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Last updated: ACS (Acute Coronary Syndrome)
on September 06, 2010

Acute Alcoholic Hepatitis/Decompensated Alcoholic Liver Disease

Key facts:


Authors: Natalie Acors and Andrew Stein
Top tip: Why are you not giving steroids? They improve mortality

Key differential diagnoses

Infection
Hepato-renal syndrome
Other causes liver dysfunction

Key Investigations

FBC, ESR, CRP
U+E, LFT/GGT, Bone, Glucose
INR
ECG, CXR
Liver/abdominal US

Key Treatment

PREDNISOLONE 40 mg od
IV PABRINEX 2 vials tds 3-6d, then THIAMINE 100 mg tds, for 1 mth

Key Management Decision

Steroids


Background


The word 'hepatitis' is a misnomer; as transaminases (AST/ALT) rarely exceed 200, and never exceed 400 U/L

Introduction

• This syndrome has only relatively recently been described. The pathogenesis is not completely understood
• It is important as severe cases have a high mortality (15-50% at 30d)
• 40% are dead at 1 year
• The diagnosis is often missed - and it is treatable.
• Many patients have cirrhosis at presentation (this may be first presentation of cirrhosis)
• Sepsis or bleeding are common precipitants, often spontaneous bacterial peritonitis

Definition

Progressive inflammatory liver injury associated with long-term heavy intake of ethanol

Terminology Try to avoid phrases like 'alcoholic' and 'alcoholism'; they are judgemental. Do you drink 'too much'? What is 'too much?. It is better to talk about alcohol dependence syndrome; or 'this patient has a high alcohol consumption'

Epidemiology

More common in non-Caucasians

Risk factors

Alcohol

Symptoms

Asymptomatic
Or, non-specifically (nausea, vomiting, anorexia and diarrhoea)
Fever (exclude infection)
Occasionally RUQ pain

Key questions

"When did your symptoms start?"
"How much alcohol do you drink (now and previously)?"

Signs

Jaundice
Enlarged tender hepatomegaly
Ascites, encephalopathy
Of liver failure/fluid overload

Investigation


Blood

FBC (Hb falling rapidly ?bleeding ?haemolysis; low platelets, ?portal hypertension/hypersplenism; anaemia and low platelets suggests cirrhosis)
± Blood film (if low platelets)
± Reticulocytes (haemolysis may occur as part of Zieve’s syndrome)
ESR/CRP, INR
U+E (Na low, ?hepato-renal syndrome (HRS); whatever cause, carries poor prognosis)
Note: HRS is rare, only occurs in patients with severe liver disease, and once established is usually fatal. Early recognition and treatment imperative
LFT/GGT: [Ref]
Note: transaminases not that elevated; usually <200; always <400; AST>ALT (vs other hepatic diseases); if v high (>10,000) think of paracetamol OD or ischaemia
Bone, Glucose (may be low)
BC
ABG, if unwell (and platelets OK)

Other

ECG
CXR (fluid overload, sepsis)
Liver/abdominal US with Dopplers (large and bright or features of cirrhosis and portal hypertension; also to exclude HCC, portal vein thrombosis as cause of deterioration)

Key investigations LFT, INR , U+E
Liver/abdo US, Ascitic tap if ascites (spontaneous bacterial peritonitis, SBP?)
Ascitic tap
Biochemistry
Protein level. Transudate has a total protein < 30 g/L - eg, cirrhosis, heart failure, nephrotic syndrome
Exudate has a total protein > 30 g/L - eg, carcinomatosis, infection, TB
Glucose: in SBP and neoplasm, decreased glucose (<3.0 mmol/L); due to increased glucose consumption
Lactate dehydrogenase (LDH): increases significantly (>500 iu/L) in SBP (and neoplasm)
Amylase: in pancreatitis (or perforated viscus) the amylase may be 5x the serum level
Cytology
Should only be performed when neoplasm is suspected
Bacteriology
WC, gram stain and culture: The diagnosis of SBP is suggested by a polymorphonuclear (PMN) cell count in excess of 250 cells per cubic millimetre; in the absence of evidence of an alternative source of infection (secondary peritonitis), such as viscus perforation or intraabdominal abscess. When mononuclear cells predominated, tuberculosis or fungal infection is likely. Gram stain may help to differentiate the organism in ascitic fluid infection. It is more frequently positive in secondary peritonitis. Dont forget to put some fluid in a BC bottle

Specialist investigations

Blood
'Hepatic screen' (Immunoglobulins, anti-mitochondrial AB, anti-smooth muscle AB; ANA/dsDNA; ferritin (may be increased in any acute illness, but iron studies and transferrin saturation may clarify), caeruloplasmin (if <45years); αFP; Anti-HA IgM, HBsAg, Anti-HCV,)
± EBV, CMV
± Tumour markers (CA 125, CA 15-3, CA19-9, CEA, AFP)
± Haptoglobin/LDH (haemolysis)

