GIT j club cirrhosis16.

1. Kurdistan Board GEH/GIT Surgery J ClubKurdistan Board GEH/GIT Surgery J Club
Supervised by:Supervised by:
Dr.Mohamed Alshekhani.Dr.Mohamed Alshekhani.

2. 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.

3. 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.

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. Medications:VAPTANS
• Selective vasopressin V2 –receptor antagonists satavaptan in
cirrhosis & ascites alleviated hyponatremia, but mortality was
higher & hepatotoxic, so not recommended.

12. 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).

13. 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.

14. 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

15. 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.

16. 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.

17. Priciples of management:
• Education,
• Lifestyle modification.
• Protecting the liver from harm (Fig. 1),
• Care coordination.

18. 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.

19. 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.

20. 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.

26. 1. Atrterial
System3. Venous
System
2. Capillary
System

27. 1. Atrterial
System3. Venous
System
2. Capillary
System
2. First
Visceral
Capillary
System3. Visceral
Venous
System
4. Second
Visceral
Capillary
System
5. Venous
System

28. Normal Liver Histology
CVCV
PVPV
6 mmHg
2-3 mmHg

34. None = 0 Portal Fibrosis = 1
Bridging Fibrosis = 3 Cirrhosis = 4

35. What is patophysiologyWhat is patophysiology
of Cirrhosis?of Cirrhosis?

60. What is natural historyWhat is natural history
of Cirrhosis?of Cirrhosis?