Julia Wendon

1. I have no financial relationship(s) to disclose relevant to my
presentation.
julia.wendon@kcl.ac.uk
All Fluids are bad
The Liverand abdominal hypertension
Julia Wendon
Consultant Intensivist and Hepatologist
Institute of Liver Studies
Kings College Hospital
London

2. A bit is good – too much – well

3. Potential Categorization of liver dysfunction in
critical care /MOF
Primary liver Injury
Acute
Acute liver Injury
Acute Liver failure
Chronic
Decompensated CLD
Critically ill cirrhotics
Surgical
Hepatectomy
Trauma
Iatrogenic
Secondary liver
Injury
Sepsis / inflammation
Ischemia/Congestion
Systemic disease
Drugs
TPN
Other…..

4. Fluids and liver disease
• 5% dextrose
• 20-50% dextrose
• N/ Saline / Hartmans / balanced crystalloids
• Colloids
• 4.5% albumin 20% albumin
• gelatins , starch

6. Haemodynamics and issues
• ALF
– Initially all volume deplete – difficult to say fluid is
bad
– Risk of pancreatitis, gut oedema
– Stiff liver, develop ascites easily
• Hepatic resection
– Initially usually run dry
– Risk of small for size syndrome
– Portal inflow excessive to outflow
– Adequate but not excess fluid required

7. Haemodynamics of cirrhosis
• Group 1
– Ascites, central hyovolaemia, total blood volume
increased, usually diuresed ++ and low na and poor
kidneys
• Group 2
– RV volume / pressure overload, ascites and oedema,
cirrhotic cardiomyopathy, No PHT, usually high CI TPG
• Group 3
– Portopulmonary syndrome with normal RA, initially
maintained CI

8. Situations for discussion
• Acute liver failure
– Plasma exchange
• Ascites and drainage of said
• Variceal haemorrhage
• Hepatorenal failure
• Continuity between right heart, hepatic veins, liver
and sinusoids and back to portal vein and hence
guts – gut oedema, translocation

9. IAP
CVP
PcwP
PeeP
Compliance 
Echo findings also predictive of mortality post TIPS

10. IAP and fluid responsiveness

11. 11
Problems related to hypotonic solutions
Replace with albumin 20% to prevent PICD
Also consider risk of variceal bleeding

13. Consider IAP and renal perfusion pressure
Options
1. Decrease IAP
2. Increase RPP
3. Improve central blood volume
RPP 61 to 67 mmHg
Potential risk of variceal
bleed ???

14. Budd^Chiari syndr
Deepak Joshi, Sujit Saha, Wi
Institute of Liver Studies, King’sColle
Keywords
abdominal compartment syndrome –
Chiari syndrome –intra-abdominal
hypertension –intra-abdominal press
Correspondence
Dr D. Joshi Institute of Liver Studies, K
College Hospital, London, SE5 9RS, U
Tel: 1 020 3299 2504
Fax: 1 020 3299 3899
e-mail: d.joshi@nhs.net
Received 16 November 2010
Accepted 12 May2011
DOI:10.1111/j.1478-3231.2011.025
Pre paracentesis
4-10 L +ive
Pressors
0.45 µg/kg/min
9 L ascites
Drained
Replaced 20%
Albumin 1.2 L
PLR : no increase

16. Terlipressin ± albumin
Ortega et al Hepatology 2002;36:941
0.5 mg 4 hrly , albumin 1g/kg/body weight day 1 then 20 - 40
g/day

17. Sanyal A Gatroenterology 2008 :134:1360
Albumin daily 1g/kg
Martin-Llahi M Gastroenterology 2008:134
Data also for norepinephrine and Ptx and NAC

18. 10 trials only type I and II
Drug ± alb vs no intervention
Vasoconstrictors + Alb : Effect on mortality at 15 days but not at
30, 90 or 180 days RR 0.6 (0.37-0.97)
Terlipressin + Albumin vs Albumin : decreased mortality in type I
RR 0.83 (0.65-1.05)

