doppler
7:20ultrasound
7:21examinations of the liver are
7:22non-invasive uncomplicated and simple to
7:24perform they give detailed information
7:27about the liver prank Emma liver blood
7:29vessels and lesions of the liver Doppler
7:32examination can demonstrate the patency
7:33or occlusion of the hepatic artery
7:35portal vein hepatic veins and the
7:38inferior vena cava lesions as small as 1
7:41centimeter can be identified with
7:43high-resolution ultrasonography and
7:45ultrasonographic imaging can guide
7:46needle biopsy with good accuracy
7:49intraoperatively ultra sonography
7:51guidance can be used to guide hepatic
7:52segments tectum ease ultrasonographer is
7:55most helpful in determining the cause of
7:57cholestatic jaundice and in locating
7:58gall stones it is less helpful in obese
8:01patients and in patients with gaseous
8:03distension of the stomach or intestines
8:07CT and MRI have advantages over
8:10ultrasound hardcopy images are produced
8:13and can be readily interpreted the
8:15spiral CT has greatly improved liver
8:17imaging because a complete scan with
8:19high resolution can be obtained during
8:21voluntary breath holding thus
8:22eliminating motion artifacts blood
8:25vessel Anatomy is enhanced with oral or
8:27intravenous contrast material CT and MRI
8:30studies also provide additional
8:32information about surrounding structures
8:34such as a spleen kidney collateral
8:36circulation and shuns CT with blood
8:39vessel enhancement provides better
8:40definition of liver segments for future
8:42resection now we'll take a look at
8:46hepatic metabolism hepatic drugget
8:51direction occurs at the level of the
8:52hepatocyte and with its dual a ferret
8:54blood flow systemically administered
8:57drugs arrive at the hepatic sinusoid via
8:58the hepatic artery whereas most orally
9:01administered drugs are absorbed in the
9:03small intestines and arrive in the liver
9:04via the portal vein when a drug is
9:07absorbed in the small intestine the
9:09liver has the opportunity to remove it
9:10from the bloodstream before the drug can
9:12exert systemic effects drugs can be
9:17divided into two groups based on the
9:18ability of the liver to remove them from
9:20circulation highly extracted lipid
9:23soluble or nonpolar compounds and poorly
9:26extracted water soluble or polar
9:27compounds in reality the distinction
9:30between these two groups is imperfect
9:32but it serves to help us understand
9:34hepatic drug clearance therefore
9:36clearance of highly extracted drugs is
9:38proportional to total liver blood flow
9:40liver disease abnormal hemodynamics and
9:43drugs can decrease both hepatic artery
9:45and portal vein blood flow and will
9:47exaggerate the systemic effects of the
9:49drug that is normally highly cleared by
9:51the liver also enter up dominance urger
9:54II and inhalational anesthetics can
9:55reduce liver blood flow by more than 80%
9:59because cirrhosis of the liver markedly
10:01decreases total hepatic blood flow as a
10:03result of fibrosis at the portal triad
10:06patients with cirrhosis can be expected
10:08to have increased sensitivity to highly
10:10extracted drugs for example propranolol
10:13which decreases total hepatic blood flow
10:15and is commonly prescribed for
10:17esophageal varices will increase the
10:19sensitivity of patients to highly
10:21extracted drugs nitroglycerin is also
10:24highly extracted it undergoes first pass
10:27hepatic clearance when it is
10:28administered orally consequently it is
10:31most effective when given sublingually
10:33or intravenously examples of other
10:36highly extracted drugs include labetalol
10:38metoprolol morphine
10:40verapamil and tylenol in practice the
10:45clearance of highly extracted drugs such
10:47as lidocaine is much more complex
10:49because of the role of protein binding
10:51protein binding limits the availability
10:53of lidocaine for hepatic extraction
10:55despite this lidocaine is highly
10:58extracted in fact very little lidocaine
11:01reaches the systemic circulation when it
11:03is administered orally
11:04lidocaine is rapidly absorbed in the
11:06small bowel and is delivered to the
11:08liver via the portal veins the near
11:10complete extraction of lidocaine is
11:12called the first pass clearance a
11:13phenomenon common to orally administered
11:15highly extracted drugs
11:17similarly systemically administered
11:20drugs that are highly extracted are
11:21rapidly cleared from the blood because
11:23the total hepatic blood flow is
11:24equivalent to about 30 percent of the
11:26cardiac output the same clearance
11:31expression can be used to understand the
11:32role of the liver and the metabolism of
11:34poorly extracted drugs hepatic
11:36microsomal enzymes are responsible for
11:38the metabolism of many of the drugs
11:40cleared by the liver because the
11:42activity of microsomal enzymes is
11:43dependent on normal hepatocellular
11:45function hepatic metabolism is decreased
11:48after hepatocellular injury and in
11:49cirrhosis of the liver the principal
11:52hepatic microsomal enzymes include the
11:54mono oxygenase Asst cytochrome c
11:56reductase and the cytochrome p450 system
12:01oxidation and hydroxylation by these
12:03enzymes convert drugs into polar
12:05water-soluble compounds alternatively
12:08alcohols can be converted into acetyl
12:10aldehydes by alcohol dehydrogenase once
12:14these reactions have occurred the drugs
12:15metabolites are conjugated with
12:16glucuronic acid and undergo active
12:19energy requiring excretion into the bile
12:21patients with cirrhosis are more
12:23sensitive to these drugs as the process
12:25can be saturated because of the
12:26compromised hepatocellular function some
12:29examples of drugs that are poorly
12:30extracted and are enzyme dependent for
12:32their metabolism include certain
12:34barbiturates benzodiazepines
12:36non-steroidal anti-inflammatory drugs
12:38caffeine theophylline and coumadin liver
12:44disease leads to
12:45other intrinsic and extrinsic effects
12:47that alter the plasma half-life are
12:48pharmacokinetic profiles of drugs first
12:52hypoalbuminemia is the characteristic
12:54finding in advanced liver disease the
12:57normal liver is capable of producing 10
12:58grams of albumin per day and this may be
13:00limited to less than 4 grams per day in
13:02advanced cirrhosis albumin is the
13:05principal plasma protein capable of drug
13:07binding severe hypoalbuminemia will
13:10increase the unbound concentration of
13:12any polar drug hypoalbuminemia and
13:15portal hypertension lead to an
