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Final FRCA – Medicine for the FRCALaura Dyal
ST6 Anaesthetics
8/5/2019
The Liver….
Learning plan
• Revise basic physiology of Liver
• Causes of Liver failure
• Acute
• Chronic
• Systemic effects of Chronic Liver disease
• Anaesthetic implications
• Acute Liver failure
• Exam practice
Liver MCQ – T/F
• The liver is one of the largest organs in the human body and undertakes multiple tasks. Regarding Liver function:
a. 70% of liver blood flow is via the hepatic artery
b. Portal tracts contain lymphatics
c. Plasma cholinesterase is produced by the liver
d. Vitamin E is stored in the Liver
e. Plasma concentrations of alanine aminotransferase increases in normal pregnancy
Anatomy of the Liver
Functional anatomy - Liver
• Bile ducts• Hepatic artery• Portal vein• Vagus nerve • Lymphatics
Functions of the Liver
1. Synthesis
2. Metabolism
3. Storage
4. Catabolism and excretion
5. Immunological / Haematological
1. Synthesis
• Proteins
• Albumin (200mg/kg/day!)
• Clotting factors
• Transport globulins
• Complement
• Plasma cholinesterase
• Alpha 1 antitrypsin
• Fats
• Triglycerides
• Cholesterol
• Bile
2. Metabolism
• Glucose homeostatis
• Glycogen synthesis and storage
• Gluconeogenesis
• Absorbs other nutrients
3. Sto
rage
Glycogen Iron
Copper
DA
EK
FOLATE
B12
4. Catabolism and excretion
• Drug metabolism
• Detoxification
• Phase 1 reactions (cytochrome P450)
• Phase 2 reactions
• First pass metabolism
• Excretion:
• Nitrogenous waste - Urea cycle
• Haem metabolism - Bilirubin
5. Immunological and Haematological• Kupffer cells – (fixed macrophages)
• Hepatocytes make
• Fibrinogen
• Heparin
• Prothrombin
Answers to MCQ
a. 70% of liver blood flow is via the hepatic artery False – 20-30% of cardiac output goes to the liver. 70% from portal vein and 30% from hepatic artery
b. Portal tracts contain lymphatics True – lymphatics and branch of vagus nerve travel with the hepatic artery, bile ducts and portal vein in portal tract
c. Plasma cholinesterase is produced by the liver True – plasma cholinesterase is synthesised by the liver
d. Vitamin E is stored in the Liver True – Vitamin E is stored
e. Plasma concentrations of alanine aminotransferase increases in normal pregnancy False – ALP increase up to 4x but ALT and AST and LDH generally do not increase.
The relevance to exams – from personal experience….12/3/15!
Liver failure
Chronic
• Viral • Hepatitis B and C
• Alcoholic Liver Disease
• Autoimmune
• Cryptogenic
• Cholestatic-• Primary billary cirrhorhosis
• -Sclerosing Cholangitis
• Venous outflow obstruction• Budd Chairi syndrome
• Metabolic • Wilsons Disease
Chronic Liver failure – systemic effects• Group work
1. Respiratory
2. Cardiovascular
3. Heamatological
4. Neurological
5. Gastrointestinal
The effects of liver disease: GI
Cardiovascular effects
• Hyperdynamic circulation
• Risk factors for IHD
• Smoking
• Hyperlipidemea
• Reduced LV workload
• Decreased SVR
• Vasodilatation
- May mask coronary artery disease
Hyperdynamic circulation in liver disease
Respiratory system
• Diaphragmatic splinting
• Hepatopulmonary syndrome
• V/Q mismatch caused by intrapulmonary shunting
• Portopulmonary syndrome (rare)
• Pulmonary hypertension due to progressive pulmonary vasoconstriction
• Remodelling causes increase PVR
Haematological
II, VII, IX, X
Increased fibrinolysis
Renal / Metabolic
• Secondary hyperaldosteronism
• Water retention
• Hyponatremia
• Treated with spironolactone (risk of hyperkalemia)
• Hepatorenal syndrome
• Renal hypoperfusion, portal hypertension, Intrabdominal hypertension (poor prognosis)
• Hypoglycemia
Neurological
• Hepatic encephalopathy increased by:
• Infection
• GI Haemorrhage
• Acid base disturbance
• Sedative drugs
• Hypoglycaemia
• Hypoxia
• Hypotension
• Excessive dietry protein
• ALD –
• risk of Vitamin B1 deficiency and Wernicke's encephalopathy
Questions so far?
