1 / 33

I have no financial relationship(s) to disclose relevant to my presentation.

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

gayora
Download Presentation

I have no financial relationship(s) to disclose relevant to my presentation.

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

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

  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 Secondary liver Injury Sepsis / inflammation Ischemia/Congestion Systemic disease Drugs TPN Other….. Surgical Hepatectomy Trauma Iatrogenic

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

  5. 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

  6. 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

  7. 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

  8. PeeP CVP PcwP Compliance ↓ IAP Echo findings also predictive of mortality post TIPS

  9. IAP and fluid responsiveness

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

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

  12. 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

  13. 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

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

  15. 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)

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

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

  18. Monescillo Hepatology 2004 ;40:793 Rx failure HVPG and CPscore • 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 6 week survival

  19. 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 alb

  20. 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

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

  22. Albumin and renal impairment in patients with cirrhosis and SBPSort P et al N Engl J Med 1999 5; 341 (6):403 • 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

  23. Budd chiari cirrhosis

More Related