13:16accumulation of extracellular fluid in
13:18the form of peripheral edema abdominal
13:21ascites and pleural effusions the
13:23apparent volume of drug distribution is
13:25increased greatly in the patients with a
13:27large volume of ascites cirrhosis
13:32secondary to chronic alcohol abuse will
13:33lead to increased effects of drugs that
13:35affect the central nervous system
13:36especially benzodiazepines this is
13:40caused not only by generalized cerebral
13:41cortical atrophy but also the
13:43accumulation of benzodiazepine like
13:45substances and ammonia in the central
13:47nervous system leading to hepatic
13:48encephalopathy benzodiazepine
13:51antagonists improve mental function in
13:53advanced encephalopathy benzo therapy
13:56for agitation should be used with
13:57caution in patients with any evidence of
13:59hepatic encephalopathy the kidneys share
14:02the load of drug excretion with the
14:03liver especially of low molecular weight
14:06conjugated compounds renal blood flow is
14:09diminished in advanced liver disease by
14:11virtue of the increased abdominal
14:12pressure seen with uncontrolled ascites
14:14acute renal failure or hepatorenal
14:17syndrome can be a complication of severe
14:20usually acute liver failure the
14:24metabolism of muscle relaxants deserves
14:26special attention sexina choline is
14:29metabolized by plasma pseudo
14:30cholinesterase patients with advanced
14:33liver disease may have decreased plasma
14:35levels of sidra cholinesterase leading
14:37to a prolonged duration of a
14:38neuromuscular blockade following sex
14:40administration pseudo cholinesterase has
14:43a high affinity for its substrate
14:44succinylcholine and metabolizes it
14:46rapidly even very low concentrations of
14:49plasma pseudo cholinesterase will result
14:51in only moderately prolonged paralysis
14:54this is an unlikely cause of clinical
14:56problems
14:57purified pseudo cholinesterase has been
15:00administered two homozygotes for a
15:01typical pseudo cholinesterase that have
15:03received Esther muscle relaxants this
15:06resulted in significant acceleration of
15:08recovery from neuromuscular blockade
15:10most of the nine depolarizing muscle
15:12relaxants are metabolized in the liver
15:14and metabolites are excreted either in
15:16bile urine or both of clinical relevance
15:19active metabolites of vecuronium
15:21accumulate in the plasma of patients
15:23with advanced liver disease now we will
15:27have a brief overview of a variety of
15:29liver diseases biliary atresia results
15:34from the destruction of bile ducts in
15:35utero infants do not survive childhood
15:38with complete atresia surgical
15:41correction of a distinct segment of
15:42biliary atresia may provide relief from
15:44severe jaundice and liver failure until
15:46liver transplantation can be performed
15:50Reye's syndrome is an acute
15:52encephalopathy precipitated by aspirin
15:54therapy for children with acute viral
15:56infection in the United States the
15:58incidence of Reye's syndrome has been
15:59tied to salicylate ingestion and the
16:01incidence has fallen as acetaminophen is
16:03substituted for salicylates in children
16:05with viral illnesses Wilson disease
16:09consists of progressive lenticular
16:11degeneration associated with cirrhosis
16:13of the liver it is an autosomal
16:15recessive abnormality of copper
16:17metabolism and results in the
16:18characteristic greenish kaiser Fleischer
16:20rings in the cornea the plasma
16:23ceruloplasmin level is decreased
16:25however Wilson disease is not a failure
16:28to produce ceruloplasmin it is a failure
16:30of copper transport followed by coupling
16:32to ceruloplasmin penicillamine therapy
16:35key lates copper leading to improvement
16:37of the neurologic symptoms and the
16:38prevention of cirrhosis fulminant
16:41hepatic necrosis can occur in 25% of
16:43cases and requires urgent liver
16:45transplantation patients with Wilson
16:47disease require uninterrupted
16:49penicillamine therapy in the
16:50perioperative period chronic
16:55of iron exposure causes hepatic fibrosis
16:56or hemochromatosis irrespective of
16:59whether the accumulation is a result of
17:01multiple transfusions or the abnormal
17:03absorption and accumulation of dietary
17:05iron hemochromatosis leads to cirrhosis
17:08and hepatocellular carcinoma hereditary
17:11haemochromatosis results in macro
17:13nodular cirrhosis diabetes from
17:15pancreatic fibrosis and cardiac iron
17:18deposition often with heart failure
17:19conduction abnormalities and coronary
17:21atherosclerosis this disease is an
17:24autosomal recessive metabolic disorder
17:26although present from birth tissue
17:29injury does not begin until age 30 to 40
17:31iron toxicity is controlled by
17:33aggressive removal of blood multiple
17:36organ like heart liver and pancreas
17:38transplantation may be required
17:42alpha-1 antitrypsin is an enzyme
17:45inhibitor produced in the liver that
17:46inhibits key proteases such as trypsin
17:48and neutrophils elastase two genes when
17:52received from each parent control the
17:53production of alpha 1-antitrypsin there
17:56are many alleles but only two are
17:58associated with the disease M is the
18:01normal allele s and z are the two
18:03alleles that are clinically significant
18:04silent genes result in complete lack of
18:07alpha 1-antitrypsin production the
18:10normal Ino type is P IMM the abnormal
18:13genotype piz z causes emphysema and in
18:16approximately 20% of patients cirrhosis
18:18the P is s and P i MZ do not cause lung
18:22disease the P is zg note i present some
18:26increased risk of lung disease liver
18:28disease may be associated with the P imz
18:31and Piz genotypes non-alcoholic fatty
18:36liver disease is prevalent in the obese
18:38population in a prospective study of
18:41eleven hundred and twenty-four
18:42asymptomatic patients referred for
18:44evaluation of abnormal liver function
18:46tests 73 of 81 patients without markers
18:49for liver disease were found to have
18:51some degree of CI ptosis on liver biopsy
18:54NAFLD is believed to be the most common
18:56cause of abnormal liver function tests
18:58in the u.s. it is most prevalent in the
19:01morbidly obese patients with type 2
19:02diabetes paradoxically it occurs
19:05frequently following bariatric surgery
19:07in its early
19:08staged NAFLD is manifested by macro
19:11vesicular fatty infiltration of less
19:13than one third of hepatocytes mostly in
19:15zone three with minimal inflammation
19:18serum transaminases are elevated and
