1. Clinical Practice Guidelines
Decompensated cirrhosis
Presented by :Hend naguib
Ass.lecturer of Hepatology
Internal Medicine

3. Clinical course of cirrhosis
Compensated cirrhosis  DC occurs at a rate of ~5–7% per year
Compensated
Stage 0: no varices, mild PH
LSM >15 and <20 or HVPG >5 and <10 mmHg
Stage 1: no varices, CSPH LSM ≥20 or HVPG ≥10 mmHg
Stage 2: varices (=CSPH)
Decompensated
Stage 3: Bleeding
Stage 4: First non-bleeding decompensation
Stage 5: Second decompensating event
Asymptomatic
Median survival: 12 years
Symptomatic
Median survival: 2 years
End stage
Stage 6: late decompensation:
Refractory ascites or jaundice, infections, renal dysfunction.
ACLF, acute-on-chronic liver failure; CSPH, clinically significant portal hypertension; DC, decompensated cirrhosis; HVPG, hepatic venous pressure gradient; LSM, liver stiffness measurement; PSE, portosystemic encephalopathy
ACLF
Death
D’Amico G, et al. J Hepatol 2018;68:56376;
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

4. AIM NOT Two alternative approaches can be taken:
Overall management of DC
AIM NOT
prevent progression
treat complications
Two alternative approaches can be taken:
Suppress aetiological factor(s)
Target key factors in the pathogenesis

5. Suppression of aetiological factor(s)
Recommendation
In patients with DC the aetiological factor should be removed, particularly alcohol consumption and hepatitis B or C virus infection, as this strategy is associated with decreased risk of decompensation and increased survival. (II-2,1).
DC, decompensated cirrhosis
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

6. Treatment of key pathogenic factors
Several strategies have been evaluated:
Targeting microbiome abnormalities and bacterial translocation to improve the gut–liver axis (i.e. Rifaximin).
Treating the inflammatory state (i.e. Statins).
Targeting portal hypertension (i.e. β-blockers).
Enoxaparin appeared to delay the occurrence of hepatic decompensation.
Pentoxifylline treatment significantly reduced the risk of liver-related complications (HE,renal impairment ,bacterial infection).
DC, decompensated cirrhosis
Further clinical research is needed
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

7. Ascites

8. Most common complication ( 5–10% )of patients
Ascites
Most common complication ( 5–10% )of patients
What is the impact ??
Impairs patient working and social life.
Frequently leads to hospitalization.
Poor prognosis (5-year survival,80% 30%).
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

9. prognosis
Development of ascites in patients with cirrhosis is associated with a poor prognosis
1-year mortality: 40%
2-year mortality: 50%
Recommendation
Since the development of grade 2 or 3 ascites in patients with cirrhosis is associated with reduced survival, LT should be considered as a potential treatment option II-2
LT, liver transplantation
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

10. Evaluation and Diagnosis
History
Physical examination
Abdominal ultrasound
Laboratory assessment : analysis of ascitic fluid
Cirrhosis is responsible for 80% of cases of ascites
Grading of ascites*
Grade 1
Mild ascites: only detectable by ultrasound examination
Grade 2
Moderate ascites: manifest by moderate symmetrical distension of abdomen
Grade 3
Large or gross ascites: provokes marked abdominal distension
*Ascites recurring on ≥3 occasions within a 12-month period despite dietary sodium restriction and adequate diuretic dosage are considered recurrent
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

11. When to do Diagnostic paracentesis ??
-All patients with new-onset grade 2 or 3 ascites.
-Patients hospitalized for worsening ascites or any complication of cirrhosis.

12. Evaluation and diagnosis
Recommendation
Neutrophil count >250 cells/µl denotes SBP (II-2;1)
Ascitic total protein <1.5 g/dl higher risk of developing SBP (II-2;1).
SAAG should be calculated when the cause of ascites is not immediately evident. (II-2;1).
Cytology should be performed to differentiate malignancy-related from non-malignant ascites. (II-2;1)
Bedside inoculation blood culture bottles with 10 ml fluid each;
SAAG ≥1.1 g/dl indicates that portal hypertension is involved in ascites formation with an accuracy of about 97%
SAAG, serum ascites albumin gradient; SBP, spontaneous bacterial peritonitis

13. Management Moderate ascites
Hospitalization not required
Correct sodium imbalance:
Dietary salt restriction and increased renal excretion with diuretics.
sodium imbalance
Recommendation
Moderate restriction of sodium intake (80–120 mmol/day, corresponding to 4.6–6.9 g of salt) is recommendeds (I;1)
Extreme sodium restriction (<40 mmol/day) should be avoided ( development of diuretic-induced hyponatraemia and renal failure) (II-2;1).
Prolonged bed rest not recommendeds (III;1)
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

14. secondary hyperaldosteronism
Which type of diuretic???

