Acute liver failure in icu

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Acute liver failure managment in Intensive care unit

Acute liver failure managment in Intensive care unit

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  • Grade 1,ii rare
    Grade iii 25-35%
    Grade iv 65-75%
    Cerebral oedema most common cause of death.
  • In america ALFSG index used which includes patient gcs,bilrubin,inr,sr phosphorus,and sr M30 (ELISA based marker of apoptosis)..Limited use as M30 not available everywhere.Better prognostic indicator than KCC.
  • Improved mortality due to orthoptic liver transplant and better critical care.
    Research difficult due to rare and heterogenous nature with rapidly progressive course but result from application of other research e.g from cerebral edema management has improved mortality.
  • Reduces IL 17 levels in Non paracetamol ALF pts.
    In pcm overdose replinishes glutathione stores and detoxifies NAPQ1 highly reactive,toxic metabolite of paracetamol overdose.
  • Most common cause of death-cerebral oedema.
  • 20_25% deaths in ALF due to intracranial hypertention and BS herniation.
    HE four compatible theories

    Cerebral vasomotor dysfunction
    Oedema secondary to ammonia toxicity
    Inflammation due to SIRS
    putative benzodiazepine-like molecules
  • Complication rate with ICP monitor 3.8%,fatal haemorrhage 1%
  • Common organisms growing klebsiella oxy, VRE, Enterococcus faecium.
  • Prophylactic antibiotics for greatest risk pts as mentioned above.

