Cirrhosis is a disease where the liver transforms into regenerating nodules surrounded by fibrous bands. Common causes include alcoholism, viral hepatitis, and non-alcoholic steatohepatitis. Complications include portal hypertension, ascites, hepatic encephalopathy, and hepatorenal syndrome. Portal hypertension is defined as a hepatic venous pressure gradient over 5 mmHg and can cause variceal bleeding, ascites, and hypersplenism. Ascites is treated initially with sodium restriction and diuretics, while refractory ascites may require paracentesis, TIPS, or liver transplant. Hepatic encephalopathy is caused by increased ammonia and treated with lactulose and rifaxim
1. Dr. Praveen Maurya Moderator:-Dr. Vinay Kumar
JR 2 Medicine (DM GASTRO)
Dept. of Medicine
GSVM Medical College, Kanpur
2. Definition
Cirrhosis is a slowly progressive disease in which diffuse
transformation of entire liver into regenerating nodules
surrounded by fibrous band and variable degree of
vascular(portosystemic) shunting.
8. Portal Hypertension (PHTN)
Definition- The elevation of the hepatic venous
pressure gradient (HVPG) to >5 mmHg.
(Normal HVPG=3-5 mmhg )
HVPG= Wedged hepatic venous pressure(WHVP) -
free hepatic venous pressure(FHVP)
It is a measure of portal sinusoidal pressure .
Obtained by catheterization of a hepatic vein via
jugular or femoral vein.
10. HVPG >10 mmhg-clinically significant PHTN( present
in > 60 % of patient with cirrhosis.)
HVPG >12 mmhg- high risk of variceal bleeding.
Portal pressure = flow x Resistance
Portal hypertension always result from increase in
both portal resistance and portal flow
11.
12. Clinical feature
Three primary complication of portal hypertension are
1-gastroesophageal varices with hemorrhage
2-ascites
3-hypersplenism
Variceal hemorrhage is an immediate life-threatening
problem with a 20–30% mortality rate associated with
each episode of bleeding.
14. Gastroesophageal Varices
40 % patients of cirrhosis have varices.
5 -15% of cirrhotics per year develop varices.
Several factor predict the risk of bleeding-
Hepatic venous pressure gradient (HVPG)
Size of varix
location of varix
Severity of cirrhosis(Child – Pugh classification)
15.
16. Treatment
Treatment for variceal hemorrhage as a complication
of portal hypertension is divided into two main
categories:
(1) Primary prophylaxis
(2) Prevention of rebleeding.
Primary prophylaxis achieved either through
1-Nonselective beta blocker :-propranolol, nadolol
2- Endoscopic variceal band ligation(EVL)
Endoscopic intervention is used as first –line treatment
17.
18. Control of Acute Bleeding
First to treat the acute bleed, which require both fluid
and blood –product replacement.
Medical management includes –
Vasoconstricting agent-
Somatostatin analogue-octreotide
Octreotide (50-100 μg/hour by continuos infusion)
Terlipressin
Endoscopic intervention is used as first –line
treatment to control bleeding acutely.
19.
20. N –Butyl cyanoacrylate (NBC) glue injection may be
superior to nonselective beta blocker and variceal
band ligation in preventing gastric variceal bleeding.
TIPS is effective in preventing gastric variceal
bleeding.
21. Transjugular Intrahepatic Portosystemic Shunt
This technique creates a portosystemic shunt by a
percutaneous approach using an expandable metal
stent,
Stent placed between portal vein and hepatic vein
Encephalopathy can occur in 20% of patients after
TIPS.
TIPS can be used for who fail endoscopic or medical
management.
22.
23. Prevention of Rebleeding
Rebleeding is defined as recurrence of bleeding after
initial control for 24 hours during which the vital signs
and Hb level are stable.
24.
25. Ascites
Ascites is the accumulation of fluid within the
peritoneal cavity.
Most common cause of ascites is portal hypertension.
Earliest/first complications of portal hypertension is
ascites
27. Clinical feature
Increase in abdominal girth and gain in weight.
