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Inpatient Management of the Cirrhotic Patient

Inpatient Management of the Cirrhotic Patient. Things You Will Learn. Background Information: -What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation : - If patient has ascites - If the patient has SBP - If patient has acute kidney injury

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Inpatient Management of the Cirrhotic Patient

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  1. Inpatient Management of theCirrhoticPatient

  2. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  3. Hepatocentric View “In the beginning, there was nothing……… Then God created the liver and gave it internal viscera and appendages to provide sustenance and mobility.”

  4. A bit about me…

  5. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  6. What is Cirrhosis? • The end stage of any chronic liver disease • HCV and EtOH are main causes in USA • Results in two major syndromes • Portal hypertension • Hepatic insufficiency • Associated with hyperdynamic circulatory state due to • Peripheral vasodilation • Splanchnic vasodilation

  7. Manifestations of Decompensation • Jaundice: hepatic insufficiency • GEV: portal HTN and hyperdynamic circulation • Ascites: sinusoidal HTN and sodium retention due to vasodilation and neurohumoral systems • HRS: peripheral dilation->renal vasoconstriction • HE: shunting through portosystemic collaterals, brain edema, and hepatic insufficiency

  8. “Status of the Liver” • 1964 – Child and Turcotte publish a system to predict mortality related to portocaval shunt surgery in cirrhosis* • 1973 – Pugh modified C-T scoring system to predict mortality related to esophageal surgery for bleeding varices (replaced ‘nutritional status” with PT)** • Child’s score = C-P score = CTP score *Child, CG, Turcotte, JG. Surgery and portal hypertension. In: The Liver and Portal Hypertension, Child, CG (Ed), Saunders, Philadelphia 1964. p.50. **Pugh RNH, Murray-Lyon IM, Dawson JL, Pietroni MC and Williams R. Transection of the esophagus for bleeding esophageal varices. Brit. J. Surg. 60: 646-654, 1973

  9. Child’s Classification Points* *Class A = 5-6 points, B = 7-9 points, C = 10-15 points

  10. Interpreting Child’s Score • These grades correlate with one- and two-year patient survival: • Class A - 100 and 85 % • Class B - 80 and 60 % • Class C - 45 and 35 % • Child’s class A are compensated • Median survival ~9-12 years • Management goals: • Treat underlying liver disease • Prevention/early diagnosis of complications • Child’s class B&C are decompensated

  11. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has renal insufficiency - If patient has portosystemic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  12. If The Patient Has Ascites • Development of ascites in cirrhosis is common (60% over 10yrs); once ascites develops mortality can reach 50% over the next 2yrs. • Ascites formation is very common in postoperative setting in patients with cirrhosis/portal HTN due to liberal use of saline IVF (this can often be the initial presentation of cirrhosis - - missed pre-op!)

  13. If The Patient Has Ascites • Clues: • Exam: palpable left/small right lobe, splenomegaly, caput medusa • Labs: • Platelets < 175,000 • Hepatic insufficiency: albumin <3.8, INR >1.3 • Imaging: nodular liver, splenomegaly

  14. If The Patient Has Ascites • Diagnostic paracentesis: • No coagulopathy cutoff, need for “reversal”, etc • Cell count and differential, albumin, and total protein • If first presentation, concern over infection, or atypical presentation • Glucose • Bedside culture • Flow cytometry • Simultaneous blood cultures (more later) • LDH • Triglycerides • Don’t forget serum albumin to determine SAAG

  15. If The Patient Has Ascites • Make the diagnosis (i.e. recognize it, then analyze the fluid - - diagnostic paracentesis) • Turn off the NS IV infusion! Think about carrier solutions for each of the patient’s IV infusions • Sodium restriction: 2gm/day (88mEq) • Oral diuretics: spironolactone alone or spironolactone/furosemide (100/40 ratio) • Goal: 300-500 ml/d (no edema) vs. 1000 ml/d (w/ edema) • Tense ascites: perform a large volume paracentesis (don’t forget the albumin - - 6-8 gm per liter ascites removed) • High risk patients with ascites should be placed on SBP prophylaxis (TP<1 and advanced liver failure)