19:20ultrasound demonstrates a diffuse
19:22increase of echogenicity zone 3 fibrosis
19:25may be focal or extensive grade 2
19:28steatosis is a more advanced form of
19:30NAFLD involving up to two thirds of the
19:33hepatocytes with extensive fibrosis in
19:35the parry portal areas grade 3 which is
19:38more than two-thirds of hepatocytes
19:40stages three and four which includes
19:42bridging fibrosis and cirrhosis is an
19:44advanced form of the disease in this
19:46respect NAFLD is difficult to
19:48distinguish from alcoholic liver disease
19:50it is hypothesized that NAFLD is an
19:53abnormality of lipid uptake synthesis
19:56degradation or secretion resulting from
19:58insulin resistance although NAFLD is an
20:02infrequent indication for liver
20:03transplantation it has the potential to
20:05be a precipitating cause a post
20:07operative liver dysfunction now we will
20:11look at some acquired liver diseases
20:15viral hepatitis is a broad collection of
20:18illnesses that have hepatic dysfunction
20:19as the only common thread the etiology
20:22modes of transmission clinical course
20:24and late complications are all different
20:26all forms of viral hepatitis showed
20:29diffuse acute inflammation with
20:30leukocyte and histo site infiltration
20:32followed by hepatic necrosis and
20:34regeneration with recovery zone 3
20:37hepatocyte suffer the greatest injury
20:39inflammation may be limited to zone 3 in
20:42mild forms of viral hepatitis or it may
20:44extend to the entire asommus and
20:46fulminant hepatic necrosis when the
20:49entire acid s is involved the patients
20:51will eventually develop post necrotic
20:52scarring with fibrosis hepatitis A is
20:57the least severe of the known forms of
20:59viral hepatitis the fecal-oral route as
21:02a contaminant of drinking water or food
21:04especially uncooked shellfish causes
21:06hepatitis A the incubation period for
21:09the disease is approximately equal to or
21:11greater than 15 days and plasma
21:13transaminases and bilirubin levels may
21:15not rise until several weeks into the
21:16course of the disease although recovery
21:19may take several weeks to months most
21:21pay
21:21with hepatitis a have an unpleasant
21:23course but uncomplicated recovery
21:25fulminant hepatic necrosis with liver
21:27failure requiring transplantation is
21:29extremely rare with hepatitis A
21:31infection hepatitis E is a form of viral
21:36hepatitis that is very similar to
21:38hepatitis A it occurs in developing
21:41countries where there is a fecal
21:42contamination of the drinking water
21:44fulminant hepatic failure following
21:46hepatitis E infection can be a serious
21:48complication of the third trimester of
21:50pregnancy hepatitis B is not often
21:55associated with jaundice however
21:57hepatitis B can lead to either fulminant
21:59hepatic necrosis and liver failure or
22:01chronic hepatitis HBS Age II was first
22:05identified in to patients who had
22:06received multiple transfusions from a
22:08haemophilia when their serum which had
22:10antibodies to HB s AG was tested in a
22:13panel that contained an antigen from an
22:15Australian Aborigine the antigen was
22:18called the Australian antigen and was
22:21subsequent identified as the antigen of
22:23viral hepatitis B the antigens and
22:26antibodies found in patients with
22:27hepatitis B form the basis for both
22:29diagnosis and prognosis HB s AG is
22:33present in the bloodstream during the
22:34acute phase of the disease and persists
22:36for more than six months if the patient
22:37becomes a carrier of hepatitis B hantai
22:40hepatitis antibodies persist in our
22:42evidence of prior hepatitis B infection
22:44or exposure hepatitis B is spread by
22:47sexual contact or exposure to blood
22:49products evidence of exposure to blood
22:52products by positive anti-hbs has been a
22:55common finding insurgents and anesthesia
22:57providers who have been in practice for
22:58years prior to the availability of the
23:00hepatitis B immunization and the
23:02adoption of universal precautions today
23:05hepatitis B vaccination of healthcare
23:07workers is mandated by institutional
23:09regulations body fluids including blood
23:12urine saliva and semen have been shown
23:14to carry hepatitis B virus DNA and
23:17samples obtained from HBS ag+ patients
23:22hepatitis D is a severe viral infection
23:25of the liver that occurs as a CO
23:27infection of a patient with acute
23:28hepatitis B or as a super infection in a
23:31patient with chronic hepatitis B but
23:33hepatitis D does not cause hepatitis
23:35independently in Western cultures it
23:37occurs most often in patients with a
23:39history of intravenous drug use but
23:41healthcare workers in transfusion
23:43recipients are also at risk as our other
23:45patients who have acquired acute or
23:47chronic active hepatitis B the virus of
23:52hepatitis C is an envelope
23:53single-stranded RNA virus immunologic
23:57identification of infection with the
23:58hepatitis C or HCV can be difficult
24:01antibodies against hepatitis C may not
24:04be present for long periods following
24:05initial infection this has important
24:08public health implications because of
24:10the prevalence of asymptomatic carriers
24:12routine testing of donated blood for HCV
24:15and HIV by polymerase chain reactions
24:17has reduced the incidence of
24:19transmission of hepatitis C and HIV to
24:21approximately one in two million
24:23transfusions PCR testing is not
24:26available for HPV thus the incidence is
24:28much higher at one in 75,000 much like
24:32hepatitis B those patients at increased
24:34risk of hepatitis C include recipients
24:37of blood products IV drug abusers
24:39hemophiliacs and health care workers
24:41following hollow needle sticks sexual
24:44transmission of hepatitis C may be
24:46possible hepatitis C rarely causes
24:51fulminant hepatic failure in fact
24:53subclinical chronic non enteric
24:55infection is fairly common unfortunately
24:58about half of the patients with acute
25:00hepatitis c infection will have evidence
25:01of ongoing hepatitis after one year at
25:04least twenty percent of these patients
25:06will eventually develop cirrhosis these
25:09patients are also at high risk of
25:10developing hepatocellular cancer through
25:12several possible immunologic and genetic
25:14events there is no vaccine yet to
25:17prevent hepatitis C infection now we'll
25:22take a look at toxic liver disease the
25:26excessive day
25:27consumption of alcohol can lead to
25:29alcoholic hepatitis especially in
