Liver Flashcards
What’s in the MELD score?
Bilirubin, INR, Creatinine
What’s the MELD score useful for? What are the cutoffs for elective surgery risk?
Cirrhosis severity score, used as predictor of 3-month survival in cirrhosis (also validated as a predictor of survival EOTH hepatitis, acute liver failure, acute hepatitis).
Was originally developed to predict mortality after TIPPS.
MELD-Na includes serum sodium, used to prioritise organ allocation for liver transplantation.
More accurate than Child’s-Pugh classification in predicting outcome in the non-transplant setting (eg. perioperatively)
MELD <10 is low risk for elective surgery, 10-15 intermediate-risk, >15= unacceptable mortality & non-essential surg should be postponed
What’s the Child-Pugh score useful for?
classifying severity of cirrhosis, 1-2 year life expectancy in cirrhosis & periop mortality among pts w cirrhosis undergoing abdo surgery
What’s the commonest indicator for hepatic transplantation worldwide?
post-hep C cirrhosis (likely to change as more effective antiviral therapies become available)
What are some considerations in the systems review & anaesthetic goals of pts for liver transplant or resection (or just a chronic liver disease pt)?
Peri-op risk depends on:
LIVER DISEASE:
*TYPE of liver disease
-Hyper-acute: time from jaundice to encephalopathy <7 days, acute 1/12, sub-acute 12 wks
-Acute liver failure= acute onset liver failure (jaundice, coagulopathy, encephalopathy) in a patient without pre-existing cirrhosis
*AETIOLOGY:
-acute eg. hepatitis, drugs eg. paracetamol
-chronic= progressive hepatic functional deterioration over >28wks–> fibrosis & cirrhosis eg. ETOH, NAFLD. May be “compensated” (asymptomatic) or “DECOMPENSATED”: ascites, jaundice, encephalopathy, variceal haemorrhages.
*SEVERITY (quantify periop mort w CPC or MELD-Na; MELD <10, 10-15 & >15 approximate CP A (5-6)/B(7-9)/C(10-15))
use for predict postop morb & mort in hepatic & non-hepatic intra-abdo surgery
*is there evidence of decompensation or concurrent sepsis?
*type of surg & if emergent, type of anaesthesia & concomitant disorders
*EXTRAHEPATIC MANIFESTATIONS
A:
-Ascites- if drained prep it’ll accumulate postop, should account for this in the fluid balance
-Pt may be unable to tolerate lying flat for induction or sedation
-aspiration risk
B:
-Hepatopulmonary syndromes: hypoxia (from impaired V/Q matching, diffusion limitation, intrapulmonary shunting) occurs in 0.5-4% of pts w cirrhotic liver disease- may require higher intra-op FiO2
-Portopulmonary syndromes: severe portal & pulmonary HTN–> RV failure & potential intra-op cardiac arrest
-Pleural effusions (CXR), hepatic hydrothorax
-use a lung-protective ventilatory strategy (low TVs, PEEP, intermittent lung volume recruitment)
-alveolar hypoventilation, reduced FRC from mech compression (ascites, hepatomegaly)
C:
-priorities= preservation of hepatic blood flow & hepatic function- consider that anaesthetic agents, PEEP, PPV & alpha & b-agonists/antagonists alter hepatic blood flow- for resection, have CVP monitored & metaraminol running- aim CVP 0-2mmHg during resection- head up, titrate metaraminol, add NAdr if metaraminol up to 20mL/hr.
-high output state due to portosystemic, pulmonary & cutaneous shunting; hyperdynamic circulation with high CO & low SVR, relative hypovolaemia & hypoT due to splanchnic & systemic vasodilation (care w neuraxial & hepatic blood flow) & cardiac failure. Goal BP w anaesthesia should be the pts baseline (may require vasopressors to achieve this & pts may have ANS dysfunction & reduced responsiveness to vasopressors)
-Varices (oesophageal, gastric, abdo wall, rectal) due to portal HTN (incr pressure gradient portal-hepatic vein (>10mmHg= portal HTN), mainfests as varices, splenomegaly, ascites) & engorgement of portosystemic anastomoses, risk acute bleed, oesophageal varices= contraindication to use of oesophageal doppler probes & oesophageal temp probes
-SBP risk
-?may have associated ETOH or cirrhotic cardiomyopathy depending on the etiology of liver failure
-smoking associated w ETOH intake- independent risk factor for CAD
-pericardial effusions & diastolic dysfunction develop in cirrhosis
ECG essential, consider echo
D:
-Encephalopathy (decr metabolism neurotoxins eg. ammonia, consent issues, risk aspiration)
-cerebral oedema/intracranial HTN
Endocrine:
adrenal insufficiency
secondary hyperaldosteronism
-Diabetes (common co-morbidity w hep C)
-autoimmiune hepatitis may be on stress steroids
Fluids: care w overload in cirrhosis (RAAS activation)- but need to maintain hepatic & renal perfusion & UO- limit if abdo surgery to limit portal pressures which may–> bleeding. Consider alb for volume expansion if ascites or hypoAlb.