Peripheral edema.
If ascitic fluid is massive, respiratory function can be
compromised, and patients will complain of shortness
of breath.
Oliguria
Muscle wasting
Excessive fatigue and weakness
Aching pain all over abdomen due to stretching.
28. Diagnosis
By physical examination
Abdominal imaging
USG-min 100 ml can be detected
Shifting dullness-500 ml
This is determined by taking patients from a supine
position to lying on either their left or right side and
noting the movement of the dullness to percussion.
Fluid thrill -1000 ml
Diagnostic paracentasis
29. The SAAG reflects the pressure within the hepatic sinusoids and
correlates with the hepatic venous pressure gradient.
SAAG ≥ 1.1 g/dL reflects the presence of portal hypertension and
indicates that the ascites is due to increased pressure in the hepatic
sinusoids.
SAAG< 1.1 g/dl ,infectious or malignant cause of ascites should be
considered.
An ascitic protein level of ≥2.5 g/dL indicates that the hepatic sinusoids
are normal.
Ascitic protein level <2.5 g/dL indicates that the hepatic sinusoids have
been damaged .
Serum ascites albumin gradient(SAAG)=serum albumin-ascitic fluid
albumin
30.
31. Treatment
Initial treatment is restriction of sodium intake to<2 g
of sodium per day,(Most average diets contain 6–8 g of
sodium per day, )
When a moderate amount of ascites is present,
diuretic therapy is usually necessary.
Spironolactone (DOC) at 100–200 mg/day as a single
dose is started,
furosemide may be added at 40–80 mg/day,
particularly in patients who have peripheral edema.
32.
33. Refractory ascites
If compliance is confirmed and ascitic fluid is not being mobilized,
spironolactone can be increased to 400–600 mg/day and furosemide
increased to 120–160 mg/day.
if ascites is still present with these doses of diuretics in patient who are
compliant with a low –sodium diet, then they are defined as having
Refractory ascites
Ascites unresponsive to sodium restricted diet and high –dose diuretic
treatment.
Managed by :-pharmacological therapy- midodrine,
clonidine
Salt free albumin (6-8 gm/L )
large volume paracentasis(LVP)
TIPS
liver transplant
34.
35. Spontaneous bacterial peritonitis
SBP is a common and severe complication of ascites
characterized by spontaneous infection of the ascitic
fluid without an intra abdominal source.
Bacterial translocation is the presumed mechanism for
development of SBP.
36. The most common organisms are E.coli .
Patients with ascites may present with fever, altered
mental status, elevated white blood cell count, and
abdominal pain .
diagnosis of Spontaneous Bacterial Peritonitis:-
Ascitic fluid culture positive
Absolute neutrophil count >250/μL.
Ascitic protein < 1 gm/dl
37. Treatment
a third-generation cephalosporin(inj .cefotaxim 2 gm
iv TDS x 5 days).
Oral ofloxacin 400 mg BD
In patients with variceal hemorrhage, the frequency
of Spontaneous Bacterial Peritonitis is significantly
increased.
38. Prophylaxis for recurrent SBP:-
Cirrhosis with GI Hemorrhage:-
inj Ceftriaxone 1 gm iv OD x 7 days
OR
Norfloxacin 400 mg BD X7 days
Prior Spontaneous Bacterial Peritonitis :-
Norfloxacin 400 mg OD untill death or liver transplant
39. Hepatorenal syndrome
HRS is a form of functional renal failure without renal
pathology
Occurs in about 10% of patients with advanced
cirrhosis or acute liver failure.
Portal hypertension splanchnic vasodilation
activate renin angiotensin system(RAAS)Severe
intra renal vasoconstriction Decrease renal
perfusion HRS
40. Criteria for HRS
1- Cirrhosis with ascites
2-Serum creatinine level ≥ 1.5 mg/dl
3-No or insufficient improvement in serum creatinine
level 48 hr after diuretic withdrawl and adequate
volume expansion with IV albumin
4-No evidence of recent use of nephrotoxic drug
5-Absence of Shock
6-Absence of structural renal disease
41. HRS I HRS II
Type 1 HRS is characterized
by a progressive impairment
in renal function and a
significant reduction in
creatinine clearance within
1–2 weeks of presentation.