25:31individuals with a low-calorie and low
25:33protein diet ingestion of 80 grams of
25:36alcohol a day places the individual at
25:38risk for alcoholic hepatitis a pre
25:40cirrhotic lesion chronic consumption of
25:43lower doses of alcohol may lead the
25:45fatty infiltration of the liver and
25:46eventually the cirrhosis of the liver
25:48alcohol is metabolized by alcohol
25:51dehydrogenase to acetyl aldehyde acetyl
25:54aldehyde dehydrogenase is the rate
25:56limiting step in eliminating acetyl
25:58aldehyde but it can be overwhelmed when
26:00large amounts of alcohol are ingested
26:04acetyl aldehyde when it cannot be
26:06rapidly eliminated is toxic to a number
26:09of cellular components and can lead to
26:10zone 3 hepatic necrosis alcohol can also
26:13be metabolized by the microsomal ethanol
26:16oxidizing system an alcohol inducible
26:18p450 system that also metabolizes
26:21acetaminophen the metabolism of acetyl
26:24aldehyde alters a reduced form of NADH
26:26nad ratio in the cytoplasm of hepatocyte
26:29s' this change in energy metabolism
26:32leads to fatty acid accumulation in
26:34zones 2 & 3 cells an early feature of
26:36alcoholic hepatitis severe hepatitis
26:40secondary to alcohol ingestion alone is
26:42rare however a fatty liver and chronic
26:45alcoholic hepatitis will lead to
26:46cirrhosis advanced cirrhosis secondary
26:51to long-term alcohol abuse is
26:53irreversible and patients will
26:54demonstrate the cardinal features of
26:56portal hypertension secondary to
26:57obliteration of portal venules in early
27:00stages patients with alcoholic cirrhosis
27:02do well as compared to other causes of
27:05cirrhosis if they can abstain from
27:06alcohol and correct their nutritional
27:08deficiencies primarily vitamins and
27:10proteins that are associated with
27:11alcohol abuse
27:12however the five-year survival rate in
27:15patients with ascites jaundice and
27:17variceal bleeding is 50% overall 40%
27:20with continued alcohol abuse and 60%
27:21with abstinence chronic alcohol abuse of
27:24greater than 90 grams per day for more
27:26than five years can lead to alcoholic
27:28cardiomyopathy in addition to cirrhosis
27:30of the liver alcohol abuse is a leading
27:33cause of non ischemic cardiomyopathy in
27:35the u.s. cardiac performance may improve
27:38with the abstinence of alcohol many
27:40patients with
27:41alcoholic cirrhosis often have
27:43concomitant risk factors for coronary
27:44atherosclerosis others may have cardiac
27:47valvular abnormalities requiring a valve
27:50replacement cardiac surgery performed
27:52using cardiopulmonary bypass has a high
27:54mortality rate in this patient
27:56population
27:59suicide attempts are the most common
28:01cause of acetaminophen induced hepatic
28:03necrosis and subsequent fulminant
28:04hepatic failure the lethal adult dose of
28:07acetaminophen is approximately 10 grams
28:09but this can be greatly reduced in
28:11patients with concomitant alcohol abuse
28:13or pre-existing liver disease
28:15acetaminophen is metabolized by the p450
28:18system in the macros ohms of hepatocyte
28:20to metabolites binding to cellular
28:22macromolecules glutathione normally
28:25binds to and clears the metabolites of
28:26acetaminophen and it's depletion may
28:28lead to the accumulation of toxic
28:30acetaminophen metabolites acetylcysteine
28:33can increase the production of
28:34glutathione and may prevent hepatic
28:36necrosis if given within the first few
28:38hours after acetaminophen ingestion
28:42fulminant hepatic necrosis and acute
28:45liver failure can occur two to three
28:46days following an acetaminophen overdose
28:49plasma transaminases are markedly
28:51elevated during the first few days after
28:53ingestion coagulopathy can become severe
28:56when the INR increases severe
28:59coagulopathy and encephalopathy are
29:01signs of a poor prognosis the outcome of
29:04acetaminophen induced hepatic necrosis
29:05can be predicted by measuring the plasma
29:08level of acetaminophen four hours after
29:10ingestion blood levels greater than 300
29:13grams per mil predict that hepatic
29:14necrosis will occur blood levels less
29:17than 120 grams per mil usually do not
29:19result in hepatic necrosis
29:21acetylcysteine is most effective when
29:24given intravenously or orally within 24
29:26hours after the ingestion of
29:27acetaminophen but it may be effective
29:29even if given up to 72 hours after
29:32ingestion many other drugs are hepato
29:36toxic their toxicity mimics other liver
29:39diseases valproic acid causes fatty
29:42infiltration of the liver drugs such as
29:44NSAIDs methyl dopa amiodarone
29:47nifedipine and isoniazid may mimic acute
29:50viral hepatitis and chronic active
29:51hepatitis methotrexate can
29:54hepatic fibrosis and portal hypertension
29:57antibiotics tranquilizers and sex
29:59hormones may cause cholestasis
30:01sex hormone therapy may also cause
30:04thrombosis of portal and hepatic veins
30:06in most cases of drug-induced hepatic
30:11dysfunction recovery occurs following
30:12withdrawal of the drug recovery may be
30:15prolonged with a drug like amiodarone
30:16because of its long half-life and the
30:18extremely long time required to
30:20eliminate metabolites furthermore some
30:23drugs can become locked into the entero
30:25hepatic circulation by the intestinal
30:27reabsorption of their toxic metabolites
30:30now we will look at autoimmune and
30:33inflammatory liver diseases autoimmune
30:36hepatitis primary biliary cirrhosis and
30:38primary sclerosing cholangitis appear to
30:41result from autoimmune mechanisms at
30:43times they are difficult to distinguish
30:45from each other or from other
30:47inflammatory diseases such as viral
30:48hepatitis patients with these autoimmune
30:51diseases often do well following liver
30:53transplantation autoimmune hepatitis is
30:58a disease characterized by Auto
30:59antibodies against a variety of liver
31:01antigens including mitochondrial and
31:04nuclear antigens
31:05it is most common in young women blood
31:08testing shows elevated gamma globulin
31:10and positive anti-nuclear antibodies
31:13early treatment with corticosteroids and
31:15anti-inflammatory drugs can slow the
31:17progression of this disease and delay or
31:19prevent the need for liver
31:20transplantation
31:22consequently it is important to
31:23distinguish autoimmune hepatitis from
31:25other forms of hepatitis with similar
31:27histology on liver biopsy patients with
31:30autoimmune hepatitis may develop
31:32cirrhosis and hepatocellular carcinoma
