Acute Liver Failure: Supporting Other Organs

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1 Acute Liver Failure: Supporting Other Organs Michael A. Gropper, MD, PhD Professor of Anesthesia and Physiology Director, Critical Care Medicine University of California San Francisco

2 Acute Liver Failure Circulatory abnormalities and shock Management of renal failure Management of respiratory failure

3 Circulatory Abnormalities Diagnosis of shock Resuscitation Goals Choice of vasopressors Goal directed therapy

4 Differentiation of Shock Cardiogenic Septic and Hypovolemic Cardiac output Normal or high Low Pulse pressure Decreased Decreased SVR Decreased Increased Temperature Up or down Unchanged or Peripheral Increased Decreased perfusion WBC count Up or down Unchanged Infection Suspected or none documented A-V DO 2 Decreased Increased

5 Therapeutic Goals in Shock Increase O 2 delivery Optimize O 2 content of blood Improve cardiac output and blood pressure Match systemic O 2 needs with O 2 delivery Reverse/prevent organ hypoperfusion

6 First, fill the tank

7 PAOP versus CVP

8 CV Mechanics in Shock Cardiac Output normal cardiogenic shock hypovolemic End Diastolic Pressure

9 Crystalloid or Colloid? Schierhout, BMJ 1998

10 Randomized, prospective trial of 4% albumin versus normal saline for fluid resuscitation 6997 patients randomized Primary outcome was 28-day mortality NEJM 2004

11 Albumin vs Saline SAFE Study: NEJM, 2004 Prospective, randomized study of 6997 patients Objective need (one): tachycardia, hypotension, low PCWP, low Urine Output Normal saline vs 4% albumin for resuscitation All other management the same Primary outcome: 28d mortality Secondary outcomes: Survival time, new organ failures, duration of mechanical ventilation, ICU LOS

12 Albumin vs Saline SAFE Study: NEJM, 2004

13 Albumin vs Saline SAFE Study: NEJM, 2004

14 FDA Medwatch on Albumin

15 If still hypotensive after fluid resuscitation, start pressors

16 Best Pressor: Dopamine? No evidence of increased renal perfusion at low doses Tachycardia more common than with norepinephrine May impair splanchnic blood flow Stimulates vasopressin secretion Does not confer clinically significant protection against renal dysfunction

17 Best Pressor: Norepinephrine? No evidence of worsening renal function Less tachycardia than dopamine More rapid and effective BP control May increase splanchnic perfusion

18 Best Pressor: Norepinephrine? Effect of norepinephrine compared with high dose dopamine and/or epinephrine on the outcome of septic shock Prospective, observational cohort N=97 Norepinephrine mortality 62% vs 82% P<0.001 RR= % CI, Martin et al, CCM 2000

19 Best Pressor: Epinephrine? 30 adult patients with septic shock MAP 60 mm Hg Norepinephrine and dobutamine vs epinephrine to MAP >80 mm Hg Results Similar effect on hemodynamics Epinephrine Lactate Lactate/pyruvate ratio Gastric phi Levy et al, Intens Care Med, 1997

20 Best Pressor: Phenylephrine? 13 patients with septic shock Treated with fluids and either low-dose dopamine or dobutamine, but remained hypotensive Phenylephrine added 0.5 to 9 µg/kg/min MAP >70 mm Hg Results Increased MAP, SVR, CI, stroke index, DO 2, VO 2 and urine output No change in HR Dose 3.7 ( ) µg/kg/min Mean duration 65 hours Gregory et al, CCM, 1991

21 What about vasopressin?

22 Vasopressin mechanism of action

23 Vasopressin plus NE versus NE alone Randomized trial of 48 patients Hemodynamic outcomes measured

24 Vasopressin administration resulted in: reduced heart rate increased MAP increased CI increased SVI increased LVSWI decreased NE requirements But: no difference in mortality no difference in organ dysfunction Increased bilirubin in AVP group Dunser et al, Circulation 2003.

25 What are the therapeutic goals?

26 What is the BP Target? BP targets are arbitrary Autoregulation is lost below MAP mmhg What is the data that we should target a MAP of 65 mmhg?

27 Crit Care Med 2005; 33:

28 How Much BP is Enough? Blood Lactate (meq/l) Oxygen Consumption (ml/min/m 2 ) Oxygen Delivery (ml/min/m 2 ) Oxygen Extraction Ratio (%)

29 How Much BP is Enough? Urine Output (ml/h) Creatinine Clearance (ml/min) Crit Care Med 2005; 33:

30 Optimizing oxygen delivery: Early goal-directed therapy

31 Randomized, prospective trial of early, goaldirected resuscitation of patients with severe sepsis Patients randomized to 6 hours of goaldirected therapy vs standard therapy 260 patients randomized In-hospital mortality was 30.5% with goaldirected therapy vs 46.5% with standard therapy Rivers et al, NEJM, 2001;345:

32 Central Venous Oximetry

33 Central Venous Oximetry

34 Supplemental oxygen + endotracheal intubation and mechanical ventilation CVP < 8 mmhg Crystalloid Colloid Central venous and arterial catheterization 8-12 mmhg MAP < 65 mmhg >90 mmhg Vasoactive agents Sedation, paralysis (if intubated), or both >65 and <90 mmhg ScvO 2 <70% Transfusion of red cells Until hematocrit > 30% >70% No >70% Inotropic agents <70% Hospital admission Yes Goals Achieved Rivers et al, NEJM, 2001;345:

