Acute liver failure following hepatic resection - JICS - The Intensive ...

© The Intensive Care Society 2013 

Review articles 

Acute liver failure following hepatic 

resection: incidence, presentation, 

prevention and management in ICU 

C Jones, L Kelliher, C Bigham, N Quiney 

The incidence of liver failure following liver resection has been reported to be between 8-32%, depending on the number 

of segments resected, the health of the patient and the incidence of hepatic ischaemic/reperfusion injury. This article 

outlines the evidence surrounding classification, prevention and management of this condition. 

Keywords: liver resection; liver failure; intensive care 

Introduction 

Mild liver dysfunction is occasionally seen following major 

surgery. Acute liver failure is much rarer. Patients at greatest 

risk of developing postoperative liver failure are those 

undergoing liver resection, where the risk can be as high as 

32%. 1 When it does occur, acute liver failure is a devastating 

complication, with a high morbidity and mortality. 

The spectrum of liver dysfunction post-hepatic resection 

encompasses everything from a transient rise in liver enzymes 

to fulminant liver failure and death. The features include 

coagulopathy, hyperbilirubinaemia, encephalopathy and 

associated multiple organ failure. The most effective way to 

reduce the impact of this complication is to prevent it 

developing in the first instance, which requires a careful and 

considered approach. Early identification of patients at risk and 

prompt and appropriate management of those developing acute 

liver failure is key. 

The incidence of liver resection surgery is increasing as a 

treatment for certain benign and malignant liver lesions. The 

most common indication in the UK is for treatment of liver 

metastases associated with colorectal cancer. Approximately 

3,600 patients per year fit into this category, a figure that will 

only increase with improvements in chemotherapy regimens. 2 

Hepatic resection is also performed in live-donor liver 

transplantation. 

Grade A 

Grade B 

Grade C 

Post-hepatectomy liver failure resulting in abnormal 

laboratory parameters but requiring no change in the 

clinical management of the patient 

Post-hepatectomy liver failure resulting in a 

deviation from the regular clinical management but 

manageable without invasive treatment 

Post-hepatectomy liver failure resulting in a deviation 

from the regular clinical management and requiring 

invasive treatment 

Table 1 ISGLS consensus severity grading of post-hepatectomy 

liver failure. 4 

This article reviews the management of post-hepatic 

resection liver failure, strategies for preventing it and some 

future directions in treatment. 

Definition and incidence 

Despite its potential severity, there is no universally accepted 

definition of postoperative liver failure 3 and therefore it is 

difficult to accurately determine its incidence. The 

International Study Group of Liver Surgery (ILSGLS) has 

recently produced this definition: 4 

‘a postoperative acquired deterioration in the ability 

of the liver to maintain its synthetic, excretory and 

detoxifying functions, which is characterised by an 

increased international normalised ratio and 

concomitant hyperbilirubinemia on or after 

postoperative day 5.’ 

The group also differentiated the severity of postoperative 

liver failure into three different grades from A to C, depending 

on the level of treatment needed. Grade A encompasses 

development of abnormal blood tests but no change in clinical 

management; grade B suggests the degree of liver failure 

needed clinical management but not invasive therapy; grade C 

is acute postoperative liver failure requiring invasive treatment 

(see Table 1). 

Other methods that have been used to define postoperative 

liver failure include the ‘50-50’ criteria. 5 A serum bilirubin 

concentration above 50 µmol/L and a prothrombin time (PT) 

which is increased by more than 50% of baseline (or INR >1.7) 

on postoperative day five is associated with a mortality of 59% 

as opposed to 1.2% if these criteria are not met (sensitivity 

69.6%, specificity 98.5%). 

Another grading system 6 used to predict the risk of 

postoperative liver failure is demonstrated in Table 2. Values 

should be present on two consecutive days during the 

postoperative course. Points score 0=no dysfunction, 1-2=mild, 

JICS Volume 14, Number 2, April 2013 133


Points 0 1 2 

Total serum bilirubin (µmol/L) ≤20 21-60 >60 

Prothrombin time 6 

(seconds above normal) 

Serum lactate (mmol/L) ≤1.5 1.6-3.5 >3.5 

Encephalopathy severity grade None 1 and 2 3 and 4 

Table 2 Severity of postoperative hepatic dysfunction score. 6 

3-4=moderate, >4= severe dysfunction. 