31:34if the autoimmune process is not
31:36controlled jaundice is not common in
31:38autoimmune hepatitis and patients often
31:40remain well nourished making them good
31:42candidates for liver transplantation
31:45corticosteroids may produce a remission
31:46in the disease and often reduce plasma
31:48bilirubin transaminases and gamma
31:51globulin levels primary biliary
31:55cirrhosis is an inflammatory disease of
31:57the intrahepatic bile ducts 90% of
32:01patients are women with onset occurring
32:02between the ages of 30 and 70 PBC is
32:05characterized by severe jaundice
32:08the other features of liver disease and
32:09thus higher bilirubin levels are used
32:11for stratification human leukocyte
32:14antigens are HLAs expressed in bile
32:16ducts appear to be the target for
32:18lymphocytes other ductal glands are also
32:21targets in this disease patients with
32:24PBC have high serum cholesterol levels
32:26they develop disabling cutaneous Xsan
32:29Thelma's of their hands and feet and
32:30severe / itis they may have other
32:33autoimmune diseases such as rheumatoid
32:34arthritis systemic lupus erythematosus
32:37scleroderma and SH Rogen's syndrome PBC
32:43can also cause interstitial lung disease
32:45and giant cell granulomas serum
32:48bilirubin levels rise dramatically as
32:50the disease progresses and are
32:51predictive of the length of survival
32:53once serum bilirubin levels exceed 6
32:56milligrams per deciliter expected
32:58survival is less than two years these
33:00patients appear clinically healthier
33:02than patients with similar levels of
33:03jaundice secondary to alcoholic
33:05cirrhosis PBC patients do well after
33:08transplantation it is unclear whether
33:11they are at risk of developing recurrent
33:12PBC in the transplanted liver primary
33:17sclerosing cholangitis or PSC is another
33:20inflammatory disease of the intra and
33:22extra hepatic bile ducts of undetermined
33:25etiology affecting more men than women
33:27it may be difficult to distinguish in
33:29the early phases from primary biliary
33:31cirrhosis serum anti mitochondrial
33:34antibodies are positive in primary
33:36biliary cirrhosis and negative in
33:38primary sclerosing cholangitis this
33:41inflammatory disease will eventually
33:43obliterate the bile ducts and cause
33:44severe jaundice and eventually liver
33:46failure colon geography reveals a
33:49characteristic beating and stenosis of
33:51the common bile duct ulcerative colitis
33:53is diagnosed in as many as 70 percent of
33:56patients with primary sclerosing
33:57cholangitis
33:58in addition PSC patients are at an
34:01increased risk of developing
34:03cholangiocarcinoma the only successful
34:06treatment of primary sclerosing
34:07cholangitis is liver transplantation
34:12hepatocellular carcinoma is rare in
34:14Western countries but common in Asian
34:16and African countries it can present as
34:19a discrete encapsulated mass
34:21as an infiltrated disease or as a
34:23multicentric disease predisposing
34:26factors for HCC include chronic active
34:28viral hepatitis and hemochromatosis
34:30although it may also be associated with
34:32other forms of cirrhosis hepatitis C is
34:35a leading risk factor for HCC in the
34:37Western world whereas hepatitis B is a
34:39leading risk factor in Asian and African
34:41patients other risk factors for HCC
34:44include long-standing heavy alcohol
34:46abuse cigarette smoking diabetes and
34:49fatty liver the incidence of HCC in
34:52Asian and African countries correlates
34:54closely with dietary exposure to a flow
34:56toxin a carcinogen produced by
34:58Aspergillus flavus a mold that
35:00contaminates food in these continents
35:04ultrasonographer CT scanning and MRI are
35:07helpful in diagnosing and localizing HCC
35:10tumors for diagnosis and biopsy but
35:12their value is decreased in patients
35:14with cirrhosis characterized by large
35:15areas of fibro nodular regeneration
35:18hepatic resection for HCC in patients
35:20with intact synthetic liver function
35:22offers a 26% five-year survival rate
35:25predictors of survival include excellent
35:28preoperative hepatocellular function the
35:30presence or absence of multiple tumors
35:32resection margins free of tumor and the
35:34need for blood transfusion during
35:36surgery liver transplantation as a
35:38therapy for limited HCC is now an
35:40established therapy : geo carcinoma is a
35:46highly malignant disease that is rare in
35:48the Western world but endemic in Asia
35:50and those regions where patients are at
35:52risk for parasitic infection with a
35:53liver fluke it is also associated with
35:56primary sclerosing cholangitis and
35:58ulcerative colitis liver transplantation
36:01is contraindicated for patients with Co
36:03NGO carcinoma patients are often
36:05jaundice and without other signs of
36:07liver failure diagnosis is established
36:10by ultra sonography and CT imaging and
36:12ERCP when the tumor involves the
36:15secondary branches of the left and right
36:17hepatic ducts
36:18it is not resectable but palliation can
36:20be achieved with stinting of the bile
36:21ducts by an endo prosthesis now we will
36:27look at
36:27causes of acute liver failure acute
36:32liver failure or fulminant hepatic
36:33failure is a catastrophic illness
36:35resulting from many of the liver
36:37diseases described in this lecture it
36:39develops within two weeks of the onset
36:41of disease and carries a poor prognosis
36:42without transplantation it occurs so
36:46rapidly that patients may not have
36:47developed jaundice sub fulminant hepatic
36:50failure with onset occurring up to eight
36:52weeks after the onset of jaundice has a
36:54better prognosis with some chance of
36:56complete recovery transaminase levels
36:59rise rapidly with fulminant hepatic
37:00failure but they may fall to normal
37:02levels after massive necrosis occurs
37:05coagulopathy can become progressively
37:07more severe the common features a
37:12fulminant hepatic failure include a
37:13severe coagulopathy metabolic acidosis
37:17hypoglycemia rapidly progressive
37:19encephalopathy and acute renal failure
37:22encephalopathy with severe cerebral
37:24edema is a usual cause of death which
37:26may occur while the patient awaits a
37:28donor liver the most common cause of
37:30fulminant hepatic failure is acute viral
37:32hepatitis fulminant hepatic failure in
37:38patients with hepatitis B can be
37:39precipitated by super infection with
37:41hepatitis D immunocompromised patients
37:44are at high risk for FH F with acute