Long case prep sheet
Summary of case Current investigations –what do they show?
Pharmacology:
1. Drugs on an effects 2. Drugs to consider
that may have issues3. Drugs to avoid
Pre operaitve
• Any more inforequired?
• Any more investigations required
• Preoptimisation
Intra operative
• Pre-induction• Induction• Airway management • Analgesia • Maintenance • Temperature
regulation• Specifics for this case
Post operative
• Post op destination (ward/HDU/ICU)
• Thromboprophylaxisis• Analgesia• Extras: eg chest
physio
Anaesthetic Implications –Group work • Pharmacology
• Pharmacology headlines in liver failure
• Specific drugs
• Induction agents
• Volitiles
• NMBD
• Opiods
• Pre-optimisation and investigations
• Intraoperative considerations
• Post operative care
Pharmacology in Liver disease
• Reduced plasma proteins
• Increased unbound fraction of protein bound drugs
• Increased distribution half life
• Increased duration of action
• Increased Volume of distribution
• Reduced metabolism
• Phase 1 reactions generally affected before phase 2 reactions
• Reduced elimination
Pharmacology Drug class Effects of liver failure Anaesthetic modifications
Induction agents
• Reduced plasma proteins -increased unbound fraction of protein bound drug
• Increased duration of action • More sensitive to sedative effects
of propofol
• Reduce dose of thiopentone• Reduce dose of propofol
(Chronic alcohol use may require higher doses of induction agent- but with
Volatileagents
Iso, sevo and des undergo minimal hepatic metabolism
Can all drop CO and MAP. Des has least hepatic metabolism and quickest emergence
Opioids • Elimination of morphine delayed • Accumulation of morphine-6-
glucuronide will occur in those with associated renal failure
• Alfentanly elimination delayed
• Remifentanyl safe• Low dose fentanyl good • Avoid morphine and
allfentanyl if possibe
NMBDs Reduced plasma cholinesterasesIncreased volume of distributionReduced protein binding Prolonged elimination (Vec /Roc)
• Metabolism of sux increased • Resistance to NMBDs • Use Cis/Atracurium
preferably
Pre-op/optimisation
• History /Examination • Check for pleural effusions/ascites
• Level of encephalopathy
Think about effects other than patient – risk of infection (viral hepatitis)
Investigations
Investigation Possible effects of Liver disease
FBC Decreased PlateletsAnaemiaIncreased MCV ( Alcohol / vit B12 def)
Clotting PT – useful indicator of hepatocellular failure
U+Es HyponateaemiaCheck for renal dysfunction
ECG If risk factors LV dysfunction
CXR Check for pleural effusions
Echocardiogram Check for underlying cardiomyopathy
Risk Stratification
Score Operative mortality risk (%)
5-6 Childs class A = low operative risk (5%)
7-9 Childs class B = Moderate risk (25%)
10-15 Childs class C = High operative risk (50%)
Intraoperative
• Elective surgery - only for well compensate chronic liver failure
• Emergency surgery – patients need urgent optimisation to include: • Intra vascular volume status
• Coagulation function
• Neurlogical assessment
• Screening for infection
• Consider blood products• PT>1.5
• Platlets <50
Intra op continued
• Induction: • Modified RSI• Propofol ( reduced dose) • Give H2 receptor blocker pre induction
• Analgesia • Remifentanil, low dose fentanyl• Avoid morphine and alfentanil
• Monitoring: (Maintaining MAP is important)• A line • CVP line • Oesophageal doppler (contraindicated?)
• Maintentence• Desflurane• Atracurium or Cis-atracurium
• IV fluids: • Crystalloids • Consider HAS in ascitic patients • Background infusion of 5-10% Dextrose to avoid hypoglycaemia
Post Operative
• Anticipate ICU/HDU requirement
• Invasive cardiac monitoring
• Careful fluid management
• Look out for
• Worsening encephlopathy
• Worsening jaundice
• Check clotting regularly
• Analgesia
• IV fentanyl PCA
Questions?