The incidence of acute liver failure following hepatic 

resection has been reported to be as high as 32% by some 

authors, 1 although others suggest it is nearer 8%. Schindl and 

colleagues believe that the risk should be quoted as less than 

1% in patients with no parenchymal disease and having small 

resections; 10% when four segments are being resected and 

30% for those having five or more segments resected. 6 

With advances in surgical and anaesthetic techniques, 

mortality rates following liver resection surgery have decreased 

from 20% in the 1970s 8 to approximately 2% today. 9 

Postoperative hepatic insufficiency/failure accounts for between 

60 and 100% of these deaths. 5,6,10-12 Morbidity following liver 

resection remains high, with rates between 15-35%. 13-15 

Causes of post-hepatic resection liver failure 

Liver dysfunction is seen occasionally after any major surgery. 

Periods of intraoperative hypoxia, hypotension, the use of 

blood transfusions or development of sepsis can all result in 

liver ischaemia and/or cellular dysfunction. Following liver 

resection, intra-operative blood loss of more than one litre with 

the need for blood transfusion increases the risk of 

postoperative liver failure and sepsis. 16,17 Sepsis has a 

detrimental effect on liver function (by inhibiting Kupffer cell 

function) and affects hepatic cell regeneration. 18 

A normal subject with no other risk factors can have up to 

75% of their liver resected safely. 19 The liver has a great 

capacity to regenerate, and the remnant can increase by 100% 

in size in as little as a week (although this is not reflected in a 

concomitant increase in synthetic function). 

The most important risk factors for postoperative liver 

failure are: 3,12 

• The size of resection 

• Evidence of preoperative liver parenchymal disease (eg 

cirrhosis) 

• Hepatic ischaemia/reperfusion injury. 

Removal of four or more segments (out of eight) is 

associated with an increased risk of postoperative liver failure. 

If the liver remnant is too small, there may not be enough 

functioning hepatocytes for adequate synthesis, excretion and 

detoxification. Another problem with small liver remnants is 

hyperperfusion; 20 the relative increase in blood flow causes 

sinusoidal dilatation, haemorrhagic infiltration, centrilobar 

necrosis and prolonged cholestasis, causing further impaired 

synthetic function and inhibition of cell proliferation. 3,20 

Underlying liver disease reduces the functional and 

regenerative capacity of the liver and therefore makes it more 

susceptible to damage. A larger remnant volume needs to be 

present at the end of surgery. 3,18 Chemotherapy also affects liver 

parenchyma and reduces its regenerative capacity. A recent 

French study looked at 101 patients undergoing intensive 

chemotherapy (≥6 cycles of the newer chemotherapy agents: 

oxaliplatin and irinotecan) prior to undergoing liver resection. 

They found that 50% of patients developed sinusoidal 

obstruction syndrome and 10% steatohepatitis on histological 

analysis (5% had both). 20 Both sinusoidal injury and steatosis 

from chemotherapy reduce the regenerative capacity of the 

liver remnant and therefore increase the likelihood of 

postoperative failure. 3,22,23 Sinusoidal injury may also occur as a 

result from ‘small-for-size syndrome,’ when dysfunction occurs 

after a living-donor partial graft. It is thought to be due to 

portal hyperperfusion of the graft, combined with poor venous 

outflow, resulting in sinusoidal congestion and endothelial 

dysfunction. 24 A similar picture can be seen after extensive 

hepatic resection with a small liver remnant. 