37:46viral hepatitis including a B herpes
37:49simplex cytomegalovirus epstein-barr
37:52virus and varicella there is another
37:54cause of fhf that needs to be considered
37:56in surgical patients alterations in
37:59total hepatic blood flow during
38:00anesthesia and surgery may precipitate
38:02fulminant hepatic failure in patients
38:04with stable underlying chronic liver
38:06disease in these patients acute liver
38:09failure is usually noticed on the second
38:11or third post-operative day and can be
38:12manifested by an unexplained
38:14encephalopathy these patients have
38:16adequate hepatocellular function
38:18preoperatively but with very little
38:20reserve to combat acute stress
38:21associated with anesthesia and surgery
38:24small decreases in hepatic oxygen supply
38:27associated with decreased total hepatic
38:29blood flow during surgery cause acute
38:31hepatocellular ischemic injury and
38:33failure the encephalopathy of fhf is
38:39different from that noted with chronic
38:40liver
38:40and the blood ammonia levels are much
38:42higher in addition amino acids which can
38:46contribute to the encephalopathy
38:47accumulate in the central nervous system
38:49and are excreted in the urine as
38:51tyrosine and leucine crystals fhf with
38:54grade three or worse encephalopathy is
38:56associated with an 80% mortality rate in
38:59contrast two-thirds of patients survive
39:01if encephalopathy does not proceed
39:03beyond grade two the principal cause of
39:06death are cerebral edema hemorrhage
39:08secondary to a severe coagulopathy and
39:10sepsis syndrome secondary to pneumonia
39:13metabolic derangement seen in fhf may
39:15include severe hypoglycemia
39:17hyperinsulinemia hyponatremia
39:20hypokalemia and lactic acidosis
39:23respiratory alkalosis may be caused by
39:25hyperventilation acute renal failure is
39:28seen in as many as fifty five percent of
39:30patients with fhf acute respiratory
39:33failure may be caused by aspiration
39:35pneumonitis or form part of the multi
39:37organ failure associated with sepsis
39:39survival is frequent with
39:41transplantation but many patients die
39:43while awaiting the availability of a
39:44donor organ now we will look at causes
39:49of chronic liver failure chronic liver
39:54failure eventually can impair most of
39:56the organ systems in the body many of
39:58the manifestations are caused by the
40:00hepatic fibrosis that follows
40:01hepatocellular injury portal fibrosis
40:05produces compression of the portal
40:06venules capillaries biliary Kenickie lie
40:09and obliteration of hepatocytes the
40:12result is portal hypertension
40:13obstructive jaundice coagulopathy
40:16encephalopathy and metabolic
40:18abnormalities if the underlying cause of
40:21fibrosis is treated effectively fibrosis
40:23of the liver may be reversible in the
40:26early stages of chronic liver failure
40:27ascites has controlled with diuretic
40:29therapy in later stages ascites is
40:32uncontrolled and patients develop the
40:34protuberant abdomen with a fluid wave on
40:36physical examination that is typical of
40:38advanced cirrhosis portal hypertension
40:41leads to abnormal renal function with
40:43Market sodium reabsorption in response
40:45to a decreased effective circulating
40:47plasma volume volume receptor
40:52stimulation increases renin secretion
40:54and aldosterone production urinary
40:57excretion of sodium is limited and total
40:59body sodium is greatly increased yet the
41:01patient show mild hyponatremia this
41:04forms the basis for therapy with loop
41:06diuretics such as lasix and aldosterone
41:07antagonists such as el doc Doane renal
41:11blood flow and GFR can be decreased in
41:13chronic liver failure because of the
41:14increased intra-abdominal pressure
41:16caused by ascites diuretic therapy and
41:18other hemodynamic abnormalities ascites
41:22is associated with spontaneous bacterial
41:24peritonitis another life-threatening
41:26complication of chronic liver failure an
41:28aerobic gram-negative organism is a
41:31usual cause of the peritonitis it may be
41:34truly spontaneous and caused by
41:35incidental bacteremia but often follows
41:38paracentesis to reduce the volume of
41:39ascites the 30-day mortality rate for s
41:42BP is approximately 32 percent one-year
41:46mortality is 78 percent survivors are at
41:49a higher risk of reoccurrence portal
41:54hypertension can lead to the development
41:55of collateral circulation with large
41:57veins in the abdominal and chest walls
41:59the mediastinum stomach and esophagus in
42:02extreme cases these venous collaterals
42:05Canon s the most with pulmonary vessels
42:06leading to portal pulmonary shunting
42:08this can produce a high blood volume
42:11high blood flow state with inter
42:12pulmonary Shen's the so called capital
42:14pulmonary syndrome or HP s the
42:17collateral circulation that occurs with
42:19portal hypertension can produce
42:20esophageal gastric and intestinal
42:22varices that are prone to rupture and
42:24bleeding obstructive jaundice is a late
42:27finding in most forms of cirrhosis and
42:29indicates a poor prognosis severe
42:31jaundice predicts death within a few
42:33years severe jaundice is usually
42:36accompanied by poor synthetic function
42:37with coagulopathy progressive
42:39encephalopathy and severe malnutrition
42:41there are two causes of the coagulopathy
42:44associated with chronic liver disease
42:46the first is decreased production of
42:48coagulation factors produced in the
42:50liver which are all accept factor 8 the
42:53second is a hypersplenism resulting from
42:55portal hypertension measuring the INR
42:58plasma fibrinogen level or direct
43:01measurement of coagulation factor
43:02activity readily assesses coagulopathy
43:04secondary to impaired synthetic function
43:07hypersplenism with sequesteration of
43:10platelets is common in advanced liver
43:11disease and results in platelet
43:13concentrations equal to or less than 70
43:15thousand bleeding from thrombocytopenia
43:18is uncommon enlisted is complicated by
43:20other causes of thrombocytopenia such as
43:22active bleeding with either a
43:23consumption coagulopathy or a dilutional
43:26coagulopathy metabolic abnormalities
43:31include hypoglycemia hyperinsulinemia
43:33amino acid emia amino acid urea
43:36respiratory alkalosis lactic acidosis
43:40hyponatremia and hypokalemia if patients
43:44require rapid multiple transfusions
43:46hypocalcemia secondary to citric
43:48toxicity may become a problem
43:50encephalopathy and chronic liver failure