Haem:
-Coagulopathy (prolonged PT, low plt, fibrinolysis)- both bleeding tendency (lack coag factors, hypofibrinogenaemia, thrombocytopenia w splenic sequestration + impaired hepatic thrombopoietin) but also distorted synthesis of anticoagulant factors (prot C, S & antithrombin) & incr vWF & FVIII)
TEG/VHA useful for global Ax. If new changes in plt or PT, seek source preop (eg. change in meds, portal vein thrombosis, infection). Care w neuraxial esp after resection w EPB catheter removal.
Bleeding more likely related to portal HTN than haemostatic factors, hypervolaemia or mucosal or traumatic bleeding related to hyperfibrinolysis
-Anaemia (which lowers plasma viscosity & further reduces effective tissue perfusion)
Infection risk (immunosuppression if chronic liver disease)- resp & urinary tract in particular, in presence of ascites SBP may–> significant sepsis
Jaundice
Kidney failure- acute or chronic, predominantly prerenal, hepatorenal syndrome is related to progressive impairment of renal perfusion & is a Dx of exclusion since Mx differs to other causes renal failure; NAdr & vasopressin may HELP, Anaes Mx involves ensuring adequate renal perfusion & urine output, avoiding hypoT, hyperK & acidosis & avoiding nephrotoxics
Nutrition:
Muscle wasting/poor nutritional state- may benefit from periop dietician input, consider
impact of reduced plasma proteins on Pk
hypoglycaemia
hypoalbuminaemia
impaired wound healing
Na: hyponatremia- should correct unless <120, correct slowly to avoid central pontine myelinolysis
Pressure injury/neuroproxia risk- if m wasting, easy bruising (care w subcut/IM which risk haematoma formation)
Decision re: proceeding:
-no absolute cut-offs, discuss w hepatologist
-acute liver injury- defer/non-OT Mx
-CTPA or MELD <10: continue w caution (10% mort)
-CTPB or MELD 10-15 consider proceed w optimisation & caution (30% periop mort)
-CTPC or MELD >15: defer/cancel/consider alt Mx-
Optimisation of pts w CLD pre-op:
-PORTAL HTN: consider decompression w TIPS if HPVG >10mmHg
consider prophylactic variceal ligation
-ASCITES: salt & H2O restriction, diuretics to optimise fluid balance, consider lg volume paracentesis for pts w grade 3 ascites (but consider vol expansion w albumin 8g/litre ascitic fluid removed to prevent post paracentesis circulatory dysfunction)
-consider TIPs for refractory ascites
-proph ABx if Hx SBP
-SBP: empiric IVABx
-encephalopathy: Rx infection, correct electroytes, consider lactulose, rifaximin, haemofiltration
-cirrhotic cardiomyopathy: fluid balance, consider periop B blockers
-hepotorenal: consider Alb, terlipressin
-other renal: fluid balance, remove risk factors
-broad spectrum ABx for any infection, consider antifungals
-coagulopathy: limit intravenous fluid & blood products perioperatively, should be guided by viscoelastic testing to avoid unecessary incr in extracellular volume, ascites, portal HTN
-No evidence for FFP to correct INR, consider prothrombin complex for vit K-dependent clotting factors, consider vit K
-correct anaemia to a Hct of >0.25
-plts to Rx thrombocytopaenia <50x10^9 immed pre-procedure
-cryo if fibrinogen <1 g/L
-only Rx hyponatremia if <120, slowly (<10mmol/L in 24hrs) as chronic
in addition to standard monitoring, CVC for major surgery pts w high CP or MELD
anticipate fluid shifts & constantly evaluate volume status (risk postop AKI & HRS
CO monitoring, UO, blood loss
isotonic crystalloids initial replacement, consider alb if >5L ascites drained, prbcs for hct >0.25, consider VHA results
haemostatic surgical & anaes principles (vol transfused correlates w postop complications & mort)
proph ABx, monitor BGL
gen avoid preop bzd (prolonged dep consciousness, precipitate encephalopahty)
reduced dose propofol
