Management The

Complications Of Cirrhosis
Presented By : Dr.Aron Berhanu(IMR1)
Outline
Introduction
Ascitis
SBP
Hepatic Hydrothorax
Hepatic Encephalopathy
HRS
Cirrhosis
• Pathologic entity defined as diffuse hepatic fibrosis with the
replacement of the normal liver architecture by nodules
.
• Although cirrhosis is strictly speaking a histologic diagnosis , a
combination of clinical, laboratory, and imaging features can help
confirm a diagnosis of cirrhosis.
Natural History
Cirrhosis has traditionally been classified as compensated or
decompensated
Stage 1 : absence of both ascites and varices;
Stage 2: presence of varices without bleeding and ascites
Stage 3 : ascites with or without esophageal varices;
Stage 4: cirrhosis is characterized by variceal bleeding
Pathogenesis
Pathophysiology of Decompensation
Management of decompensated
cirrhosis
The overall management of decompensated cirrhosis can
be addressed using two approaches.

a)First approach is the suppression of the aetiological factor(s)

b)Second based on targeting key factors of pathogenesis of

cirrhosis decompensation and progression

Management of decompensated
cirrhosis
Several strategies have been evaluated to prevent disease
progression in patients with decompensated cirrhosis, including i)
targeting microbiome abnormalities and BT, to improve gut-liver
axis; ii) improving the disturbed circulatory function; iii) treating
the inflammatory state; and iv) targeting portal hypertension
Ascitis
Ascites is the most common cause of decompensation in cirrhosis.

The mainstay of ascites formation is renal sodium retention due to the activation

of sodium retaining systems

Five-year survival drops from about 80% in compensated patients to about 30%

in patients with decompensated cirrhosis and ascites

Diagnostic Workup
Management Of Grade 2 Ascites
Management of Grade 2 Ascites
Management Of Grade 3 Ascites
Refractory Ascites
Management Of Refractory Ascites
 Spontaneous Bacterial Peritonitis
Bacterial infection of ascitic fluid without any intra-abdominal surgically treatable source of infection.
Half the episodes of SBP are present at the time of hospital admission while the rest are acquired during
hospitalisation
Present with : a) local symptoms and/or signs of peritonitis , b) signs of systemic inflammation ,
c)worsening of liver function; d) HE; e) shock; f) renal failure; and, g) GI bleedin g
The diagnosis of SBP is based on neutrophil count in ascitic fluid of >250/mm 3

Ascitic fluid culture positivity is not a prerequisite for the diagnosis of SBP, culture should be
performed in order to guide antibiotic therap y
Management
Empirical antibiotic treatment
should be based on the following: (1) risk of multidrug resistant (MDR) bacteria;
(2) severity of the infection; and (3) local epidemiology
Community-acquired infections, :most common bacteria that cause SBP are Gram-
negative organisms( cephalosporins).

MDR: risk for these organisms include repeated hospitalizations or repeated

contact with the healthcare environment, noninvasive procedures, and recent
antibiotic treatment, (nosocomial and health care associated settings) .
Mangagement
A five-day therapy is as effective as a 10-day treatment.

Efficacy of antibiotic treatment should be monitored

by performing another diagnostic paracentesis 48 hours after
the initiation of therapy.

Decreased by at least 25% from the pretreatment value,

indicative of response.
Mangagement
SBP without septic shock may lead to a further circulatory
dysfunction, thereby increasing the risk of development of HRS.
Albumin, 1.5 g/kg intravenously at diagnosis and 1 g/kg
intravenously on day 3.
Particularly effective in patients with baseline serum bilirubin ≥ (4
mg/dl) or SCr ≥ (1 mg/dl)
Prophylaxis
Three high-risk patient populations have been identified:

i) Acute GI haemorrhage;

ii) patients with low total protein content in ascitic

fluid and no prior history of SBP (primary prophylaxis),

iii) patients with a previous history of SBP (secondary prophylaxis)

Prophylaxis
Prophylaxis
Ascitis(continued)

Hepatic Hydrothorax: accumulation of transudate in the pleural

space of patients with decompensated cirrhosis in the absence of
cardiac, pulmonary or pleural disease
Formation is secondary to small diaphragmatic defects,
Can lead to respiratory failure and can be complicated by
spontaneous bacterial infections (empyema )
Diagnostic criteria same for ascites. (protein content of pleural
effusion is low and the serum to pleural fluid albumin gradient is
greater than 1.1 g)
Ascitis(continued)
Ascites(continued)
The first-line management relies on the treatment of ascites
with diuretics and/or LVP
Therapeutic thoracentesis is required to relieve dyspnoea.
Chest tube should not be inserted, because of the high risk of complications.
TIPS has been effectively employed as definitive treatment or bridge to
transplantation for refractory hepatic hydrothorax.
LT represents the best option for patients with refractory hepatic hydrothorax.
Hepatic Encephalopathy

Hepatic encephalopathy (HE) is broadly defined as brain dysfunction caused

by liver insufficiency and/ or portal-systemic shunting, which manifests as a
wide spectrum of neurological or psychiatric abnormalities.
Defined as a metabolic disorder, HE is widely considered to
be reversible following LT.
Notion is changing: Neuroinflammation and neuronal cell death.
Hepatic Encephalopathy
Underlying liver disease :Types A, B and C.

