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home - Liver - Liver Failure - Other Drug Injury Written by Dr Sebastian Zeki

Assesses the severity of liver dysfunction and its prognostic
significance following haemorrhage

Knows importance of correcting hypovolaemia preventing
complications of GI bleeding and deterioration of liver function and
stopping bleeding

Knows the potential use of blood & clotting factors the role of
antibiotics the use of vasoconstrictors therapeutic endoscopy the
indication for transjugular intra-hepatic portosystemic shunt (TIPS) or
surgical shunt surgery

Aware of the specific complications of bleeding in cirrhotic patients –
including hepatic encephalopathy need for airway protection
nutrition identification of alcohol withdrawal

Shows proficiency in endoscopy – including emergency endoscopic
techniques of variceal band ligation endoscopic sclerotherapy
injection of cyanoacrylate glues for gastric varices

Can place safely and manage a Sengstaken tube in refractory
variceal bleeding

Can prevent and treat complications including hepatorenal failure
ascites spontaneous bacterial peritonitis and hepatic encephalopathy

Appreciates criteria for referral to specialist centre when appropriate –
such as with bleeding gastric or ectopic varices or consideration of

Appreciates need to treat patients using a multi–disciplinary approach
Shows understanding of an empathic approach which may involve


Knows risks and prognosis of recurrent variceal bleeding in cirrhotic

Aware of role of secondary prophylaxis with either non–selective ?-
blockers endoscopic ligation or both

Can select suitable endoscopic therapy and perform the appropriate
procedure competently

Appreciates the potential role of other specialists e g interventional
radiologists and nurse specialists



Understands the mechanisms of biliary metabolism the various
abnormalities that lead to hyperbilirubinaemia and knows and
recognises the causes of the various forms of jaundice

Selects and interprets appropriate investigations and formulate
management plans

Approaches patients presenting with jaundice in a logical and
methodical manner


Can define the different types (I and II) of hepatorenal

Knows the differential diagnosis of different types of renal
failure/impairment in liver disease

Understands the major and minor criteria in diagnosis of HRS and be
able to differentiate between HRS and acute kidney injury

Appreciates the prognostic significance of renal impairment in
patients with chronic liver disease

Knows the options for management and treatment of HRS the role of
colloids and vasoconstrictors as well as renal supportive treatment by

Uses and interprets result of sometimes complex investigations

Can judge when to involve other specialists especially nephrologists
radiologists and intensivists



Understands the pathogenesis of hepatic encephalopathy (HE)
Knows the differential diagnosis of HE including the existence of risk
factors for its causation including metabolic disorders and intracranial
structural disorders (such as subdural haematomas)

Knows factors that may precipitate HE including bleeding electrolyte
disturbance drugs or other organ failure

Knows the various treatment options appropriate for grade of severity

Can grade the mental state (Glasgow coma score and West Haven

Shows ability to differentiate between acute and acute on chronic liver

Can identify the patient at risk of raised intracranial pressure and
cerebral oedema

Selects and use investigations appropriately and determine timing of
airway protection

Appreciates the role of other specialists and interacts in a
professional manner with intensivists neurologists
neurophysiologists radiologists and other specialists

Makes referral where appropriate to specialist centre for liver



Understands the causes of acute hepatitis including viral druginduced alcohol-induced and auto-immune liver disease

Knows the appropriate plan of investigation and management of
specific diseases including the role of serological investigations and
liver biopsy

Takes an accurate history from patients with acute liver disease and
performs detailed clinical examination

Utilises investigation in a structured manner
Considers all therapeutic modalities and preparedness to refer to
specialist centre where diagnosis remains in doubt or appropriate
management cannot be performed


Methods GMP
Recognises and knows how to diagnose acute and chronic drug
induced liver injury and dysfunction
SCE 1,2
Aware of methods of diagnosis, role of liver biopsy and therapy
including role of steroids in treatment in selected cases
SCE, CbD 1
Understands the role of both prescription and recreational drugs and
the aetiology of a wide variety of liver disease and dysfunction often
requiring prompt intervention or involvement of specialist services
SCE, CbD 1,2,3
Has awareness of the range of iatrogenic liver dysfunction SCE, CbD 1,2,3
Able to interact with specialist pharmacy services. Can use yellow
card reporting system of potential adverse effects of drugs.