Vascular occlusive techniques used to reduce intraoperative 

bleeding comprise either total occlusion of both inflow and 

outflow, or total inflow occlusion. The ‘Pringle’ manoeuvre 

refers to the total occlusion of inflow, ie occlusion of hepatic 

artery and portal vein inflow to the liver. This limits blood 

supply to the liver, with the result that bleeding will principally 

be a result of hepatic venous pressure, which itself can be 

reduced by maintaining a low CVP intraoperatively. Occlusion 

induces ischaemia in the liver remnant, 25 resulting in hepatic 

ischaemia/reperfusion injury, the generation of free radicals and 

subsequent liver dysfunction. For this reason, the Pringle 

manoeuvre is now used much less frequently 26 and for less 

than forty-five minutes in total during surgery. 27 

Other risk factors for postoperative liver failure include 

age over sixty-five, as the ability of the liver to regenerate 

decreases with age, 28 diabetes mellitus and poor nutritional 

status. 3,18 Being male doubles the risk of developing 

postoperative liver failure. 29 

Rarely, postoperative liver failure can result from altered 

vascular supply. Portal or hepatic vein obstruction can occur 

either through thrombosis, torsion or surgical injury. It is 

worth considering these options and excluding them with an 

ultrasound scan. Postoperative cholestasis can also ‘muddy the 

waters.’ It is often drug-induced (eg penicillin, erythromycin 

and NSAIDs), but can occasionally be a result of the surgery 

itself, or following total parenteral nutrition on the intensive 

care unit. Occasionally an isolated increase in bilirubin can 

occur, for example following a blood transfusion or in a patient 

with Gilbert’s syndrome. Gilbert’s syndrome is present in 2-5% 

of the population. A decreased activity of hepatic glucuronyl 

transferase leads to an increase in unconjugated bilirubin. 

Preventative strategies 

Careful patient selection to ensure adequate 

residual liver volume 

In patients with normal liver parenchyma, a remnant as small 

as 26% of the original liver’s volume can be safely left. 6 

However those with parenchymal diseases require a larger 

residual volume (approximately 40%) to avoid postoperative 

liver failure; 19 a similar volume has been suggested for those 

patients who have received intensive chemotherapy treatment 

134 

Volume 14, Number 2, April 2013 JICS


(>6 cycles) prior to liver resection surgery. 21 In that study, the 

authors found that residual volumes of 44.8%, 43.1% and 

37.7% were independent predictors of overall morbidity, sepsis 

and liver failure respectively. 

In patients with cirrhosis, resections should only be offered 

in those with stable disease (ie Child-Pugh class A); only very 

small resections in selected patients should be offered to patients 

with Child-Pugh class B, and avoided in class C patients. 

Where an extensive resection is planned, avoiding the 

problems associated with a potentially small remnant can be 

achieved by employing strategies such as preoperative 

neoadjuvant chemotherapy to reduce the volume of tumour, 

performing a staged hepatectomy or a preoperative portal vein 

embolisation (PVE). PVE is one of the most useful strategies 

there is in preventing postoperative liver dysfunction and 

involves embolising one of the portal veins to induce liver 

atrophy on the operative side and hypertrophy in the intended 

remnant section. 30 

Choice of anaesthetic agents 

The volatile anaesthetic agents metabolised in the liver are 

known to alter hepatic blood flow and induce transient 

changes in liver enzymes. The use of halothane, which on 

repeated exposure may cause hepatitits (so-called ‘halothane 

hepatitis’) is now uncommon. Other volatile agents, including 

isoflurane, sevoflurane and desflurane, have minimal hepatic 

metabolism and there is a lack of evidence demonstrating 

hepatotoxicity. 31 Total intravenous anaesthesia (TIVA) has been 

advocated by some as a preferred option in liver surgery, but to 

date there is no evidence to support this. 

Minimise blood loss 

Postoperative blood transfusions have an immunosuppressive 

effect 16 and, as stated above, the requirement for blood 

transfusion following major blood loss increases the risk of 

postoperative liver failure. 16,17 Strategies to reduce blood loss 

include: maintaining a low central venous pressure 

(


there are localising signs. Cerebral oedema is a worrying 

complication, which is more prevalent the more acute the liver 

failure. Increased ammonia may be involved in the 

development of cerebral oedema by both cytotoxic and 

vasogenic mechanisms. 

Cardiovascular 

Distributive shock develops with severe peripheral shunting. A 

high cardiac output, decreased oxygen extraction, and low 

systemic vascular resistance are all features. The origin of the 

peripheral shunting is unclear. It may be the result of 

platelet/fibrin plugs, and abnormal vasomotor tone. 44 The 

result is poor peripheral extraction of oxygen. 

Renal 

Acute kidney injury is common. This is multifactorial; the 

common reasons are pre-renal renal failure and acute tubular 

necrosis. Hepato-renal syndrome (HRS) can occur in fulminant 

liver failure and is associated with high morbidity and 

mortality. 45 HRS is more typically associated with 

decompensated chronic liver disease, portal hypertension and 

spontaneous bacterial peritonitis. Differentiating HRS from prerenal 

failure that progresses to ATN can be difficult. Urine 

sodium analysis and microscopy can be helpful. HRS typically 

takes longer to resolve, if it does at all, being associated with 

greater than 50% mortality. When acute liver failure develops 

following a resection, it will be acute (within 28 days), 

so manifestations more commonly linked to chronic liver 

disease are less likely to be present, such as portal hypertension 

and tense ascites. However, if they occur (as the underlying 

architecture of the remaining liver may be compromised) 

then they should be managed appropriately. If tense ascites 

is present, then reducing intra-abdominal pressure can 

improve renal function. Hypophosphataemia can also 

sometimes be seen after liver resection due to increased renal 

excretion of phosphate. 