  16. If The Patient Has Ascites • Do NOT use furosemide alone • Sodium not taken up in LoH absorbed in DCT/CT due to hyperaldosteronism • Do NOT use IV diuretics • No evidence that other diuretics (metolazone, thiazides, torsemide) offer advantage of spironolactone +/- furosemide

  17. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  18. If The Patient Has SBP • Most common infection in cirrhosis • Occurs in 10-20% of hospitalized patients with cirrhosis and ascites • Mortality 10-20% (was 80% when first described) • Early diagnosis is KEY to management and reduction of complications • Diagnostic paracentesis in any patient with cirrhosis and ascites: • Upon hospital admission • Who develops S/Sx compatible with SBP (abd pain, F/C) • With worsening renal or liver function

  19. If The Patient Has SBP • Diagnosis established: • Ascites PMN cell count >250 • Ensure bedside cultures collected • Simultaneous BCx should also be drawn (>50% SBP also have bacteremia) • Traumatic tap if >10,000 RBC • Subtract 1 PMN for every 250 RBC

  20. If The Patient Has SBP • Do not wait on culture results to start Abx • Cefotaxime most studied (2g q12hr) • 3rd generation cephalosporine (ceftriaxone 1-2g q12hr) • “Quinolone” ok if community-acquired, uncomplicated • Extended spectrum Abx (carbapenems, piperacillin/tazobactam) if nosocomial SBP • Can change to PO in 48hrs if improving • 5 day course of Tx minimum, 8 days preferred, thus 7 days reasonable • Repeat paracentesis/broaden coverage if not improving in 48hrs (expect at least 25% PMN decrease)

  21. If The Patient Has SBP • Albumin to prevent renal dysfunction (10% vs. 3%) and 3 month mortality (41% vs. 22%) • 1.5g/kg on day #1 within 6 hours of Dx • 1.0g/kg on day #3 (reasonable to tailor to renal fx) • What NOT to do: • Avoid aminoglycosides • No large volume paracentesis • Avoid diuretics (stop them if Pt is taking them)

  22. Cuban Rock Iguana

  23. Cuban Rock Iguana

  24. Cuban Rock Iguana

  25. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  26. If The Patient Acute Kidney Injury (AKI) • AKI occurs in ~19% hospitalized patients with cirrhosis • Pre-renal ~68% of these • Intra-renal next most common (ATN vs. GN) • Post-renal <1% • Hepatorenal syndrome (HRS) is a form of pre-renal failure: systemic/splanchnic vasodilation and reduced EAV->renal vasoconstriction • HRS ~33% of pre-renal AKI (1/5 of cirrhotics hospitalized with AKI) • Development of HRS-1 median survival ~2wks

  27. Dec. Effective Arterial Pressure(inc. CO/CI, dec. SVR, splanchnic vasodilation) Endotoxemia Nitric Oxide Carotid/Renal Baroreceptors Sense Dec. Perfusion Activation of Endogenous Vasoconstrictors Dec. renal PG’s synthesis and effect Non-Osmotic Loss of local renal vasodilators R.A.A.S S.N.S ADH AgII Dec. PGE2 Aldo V2 Receptor Inc. Renal Vascular Tone H2O Retention Abnml Renal Hemodynamics Na+/H2O Retention

  28. If The Patient Has AKI • Definition of HRS shifting target • Consensus conferences: Cr double to >2.5 • Suggested that Tx initiated earlier, with only 1.5-fold increase in Cr from baseline • Key to success is the early recognition and Tx of this condition

  29. If The Patient Has AKI • D/C medications that decrease blood volume • Diuretics • Lactulose • Vasodilators • Expand intravascular volume • Albumin 1g/kg up to max 100g • NS if over-diuresis is suspected

  30. If The Patient Has AKI • Search for and Tx AKI precipitants • Infection • Fluid loss • Blood loss • If no improvement or continued worsening • Renal U/S to R/O post-renal AKI • Urinary sediment to R/O intrinsic AKI • Proteinuria/hematuria suggests GN • Granular/epithelial casts suggests ATN • Historical clues such as sepsis, hypovolemia, recent nephrotoxins, contrast dye help sort out ATN vs. HRS

