Kurdistan Board GEH/GIT Surgery J ClubKurdistan Board GEH/GIT Surgery J ClubSupervised by:Supervised by:

Dr.Mohamed Alshekhani.Dr.Mohamed Alshekhani.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Medications:VAPTANS• Selective vasopressin V2 –receptor antagonists satavaptan in

cirrhosis & ascites alleviated hyponatremia, but mortality was higher & hepatotoxic, so not recommended.

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).

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.

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

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.

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.

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

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.

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.

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.

1. AtrterialSystem3. Venous

System

2. CapillarySystem

1. AtrterialSystem3. Venous

System

2. CapillarySystem

2. FirstVisceralCapillarySystem3. Visceral

Venous System

4. SecondVisceralCapillarySystem

5. VenousSystem

Normal Liver Histology

CVCV

PVPV

6 mmHg

2-3 mmHg

None = 0 Portal Fibrosis = 1

Bridging Fibrosis = 3 Cirrhosis = 4

What is patophysiology What is patophysiology of Cirrhosis?of Cirrhosis?

What is natural history What is natural history of Cirrhosis?of Cirrhosis?