Liver failure

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Liver failure

Hyper - acute liver failure

Acute liver failure

Greatest risk of cerebral

oedema, CVS failure

Greatest chance of

spontaneous survival







Sub - acute liver failure

Lowest risk of cerebral

oedema/ encephalopathy

Easily confused with CLD

Ascites

Lowest chance of

spontaneous survival

Principle Causes of Acute Liver Failure

Cause Agent responsible



Viral Hepatitis A, B, D E, others

Drug related Idiosyncratic and dose related



Toxins Carbon tetrachloride, Phosphorous

Amanita phalloides

Vascular events Ischemic hepatitis, Budd-Chiari, VOD, heat

shock liver

Other Pregnancy related, Wilson disease, lymphoma



No previous liver disease

Various definitions

Jaundice or symptoms to encephalopthy

• Decompensated chronic liver disease

– Decompensation with sepsis

· Bacterial peritonitis : Rx as “peritonitis”

· Bacteraemia, chest, urine

– Variceal bleed : frequently septic, endoscopic skills ± TIPS

– Encephalopathy

– Hepatorenal failure

– Alcoholic hepatitis : steroids, pentoxifylline, feed, delta bilirubin



Differential with ALF :

History

Pattern of LFT‟s

Imaging : ultrasound, CT scan

Biopsy : vary rarely indicated



• Liver trauma

Multi system disease

Coagulopathy

· INR important prognostic indicator in established ALF

· Platelet dysfunction DIC - rare

Metabolic

· Insulin resistance : Clarke et al Hepatology

· Hyperlactataemia :Bernal et al Lancet 2002 : useful to track

· Liver net producer of lactate Murphy et al Crit Care Med 2001

· P04, Mg, Na, glucose, K, pH

· High incidence of pancreatitis

Nutrition

· Frequent poor recent oral intake ± vomiting

· No evidence for protein restriction in either acute or CLD

· Gastric prophylaxis

· Increased metabolic requirements Walsh et al CCM

2000;28(3):649-54

Renal failure

• Common 45% of all cases

• Multifactorial - frequently pre renal, ATN rather than

HRS

• Role of intra-abdominal pressure

• Specific associations with viral disease, alcohol,

auto-immune

• CRRT or slow haemodialysis is ideal



• Anticoagulation

– epoprostenol, heparin, regional anticoagulation,

citrate

Infection : ALF

• Impaired innate and cellular immunity

• Bacterial infection 335 of 887 patients (550 episodes)

• Severe sepsis 58% mortality

• Septic shock 98% mortality

• Fungal infection 99 of 887 : 11% : 64% mortality

• Rolando et al Hepatology 2000 32:734, 31(4):872

• Components of SIRS associated with encephalopathy

• Rolando et al Hepatology 2000;32:734-9, Vaquero et al Gastroenterology

2003;125:755-64, Shawcross D et al J Hepatol inpress

• Cultures +++

• Antibiotics : broad initially - 5/7 course Antifungals

• No benefit to routine prophylaxis or Selective gut decontamination

• Rolando et al Semin Liver Dis 1996;16:389-402, Rolando et al Liver Trans

Surg 1996;2:8-13

Vasopressors in ALF

• What mean arterial pressure ?

– Clinical examination ….invasive

– Determined by JV saturation and ICP : autoregulating or not ?



• Which drug?

– Determine fluid responsiveness initially

· Whatever you can get your hands on

– In sepsis and MOF epinephrine may be detrimental

· increases splannchnic V02 : glucose turnover Meier Hellman et al 1997

Crit care Med

– Phenylephrine : decreased flow with decrease in spl V02 Reinelt

Crit Care Med 1999,27:325





– Norepinephrine as first choice

– Vasopressin may be potentially detrimental : cerebral

complications and potential splanchnic ischaemia

Results stratified according to blood pressure on day of SST

Harry et al Hepatology 2002

–57% of patients have abnormal synacthen response

–hypotension associated with lower baseline and increment (p65 : frequently not autoregulating - need to measure ICP

• Treat “ICP” - pupillary abnormalities

– Mannitol 150 ml 20% (osmolarity 150, pressors, fever, hyperacute and acute, pupilllary

abnormalities

• Temperature - avoid fever : hypothermia should not be undertaken routinely

Currently available…

Phase III study with BAL Demetriou et al Ann Surg 2004;239 660-670

MARS Therapy

Mitzner et al Liver Transpl 2000;6:277-286, Heemann et al Hepatology 2002;36:949-58





24 patients with CLD and „acute liver injury‟

• MARS group: reduced bile acids, bilirubin, encephalopathy

• Controls: biochemistry static, worsening

encephalopathy

– MARS 11/12 , SMT 6/12 (P90, pressors, 8/30 30 day survival (median 21)

Clinical jaundice > 92% 1month Ventilated survival 0/15

Mortality vs 11% in those with 3.0 day 2 or > 4.0 thereafter INR >1.8

oliguria and/or elevated creatinine oliguria/renal failure

altered conscious level encephalopathy

hypoglycaemia hypoglycaemia

shrinking liver size

300 µmol/l



Budd Chiari



Pregnancy related

Paracetamol Non-Paracetamol

pH 6.5

within 24 hrs

PT > 100 INR > 6.5 any 3 of :

Creatinine > 300 µmol/l seronegative hepatitis or

grade 3 - 4 encephalopathy drug related / halothane

Bilirubin > 300 µmol/l

Low P04 : good prognosis

Alpha feta protein INR > 3.5

Age 40 yrs

Lactate : 4 hrs > 3.5 OR 43 p 7 days

Lactate : 12 hrs > 3.5 OR 63 p 30

Children - coagulopathy INR > 4.5 Encephalopathy +

Factor V 30 yrs of age

The future:

Increasing liver disease

alcohol, HCV, NAFLD

HCC



Treatment changing

Innovative treatment options

liver support systems - further

Controlled trials required



Transplantation is a real option

Early discussion



Assume fluid deplete: time is tissue

Infection is common

Agitation=HE



Close observation



julia.wendon@kcl.ac.uk


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