  31. If The Patient Has AKI • OLT is only definitive Tx that provides long-term survival • Arteriolar vasoconstrictors bridge to OLT • Terlipressin most studied but not available in USA • Midodrine plus octreotide most common in USA • Midodrine: start 5-7.5mg PO TID and increase to 12.5-15mg TID • Octreotide 100mcg SQ TID and increase to 200mcg SQ TID(continues infusion or used as sole therapy->no benefit) • Should be coupled with albumin infusions

  32. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  33. If The Patient Has Hepatic Encephalopathy (HE) • HE (or portosystemic encephalopathy: PSE) is a clinical spectrum of reversible abnormalities in neuropsychiatric function of patients with advanced liver disease • Continuum of neuropsychiatric alteration: • Episodic (acute): either precipitated or spontaneous • Recurrent : 2 or more acute episodes per year • Persistent (chronic): persistent deficits negatively affect social/occupational function • Minimal (subclinical): only found with careful testing

  34. If The Patient Has HE • Precipitating Factors: • Infection • Recent TIPS placement • Non-compliance • HCC • HV/PV thrombosis • Hypovolemia • GI bleeding • Hypokalemia • Metabolic alkalosis (diarrhea) • Hypoxia • Sedatives • Hypoglycemia

  35. Asterixis

  36. If The Patient Has HE

  37. If The Patient Has HE Psycodynamic or “Trail test”

  38. If The Patient Has HE Therapy: • Fix/Remove the precipitating factors • Lactulose: 30-50ml q2h initially, then TID (goal 3-5 soft BM/d); can use 300ml retention enemas also • Antibiotics: rifaximin 200-600mg TID • No evidence that combo with lactulose is better • Use in patients who can’t tolerate or don’t respond to lactulose • Flumazenil: 0.4-2.0 mg IV (lasts 2-4 hrs only) • Don’t restrict protein (1.0 -1.2 g/kg/day) • If recent TIPS may need reduction/occlusion

  39. Hutia a.k.a “Banana Rat”

  40. “Banana Rat: The Other White Meat”

  41. Things You Will Learn Background Information:-What is cirrhosis - What is compensated versus decompensated cirrhosis Admission Evaluation: - If patient has ascites - If the patient has SBP - If patient has acute kidney injury - If patient has hepatic encephalopathy - If patient has gastrointestinal bleeding - Pain management Preoperative Evaluation: - Risk Factors for morbidity/mortality - “Status” of the Liver - Type of Surgery - Contraindications to Surgery

  42. Acute Gastrointestinal Bleeding • Liver involved in all 3 systems (coagulation, fibrinolysis and protein C dep. pathway) • Nearly all proteins involved in hemostasis are produced in the liver (exceptions: Factor VIII, vWF, thrombomodulin) • Impaired production and clearance effect fibrinolytic system (dec. clearance t-PA, PAI-1) • Clinical importance of PLT dysfxn in cirrhosis unclear; thrombocytopenia is due to splenic sequestration

  43. Acute Gastrointestinal Bleeding • Overall have impaired thrombin generation and less stable fibrin structure with increased fibrinolysis (“defective hemostatic plug”) • Hemostatic disturbances in cirrhosis are similar to those described for DIC

  44. Acute Variceal Hemorrhage • Acute variceal hemorrhage mortality 15-20%

  45. Acute Variceal Hemorrhage • Volume expansion: colloids over crystalloids • SBP 90-100mm Hg • HR<100 bpm • Transfusion of blood products to maintain • Hgb ~8g/dl (higher increases re-bleeding/mortality) • Platelets ~50,000 • INR to 1.3 • Consider prophylactic intubation if massive bleeding and decreased LOC

  46. Acute Variceal Hemorrhage • Initiate somatostatin analog (octreotide) as soon as diagnosis suspected • 50 mcg IV bolus followed by 50 mcg/hr infusion • Continued for 5 days • Antibiotic prophylaxis for 3-7 days with cipro vs. ceftriaxone (ascites, PSE, bilirubin >3, malnutrition) • Endoscopic evaluation within 12 hours

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