roc or vec prolonged elimination phase, atrac or cis commonly used but may need incr doses (VD incr, PB altered), sux long duration
prop or volatile, remi, consider alf or fent
fent pref postop as no active metabolite & is excreted renally
avoid morphine, carefuly dose oxy or tramadol (sedation/encephalopathy risk)
avoid NSAIDs (nephrotox, plt dysfunction, GI haemorrhage)
can use paracetamol reduced doses unless it’s the aetiology of ALF
can use regional, consider epidural if VHA normal, INR <1.5, plt >100
reduced doses & shorter infusions (LAST risk)
postop often HDU
monitor renal, fluids, electrolytes, glucose
carefully titrate sedatives & analgesia
aggressively Mx sepsis (broad-spectrum ABx)
coagulation status
signs jaundice, encephalopathy, ascites, coagulopathy
consider VTE prophylaxis
What’s portopulmonary HTN & proposed mechanism?
Pulmonary arterial HTN (group 1 pulm HTN), associated with portal HTN. Thought to be due to a humoral substance which would normally be degraded by the liver, reaching pulm circulation through portosystemic collaterals.
What’s hepatopulmonary syndrome? Cause?
Abnormal arterial oxygenation caused by intrapulmonary vascular dilatations in the setting of liver disease, portal HTN or congenital portosystemic shunts. Thought to be related to bacterial translocation & toxin release from portal HTN which may stimulate the release of vasoactive mediators, or failure of the damaged liver to clear circulating pulmonary vasodilators.
What’s the main indication for hepatic resection?
Metastatic colorectal adenocarcinoma
Which drugs should be avoided or dosages considered for hepatic resection? why?
Those relying heavily on hepatic metabolism, eg. lignocaine, or those which may compound post-operative hepatic encephalopathy (eg. BZD *midaz intermediate ER so metabolism is slowed by liver disease, age, CYP3A4 inhibitors- renal Cl & has an active metabolite so DOA prolonged by impaired renal fn)
What proportion of functional hepatic tissue is removed during major liver resection?
30-75%
Does lignocaine have a high HER?
yes- so hepatic blood flow is a limiting factor in it’s metabolism & rate is slower if pts have CCF or hepatic insufficiency
After how many half lives is the plasma [] of a drug below a clinically relevant level?
4-5 (by this point, 94-97% of the drug has been eliminated)
How much data falls within 1, 2 & 3 standard deviations of the mean?
68%, 95% & 99.7%
What are the possible sources of bleeding for hepatic resection?
either from vascular inflow (portal vein, hepatic artery) or venous back-bleeding
What’s the Pringle manoeuvre? What are it’s risks? How can these be minimised?
Intermittent cross-clamping of the structures of the porta-hepatis to limit vascular inflow to the liver, helping control bleeding. risks ischaemia-reperfusion injury to the liver & postop hepatic dysfunction. Can minimise with ischemic preconditioning & using intermittent vs continuous clamping.
Steps for liver resection?
Perihepatic dissection, identify vascular anatomy, may use intro US to pinpoint lesions for resection, ligate branches of the PV/HA supplying the resection segments (may reduce remaining inflow bleeding by intermittent X-clamp of the structures of Porta hepatic w Pringle manoeuvre)
What’s in the porta hepatis?
PV, R&L HA & R&L HDs
What’s a concern with using thoracic epidurals for liver resections?
pre- or post-op hepatic dysfunction & coagulopathy, bleeding risk
What’s preconditioning? Which agents we use can help?
Complex evolutionary response leading to more effective glycolysis & mitochondrial respiration & reduced apoptosis, allowing tissues to adapt to stress (eg. ischemia/reperfusion injury). Volatiles & lignocaine may activate receptors influence mitochondria.