Infection 

Immunocompromise is a feature of acute liver failure 12 and 

consequently bacterial and fungal infections are more 

prevalent. Infection can also be harder to detect as there 

is a blunted systemic inflammatory response in this population. 

A high index of suspicion is required; for management, 

see below. 

Pharmacology 

A number of drugs are metabolised in the liver. This results in 

prolonged effects of sedation, certain neuromuscular blockers 

and a number of ‘housekeeping’ ICU drugs, eg omeprazole. 

Supportive management of acute liver failure 

In most centres, patients undergoing liver resection will be 

admitted to a level 2 bed for initial postoperative care. The 

majority of patients will pass through without complication. If 

acute liver failure develops, then supportive management 

(Table 3) is required until either the liver regenerates, a 

treatable cause of the liver failure is established or (if 

appropriate) an orthotic liver transplant is performed. 

Airway 

Intubation will be required when the airway is no longer 

protected in grade 3/4 encephalopathy, or if the airway is 

compromised in another way. 

Respiratory 

Hypoxia may be a problem due to concomitant pneumonia, 

pulmonary oedema or pulmonary haemorrhage. Due to the 

concern over the possibility of cerebral oedema, PaCO 2 will 

have to be controlled tightly at 4.5-5 kPa and minimal 

achievable PEEP should be used. 

Cardiovascular 

Distributive shock usually develops and appropriate fluid 

loading and vasopressors will be needed. A cerebral perfusion 

pressure of 50-60 mm Hg will be required for neuroprotection. 

Neurological 

As previously stated, encephalopathy, cerebral oedema, 

intracranial haemorrhage and seizures can occur. In acute liver 

failure, the level of encephalopathy and degree of oedema are 

closely linked. If cerebral oedema is suspected, neuroprotective 

strategies should be implemented such as the aforementioned 

control of carbon dioxide levels and arterial blood pressure 

control. Other aspects include maintaining blood sugar levels 

of less than 10 mmol/L (avoiding hypoglycaemia), keeping the 

head up at 30 degrees and avoiding ties for the endotracheal 

tube. An intracranial pressure monitor may be inserted; 

however, risks of intracranial bleeding and infection are higher 

in the liver failure population. It can be a useful monitor 

provided that it is used to guide use of aggressive therapy, such 

as hypertonic saline to achieve a sodium level of 145- 

155 mmol/L, mannitol, cooling to 32-34 degrees or deep 

sedation to achieve burst suppression. Other monitors can also 

be used, such as the transcranial Doppler or jugular bulb 

oxygen saturation monitor, to guide therapy. Encephalopathy is 

typically graded from 0 to 4, and is thought to result from a 

number of metabolites not cleared by the liver; this improves 

as liver function returns. Administration of regular lactulose 

may be helpful. Seizures should be initially controlled with 

phenytoin and minimal doses of benzodiazepines (due to their 

prolonged action). An electroencephalogram may be required 

to prove termination of seizures if any doubt exists. The cause 

for the seizures should be established, including brain imaging. 

Biochemistry 

Bicarbonate infusions can be used, but often, renal replacement 

therapy is required to provide the appropriate support for 

acidosis, fluid and electrolyte control. Anticoagulation of the 

filter circuit may not be required or, depending on the platelet 

count, prostacyclin may be used. 

Coagulopathy 

In the early postoperative period, it is reasonable to treat an 

INR of >1.5. However, others suggest that it is not necessary to 

correct clotting abnormalities (provided there is no bleeding) 

unless invasive procedures are planned or the coagulopathy is 

profound. 2 In fulminant liver failure, coagulopathy can be 

profound (and resistant to Vitamin K). In this unit, we correct 

136 



Problem 

Circulatory disturbances 

Management/Aim 

CVP 8-12 mm Hg 

MAP 65-90 mm Hg 

Haematocrit ≥30% 

Central venous oxygen saturation ≥70% 

Respiratory dysfunction Arterial oxygen saturation ≥93% 

Renal dysfunction 

Liver protection 

Sepsis 

Urine output ≥0.5 mL/kg/hr 

N-acetylcysteine infusion for 72 hours: 150 mg/kg loading dose over 

one hour, 12.5 mg/kg/hr for four hours, 6.25 mg/kg/hr subsequently 

Septic screen: CXR, sputum, urine and blood culture 

Ascitic fluid from drain site 

Consider CT abdomen 

Start antibiotics if worsening of encephalopathy or SIRS parameters 

Coagulopathy Platelet count ≥50 x 10 9 /L 

(correct if bleeding or invasive procedure) International standardised ratio ≤1.5 

