git j club cirrhosis16
TRANSCRIPT
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Kurdistan Board GEH/GIT Surgery J ClubKurdistan Board GEH/GIT Surgery J ClubSupervised by:Supervised by:
Dr.Mohamed Alshekhani.Dr.Mohamed Alshekhani.
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Definition:• Irreversible fibrosis of the liver, the end stage of a final shared
pathway in chronic damage to a major vital organ. • It the 13th leading cause of death globally, with worldwide
mortality • The pathophysiological features of cirrhosis involve progressive
liver injury&fibrosis resulting in portal hypertension& decompensation, including ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, variceal hemorrhage, the hepatorenal syndrome&hepatocellular carcinoma.
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Definition:• The major causes:• HBV• HCV• Alcoholism• NAFLD/NASH. • HCV/NASH primarily responsible for the growing burden of
cirrhosis in health care. • NASH is predicted to surpass HCV-related cirrhosis as the most
common indication for orthotopic liver transplantation. • Chronic injuries to the liver are synergistic; not unusual to see
cirrhosis due to a combination of chronic viral hepatitis, obesity, & alcoholism.
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Causes:• The major causes:• HBV• HCV• Alcoholism• NAFLD/NASH. • HCV/NASH primarily responsible for the growing burden of
cirrhosis in health care. • NASH is predicted to surpass HCV-related cirrhosis as the most
common indication for orthotopic liver transplantation. • Chronic injuries to the liver are synergistic; not unusual to see
cirrhosis due to a combination of chronic viral hepatitis, obesity, & alcoholism.
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Causes:• Compensated cirrhosis is associated with a risk of death *4.7 the
risk in the general population&ecompensated cirrhosis *9.7.• The average life expectancy of a patient with compensated
cirrhosis is 10 - 13 years, as low as 2 years if decompensation. • Alcoholic cirrhosis, 65% who abstain from drinking are alive at 3
years, as compared with 0% who continue • The economic burden of cirrhosis is bifg• In patients with compensated cirrhosis, the 10-year probabilities
of ascites, hepatic encephalopathy, GIB, 47%, 28%, 25%, respectively.
• 15% with ascites die within 1 year, 44% within 5 years. • Esophageal varices develop in > third within 3 years after
diagnosis, annual incidence of HCC is 5% with median survival 2 years if limited & 6 months if advanced.
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Nutrition:• Malnutrition occurs in 20 - 60%. • Daily protein intake of 1.0 - 1.5 g / kg body weight. • High-protein diets tolerated &associated with sustained
improvement in mental status, but restriction does not have any beneficial effect in patients with acute HE, so avoid protein restriction, regardless of whether they have a history of HE.
• Because of hypermetabolism, overnight fasting causes musc waste• Late-night meal improve nitrogen balance without exacerbate HE• Two cans of high-protein nutritional supplement (474 ml per can)
nightly resulted in sustained increases in total body protein.• A 2000-mg limit in daily sodium intake is mandatory for ascites. • Fluid restriction only when S Na<120 mm/ lit &needs fluid intake
<urinary volume, but the urinary volume is so low in cirrhosis that adequate fluid restriction is nearly impossible to achieve.
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Medications:HT Drugs• Hypotension < 82 is associated with poor survival.• Because of these hemodynamic changes, antihypertensive agents
should be discontinued in patients who have decompensated cirrhosis with ascites or hypotension.
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Medications:NSBBs• Nonselective beta-blockers reduce portal pressures&used in the
primary & secondary prophylaxis of variceal hemorrhage. • Caution needed in the the use of beta-blockers in decompensated
cirrhosis with refractory ascites,1 spontaneous bacterial peritonitis& alcoholic hepatitis.
• The “window hypothesis,” postulates that beta-blockers are associated with higher rates of survival only within a clinical window.
• In patients with stable hypotension, midodrine improve splanchnic / systemic hemodynamics, renal function, Na excretion.
• Octreotide/ midodrine is beneficial with T1HRS &without.• Baveno guidelines recommend discontinuation of NSBBs when
SBB <90-100 mm Hg, Na <120 mm/liter, or AKI developed.
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Medications:Paina&sedatives• Because of the risk of acute renal failure &GIB ,NSAIDs are
contraindicated, except for low-dose aspirin in patients in whom the severity of CVD>severity of cirrhosis.
• Opiates should be used cautiously or avoided, because they may precipitate or aggravate HE.
• Tramadol is safe in low doses&topical medications such as lidocaine patches are generally safe.
• Acetaminophen is effective / safe in 2-4 gms/day, provided that the patient does not drink alcohol.
• Benzodiazepines should be avoided in HE.• For hepatitis or cirrhosis &severe symptoms of acute alcohol
withdrawal, short-acting benzodiazepines such as lorazepam/oxazepam are preferred.
• For insomnia, hydroxyzine 25 mg /trazodone100 mg at bedtime.
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Medications:STATINS• Can be safely started/continued &have established CV benefits in
NAFLD.• The overall statin-induced acute liver failure is 0.2- 1/million.• Routine monitoring of ALTin patients is no longer
recommended.
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Medications:VAPTANS• Selective vasopressin V2 –receptor antagonists satavaptan in
cirrhosis & ascites alleviated hyponatremia, but mortality was higher & hepatotoxic, so not recommended.