Transcript

  • 1. Acute Liver failure Wahid Altaf
  • 2. Case…Thursday evening call from AnE registrar  Mr C.E. 56 Year old male.  Presenting complaint of Jaundice Confusion Feeling unwell  Background history, liver transplant 8yrs ago with normal liver functions untill 20 days back.
  • 3. Further questioning  Hypotension  Tachycardia  Vasodilatory shock  Severe Compensated Metabolic acidosis Ph 7.37 HCO3 14 lactate 8  Blood Glucose 2.5  Deranged Liver functions.( Bilirubin 116, ALP 357, GGT 103,AST 1241,ALT 873).
  • 4. Definition of Liver failure “The abrupt loss of hepatocellular function in a patient with previously normal liver function, the expression of which includes coagulopathy and encephalopathy.” AASLD…“Evidence of a coagulation abnormality (INR>1.5) and mental alteration (encephalopathy) in a patient without pre-existing cirrhosis and with an illness of <26wks duration”
  • 5. Encephalopathy
  • 6. Classification
  • 7. Parradox  Rapid onset ALF ----> higher risk of cerebral edema but better prognosis for recovery  Classic example: Paracetamol OD  Slow onset ALF -----> lower risk of cerebral edema, higher risk of portal hypertensive problems (e.g. ascites, variceal bleeding), and ultimately poorer prognosis (w/o transplant)  Classic example: NANB hepatitis
  • 8. Etiology
  • 9. Common drugs causing ALF  Isoniazid  Sulfur Antibiotics  Nitrofurantoin  Azole antifungals  Antiepileptics- Phenytoin, sodium valproate.  Herbals-ex kava kava,ma huang,comfrey.  Ibuprofen  Statins
  • 10. Prognosis…family
  • 11. Poor prognosis  Phone a friend, call Your consultant Don’t hesitate to call St. Vincent University Hospital.
  • 12. Mortality  Hospital survival Mid 1970”s ….. 17% Mid 2000”s …... 62%
  • 13. Pathophysiology  Death of a mass of hepatocytes.  Loss of vital synthetic and metabolic hepatic functions.  Sterile inflammatory condition leading to SIRS.  Aim of management is to halt progression from hepatic impairment to MODS.
  • 14. Investigations  ALT, AST, ALP,GGT.  Bilirubin, Ammonia, Lactate.  Blood glucose, Coags: PT, aPTT, INR, Albumin.  Electrolytes, Mg, Phos.  Arterial blood gas  FBC with differential.  Drug screening, paracetamol levels
  • 15. Investigations.  If under 35 years of age Ceruloplasmin, Serum & urine copper  Anti HAV IgM  Anti HBc IgM/ Anti HBsAg  Anti-HCV  Pregnancy test  Autoimmune markers – ANA, ASMA, Ig levels  HIV status  Amylase & lipase
  • 16. Invstg  Diagnostic imaging  Liver biopsy
  • 17. Imaging  Microbiology : Strep parasanguinus and candida.
  • 18. Ammonia levels  >75 mcg/l …Encephalopathy  >200 mcg/l…Cerebral oedema and raised ICP.
  • 19. Cause-Specific therapy
  • 20. Cause-specific therapy
  • 21. N-Acetylcysetine •May improve circulatory function and oxygen delivery •No improvement in overall survival but significant improvement in transplant-free survival with encephalopathy grade 1-2. Time to NAC administration important Time in hrs Mortality (%) <12 0.4 >12 6 >24 13 >48 19 •Now generally recommended for all patients with ALF
  • 22. When to pick up the phone in paracetamol overdose  D2-  pH <7.3  INR>3  Cr >200  Hypoglycaemia  D3-  HE  Cr>200  INR >4.5  D4-  Any rise in INR  Cr >250  HE
  • 23. Good ICU housekeeping  Stress ulcer prophylaxis  No DVT prophylaxis  Feeding  Blood glucose management  Electrolytes like phosphate and magnesium.
  • 24. Lines  Ultrasound guided  No correction of coagulopathy  Arterial line  Central line  Vascath
  • 25. Severe Vasodilatory shock  Optimise cardiac filling pressures –Haemodynamics can be challenging to determine given the disruptive effects of liver failure on the vasculature  Saline challenge, albumin.  Vasopressors
  • 26. Vasopressors  Nor-Adrenaline  Terlipressin  Vasopressin..no evidence of splanchnic ischemia.
  • 27. Sedation  Avoid if possible  Propofol/Remifentanyl is reasonable
  • 28. Pulmonary considerations  Airway –Elective intubation –Elective intubation once in grade 3 encephalopathy  Rapid intubation technique –Avoid spikes in ICP or decreased CPP  Pneumonia –Commonest site of sepsis  Acute lung injury/ARDS –In one third of patients
  • 29. Renal failure  Renal failure in 50%  Particularly common with paracetamol overdose –Liver and renal metabolites
  • 30. Management  Volume control  Maintenance of blood pressure  Prevention/treatment of sepsis  Judicious selection of drugs  Early use of renal replacement therapy –Before fluid problems aggravate cardiovascular status and ICP –Sodium management –Better ammonia level management
  • 31. Complications of acute liver failure and management
  • 32. Management of complications  Cerebral edema  Sepsis  Coagulopathy
  • 33. Cerebral oedema
  • 34. Predictors of cerebral edema •Rapid onset ALF ―Rapid accumulation of glutamine overwhelms astrocytes' ability to exclude organic osmolytes •Grade 3-4 encephalopathy ―High ammonia concentrations •Infection and/or SIRS ―Case for prophylactic antibiotics •Vasopressor therapy •Renal replacement therapy
  • 35. Invasive monitoring of ICP
  • 36. Delaying the onset of raised ICP
  • 37. Delaying the onset of raised ICP
  • 38. Delaying the onset of raised ICP
  • 39. Two principles in management of cerebral oedema
  • 40. Raised ICP management  1st line Mannitol  2nd line Hyperventillation to PaCO2 25-35mmhg  3rd line Hypertonic saline, Hypothermia  4th line Barbiturates, Anticonvulsants  Other considerations Transplantation, total hepatectomy.
  • 41. Infection •Infection is near-universal –Failing liver results in failed host defences –Infection precipitates MOSF, cerebral oedema –Frequent cause of death •Organisms –Bacterial and fungal –Gram negative organisms (52%) more frequent than Gram-positive organisms (44%) and Candida Infection
  • 42. Sites of sepsis
  • 43. Recommendations  Minimize invasive procedures, strict asepsis  Daily chest radiograph and surveillance cultures  Empiric broad spectrum antibiotics for those patients at greatest risk: –Grade 3-4 encephalopathy –Renal failure –Any component of SIRS –Planned transplantation (includes antifungals)
  • 44. Coagulopathy  Increased INR present by definition  Thrombocytopenia present in up to 70%  TEG is reassuring
  • 45. Is there bleeding diathesis?  Significant bleeding is uncommon: 5% –Anticoagulant proteins decrease in parallel with coagulation factors –Spontaneous intracranial haemorrhage is rare  Less clinically-significant bleeding may occur from several sites –Gastric mucosa –PPIs  Invasive procedures offer the greatest risk
  • 46. Correcting coagulopathy before invasive procedures  Correction itself carries risks –Volume overload –Aggravation of ICP –Transfusion-related acute lung injury –Thromboembolism (particularly with recombinant Factor VIIa)  Commonly used goal of INR <1.5 untested, lacks scientific basis  Correction obscures underlying trends in INR which are important prognostically.
  • 47. Correcting coagulopathy before invasive procedures  FFP not encouraged except to correct coagulopathy before invasive procedure –Effect modest, short-lived –Does not improve survival  Platelet transfusions –Rarely necessary  Recombinant activated Factor VII –Is effective –Cost –Short-lived effect –Prothrombotic
  • 48. Other options  Liver transplant  MARS.. Extracorporeal support, dialysis against albumin.  CRRT against albumin.
  • 49. Liver transplant Accepted Indications Absolute contraindications Acute Liver Failure Brainstem herniation Decompensated cirrhosis with MELD>15 Severe intracranial hypertention (ICH>50) Hepatocellular criteria with Milan criteria Advanced cardiopulmonary disease.Haemodynamic unstability,requiring high dose pressors Hilar cholangiocarcinoma Uncontrolled infection Hepatopulmonary syndrome Multiorgan failure Portopulmonary hypertention Current/Recent extrahepatic malignancy unless tumour free>2yrs Primary hyperoxaluria Untrated alcoholism/Drug use Cystic fibrosis with liver involvement Severe uncontrolled mood disorders
  • 50. Palliate  Declined by liver services  Refractory ICP  Blown pupils  Communication skills  Don’t forget morphine infusion.
  • 51. In summary •Causes •Help •Bloods •NAC •Early lines, don’t be afraid •Drugs, dialysis •Raised ICP •Coagulation •Manage Infections •Transplant •Palliate