Other
Liver biopsy (Transjugular biopsy may be required)

Differential diagnosis

Infection; 10% will have sepsis even in the absence of clinical signs; fever may be a reflection of SIRS
Hepato-renal syndrome
Consider alternative causes of liver dysfunction
(viral hepatitis, haemochromatosis) or acute liver insult on background of alcoholic liver disease (paracetamol OD, ischaemia)

Treatment


Treatment
(first line)

STOP ALCOHOL CONSUMPTION


Drugs
IV PABRINEX 2 vials tds, for 3-6d; give over 30 mins (resus equipment to hand); before changing to oral treatment (PO THIAMINE 100 mg tds, for one month)
± IV GLUCOSE, 20 mls 50%, if BG <4 mmol/L
Note: GLUCOSE increases risk of Wernicke's encephalopathy, so give IV PABRINEX first
± IV CO-AMOXICLAV 1.2 g tds (to cover Spontaneous Bacterial Peritonitis (SBP))
± PO CHLORDIAZEPOXIDE 20-40 mg qds, gradually reducing over 7-14d (Rx DTs/agitation); prescribe PRN doses as well; many clinicians start at dosages that are too low

± Rx of seizures
Avoid sedatives if encephalopathy present
Avoid nephrotoxic drugs and diuretics

Procedures
IV
Daily weights
High calorie, low salt, high protein diet
Monitor LFT, U+E, INR
Fluid restrict if Na <125
Diagnostic ascitic tap (WC > 250 neutrophils indicates SBP)

Prescribing issues Significant risk of anaphylaxis with PABRINEX

Key management decision

Prednisolone/not
[Ref]

Stop

Alcohol

Treatment
(second line)

Drugs
• PREDNISOLONE 40 mg od for 5/7, then tapered over 28d. There is some evidence that a subset of patients with severe alcoholic hepatitis benefit from prednisolone. But all patients with GI bleeding, sepsis or renal impairment were excluded from the trials
Note: prednisolone should not be started if there is any suspicion of sepsis (10% will have sepsis even in the absence of clinical signs. Full sepsis screen must be completed before prednisolone considered
• If suspected variceal bleeding, give IV TERLIPRESSIN 2 mg stat, then 1-2 mg qds (provided no active cardiac ischaemia); for upto 72h
• Give 4.5% HAS if renal impairment is present. If no response, IV TERLIPRESSIN 0.5 mg qds
Procedures
If unwell, urinary catheter, CVP line, arterial line (if clotting/platelets OK)
Endoscopy

Admit?

Usually

Bed plan

Medical admission ward
± Gastroenterology
± ITU

Referrals

Medical
Hepatology
± ITU

Other
Dietitian
Community alcohol service

The Rest


Complications Cirrhosis, variceal haemorrhage, sepsis (including SBP), hepato-renal failure

Follow-up

• Hepatology/gastroenterology
• Community alcohol service

Prognosis

• 30-day mortality = 15% (severe liver disease 50%)
• If no encephalopathy, jaundice, or coagulopathy, 30-day mortality < 5%
• 1-year mortality rate after hospitalization for AAH = 40%
Note: worse if female, older, WC increased, or abnormal clotting; long-term prognosis depends heavily on whether patients have established cirrhosis and whether they continue to drink

Risk stratification
(who can be managed as outpatient)

If patient well with no melaena, ascites or encephalopathy, and bilirubin <100, they can be managed as outpatient

2° Prevention
+ Health promotion

•Encourage attendance at community alcohol service, and Alcoholics Anonymous
• To most patients, advise NO aclohol consumption for 6 months, in first instance
•If no end-organ damage, then normal 'safe' alcohol limit is advised (<4 units a day for male, <3 for female). If end-organ damage, patient should remain teetotal
• ACAMPROSATE – helps relieve intense anxiety, cravings and insomnia
• DISULFIRAM – causes unpleasant side effects with alcohol ingestion

'Safe' alcohol consumption

Don't forget

• To consider prednisolone
• SBP .. ie, if in doubt, give antibiotics as well
• Community alcohol service referral at discharge

Red flags

• Reduced conscious level
• GI Bleeding
• Hyponatraemia or renal impairment
• Continued drinking

References


national guidelines UK/BSG: Guidelines on the management of ascites in cirrhosis. Moore KP and Aithal GP. Gut 55; 1-12, 2006

review Alcohol abuse in the critically ill patient. Moss M et al. Lancet; 368: 2231�42, 2006 (pdf)