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Invasive procedures:Surgery• Intraabdominal surgery should be avoided in patients with
decompensated cirrhosis unless the procedure confers more benefit than risk, as is the case with orthotopic liver transplantation.
• Cholecystectomy in particular is associated with high morbidity / mortality among patients with decompensated cirrhosis.
• MELD used to predict 30-day postoperative mortality in patients planning to undergo non-transplantation surgeries & if < 14 is better than Child–Pugh class C in predicting a high risk of death associated with abdominal surgery.
• In major digestive, ortho,heart surgery, MELD, age, ASA class were independent predictors of surgical mortality.
• Online risk calculator (www.mayoclinic.org/medical-professionals/ model-end-stage-liver-disease/ post -operative-mortality-risk-patients-cirrhosis).
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Invasive procedures:endoscopy• Endoscopic procedures are relatively safe &antibiotic prophylaxis
is not indicated for routine endoscopy, except for acute GIB.• PEG is associated with a high risk of death with ascites &
contraindicated.
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Invasive procedures:Paracentesis• Indications:• All patients with new-onset ascites• Existing ascites who are admitted to the hospital, and in• Clinical deterioration (fever, abdominal pain, hepatic
encephalopathy, leukocytosis, renal failure, or metabolic acidosis). • Spontaneous bacterial peritonitis is diagnosed when the
neutrophil count in ascitic fluid is at least 250 cells/cubic millimeter & secondary bacterial peritonitis is ruled out
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Invasive procedures:Paracentesis• Is relatively safe, even in marked coagulopathy, including an INR
as high as 8.7 & platelets low as 19,000 /cubic millimeter.• Bloody ascitic fluid is typically due to a traumatic paracentesis,
but excessive blood is suggestive of ruptured HCC;often associated with hemodynamic instability &requires urgent embolization.
• In patients with diuretic-sensitive ascites, the removal of 5 liters of fluid is sufficient to reduce intraabdominal pressure, at which point sodium restriction&diuretics are continued.
• With diuretic-refractory ascites, the goal is to remove as much fluid as possible& if > 8 lits needed to be removed frequently found to be nonadherent to the prescribed dietary regimen.
• It is important not to delay paracentesis in patients with suspected spontaneous bacterial peritonitis.
• Rrecommended 6 - 8 g of albumin given / lit removed if > 5 lits.
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Invasive procedures:Paracentesis• In SBP, albumin 1.5 g /kilogram be given within 6 hours after
diagnosis+1 g / kilogram on day 3. • Albumin in SBP can be restricted to patients who have a higher
risk of death serum creatinine >1 mg per deciliter ,BUN>30 mg/ deciliter ,bilirubin >4 mg / deciliter, because the probability of survival is not higher when albumin is given to patients who have a low risk of death.
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Priciples of management:• Education,• Lifestyle modification.• Protecting the liver from harm (Fig. 1),• Care coordination.
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Priciples of management:• “Recompensation”/ reversal of cirrhosis described in patients
with alcoholic cirrhosis who abstained from alcohol, patients with HBV/HCV infection who underwent antiviral therapy& patients with nonalcoholic steatohepatitis who underwent bariatric surgery.
• Public education efforts are needed to discourage obesity, needle sharing, excessive alcohol consumption.
• Screening is very useful in high-risk groups.• All patients with cirrhosis undergo surveillance for HCC with
Abd U/S or CT every 6 months.• Serum alpha-fetoprotein with abd U/S may improve the
effectiveness of surveillance.• But not for HCV , NAFLD, or NASH without cirrhosis.
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Priciples of management:• Patients with a history of SBP or among hospitalized patients
with an ascitic-fluid protein<1.5 g /deciliter of ascitic fluid, selective intestinal decontamination with trimethoprim–sulfamethoxazole or cipro or norfloxacin increases the rate of short-term survival & reduces the overall risk of bacterial inf
• Among patients with AGIB, ceftriaxone at a dose of 1 g daily for 7 days is effective in the prophylaxis of bacterial infections, including SBP.
• Patients with alcoholism are prone to relapse because of cravings /anxiety& baclofen frecommended or the suppression of alcohol cravings.
• Evaluation for transplantation is indicated for decom cirrhosis when the MELD score is 17 or more.
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Priciples of management:• Care coordination:• Improve quality & clinical outcomes while reducing readmission
rates /expenditures.• Care coordinators facilitate inpatient-clinic transitions, reconcile
medications, call ptients to prevent unnecessary visits to the ER, place “smart scales” in homes to monitor body weight remotely, facilitate interaction with other health care professionals&arrange referrals to nursing facilities or hospice.
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1. AtrterialSystem3. Venous
System
2. CapillarySystem
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1. AtrterialSystem3. Venous
System
2. CapillarySystem
2. FirstVisceralCapillarySystem3. Visceral
Venous System
4. SecondVisceralCapillarySystem
5. VenousSystem
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Normal Liver Histology
CVCV
PVPV
6 mmHg
2-3 mmHg
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None = 0 Portal Fibrosis = 1
Bridging Fibrosis = 3 Cirrhosis = 4
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What is patophysiology What is patophysiology of Cirrhosis?of Cirrhosis?
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What is natural history What is natural history of Cirrhosis?of Cirrhosis?
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