TIPS procedure
SBA 1
• You are asked to anaesthetize a 34-year-old lady for insertion of a transjugular intrahepatic porto-systemic shunt. She is suffering from Budd–Chiari syndrome and has large tense ascites. She has no other past medical history and gives no history of reflux. The procedure has been attempted twice under local anaesthesia, but she was unable to tolerate the procedure due to discomfort. Your anaesthetic plan is to:
a. Ask the physicians and radiologists to attempt the procedure under local anaesthesia again, with larger volumes of local anaesthetic
b. Ask the physicians to improve her respiratory function by draining the ascites first
c. Ask the physicians to perform the procedure again with sedation d. Provide regional anaesthesia with a cervical plexus block, a large iv
access, invasive arterial monitoring and cardiovascular stability, with blood products available
e. Provide general anaesthesia with an ETT, a large iv access, invasive arterial monitoring and cardiovascular stability, with blood products available
SBA 1 answer
• Answer: e
It is unlikely that they will succeed with local anaesthesia if they have tried twice before and it is unfair to the patient if she finds it distressing or uncomfortable. The question states the procedure was terminated twice due to discomfort, not hypoxia. However, this does have to be borne in mind for people with large, tense ascites. Sedation is an option, but the potential for the respiratory depressant effects of sedation on patients with liver disease with pulmonary dysfunction (from ascites or porto-pulmonary associations), as well as their prolonged action of sedative drugs, the risk of aspiration, the risk of precipitating encephalopathy and a prolonged procedure make a general anaesthetic with a secure airway the treatment of choice.
Acute Liver Failure
• SBA
• Definitions
• Multisystem effects
• Transplant criteria ( Kings College Criteria)
SBA 1
• The incidence and prevalence of liver disease is increasing worldwide. What is the most common cause of acute hepatic failure in the UK?
a. Ethanolb. 3, 4-methylenedioxymethamphetaminec. Amanita phalloides
d. Viral hepatitis
e. Acetaminophen
SBA 1 Answer = E
In the UK acetaminophen overdose is the most common cause of acute hepatic failure (70%) while worldwide it is viral hepatitis. Alcohol and other drugs are implicated while Amanita phalloides is a poisonous mushroom and a rare cause of acute hepatic failure.
Acute Liver Failure
• Acute liver failure (ALF) is a devastating syndrome that triggers a cascade of events, leading to multiple organ failure and often death.
• In those patients with high grades of encephalopathy, the chances of survival are less than 20% with medical management alone.
• Early deaths: cerebral oedema or cardiovascular collapse• Late deaths: sepsis and multiple organ failure • Liver transplantation is the only current definitive
treatment in those failing supportive medical management.
Acute Liver failure Classification• ALF – syndrome defined by the occurrence of encephalopathy,
coagulopathy and jaundice in an individual with a previously normal liver.
• Hypeeracute – within 7 days
• Acute – 8-28 days
• Subacute – 5-26 weeks
Liver failure
Chronic
• Viral • Hepatitis B and C
• Alcoholic Liver Disease
• Autoimmune
• Cryptogenic
• Cholestatic-• Primary billary cirrhorhosis
• -Sclerosing Cholangitis
• Venous outflow obstruction• Budd Chairi syndrome
• Metabolic • Wilsons Disease
Acute
• Paracetamol overdose
• Viral hepatitis
• Circulatory shock
• Drugs• Aspirin
• Rifampicin
• Acute fatty liver of pregnancy
Systemic effects –Neuro
• Encephalopathy
• Mortality higher in those with Grade III or IV
• Cerebral oedema
• In up to 80%
• More in hyperacute ALF
• Raised ICP
Systems effects – CVS
• Similar picture to sepsis
• Hypotension
• Low SVR
• High Cardiac output
Systemic effects - Renal
• Oliguric renal failure
• Occurs in 75% of paracetamol overdose patients
• 30-50% in other causes
• Usually indicator of poor prognosis
Systemic effect – Immune
• Decreased complement synthesis
• Kuffer cell dysfunction
• Increased suseptibility to infection
• Increased risk of fungal infections
Kings Criteria
References
• Vaja R (2010) Anaesthesia for patients with liver failure, Continuing Education in Anaesthesia, Critical Care & Pain | Volume 10 Number 1, BJA, oxford University Press
• Lai et al, (2004),Management of Acut Liver failure Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4, Issue 2 April 2004 Pags 40-43
• Ebrahim et al (2013) (Practice Single Bset Anser questions for the Final FRCA – A revision guide. Cambrige Univerisyt Press,P65 and 132