15. Diuretics
Mainstay of medical treatment are anti-mineralocorticoid drugs.
Recommendation
First episode of grade 2 ascites
Anti-mineralocorticoid drug alone 100 mg/day with stepwise increase every 72 hours to a maximum of 400 mg/day if no response to lower doses) (I;1)
patients who do not respond to anti-mineralocorticoids or develop hyperkalaemia, furosemide (from 40 mg/day with 40 stepwise increases to 160 mg/day) (I;1)
Long-standing or recurrent ascites
Combination of an anti-mineralocorticoid drug and furosemide(I;1).
Torasemide can be given for a weak response to furosemide(I;2)
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep
Maximum weight loss: 0.5 kg/day in patients without oedema,
1 kg/day in patients with oedema (II-2;1)

16. First weeks of treatment patients should undergo frequent clinical and biochemical monitoring (I;1)

17. considerations prior to initiating diuretics
Diuretic therapy is generally not recommended in patients with persistent overt hepatic encephalopathy (III;1)

18. Monitoring of patients receiving diuretics
Loop diuretics can lead to hyponatraemia , hypokalemia and hypomagnesemia. Muscle cramps
Recommendation
Discontinue severe hyponatraemia, AKI, worsening hepatic encephalopathy, or incapacitating muscle cramps(III;1)
Discontinue furosemide for severe hypokalaemia (<3 mmol/L )
Discontinue anti-mineralocorticoids for hyperkalaemia (>6 mmol/L) (III;1)
Albumin infusion are recommended in patients with muscle cramps(I;1)
AKI, acute kidney injury *
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

19. Management of Grade 3 ascites
Grade 3 or large ascites
LVP, is the treatment of choice. (I;1)
- Plasma volume expansion should be performed by albumin. infusion (8 g/L ascites). (I;1)
- After LVP, patients should receive the minimum dose of diuretics necessary to prevent re-accumulation of ascites. (I;1)
AKI, acute kidney injury; LVP, large-volume paracentesis; PPCD, post-paracentesis circulatory dysfunction; SBP, spontaneous bacterial peritonitis
*Grade of evidence I, grade of recommendation 1
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

20. Contraindicated drugs
Increase risk of renal impairment.
Recommendation
NSAIDs should not be used (II-2;1)
Angiotensin-converting enyzme inhibitors, angiotensin II antagonists(II-2;1)
Aminoglycosides are discouraged (increased risk of AKI). (II-2;1)
AKI, acute kidney injury; DC, decompensated cirrhosis; NSAID, non-steroidal anti-inflammatory drug
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

21. Refractory ascites: definition
“Ascites that cannot be mobilized or the early recurrence , (after LVP)which cannot be prevented by medical therapy”
Refractory ascites
Diuretic resistant
Diuretic intractable
lack of response to sodium
restriction and diuretic treatment
Development of diuretic-induced
complications that preclude the use of an effective diuretic dosage
LVP, large-volume paracentesis
Refractory ascites is associated with a poor prognosis
Median survival around 6 months
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

22. Refractory ascites: diagnostic criteria
Treatment duration
Intensive diuretic therapy for at least 1 week and on a salt-restriction.
Early ascites recurrence
Reappearance of grade 2 or 3 ascites within 4 weeks of initial mobilization
Diuretic-induced complications
HE:
Renal impairment: increase of serum creatinine to a value >2 mg/dl .
Hyponatraemia: a decrease of serum sodium <125 mmol/L
Hypo- or hyperkalaemia: a change in serum potassium to <3 mmol/L or >6 mmol/L despite appropriate measures
Incapacitating muscle cramps
HE, hepatic encephalopathy

23. Refractory ascites: management
Recommendation
Repeated LVP plus albumin (8 g/L of ascites removed) are recommended as first-line treatment for refractory ascites(I;1).
High doses of NSBB should be avoided (i.e. propranolol >80 mg/day) (II-2;1)
Carvedilol can not be recommended at present(I;2)
Addition of midodrine to diuretic treatment cannot be recommended (III;1)
LVP, large volume paracentesis; NSBB, non-steroidal β-blocker; PPCD, post-paracentesis circulatory dysfunction
*See also section on gastrointestinal bleeding EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

