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Acute liver failure in icu
This document summarizes the case of a 56-year-old male with acute liver failure who underwent liver transplantation 8 years ago. He presents with jaundice, confusion, and feeling unwell. On examination he has hypotension, tachycardia, and signs of vasodilatory shock. Blood tests show deranged liver function and metabolic acidosis. The document defines acute liver failure and outlines its etiology, prognosis, pathophysiology, investigations, treatment of complications including cerebral edema and infection, and the role of liver transplantation.
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Acute liver failure in icu
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- 2. Case…Thursday evening callfrom 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 Liverfailure “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”
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- 7. Parradox Rapid onsetALF ----> 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
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- 9. Common drugs causingALF Isoniazid Sulfur Antibiotics Nitrofurantoin Azole antifungals Antiepileptics- Phenytoin, sodium valproate. Herbals-ex kava kava,ma huang,comfrey. Ibuprofen Statins
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- 11. Poor prognosis Phonea friend, call Your consultant Don’t hesitate to call St. Vincent University Hospital.
- 12. Mortality Hospital survival Mid1970”s ….. 17% Mid 2000”s …... 62%
- 13. Pathophysiology Death ofa 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 under35 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 >75mcg/l …Encephalopathy >200 mcg/l…Cerebral oedema and raised ICP.
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- 22. N-Acetylcysetine •May improve circulatoryfunction 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
- 23. When to pickup 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
- 24. Good ICU housekeeping Stress ulcer prophylaxis No DVT prophylaxis Feeding Blood glucose management Electrolytes like phosphate and magnesium.
- 25. Lines Ultrasound guided No correction of coagulopathy Arterial line Central line Vascath
- 26. 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
- 27. Vasopressors Nor-Adrenaline Terlipressin Vasopressin..no evidence of splanchnic ischemia.
- 28. Sedation Avoid ifpossible Propofol/Remifentanyl is reasonable
- 29. Pulmonary considerations Airway –Electiveintubation –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
- 30. Renal failure Renalfailure in 50% Particularly common with paracetamol overdose –Liver and renal metabolites
- 31. 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
- 32. Complications of acuteliver failure and management
- 33. Management of complications Cerebral edema Sepsis Coagulopathy
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- 35. Predictors of cerebraledema •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
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- 37. Delaying the onsetof raised ICP
- 38. Delaying the onsetof raised ICP
- 39. Delaying the onsetof raised ICP
- 40. Two principles inmanagement of cerebral oedema
- 41. 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.
- 42. Infection •Infection is near-universal –Failingliver 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
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- 44. Recommendations Minimize invasiveprocedures, 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)
- 45. Coagulopathy Increased INRpresent by definition Thrombocytopenia present in up to 70% TEG is reassuring
- 46. Is there bleedingdiathesis? 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
- 47. Correcting coagulopathy before invasiveprocedures 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.
- 48. Correcting coagulopathy before invasiveprocedures 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
- 49. Other options Livertransplant MARS.. Extracorporeal support, dialysis against albumin. CRRT against albumin.
- 50. Liver transplant Accepted IndicationsAbsolute 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
- 51. Palliate Declined byliver services Refractory ICP Blown pupils Communication skills Don’t forget morphine infusion.
- 52. In summary •Causes •Help •Bloods •NAC •Early lines,don’t be afraid •Drugs, dialysis •Raised ICP •Coagulation •Manage Infections •Transplant •Palliate
Editor's Notes
- #6 Grade 1,ii rare Grade iii 25-35% Grade iv 65-75% Cerebral oedema most common cause of death.
- #11 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.
- #13 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.
- #23 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.
- #34 Most common cause of death-cerebral oedema.
- #35 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
- #37 Complication rate with ICP monitor 3.8%,fatal haemorrhage 1%
- #43 Common organisms growing klebsiella oxy, VRE, Enterococcus faecium.
- #45 Prophylactic antibiotics for greatest risk pts as mentioned above.