Ascites 

Encephalopathy/cerebral oedema 

If grade 3-4 

Paracentesis if severe pain or respiratory/renal compromise 

Start lactulose 

Neuroprotective strategies: keep PaO 2 >10 kPa, PaCO 2 4.5-5 kPa, 

cerebral perfusion pressure >50-60 mm Hg, blood sugar 6-10 mmol/L, 

head up, no neck ties 

Consider ICP monitor and/or other cerebral monitoring tools. 

Resistant ICP treatments include hypertonic saline, mannitol and 

cooling to 32-24°C 

Nutrition 

Stress ulcer prophylaxis 

Enteral energy supply of 2,000 kcal/day 

Enteral is preferred to parenteral route 

Maintain euglycaemia and other electrolytes within normal 

range (K + /PO -3 4 /Mg ++ ) 

Start proton pump inhibitor 

Table 3 Goal directed therapy, adapted from: van den Broek, 48 Hammond. 3 

the coagulopathy if haemostasis is required or for 

interventional procedures. Fresh frozen plasma (FFP) and 

cryoprecipitate can be used, but give a significant volume load. 

Consequently, recombinant factor VIIa and fibrinogen 

concentrate can be useful. Early thrombocytopenia is often not 

corrected until levels are below 50 x 10 9 /L and haemostasis is a 

concern. Thrombocytopenia that develops later can have lower 

limits prior to correction. Platelet dysfunction can be 

quantified by using appropriate thrombo-elastogram 

preparations or platelet function analysers. 

Renal dysfunction 

Acute kidney injury should be managed by the three basic 

principles: 

• Providing an adequate blood pressure 

• Optimal cardiac output with appropriate fluid loading 

• Avoiding nephrotoxic drugs. 

If severe liver failure develops, continuous haemofiltration is 

usually required for a number of reasons, most commonly, 

profound acidosis. It is not clear whether haemodiafiltration or 

high volume exchanges provide any significant survival 

advantage. If HRS is suspected, then there is limited evidence to 

suggest that terlipressin is a useful vasopressor and that albumin 

is a useful replacement fluid. 46 This can be 4.5% albumin if 

hypovolaemia is suspected and 20% albumin otherwise. 

In the event of tense ascites, drainage should be performed 

to prevent a high intra-abdominal pressure, but it is unclear 

whether high-volume or low-volume ascites removal (with 

appropriate albumin replacement) is beneficial. 

Infection 

Patients with liver failure are at particular risk of developing 

sepsis due to a combination of immunoparesis, poor 

nutritional status and increased gut translocation. Sepsis can 

arise as a result of both bacterial and fungal pathogens (see 

Table 4). Some studies have demonstrated that prophylactic 

antibiotics can reduce the incidence of infective complications 

in patients with established postoperative liver failure, 3,7,47,48 

however they are not routinely recommended as they have not 

been shown to improve outcomes or survival. 3,49,50 Equally, 

some studies have suggested a role for routine antifungal 

prophylaxis, although conclusive evidence is lacking. 51 



Fungal 

Candidia albicans 

Aspergillus 

Bacterial 

Escherichia coli 

Staphylococcus 

Pseudomonas 

secondary to relative hyperperfusion may be successfully 

managed by decreasing portal venous inflow through 

embolisation of the splenic artery as described in two case 

series. 67,68 Surprisingly, neither of these reported any serious 

complications such as splenic infarction, but this was not 

been replicated in another, smaller case series. 69 

Table 4 Commonest pathogens in liver failure. 52 

Diagnosing sepsis in this population is difficult and regular 

surveillance cultures are recommended with an early escalation 

of antibiotic therapy and antifungals. 

Nutrition 

Poor nutritional status can affect outcome after major cancer 

surgery. 53 It is associated with an altered immune response and 

can reduce regeneration of liver cells. 54-56 Early enteral feeding 

can preserve the integrity of the gut barrier and so reduce 

postoperative infection rates. 57,58 Those developing liver failure 

should have regular high-dose lactulose (start at 20 mL tds) to 

produce 3-4 soft stools per day. 