What are the benefits & risks of maintaining low CVP during resection?
Substantially reduces bleeding & transfusion requirements without adverse consequences despite theoretically increased risk of air embolus
What techniques can be used to reduce CVP during hepatic resection?
reverse trendelenburg (head up), epidural boluses
What CVP aim for in hepatic resection?
0-2mmHg
When is the peak time for disturbances in clotting after hepatic resection?
D2-3 postop (& may take 5+ days to resolve)- so care if put in epidural catheter for postop pain control after hepatic resection- check plt & INR before remove- only consider epidural if 60-70% total liver volume expected to remain. Alternatives= single shot spinal w ITM or peripheral blocks.
Why active warming important during hepatic surgery?
minimise coagulopathy
What’s the liver blood flow? % from PV & HA?
1.5L/min, 80% & 20%
Is cell salvage useful for hepatic resection?
Not likely as if loose blood it’s a sudden major bleed & need products ready (vs steady trickle)
What would be the reduction in CO if clamping supra- & infra-hepatic IVC & hepatic pedicle?
60%
What’s the reduction in CO if occlude HA & PV? And the increase in LV afterload?
10%, 20-30%
What is the principle of fluid management pre-resection?
running the pt dry- UO 0.5mL/kg/hr
Should nmbds be based on actual or ideal BW?
sux actual, others ideal (which is 22 x (height in m^2))
What’s the initial & maintenance doses of vecuronium?
0.1mg/kg & 0.01mg/kg
Should induction & maintenance w propofol be based on lean or total body weight?
induction lean body weight & maintenance infusion total body weight
What’s acute liver failure?
Acute hepatocellular dysfunction with coagulopathy & encephalopathy in a pt without prior known liver disease
What’s the transplant-free survival of hyper acute (<=7/7), acute (8-28d) & subacute (28/7-6/12) liver failure?
30, 33 & 14%
What’s the commonest cause of acute liver failure? proportion?
Other causes?
Paracetamol excess (up to 70% of cases) Viral hepatitis (Heps A-G, CMV, EBV, HSV) Autoimmune hepatitis Toxins (eg. carbon tetrachloride) Acute fatty infiltration of pregnancy HELLP syndrome Wilson's disease Reye's syndrome
What’s the manifestation of acute liver failure & metabolic derangements?
Encephalopathy, cerebral oedema
Severe coagulopathy with active fibrinolysis
Metabolic acidosis, hypokalaemia, hypoglycaemia, hyponatremia
High cardiac output state with reduced SVR, risk of raised ICP, ARDS & renal failure
Can elective surgery proceed in a patient with active hepatitis?
No. It’s a contraindication to elective surgery due to high periop mortality.
Delay (unless true emergency) until 30d after LFTs have normalised.
What are some anaesthetic concerns for acute hepatitis?
A: pts w grade 3/4 encephalopathy require intubation to protect their airway
B: at risk of ARDS
C: high CO state
Hypotension & hypovolaemia- Mx w IVT, vasopressors/inotropes (NAdr= first line)
Maintain BP within 10-20% of pre-op baseline
D: encephalopathy
May require ICP monitoring (?+/- bicarbonate-buffer haemofiltration)
E: temp management (coagulopathy)
hyponatremia, hypokalaemia, metabolic acidosis (correct), risk of renal failure
G: hypoglycaemia common- need to correc
H: severe coagulopathy with active fibrinolysis- reverse for surgery. May need ICU
K: renal failure with hepatic failure confers high mortality- up to 50% of pts w ALF also have ARF. Avoid intra-op hypoT, maintain UO 1mL/kg/hr, avoid nephrotoxins.
Personnel: hep B/C contagious- universal precautions
Discuss w specialist liver unit (?considering transplantation)
Require management of cause: delivery if pregnancy-related, NAC if paracetamol OD, orthotropic liver transplant may be definitive Rx
What’s the first line vasopressor for acute liver failure?
Noradrenaline
What’s the Kings criteria for transplant referral in acute liver disease?
Paracetamol: pH <7.3 of ALL of: PT>100 or INR >1.5 Cr >300 Grades 3-4 encephalopathy Non-paracetamol: PT>100 OR any 3 of: age<10 or >40 PT>50 bili >300
What’s chronic hepatitis? what can be the sequelae?