19. MAP no relationship to
changes in GFR
MAP increased (>85)
Reversal of RAA, NE levels
Creatinine is
Dreadful measure
Of renal function

20. Airway
Breathing
Circulation
fluids - coagulation factors ??
others ?
Na issues
IAP – ascites & endoscopy
Terlipressin / somatostatin
Watch right sided pressures

21. • 116 patients with cirrhosis and variceal bleed
• Endoscopy and sclerotherapy
• HVPG measured within first 24 hours: < or > 20
mmHg
• If > 20 randomized to TIPS or medical Rx
Monescillo
Hepatology
2004 ;40:793
Rx failure
HVPG and CPscore
6 week survival

22. alb
Given over 6 hours for 20% albumin and 18 hrs for HES 6%
1.5 g/kg at day 1 and 1.0 g/kg at day 3

30. 1235 patients screened : 101 RV > 50 mmHg
MPAP > 25 mmHg in 90%
PPS observed in 55%
Remainder relate to increased MPAP in response to increased flows
Calculate transpulmonary gradient (MPAP-PAOP)
Poor correlation
with MELD

31. IAP 11.8±3.6
PDR 26.6 ± 13 vs 21.8± 7.8 (NS)
CVP 9.3±4.6 vs 15.7±4.7 (p<0.001)
Individual variation was
however observed

32. • SBP frequently associated with renal failure
• Associated with decreased effective blood volume
and high mortality
• 126 patients iv cefotaxime or iv cefotaxime plus
albumin (1.5g/kg) at day 0 and day 3 (1.0 g/kg)
• 94% and 98 % had resolution of infection
• Renal failure in 21 (33%) cef grp vs 6 (10%) in
alb/cef grp p=0.002
• Mortality 18 (29%) vs 6 (10%)
• At 3 months the mortality was 41% vs 22% p=0.03
Albumin and renal impairment in patients with
cirrhosis and SBPSort P et al N Engl J Med 1999 5; 341 (6):403