24. Refractory ascites: indications for TIPS
Recommendation
Patients should be evaluated for TIPS insertion when:
There is refractory or recurrent ascites (I;1)
PTFE, polytetrafluoroethylene; TIPS, transjugular intrahepatic portosystemic shunt
*By shunting an intrahepatic portal branch into a hepatic vein
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

25. Alfapump implantation in patients with refractory ascites not amenable to TIPS insertion is suggested in experienced centres. However, close patient monitoring is warranted because of the high risk of adverse events including renal dysfunction and technical difficulties (I;2)

26. Hepatic hydrothorax: definition and diagnosis
Accumulation of transudate in the pleural space.
In the absence of cardiac, pulmonary or pleural disease
Ascites moves through small diaphragmatic defects.
Can be complicated by spontaneous bacterial infections .
Associated with poor prognosis
Median survival: 812 months
*Grade of evidence III, grade of recommendation 1
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

27. Hepatic hydrothorax: treatment
Treatment of ascites with diuretics and/or LVP. (III;1)
Therapeutic thoracentesis is required to relieve dyspnoea. (III;1)
What beyond diuretics and thoracentesis ?
LT, liver transplantation; LVP, large volume paracentesis
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

28. Hepatic hydrothorax
Recommendation
TIPS insertion for recurrent symptomatic hepatic hydrothorax is recommended(II-2;1)
Pleurodesis can be suggested to patients with refractory hepatic hydrothorax not amenable to LT or TIPS insertion (III;1)
Mesh repair of diaphragmatic defects(II-2;2)
LT, liver transplantation; TIPS, transjugular intrahepatic portosystemic shunt
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

29. Hyponatraemia
Serum sodium concentration <130 mmol/L.
Hypo- and hypervolaemic hyponatraemia can occur.
Recommendation
Patients with cirrhosis who develop hyponatraemia should be evaluated for LT(II-2,1).
Removal of the cause and administration of normal saline are recommended in the management of hypovolaemic hyponatraemia(III;1)
Fluid restriction to 1,000 ml/day is recommended in the management of hypervolaemic hyponatraemia. (III;1).
LT, liver transplantation
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

30. Albumin can be administered but data are very limited .
Hypertonic saline should be limited to rare patients with life-threatening complications. It can be considered in patients with severe hyponatraemia who are expected to undergo LT within days.
Correction should be slow to avoid irreversible neurological sequelae .
Albumin can be administered but data are very limited .
vaptans should be limited to clinical trials .

31. Variceal haemorrhage

32. Variceal haemorrhage: pathophysiology and natural history
70% of GI bleeding events result from VH
Recommendation
Patients with DC are at high risk and should have an Endoscopy to screen for varices.
If OGD is performed, the presence, size and presence of red wale marks should be reported
In patients without varices in whom aetiological factor persists and/or remain decompensated, screening OGD should be repeated yearly .
DC, decompensated cirrhosis; GI, gastrointestinal; OGD, oesophago-gastroduodenoscopy; VH, variceal haemorrhage
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

33. Variceal haemorrhage: prevention and treatment
Recommendation
Primary prophylaxis for detection of high-risk varices.(small varices with red signs, small varices in Child C patients and medium or large varices irrespective of Child class)
Patients with small varices with red wale marks or Child–Pugh C should be treated with NSBBs
Patients with medium–large varices should be treated with either NSBBs or EBL
Choice of treatment can be based on local resources and expertise, patient preference, contraindications and AEs
NSBBs could be preferred for lowering portal pressure, they also exert other potential beneficial effects
AE, adverse event; DC, decompensated cirrhosis; EBL, endoscopic band ligation; NSBB, non-steroidal β-blocker; VH, variceal haemorrhage
EBL
NSBBs
equally effective

34. NSBBS
Ascites is not a contraindication for NSBBs. (propranolol and nadolol)
Caution in cases of severe or refractory ascites
The use of carvedilol can not be recommended
progressive hypotension<90
bleeding, sepsis,
SBP , AKI, hyponatremia
After recovery, reinstatement of NSBBs can be attempted

35. Is the concept of titration of NSBBs will be a target heart rate of 50–55 bpm???

36. Prevention of variceal rebleeding(secondery prophylaxis)
Monotherapy
NSBBs and EBL in combination
Covered TIPS placement is recommended in patients who continue to be intolerant to NSBBs
EBL, endoscopic band ligation; NSBB, non-steroidal β-blocker; TIPS, transjugular intrahepatic portosystemic shunt
*Provided that there are no absolute contraindications
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