When MAY transplantation be considered?
Any hepatitis lasting >6/12.
Inflammation can –> fibrosis & may lead to nodular regeneration & disruption of liver architecture (cirrhosis) which may lead to portal HTN.
Compensated= liver function maintained
decompensated (eg. triggered by infection)= deterioration in liver function. If unable to remain compensated w Rx of the cause (which can sometimes reverse fibrosis), consider transplantation.
What are the main etiologies of chronic liver disease? And less common?
ETOH, HBV, HCV & fatty liver disease
Less common:
Inherited (haemachromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency)
Immune-mediated (primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis)
Vascular disease (budd-chiari, veno-occlusive)
Drugs (isoniazid, methyldopa)
What’s the main route of transmission of HBV? What’s the risk of developing chronic HBV?
Vertical transmission- falling numbers due to routine vaccination of babies
95% risk developing chronic HBV if infected @ birth, when infected as an adult 3% chance developing chronic HBV
What’s the risk of developing chronic HCV infection? Main risk factor?
75%. IVDU (less common w blood products now all donors screened)
What’s a rising cause of cirrhosis in the west?
Non-ETOH liver disease w rising obesity levels, esp in pts w T2DM & HTN
What are some perioperative considerations of a pt with known Hx ETOH excess:
Acute intoxication:
- Consent issue. Avoid non-emergency surgery.
- May have vomiting, hypoglycaemia & delayed gastric emptying: RSI
- Binge drinking (associated with vomiting & fasting) may be associated with ketoacidosis
- Ensure adequate rehydration, check for electrolyte & glucose disturbance, consider IV vit-B (slow BD for 3-5 days)
Chronic ETOH excess:
- Tolerance to GA, 2-5x increased risk of postop complications
- Anticipate ETOH withdrawal symptoms but don’t complicate management by attempting to withdrawal perioperatively; most pts can tolerate 24hr abstinence- monitor & prescribe regular BZD
- Seizures are most commonly 6-48hrs after drinking cessation- several fits over a period of days are common & may be predisposed by low K+ & Mg++. May be preceded by disorientation & agitation (DTs). Rx w BZD (eg, diazepam 10mg IV), repeat as required
- ETOH cardiomyopathy
- ETOH liver disease
What’s ETOH cardiomyopathy characterised by?
Dilated, hypokinetic LV & reduced EF
May have CCF & oedema, exacerbated by low serum Alb
Consider echo
What’s the progression of ETOH liver disease?
Reversible fatty liver, then ETOH hepatitis (abdo pain, wt loss, jaundice, fever) later cirrhosis (jaundice, ascites, portal HTN, hepatic failure)
What are some of the more common causes of periop mortality in chronic liver disease?
sepsis, bleeding, renal failure, worsening hepatic failure with encephalopathy
What are the elements of the Child’s-Pugh classification?
Bilirubin Albumin PT Ascites Encephalopathy
Which clotting factor dose the liver NOT synthesise?
VIII
What are 5 mechanisms for coagulopathy in liver disease? Describe the vitamin K issue.
Decreased synthesis of clotting factors
Decreased clearance of activated clotting factors
Quantitative & qualitative platelet abnormalities
Hyperfibrinolysis
Vitamin K deficiency (due to obstructive jaundice- this will prolong the PT. No vit K assay so a trial IV vit K may improve PT if it’s the cause, no improvement if the coagulopathy due to impaired liver synthetic function)
What’s encephalopathy due to? What are the grades of encephalopathy?
Buildup of toxins (esp ammonia due to deranged amino acid metabolism), may be precipitated by sedatives, GI bleed, infection, surgery, trauma, postop ileus (HENCE PRESCRIBE CONCURRENT LACTULOSE W POSTOP OPIOIDS as constipating agents may precipitate encephalopathy), hypokalaemia.
Grade 0= alert & oriented
1= drowsy & oriented
2= drowsy& disoriented
3= rousable stupor, restless
4= coma
Intubate if Gd 3/4 or if cerebral oedema develops
Cause & management of hypoglycaemia in liver disease?
Impaired glycogen storage. Monitor BGL, give 30mL of 50% glucose (15g) as slow IV push 15-minutely until BGL >4, monitor plasma potassium.