35 Evidence: The Importance of Early Goal Directed Therapy Early goal-directed therapy in patients with severe sepsis produced: 42% in relative risk of in-hospital and 28- day mortality (P=0.009, =0.01) 33% in relative risk of death at 60 days (P=0.03) NNT to prevent 1 event (death) = 6 to 8 Rivers E, et al. N Engl J Med 2001;345:

36 Management of Renal Failure

37 Impact of ARF on Mortality in Critically Ill Patients Metnitz et al, Critical Care Medicine, 2002

38 Acute Renal Failure Prerenal Failure Intrinsic Renal Postrenal Failure Vascular Acute Glomerulonephritis Acute Interstitial nephritis Acute Tubular Necrosis Obstruction of collecting system Decreased effective Blood volume HRS Ischemic Nephrotoxic HRS Exogenous Endogenous

39 Acute Tubular Necrosis Lamiere et al, Lancet: 2005

40 Hepatorenal Syndrome: Consensus Definition, International Ascites Club Major Criteria Acute/chronic liver disease with hepatic failure and portal hypertension Low GFR: serum Cr > 1.5 mg/dl or 24 hour creatinine clearance < 40 cc/min Absence of shock, ongoing infection, fluid loss, treatment with nephrotoxins No improvement in renal function following withdrawal of diuretics, expansion of plasma volume with 1.5 L isotonic saline Proteinuria < 500 mg/d and no ultrasonographic evidence of obstructive uropathy or parenchymal disease Minor Criteria Urine volume < 500 cc/d Urine Na < 10 meq/d Urine osm > Plasma osm Urine RBC < 50/hpf Serum Na < 130 meq/l Arroyo et al, Hepatology 23(1996):

41 Hepatorenal Syndrome Type I: Doubling of serum Cr to > 2.5 mg/dl or a 50% reduction of initial GFR to less than 20 cc/min within 2 weeks Type II: Moderate and stable reduction in GFR without a rapidly progressive course

42 When To Initiate CRRT? Oliguria with <200 ml in 12h Anuria: urine output <50mL in 12h Hyperkalemia: potassium >6.5 mmol/l Severe acidemia: ph<7.0 Azotemia: urea concentration >30mmol/L Uremic encephalopathy Uremic neuropathy/myopathy Uremic pericarditis Plasma sodium >155 mmol/l or <120mmol/L Hyperthermia Drug overdose with dialysable toxin

43 Hemodialysis Movement of small molecules across a selective membrane Forni. NEJM, 1997

44 Hemofiltration Movement of water and small molecules across a selective membrane, with selective fluid replacment Forni. NEJM, 1997

45

46 IHD vs CRRT Lamiere et al, Lancet: 2005

47 Continuous Renal Replacement Therapy

48

49 Slow removal of excess intra/extravascular volume

50 Convective solute clearance without dialysis

51 Dialysis with solute and nitrogen removal

52 Solute and nitrogen clearance, with fluid replacement

53 Does dialysis dose matter? Ronco et al, Lancet: 2000

54 Dialysis Dose and Mortality Ronco et al, Lancet: 2000

55 Management of Respiratory Failure

56 Respiratory Abnormalities in ALF Hepatopulmonary syndrome (HPS) Portopulmonary hypertension (PPH) Acute lung injury and the acute respiratory distress syndrome (ALI/ARDS)

57 Hepatopulmonary vs Pulmonary Hypertension Herve et al, Eur Resp J, 1998

58 Hepatopulmonary Syndrome Defined as: Presence of liver disease Hypoxemia on room air Intrapulmonary vascular dilation

59 Portopulmonary Hypertension Defined as: Histologic changes in the pulmonary circulation leading to increased vascular resistance. Mean PAP > 25 mmhg, with PCWP > 15 mmhg Evidence of portal hypertension

60 Definition of ARDS Clinical syndrome characterized by: oxygenation defect (PaO 2 /FiO 2 <200mmHg) bilateral infiltrates on CXR No evidence of CHF PCWP < 18 mmhg Acute Lung Injury (ALI) above, except (PaO 2 /FiO 2 <300mmHg)

61 Pressure-volume relationship appropriate V t V excessive V t protective V t P flex P aw

62 CT in Early ARDS Normal lung Consolidated lung Pleural Effusion

63

64 PaO 2 / FiO P/F * * Study Day 6 ml/kg 12 ml/kg ARDSnet, NEJM 2000

65 Median Organ Failure Free Days * * * * = 6 ml/kg = 12 ml/kg ARDSnet, NEJM 2000

66 Ventilator-Free Days ml/kg 12 ml/kg ml/kg 12 ml/kg ARDSnet, NEJM 2000

67 Mortality Prior to Hospital 50 Discharge 40 P= Mortality (Percent) ml/kg 12 ml/kg ARDSnet, NEJM 2000

68 Conclusions Shock resuscitation is time-sensitive Consider central venous oxygen saturation as a resuscitation target Continuous renal replacement therapy is a powerful tool for achieving homeostasis in acute renal failure Use a protective ventilation strategy in patients with acute lung injury

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