37. Variceal haemorrhage: management of acute GI bleeding
Medical emergency
Acute GI bleed + portal hypertension
Airway
Breathing
Circulation
Volume replacement with colloids and/or crystalloids .
target HB range 7–9 g/dl) (I;1)
Initial assessment* and resuscitation
Immediate start of vasoactive drug therapy
Antibiotic prophylaxis (I;1)
Early diagnostic endoscopy (<12 hours)
Balloon tamponade or oesophageal stenting
(if massive bleeding)
ENDOSCOPY
Confirm variceal bleeding
ENDOSCOPY
Endoscopic band ligation +
Maintain drug therapy for 3–5 days and antibiotics‡
BID, twice daily; DC, decompensated cirrhosis; GI, gastrointestinal; Hb, haemoglobin; TIPS, transjugular intrahepatic portosystemic shunt
Control
(~85% of cases)
Further bleeding
(~15% of cases)
Consider early TIPS in high risk patients
Rescue with TIPS

38. Ceftriaxone (1 g/24 h) for up to seven days
Terlipressin is 2 mg/4 h during the first 48 h, followed by 1 mg/4 h thereafter.
Somatostatin is a continuous infusion of 250 µg/h (that can be increased up to 500 µg/h) with an initial bolus of 250 µg.
Octreotide is a continuous infusion of 50 µg/h with an initial bolus of 50 µg.
Ceftriaxone (1 g/24 h) for up to seven days

39. Acute variceal haemorrhage: treatment
Early covered TIPS (placed within 24–72 hours) can be suggested for child–Pugh class C with score <14.
PPI after EBL may PPI after EBL may reduce the size of post-banding.
β-blockers should be avoided during the acute bleeding episode
TIPS, transjugular intrahepatic portosystemic shunt; VH, variceal haemorrhage
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

40. persistent bleeding!!!??

41. Management of persistent bleeding
-TIPS should be used as the rescue therapy of choice in cases of persistent bleeding or early re-bleeding.
-Balloon tamponade should be used in case of uncontrolled bleeding as a temporary ‘‘bridge” (max 24 hours)
EBL, endoscopic band ligation; TIPS, transjugular intrahepatic portosystemic shunt
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

42. Overall bleeding risk without treatment
Gastric Varices
Type
Definition
Relative frequency
Overall bleeding risk without treatment
Gastro-oesophageal varices (GOV)
GOV type 1
OV extending below cardia into lesser curvature
70%
28%
GOV type 2
OV extending below cardia into fundus
21%
55%
Isolated gastric varices (IGV)
IGV type 1
Isolated varices in the fundus 7%
78%
IGV type 2
Isolated varices else in the stomach 2% 9%
-Gastro-oesophageal varices type 1, managed as oesophageal varices.
-Cyanoacrylate is the recommended treatment for (gastro-oesophageal varices type 2 or isolated gastric varices type 1).

43. Portal hypertension gastropathy
Recommendation
NSBB and iron supplementation and/or blood transfusion, are recommended as first-line therapy for chronic haemorrhage from PHG
Acute PHG bleeding may be treated with somatostatin analogues or terlipressin .
DC, decompensated cirrhosis; NSBB, non-selective β-blockers; PHG, portal hypertension gastropathy; TIPS, transjugular intrahepatic portosystemic shunt
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

44. It is important to distinguish PHG from GAVE

46. Spontaneous bacterial peritonitis
Definition: bacterial infection of ascitic fluid without any intra-abdominal surgically treatable source of infection.
: all patients with cirrhosis and ascites are at risk.
: mortality exceeded 90% when first described.
DEFINITION
Prevalence
Prognosis
BT, bacterial translocation
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

47. However: SPB may be asymptomatic, particularly in outpatients
Diagnosis????
Signs/symptoms of peritonitis: abdominal pain, tenderness, vomiting or diarrhoea, ileus
Signs of systemic inflammation: hyper- or hypothermia, chills, altered WBC count
Worsening liver function, HE, shock, renal impairment, GI bleeding
GI, gastrointestinal; HE, hepatic encephalopathy; SBP, spontaneous bacterial peritonitis; WBC, white blood cell
However: SPB may be asymptomatic,
particularly in outpatients
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

48. Spontaneous bacterial peritonitis: diagnosis
Diagnosis is based on diagnostic paracentesis
Recommendation
SBP diagnosed by a neutrophil count in ascitic fluid >250/mm3.
Ascitic fluid culture positivity is not a prerequisite for SBP diagnosis.(negative 60%) is done to guide for antibiotic.
GI, gastrointestinal; HE, hepatic encephalopathy; SBP, spontaneous bacterial peritonitis; WBC, white blood cell
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

49. Antibiotic resistance Piperacillin/tazobactam, Carbapenem
Management of SBP
Empirical IV antibiotics should be started immediately following diagnosis
Antibiotic resistance Piperacillin/tazobactam, Carbapenem
Third-generation cephalosporins
1 st line ( I,1).
At least 5–7 days
Check efficacy for second paracentesis after 48 hours at least 25%) reduction in leucocyte count .