33. Haemodynamicresponse to abdominal decompression in acute
Budd^Chiari syndrome
Deepak Joshi, Sujit Saha, William Bernal, Nigel Heaton, Julia Wendon and Georg Auzinger
Institute of Liver Studies, King’sCollege Hospital, London, UK
Keywords
abdominal compartment syndrome – Budd-
Chiari syndrome – intra-abdominal
hypertension – intra-abdominal pressure
Correspondence
Dr D. Joshi Institute of Liver Studies, King’s
College Hospital, London, SE5 9RS, UK.
Tel: 1 020 3299 2504
Fax: 1 020 3299 3899
e-mail: d.joshi@nhs.net
Received 16 November 2010
Accepted 12 May 2011
DOI:10.1111/j.1478-3231.2011.02557.x
Abstract
Background: Intra-abdominal hypertension (IAH) and abdominal compart-
ment syndrome commonly occur in patients with liver disease. Aims: We
compared haemodynamic variables pre- and post-abdominal decompression
in patientswith acuteBudd–Chiari syndrome(BCS) and patientswith chronic
liver disease(CLD), ascitesand IAH. Methods: Patientswith IAH admitted to
theLiver ICU, King’sCollegeHospital werestudied. Transpulmonary thermo-
dilution cardiac output (CO) monitoring was performed with the PiCCOs
system. Results: Ten patientswith decompensated BCS(median age39 years,
20–52) and eight patients with CLD (59 years, 33–65) and tense ascites
requiring paracentesis were studied. Intra-abdominal pressure (IAP) was
raised in both groups pre-intervention (BSC 23mmHg, 17–40; CLD 26,
20–40). Intrathoracic blood volume (ITBVI) waspersistently low in the BCS
group (632ml/m2
, 453–924) despite volumeresuscitation. Post-intervention,
reduction in IAPwasnoted in both groups(BCSPo 0.001, CLD Po 0.0001).
TheITBVI increased (P= 0.001) in theBCSgroup only. An increasein cardiac
index (CI) and strokevolumeindex (SVI) wasnoted in both groups(BCS: CI
P= 0.003, SVI: P= 0.007; CLD: CI P= 0.005, SVI P= 0.02). Thecentral venous
pressuredid not changein either group and did not correlatewith markersof
flow (CI, SVI) or IAP. Both groups demonstrated an inverse relationship
between IAP, CI and SVI. Conclusion: Patients with BCS and IAH have
evidence of central hypovolaemia. In addition to raised IAP, hepatic venous
obstruction and caudatelobehypertrophy limit venousreturn in patientswith
BCS. Reduction in IAP and re-establishment of caval flow restores preload
with improvement in CO.
Intra-abdominal hypertension (IAH), (sustained elevation
of intra-abdominal pressure, IAP, Z 12mmHg) and ab-
dominal compartment syndrome(ACS) (IAPZ 20mmHg
with evidence of new organ dysfunction) are associated
with decreased survival and a high prevalence of multi-
organ failurein critically ill patients(1–3). IAP isaffected
by the volume of intra-abdominal organs, presence of
spaceoccupying lesions(solid or liquid) within theabdo-
men and conditions limiting abdominal wall expansion.
ACSleft untreated can result in pulmonary, renal and liver
including the respiratory, renal, intestinal, cerebral and in
particular the cardiovascular system (8, 9), where it is
associated with a reduction in cardiac preload caused by
reduced venous return from intra-abdominal venous ca-
pacitance vessels. Studies have demonstrated that static
fillingpressuressuch ascentral venouspressure(CVP) and
pulmonary artery occlusion pressurecorrelatepoorly with
true cardiac filling (10). They may be falsely raised in
critical illness because of changes in thoraco-abdominal
compliance such as during positive pressure ventilation
Budd^Chiari syndrome
Deepak Joshi, Sujit Saha, William Bernal, Nigel Heat
Institute of Liver Studies, King’sCollege Hospital, London, UK
Keywords
abdominal compartment syndrome – Budd-
Chiari syndrome – intra-abdominal
hypertension – intra-abdominal pressure
Correspondence
Dr D. Joshi Institute of Liver Studies, King’s
College Hospital, London, SE5 9RS, UK.
Tel: 1 020 3299 2504
Fax: 1 020 3299 3899
e-mail: d.joshi@nhs.net
Received 16 November 2010
Accepted 12 May 2011
DOI:10.1111/j.1478-3231.2011.02557.x
Abstract
Background:
ment syndrom
compared hae
in patientswi
liver disease(
theLiver ICU
dilution card
system. Resul
20–52) and
requiring par
raised in bot
20–40). Intra
group (632m
reduction in I
TheITBVI in
index (CI) an
P= 0.003, SVI
pressuredid n
flow (CI, SV
between IAP,
evidence of c
obstruction a
BCS. Reducti
with improve
Intra-abdominal hypertension (IAH), (sustained elevat
of intra-abdominal pressure, IAP, Z 12mmHg) and
dominal compartment syndrome(ACS) (IAPZ 20mm
with evidence of new organ dysfunction) are associa
with decreased survival and a high prevalence of mu
organ failurein critically ill patients(1–3). IAP isaffec
by the volume of intra-abdominal organs, presence
spaceoccupying lesions(solid or liquid) within theabd
men and conditions limiting abdominal wall expansi
ACSleft untreated can result in pulmonary, renal and li
dysfunction (4–7). ACScan complicatethediseasecou
of decompensated chronic liver disease (CLD) if por
hypertension, ascites, and less frequently bleeding fro
abdominal, as well as extra abdominal organ function
Liver International (2011)
c 2011 John Wiley & SonsA/S
cirrhosis
Budd chiari