N-acetylcysteine (NAC) 

Glutathione is an anti-oxidant found in the liver and plays an 

important role in the cellular defence mechanisms against 

oxidative damage from free radicals. 59,60 Glutathione is oxidised 

by oxygen-free radicals; its oxidised form is then reduced by 

NADPH (reduced nicotinamide adenine dinucleotide 

phosphate) forming an oxidation/reduction cycle that serves to 

‘mop up’ harmful free radicals. During hypoxia, glutathione 

stores are consumed, which can add to oxidative injury on 

reperfusion. 61,62 NAC is a precursor to glutathione and, when 

given as an infusion postoperatively, may reduce liver 

dysfunction. NAC also has an anti-inflammatory action 

inhibiting chemotaxis. This, in turn, decreases the generation 

of oxygen-free radicals by phagocytic cells. 63 In other nonparacetamol-induced 

causes of acute liver failure, both 

intravenous and oral NAC have been shown to improve 

transplant-free survival and appear safe and well tolerated. 64,65 

However, the evidence for the routine use of NAC to reduce 

ischaemia/reperfusion injury and prevent complications after 

major surgery is inconclusive. 62 Many units still use this as a 

routine therapy until normal liver function has returned. 35 

Acute postoperative liver failure amenable to 

treatment 

It is important to rule out any treatable cause of post-resection 

liver failure: 

• Portal vein thrombosis: This will give rise to ischaemia and 

possible infarction. The diagnosis can be made using either 

ultrasound Doppler or CT scan. The debate over whether 

early postoperative portal vein thrombosis is best managed 

with surgical de-obstruction or anticoagulation remains 

unresolved. 24 

• Venous outflow obstruction: Where this is due to rotation of 

the remnant liver segment, surgical intervention is 

indicated. There is also a role for endovascular stenting to 

improve venous outflow. 66 

• ‘Small-for-size’ remnant: There is some evidence that 

patients with a small remnant and venous congestion 

Liver transplantation 

Liver resection is often performed for the removal of metastatic 

malignancy and in these circumstances, consideration for liver 

transplant is often not appropriate. However, provided there 

are no contraindications, liver transplantation can be 

considered and has been successfully used as the treatment of 

postoperative liver failure. 24 The Milan criteria, developed in 

patients undergoing resections for hepatocellular carcinoma to 

help identify those suitable for transplantation, are as follows: 

• Single lesion hepatocellular carcinomas of


system, which also uses the principle of albumin dialysis, 

where lipophilic albumin-bound toxins (eg bilirubin, etc) are 

filtered and then adsorbed with a second circuit, to clean the 

albumin before being returned to the patient. SPAD is a Single- 

Pass Albumin Dialysis system which uses a similar circuit to 

MARS ® , except it uses normal machines and no perfusion 

pump systems, and uses a counter-current flow of albumin 

solution. Studies have shown that SPAD can achieve greater 

clearance of ammonia and bilirubin than MARS ® , although 

clearance of water-soluble substances was similar between the 

two methods. 76 

Conclusion 

Despite vast improvements in the perioperative care of patients 

undergoing liver resection surgery, there remains a significant 

risk of developing postoperative liver failure. Best estimates 

place the incidence at about 8%. Preoperative liver function 

and resection size are the most important factors in the risk 

associated with postoperative liver failure, although a number 

of pre- and peri-operative factors are also important, such as 

the presence of diabetes mellitus or the use of vaso-occlusive 

techniques. With advances in chemotherapy, patients who 

traditionally would not have been considered operable are 

becoming amenable to surgical treatment. Careful patient 

selection and optimisation, for example using portal vein 

embolisation, are important in reducing the incidence of 

postoperative liver failure. 

If acute liver failure occurs, then treatable conditions (such 

as segment torsion) should be considered and appropriate 

supportive care provided. Preventing and managing 

complications (commonly infective or haemorrhagic) are also 

an important aspect of care. Fulminant post-resection liver 

failure has a very poor prognosis, accounting for the majority 

of post-liver resection deaths. 

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Chris Jones Clinical Research Fellow 

drchrisnjones@yahoo.co.uk 

Leigh Kelliher Clinical Research Fellow 

Colin Bigham Locum Consultant in Anaesthesia and Intensive 

Care 

Nial Quiney Consultant in Anaesthesia and Intensive Care 

Royal Surrey County Hospital NHS Foundation Trust 

140

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