Time course: 1) Episodic, recurrent HE (multiple episodes within a time interval of 6

months), and (2) Persistent (altered behavior always present with relapses of overt HE)

Spontaneous HE or Secondary HE

West-Haven

Overt HE vs Covert HE
Pathophysiology

Neurological impairment and cognitive decline provoked by liver

dysfunction are the result of blood-derived factors influencing the
permeability and/or altering the integrity of the BBB.
Ammonia :the best described neurotoxin involved in HE.
Elevated in 90% of patients with HE, although serum levels are neither a
sensitive nor specific indicator of its presence.
Ammonia exerts its deleterious effects through multiple pathways including
cellular swelling, inflammation, oxidative stress, mitochondrial dysfunction,
disruption of cellular bioenergetics, changes in pH and alterations in
membrane potential.
Pathophysiology
Neuropathophysiology
Increased sensitivity of the astrocyte (peripheral-type) benzodiazepine receptor(GABA)

CSF composition is significantly different in cirrhotic patients with HE compared to those

without.

Increases in concentrations of neurosteroid,further activates the GABAa-benzodiazepine

receptor system.

NH3 enters astrocytes, metabolized via glutamine synthetase into glutamine, this
increases astrocyte osmolality and causes cell swelling.

Neuronal cell death: Neurodegeneration is probably the operative mechanism

Management Of HE

1) Initiation of care for altered consciousnes (ABC’s)

2)Evaluation of alternative causes of altered mental status .

3) Identification and correction of precipitating events.

4)Treating HE
Management Of HE
Lactulose:Nonabsorbable disaccharide,
Exerts its effects through catharsis and reducing intestinal pH,ammonia
production is reduced in the gut, faecal excretion is increased thereby
inhibiting ammonia absorption.
Dosing of lactulose can be started at 15–20 ml every 12 hours until 2 soft
stools are passed, followed by titration to 2–3 semi-soft stools/day
.
Management Of HE

Rifaximin is a semisynthetic, non-aminoglycoside, is minimally

absorbed (>4%),
Exerts its effect through reducing secondary bile acid
production;
The most solid evidence for the its use as an add-on to
lactulose to prevent recurrence of HE
Management Of HE
Agents that may modify intestinal flora and modulate the generation or intestinal absorption of

ammonia

Acarbose : intestinal α-glucosidase inhibitor

Probiotics: live bacteria which are believed to improve gut dysbiosis and negatively impact

ammonia production.

Polyethylene glycol — solution is a cathartic that may help treat hepatic encephalopathy by

increasing excretion of ammonia in the stool.

Management Of HE
Branched-chain amino acids (BCAA): have been documented to
promote muscle protein synthesis and improve muscle mass
loss,
L-ornithine L-aspartate (LOLA ):lowers plasma ammonia
concentrations by enhancing the metabolism of ammonia to glutamine,
Prophylaxis for HE
Lactulose is effective at preventing the subsequent episodes
of overt HE in patients with cirrhosis.
Rifaximin as add-on to lactulose is more effective than
lactulose alone.
VSL#3, a probiotic preparation has also been shown to
effectively prevent subsequent episodes of overt HE,
Hepatorenal Syndrome (HRS)
A functional renal failure caused by intrarenal
vasoconstriction which occurs in patients with end-stage
liver disease as well as in patients with acute liver failure
or alcoholic hepatitis
Type 1 : Corresponds to HRS-AKI
Type 2: include renal impairment which fulfills the criteria
of HRS but not of AKI, namely non-AKI-HRS (NAKI),
Diagnosis
Management
Complete response to the treatment should be defined
by a final SCr within 0.3 mg/dl from the baseline value.

Partial response should be defined by the regression of

AKI stage to a final SCr ≥0.3 mg/dl from the baseline
value
References
Hepatic encephalopathy: Novel insights into classification,
pathophysiology and therapy , Journal of Hepatology

Sleisenger and Fordtran’s Gastrointestinal and Liver Disease

11th edition

EASL Clinical Practice Guidelines for the management of

patients with decompensated cirrhosis, 2018
Uptodate 2018
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