50. 1.5 g/kg at diagnosis and 1 g/kg on Day 3
Albumin is
1.5 g/kg at diagnosis and
1 g/kg on Day 3
The incidence of HRS1 and mortality

51. Primary prophylaxis of SBP
Primary prophylaxsis with norfloxacin (400 mg/day) is recommended in patients with:
Child–Pugh score ≥9 and serum bilirubin level ≥3 mg/dl.
Ascitic fluid protein lower than 15 g/L
SBP, spontaneous bacterial peritonitis
1. Wiest R, et al. Gut 2012;61:297–310;
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

52. Secondary prophylaxis
In patients who survive an episode of SBP, the recurrence rate at 1 year is approximately 70%
Prophylactic norfloxacin (400 mg/day, orally) is recommended in patients who recover from an episode of SBP.
PPIs may increase the risk for the development of SBP, their use should be restricted to those with a clear indication.
HE, hepatic encephalopathy; LT, liver transplantation; PPI, proton pump inhibitor; SBP, spontaneous bacterial peritonitis
1. Rimola A, et al. J Hepatol 2000;32:142–53;
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

53. Management of other infections
Non-SBP infections, as well as SBP, are known as common precipitating factors for ACLF.
C reactive protein and procalcitonin can be used for detecting infection
High bacterial resistance to antibiotics, carbapenem alone or in combination with other antibiotics should be preferred.
Routine use of albumin not recommended in infections other than SBP
SBP, spontaneous bacterial peritonitis; XDR, extensively drug resistant
*Carbapenem alone or in combination with other antibiotics proved to be superior to third-generation cephalosporins in healthcare-associated infections other than SBP
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

54. prognostic scores Sequential Organ Failure Assessment (SOFA) score
Organ/system* 1 2 3 4
Liver (bilirubin mg/dl)
<1.2
≥1.2–<2.0
≥2.0–<6.0
≥6.0–<12.0
≥12.0
Kidney (creatinine mg/dl)
≥2.0–<3.5
≥3.5–<5.0
≥5.0
Cerebral (HE grade)
NO HE
Grade I
Grade II
Grade III
Grade IV
Coagulation (INR and PLT count)
<1.1
≥1.1–<1.25
≥1.25–<1.5
≥1.5–<2.5
≥2.5 or PLT ≤20,000/mm3
Circulation (MAP mmHg and vasopressors†)
≥70
<70
Dopamine ≤5 or dobutamine or terlipressin
Dopamine >5 or A ≤0.1 or NA ≤0.1
Dopamine >15
or A >0.1 or NA >0.1
Lungs
PaO2/FiO2, or
>400
>300–≤400
>200–≤300
>100–≤200
≤100
SpO2/FiO2
>512
>357–≤512
>214–≤357
>89- ≤214
≤89
A, adrenaline; FiO2, fraction of inspired oxygen; HE, hepatic encephalopathy; INR, international normalized ratio; MAP, mean arterial pressure; NA, noradrenaline; PaO2, partial pressure of arterial oxygen; PLT, platelet; SpO2, pulse oximetric saturation; WBC, white blood count
*Bold text indicates the diagnostic criteria for organ failures; †μg/kg/min
1. Jalan R, et al. J Hepatol 2015;62:831–40;
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

55. Assessing severity of infection
qSOFA and Sepsis-3 criteria have been validated in patients with cirrhosis.
Is baseline SOFA score available?
Apply sepsis-3 criteria
Apply sepsis-3 criteria and qSOFA
Sepsis-3 positive and qSOFA negative
Good outcome
Grey zone Monitoring SOFA score is required
Sepsis-3 and qSOFA negative
Sepsis-3 and qSOFA positive
Positive
Negative
Poor outcome Patient with need for transfer to ICU
Yes No
ICU, intensive care unit; qSOFA, quick Sequential (sepsis-related) Organ Failure Assessment
1. Singer M, et al. JAMA 2016;315:801–10; Figure adapted from Piano S, et al. Gut 2017; doi: /gutjnl [Epub ahead of print]; EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