43:52is associated with an elevation of the
43:54plasma ammonia level however
43:57encephalopathy and neurological
43:59manifestations of chronic liver disease
44:01are much more complex than simple
44:03ammonia intoxication ammonia is only one
44:06of the many potentially neurotoxic
44:08compounds that are produced in the
44:09intestines and reach the brain by virtue
44:11of the collateral portosystemic shunt
44:12thing of chronic liver disease normally
44:16the liver extracts all of these
44:17compounds from portal vein blood central
44:20nervous system gaba amino butyric acid
44:22and inhibitory neurotransmitter is also
44:25increased in chronic liver disease as
44:27our GABA and benzodiazepine receptors in
44:30the brain there are other
44:34of abnormal neurologic findings in
44:36chronic liver disease there can be
44:38generalized cortical atrophy and the
44:40increased presence of astrocytes often
44:42associated with Alzheimer's disease the
44:45EEG shows generalized slowing vitamin
44:49deficiencies can lead to Wernicke
44:50encephalopathy which is inadequate
44:52thiamine and b1 and also contributes to
44:54the neurologic findings of chronic liver
44:56disease portal systemic encephalopathy
44:59is characterized by depressed
45:00consciousness personality changes
45:02slurred speech apraxia and a flapping
45:05tremor severity is graded from minimal
45:08confusion through coma Grade four coma
45:11is usually a terminal event the
45:16circulation and chronic liver disease is
45:18hyper dynamic and characterized by a
45:19markedly increased cardiac index a low
45:22systemic vascular resistance mild
45:24tachycardia a normal to increased stroke
45:26volume a high mixed venous oxygen
45:28saturation and a poor oxygen extraction
45:31ratio patients with the normal cardiac
45:34index at cardiac catheterization should
45:36be considered to have a cardiomyopathy
45:37and the differential diagnosis should
45:39include ischemic cardiomyopathy
45:41alcoholic cardiomyopathy and
45:43cardiomyopathy secondary to
45:45hemochromatosis systemic pre capillary
45:48AV shunting can cause a hemodynamic
45:50changes seen in the chronic liver
45:51disease circulating blood volume is
45:54reduced an extracellular fluid volume is
45:56often markedly increased coronary artery
45:58disease in patients with advanced liver
46:00disease may require coronary
46:01revascularization - pulmonary syndromes
46:07are noted in patients with advanced
46:08liver disease the first is the HP s the
46:11second is portal pulmonary hypertension
46:13or pph HBS is characterized by pulmonary
46:17pre capillary and capillary vaso
46:19dilatation and direct pulmonary AV
46:21communications this syndrome is
46:23associated with a three-fold elevation
46:25of exhaled nitric oxide as compared to
46:28control subjects the patients are short
46:30of breath cyanotic and display systemic
46:33arterial hypoxemia dyspnea and tachypnea
46:36and oxygen desaturation is worsened in
46:39the upright position a syndrome
46:40described as Platini a' and orthodoxy a'
46:43this is a high-volume low-pressure
46:45pulmonary blood state with normal
46:48ventricular function and a low pulmonary
46:50vascular resistance pph on the other
46:55hand is a high pressure state similar to
46:57primary pulmonary hypertension the right
47:00ventricle is often dilated cyanosis is
47:02absent right ventricular ejection
47:04fraction is low and systemic hypoxia is
47:07rare these patients may acutely respond
47:10to inhaled nitric oxide patients with
47:13HBS fare better after liver
47:14transplantation then do those with pph
47:20hepatorenal syndrome is a form of renal
47:22failure associated with liver disease it
47:24is more common in acute liver failure
47:26but also occurs in patients with chronic
47:28liver failure hepatorenal syndrome is
47:31the result of intense renal arteriolar
47:33vasoconstriction in response to the
47:35functional hypovolemia caused by splenic
47:37vaso dilatation and other physical
47:39changes of liver failure type 1
47:42hepatorenal syndrome typically evolves
47:44over less than one week and is an
47:45indication for urgent liver
47:47transplantation type 2 hepatorenal
47:49syndrome develops over a period of a
47:51month and is less of an emergency
47:53standard treatment of hepatorenal
47:55syndrome includes intravascular volume
47:57expansion with administration of albumin
47:59and the reduction of intra-abdominal
48:01pressure by relieving 10 societies the
48:04administration of a vasopressin analog
48:06turley pressin may improve renal
48:08function by its action as a splenic
48:10vasoconstrictor portal venous pressure
48:13reduction by tips has been used for
48:14hepatorenal syndrome but it is not
48:16recommended on the basis of controlled
48:18clinical trials the prognosis of
48:21hepatorenal syndrome is poor now we will
48:26look at the approaches to management FFP
48:31infusion and/or cryoprecipitate
48:32administration greatly improves the
48:34coagulopathy of either acute or chronic
48:36liver failure recombinant factor 7 may
48:39also improve the coagulopathy therapy
48:42should be guided by measurement of the
48:44INR plasma fibrinogen levels and
48:46specific coagulation factor analysis
48:48when available patients may require
48:50infusions of large volumes of FFP which
48:53can itself contribute to circulatory
48:55overload it is important to avoid the
48:58inadvertent administration of small
48:59doses of heparin via monitoring lines to
49:01patience with the coagulopathy secondary
49:03to liver disease platelet transfusion is
49:06not indicated unless a platelet count is
49:08less than 70,000 platelets can be
49:10sequestered in the spleen when the
49:12patient has hypersplenism endoscopic
49:17band ligation therapy is the mainstay of
49:19treatment to reduce esophageal varices
49:20and prevent variceal hemorrhage
49:23treatment with nonspecific beta
49:25adrenergic blockers particularly
49:27propranolol and natal off may decrease
49:28the size of esophageal varices
49:31however these agents do not reduce the
49:33portal hypertension which caused the
49:35development of the varices in the first
49:36place
49:37portal decompression can be accomplished
49:39surgically through a portal cable shunt
49:41bezel cable shunt or splenorenal shunt
49:43or by means of a trance jag euler
49:45intrahepatic portal vein to hepatic vein
49:48shut to high complication rate and a
49:51mortality rate that is similar to that
49:52reported by centers with extensive
49:54experience in surgical shunting