Bad prognosis
Without transplant median
survival-4-6 week
Type 2 HRS is characterized
by a reduction in glomerular
filtration rate(GFR) with an
elevation of serum creatinine
level,
present as refractory ascites
Without transplant median
survival-4-6 month
42. Management of Hepatorenal Syndrome (HRS)
Measures to prevent variceal bleeding
Pentoxifylline for severe alcoholic hepatitis
Avoid intravascular volume depletion (diuretics,
lactulose, GI bleeding, LVP ).
Prompt diagnosis and treatment of infections
43. Stop all nephrotoxic agents (ACEIs, ARBs, NSAIDs,
diuretics)
Antibiotics for infections
IV albumin—bolus of 1 g/kg/day on presentation
(maximum dose, 100 g daily).
Continue at dose of 20-60 g daily
44. Vasopressor therapy
Terlipressin*—start at 1 mg IV every 4 hr
Increase up to 2 mg IV every 4 hr if baseline serum creatinine
level does not improve by 25% at day 3 of therapy
OR
Midodrine —begin midodrine at 2.5-5 mg orally TDS
increase to a maximum dose of 15 mg TDS.
+
Octreotide- at 100 µg subcutaneously TDS
and increase to a maximum dose of 200 µg subcutaneously 3
times daily,
or
begin octreotide at a 25-µg IV bolus and continue at a rate of 25
µg/hr
45. Norepinephrine—0.1-0.7 µg/kg/min as an IV infusion.
Duration of vasopressor treatment is generally a maximum
of 2 weeks until reversal of hepatorenal syndrome or liver
transplantation.
46. Hepatic encephalopathy
Portosystemic encephalopathy
Defined as an alteration in mental status and
cognitive function occurring in the presence of liver
failure.
47. Liver dysfunction No urea cycle ammonia in
circulation enters brain astrocyte
in astrocyte –glutamate +NH3 Glutamine
glutamine enters in neuron
Converted to Glutamate Act on NMDA receptor
Neurotoxicity
50. Treatment
Manage precipitating factor
Mainstay of treatment-Lactulose-
Goal of lactulose therapy-promote 2-3 soft stool per
day.
Rifaximine -550 mg BD very effective
Zinc supplimentation
L- ornithine L-aspartate-promote detoxification of
ammonia.
51. Hepato pulmonary syndrome
Clinical triad
1- liver disease(PHTN with or without cirrhosis)
2-Hypoxemia
3-Intra pulmonary vascular vasodilation
Pathogenesis-
Nitric oxide Intrapulmonary vasodilation +shunting
of alveolar capillary Connect pulmonary artery to
pulmonary vein Deoxygenated blood in vein
Affect diffusion Hypoxia
52. Clinical feature –platypnea(dyspnea worsened by erect
position and improved by supine position )
Orthodeoxia(Fall in oxygen saturation by > 4% on
standing ).
IOC- Bubble echocardiography
Treatment-liver transplant
53. Malnutrition in cirrhosis
Cirrhotic patients are more catabolic and muscle
protein metabolized(cirrhotic sarcopenia-severe
muscle depletion)
Multiple factor-poor dietary intake,
- alteration in protein metabolism,
-alteration in gut nutrient absorption.
54. Coagulopathy
Almost universal in patient with cirrhosis.
Decrease synthesis of clotting factor-vitamin K
dependent(II,VII,IX,X) is more common.
Vitamin K absorption is diminished.
Under these circumstances administration of
parenteral Vitamin K does not improve prothrombin
time.
55. BONE Disease in cirrhosis-osteoporosis is common
because malabsorption of Vitamin D and decrease
calcium ingestion.
Hematological abnormality in cirrhosis-Anemia,
Neutropenia