56. Choice of empirical antibiotic therapy should be based type of infection (I;1).
Cellulitis
Community-acquired
Healthcare-associated
Nosocomial
Piperacillin-tazobactam
or 3rd-gen
cephalosporin +
oxacillin
AREA DEPENDENT:
Like nosocomial
infections if high
prevalence of MDROs
or if sepsis
3rd-gen
cephalosporin or
meropemen + oxacillin or glycopeptides or
daptomycin or
linezolid
Most clinically relevant
Pneumonia
UTI
Community-acquired
Healthcare-associated
Nosocomial
Community-acquired
Healthcare-associated
Nosocomial
Piperacillin-tazobactam
or ceftriaxone +
macrolide or
levofloxacin or
moxifloxacin
AREA DEPENDENT:
Like nosocomial
infections if high
prevalence of MDROs
or if sepsis
Ceftazidime or
meropemen +
levofloxacin ±
glycopeptides or
linezolid
UNCOMPLICATED:
ciprofloxacin or
cotrimoxazole
IF SEPSIS: 3rd-gen cephalosporin
or piperacillin-tazobactam
AREA DEPENDENT:
Like nosocomial
infections if high
prevalence of MDROs
or if sepsis
UNCOMPLICATED:
fosfomycin or
nitrofurantoin
IF SEPSIS:
meropemen +
teicoplanin or
vancomycin
Gen, generation; MDRO, multidrug resistant organism; UTI, urinary tract infection
Adapted from Jalan R, et al. J Hepatol 2013;60:1310–24;
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

57. Renal impairment

58. Renal impairment
In patients with liver diseases, even a mild increase in SCr should be considered since it may underlie a marked decrease of GFR (II,1)
First step is to establish CKD, AKD, AKI .(II,1)
Screening and treatment of infection are most important(II,1)
Diuretics and/or β-blockers should be immediately stopped(II,1)
In patients with AKI and tense ascites, therapeutic paracentesis ( with albumin infusion even with a low volume paracentesis)
AKD, acute kidney disease; AKI, acute kidney injury; CKD, chronic kidney disease; GFR, glomerular filtration rate; KDIGO, Kidney Disease: Improving Global Outcomes; SCr, serum creatinine
*Proteinuria/haeamaturia/ultrasonography abnormalities. †Stage 1A (sCr <1.5mg/dl), Stage 1B (sCr ≥1.5mg/dl)
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

59. Renal impairment: definitions of kidney disease
Kidney Disease: Improving Global Outcomes (KDIGO) group definitions:
Definition
Functional criteria
Structural criteria
AKI
Increase in sCr ≥50% within 7 days, OR
increase in sCr ≥0.3 mg/dl within 2 days
No criteria
AKD
decrease in GFR ≥35% for <3 months,
increase in sCr ≥50 % for <3 months
Kidney damage
for <3 months
CKD
GFR <60 ml/min per 1.73 m2 for ≥3 months
for ≥3 months
SO…
AKD, acute kidney disease; AKI, acute kidney injury; CKD, chronic kidney disease; GFR, glomerular filtration rate; KDIGO, Kidney Disease: Improving Global Outcomes; sCr, serum creatinine
Baseline sCr
sCr obtained within 3 months prior to admission.
*International Club of Ascites-recommended adaptation of KDIGO group criteria
EASL CPG decompensated cirrhosis. J Hepatol 2018;doi: /j.jhep

60. ICA diagnostic criteria for HRS-AKI
Cirrhosis and ascites
No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g per kg of body weight
Absence of shock
No use of nephrotoxic drugs (NSAIDs,aminoglycosides, iodinated contrast media)
No macroscopic signs of structural kidney injury:
Absence of proteinuria (>500 mg/day)
Absence of microhaematuria (>50 RBCs per high power field)
Normal ultrasonography
AKI, acute kidney injury; HRS, hepatorenal syndrome; ICA, International Club of Ascites; NSAID, non-steroidal anti-inflammatory drug; RBC, red blood cell

61. First-line therapy is terlipressin plus albumin 1 g /kg (I,1)
Terlipressin IV bolus
(1 mg / 4–6 hours)( I,1)
Response (decrease in SCr <25% after 2 days).
Midodrine + octreotide can be an option when terlipressin or noradrenaline .
LT is the best therapeutic option for patients with HRS regardless of the response to drug therapy.
RRT should be based on the individual severity of illness