49:56pre-existing encephalopathy may preclude
49:58any form of portal shunting because of
50:01the decrease in ammonia extraction that
50:02follows a decrease in portal vein blood
50:04flow to the liver octreotide is a
50:07somatostatin analog that has been used
50:09for control of non variceal upper and
50:11lower gastrointestinal bleeding
50:12secondary to portal hypertension it is
50:15administered as a continuous infusion
50:17and produces vasoconstriction of the
50:19portal circulation vessels ascites is
50:24the accumulation of an extracellular
50:25colloidal fluid in the abdominal cavity
50:27as a result of long-standing portal
50:29hypertension it is a consistent finding
50:32in patients with cirrhosis and it is a
50:34poor prognostic finding as only 50% of
50:36patients with societies will survive for
50:38two years the diagnosis of ascites can
50:41be made by ultra sonography when it is
50:42not apparent on physical examination
50:45ascites can be controlled by restriction
50:47of sodium intake in the diet by the
50:49administration of diuretics or by
50:50abdominal paracentesis dietary sodium
50:54restriction is often difficult to
50:55maintain because of non-compliance
50:58diuretic therapy includes the use of
51:00furosemide and al Doc tone optimal
51:03diuretic therapy requires several weeks
51:04during which time the balance of sodium
51:06intake versus renal excretion of sodium
51:08is monitored potassium balance is
51:11achieved with the use of potassium
51:13wasting diuretics like lasix and
51:15I am sparing diuretics like albick tone
51:17if diuretic therapy is ineffective
51:19invasive procedures may be necessary to
51:21relieve tense abdominal swelling these
51:24procedures include large volumes of
51:26fluid removal by paracentesis peritoneum
51:29venous shunting or tips large volume
51:32paracentesis leads to progress of
51:34wasting a protein but not usually the
51:36hemodynamic instability slow removal of
51:39ascites by paracentesis can relieve the
51:41symptoms of massive ascites and improve
51:43the quality of life for these patients
51:45currently peritoneum venous shunting is
51:48performed infrequently because of the
51:50risk associated with the procedure and
51:51the lack of advantages over paracentesis
51:53and tips the risk include hepatic
51:56failure secondary to a major surgical
51:58procedure in patients with marginal
52:00hepatocellular function the risk of
52:02bacterial contamination with subsequent
52:04peritonitis and the risk of a
52:06post-operative ascites leak the
52:08procedure can be complicated by
52:10thrombosis followed by non function of
52:12the shunt encephalopathy is present in
52:17the majority of patients with cirrhosis
52:19although at times it may only be
52:21demonstrated by psychometric testing
52:23because encephalopathy can progress
52:25rapidly from subclinical findings to
52:27overt coma it should be anticipated in
52:29any patient with cirrhosis undergoing
52:31surgery encephalopathy is graded
52:34according to the level of consciousness
52:35personality and intellectual features
52:37neurologic signs and
52:40electroencephalographic findings
52:42standard therapy for the cerebral edema
52:44contributing to grade 3 and grade 4
52:46encephalopathy include endotracheal
52:47intubation moderate hyperventilation and
52:50monitoring and control of intracranial
52:52pressure ICP monitoring involves
52:55substantial risk of intracranial
52:56hemorrhage and coagulopathy patients
52:58control of ICP may prevent seizures
53:01which lead to elevated ICP
53:04encephalopathy can be improved in the
53:06short term by limiting protein in the
53:07diet
53:08obviously this counters the objective of
53:10improving protein nutritional status and
53:12chronic liver disease but limitation of
53:14protein in the diet will decrease the
53:16amount of nitrogenous waste and ammonia
53:18produced in the bowel ammonia is an
53:21uncharged molecule that readily passes
53:22into the blood from the gut it can be
53:25converted to ammonium ion in the
53:27presence of excess hydrogen ions
53:29ammonium ion does not cross the gut
53:31mucosa conversion of ammonia to ammonium
53:35ion can be achieved by the oral
53:36administration of lactulose an enzyme
53:39that increases the acid content of the
53:40colon acidification of the stool traps
53:44ammonia as ammonium ion in the gut
53:45contents neomycin can reduce the number
53:49of bacteria producing ammonia from
53:50protein
53:51if encephalopathy is life-threatening
53:53charcoal hemoperfusion can be used to
53:56eliminate the responsible metabolites
53:57from the blood so can exchange
54:00transfusion and extracorporeal organ
54:02perfusion however these are experimental
54:05therapies used as a strategy that may
54:07worsen the coagulopathy and are only a
54:09bridge until transplantation can occur
54:12in conclusion the liver is a complex
54:16organ that serves multiple functions
54:18including protein synthesis carbohydrate
54:20and lipid metabolism the excretion of
54:22waste products drug metabolism and
54:24phagocytosis recognizing that each of
54:28these vital functions can be impaired
54:29with liver disease leads to an
54:31understanding of the primary feature of
54:32liver failure namely ascites jaundice
54:35coagulopathy encephalopathy altered
54:38metabolism and abnormal fluid balance
54:41cirrhosis is the final common
54:43manifestation of most forms of liver
54:45disease the clinical features are the
54:47degree of malnutrition the control of
54:49ascites and the history of
54:50encephalopathy laboratory assessments
54:53are the determination of the INR plasma
54:56albumin and bilirubin levels
54:58preoperative preparation includes the
55:00correction of coagulopathy by the
55:01administration of FFP or cryo the
55:04control of ascites with diuretic therapy
55:06or paracentesis and the correction of
55:08encephalopathy by limiting protein
55:10intake and the administration of
55:11lactulose transfusion of pak red blood
55:14cells may be necessary to correct blood
55:16loss from bleeding esophageal varices
55:18preoperative platelet transfusion is
55:20usually unnecessary unless the platelet
55:22count is less than 70,000 the prevention
55:25of sepsis by minimising invasive
55:27procedures and the use of strict sterile
55:29technique for the insertion of lines and
55:31surgery is extremely important these
55:33steps may reduce a risk of complications
55:35or death for surgical patients with
55:37acute or chronic liver disease
55:46you

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