Understands the causes and pathophysiology of acute liver failure
Can plan appropriate investigation evaluate prognosis and construct
a detailed management plan

Identifies those potentially suitable for emergency liver transplantation
Develops ability to make accurate evaluation of patients with liver
failure at the stage of initial presentation

Can deliver management plan appropriately evaluate changes in
patient’s condition and react accordingly

Utilises the range of medical interventions necessary to support
critically ill patients

Demonstrates ability to identify patients at risk of developing acute
liver failure and understand the criteria for referral to specialist centres

Works collaboratively with nurses and all ITU staff as well as
colleagues in other clinical disciplines to deliver the highest standard
of clinical care

Communicates effectively and relates with empathy to family and
close friends of patients

Other Drug Injury

Biliary sclerosisUsually occurs after therapy of metastatic carcinoma with floxuridine.This looks like PSC.Clinical presentation is with RUQ pain, LOW, and jaundice. Chronic intrahepatic cholestasis —This presents as PBC without AMA.It can evolve from acute drug-induced cholestasis.It usually resolves with drug withdrawal- can take months.It can progress to vanishing bile duct syndrome and liver failure. Drug Induced Chronic cholestasis Peliosis hepatis This is rare.Histology demonstrates multiple, small, dilated blood-filled cavities in hepatic parenchyma.It is usually associated with hepatic tumors or with cholestatic jaundice.Drug associations include anabolic steroids, arsenic, azathioprine, mercap-topurine, OCP danazol, diethylstilbestrol, tamoxifen, vitamin A, and hydroxyurea.It usually resolve on withdrawal. Sinusoidal obstruction syndrome (veno-occlusive disease) Clinically this presents as Budd-Chiari syndrome. This is due to the occlusion of the terminal hepatic venules and hepatic sinusoids rather than the hepatic veins and inferior vena cava.Associated Drugs include Pyrrolizidine alkaloids (found in herbal remedies) , Azathioprine; Mercaptopurine; Vitamin A; OCP; Cyclophospha-mide; Tetracycline ; Chemotherapy. Hepatic vein thrombosis Most common implicated medication is the OCP. Granulomatous disease Noncaseating granulomas are usually located in the periportal and portal areas.Drug associations include Allopurinol; Amiodarone; Carbamaz-epine; Diazepam; Diltiazem; Isoniazid; Methyldopa,; Phenytoin; Procainamide; Quinidine; Sulfonamides; Sulfonylureas.Drugs can be associated with hepatocellular injury (granulomatous hepatitis) or cholestasis, but normally silent.Clinical presentation includes a low-grade fever and chronic fatigue.Jaundice is rare.The injury is usually transient without significant sequelae. AngiosarcomaThis is rare.It is associated with thorotrast (contrast used in the 1930s to 1950s), arsenic, potassium arsenite, radium, inorganic copper, and polyvinyl chloride, and anabolic steroids.There is a mean life expectancy of 6m after diagnosis. Hepatocellular carcinomaDrug associations include aflatoxin, OCP, and alcohol. Hepatic adenoma This is increased in females on the OCP (esp >5 yrs) and males on anabolic steroids (which regress when drug stopped). Drugs:Amitriptyline; Ampicillin; Amoxicillin-clavulanate; Carbamazepine; Chlorpromazine; Cyprohepta-dine; Crythromycin estolate; Haloperidol; Imipramine; Organic arsenicals; Prochlorperazine; Phenytoin; Trimethoprim; Sulfamethoxazole, Thiabendazole; Tolbutamide; Tetracycline; OCP Anabolic steroids.Drugs implicated in chronic intrahepatic cholestasis and also ductopenia include carbamazepine,; Chlorpromazine; Chlorpropamide; Co-trimoxazole,; Haloperidol, Thiabendazole, and TCA’s. Written by Dr Sebastian Zeki

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