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4 What Can We Do to Treat PLF

4 What Can We Do to Treat PLF

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Postsurgical Liver Failure


avoidance of water overload. Coagulopathy may occur after major liver resection.

In the absence of bleeding, usually it is not necessary to correct clotting abnormalities except for invasive procedures or when coagulopathy is severe. Vitamin K may

be given but there is no support by clinical trials. Thrombocytopenia may complicate liver failure. Indications for platelet transfusion in acute liver failure include

bleeding, severe (<20 × 106/L) thrombocytopenia, or when an invasive procedure is

planned. A platelet count >70 × 106/L is deemed safe for interventional procedures.

Nutrition is important and supplementation should be established early in patients

with liver failure. Enteral nutrition is the preferred route as it improves gut function

and restores normal intestinal flora. Cerebral edema and intracranial hypertension

may occur as a result of PLF. Cerebral edema is unlikely in patients with grade 1 or

2 encephalopathy. With progression to grade 3 encephalopathy, a head CT should be

performed to exclude intracranial hemorrhage or other causes of declining mental

status [13, 19, 27].

Extrahepatic assistance devices have been developed in the last years. They fall

into two categories: artificial and bioartificial systems. Artificial devices use combinations of hemodialysis and adsorption over charcoal or albumin to detoxify plasma.

Bioartificial devices use human or xenogeneic hepatocytes maintained within a bioreactor to detoxify and provide synthetic function.

These systems have not been evaluated extensively in patients with PLF. Outcomes

for the use of these different devices in the management of acute liver failure are

also unclear [10]. Therefore, currently, their role in PLF is undefined.

Liver transplantation is the only radical treatment in patients with end-stage

liver disease. However, patients with PLF are rarely eligible for it because of tumor

or the severity of their comorbid conditions. Moreover, liver transplantation for

PLF is associated with significant morbidity. Therefore, the use of a rescue hepatectomy and subsequent liver transplantation in patients suffering from PLF may

be of value in desperate situations where conventional measures fail. It is based on

the concept that the “necrotic liver” is the source of unknown humoral substances

that contribute to the systemic inflammatory response syndrome [33]. The use of

salvage hepatectomy and orthotopic liver transplantation for PLF has been reported

in a case series of seven patients who underwent liver resection for cancer with an

overall 1-year (88 %) and 5-year (40 %) survival promising rates [18]. However, it

has been suggested to limit liver transplantation to patients below the age of 70

years, with HCC and no macrovascular invasion, and, possibly, a small cholangiocarcinoma (less than 3 cm) without lymph node invasion. There is no indication for

transplantation in patients with liver metastasis, except those with neuroendocrine

tumors [13].


PLF is a serious and life-threatening complication in patients undergoing major

liver resections or limited functional reserve due to preexisting liver disease.

Adequate preoperative risk assessment of liver function and general condition,

parenchyma-sparing surgery, and optimal intra- and postoperative management and treatment are essential for preventing PLF. Early diagnosis of this


G. Biancofiore

complication can help initiate early treatment in the ICU aiming at optimizing

and recovering both hepatic and extrahepatic organ function. Extracorporeal

liver devices are still experimental in this particular clinical setting. The anesthetists, in their quality of leaders of the perioperative process of patients

undergoing complicated surgery, play a key role in the management of this

class of patients and are called to address the knowledge gap that still characterizes this particular clinical setting.


1. Balzan S, Belghiti J, Farges O, Ogata S, Sauvanet A, Delefosse D et al (2005) The ‘50-50

criteria’ on postoperative day 5: an accurate predictor of liver failure and death after hepatectomy. Ann Surg 242:824–829

2. Beck-Schimmer B, Breitenstein S, Urech S, De Conno E, Wittlinger M, Puhan M, Jochum W,

Spahn DR, Graf R, Clavien PA (2008) A randomized controlled trial on pharmacological preconditioning in liver surgery using a volatile anesthetic. Ann Surg 248:909–918

3. Beck C, Schwartges I, Picker O (2010) Perioperative liver protection. Curr Opin Crit Care


4. Behrns KE, Tsiotos GG, DeSouza NF, Krishna MK, Ludwig J, Nagorney DM (1998) Hepatic

steatosis as a potential risk factor for major hepatic resection. J Gastrointest Surg 2:292–298

5. Cescon M, Cucchetti A, Grazi GL, Ferrero A, Vigano L, Ercolani G, Zanello M, Ravaioli M,

Capussotti L, Pinna AD (2009) Indication of the extent of hepatectomy for hepatocellular carcinoma on cirrhosis by a simple algorithm based on preoperative variables. Arch Surg 144:57–63

6. Clavien P-A, Petrowsky H, DeOliveira ML, Graf R (2007) Medical progress: strategies for

safer liver surgery and partial liver transplantation. N Engl J Med 356:1545–1559

7. de Liguori Carino N, O’Reilly DA, Dajani K, Ghaneh P, Poston GJ, Wu AV (2009) Perioperative

use of the LiMON method of indocyanine green elimination measurement for the prediction

and early detection of post-hepatectomy liver failure. Eur J Surg Oncol 35:957–962

8. Dello SA, van Dam RM, Slangen JJ, van de Poll MC, Bemelmans MH, Greve JW et al (2007)

Liver volumetry plug and play: do it yourself with ImageJ. World J Surg 31:2215–2221

9. del Olmo JA, Flor-Lorente B, Flor-Civera B et al (2003) Risk factors for nonhepatic surgery in

patients with cirrhosis. World J Surg 27:647–652

10. Faybik P, Krenn CG (2013) Extracorporeal liver support. Curr Opin Crit Care 19:149–153

11. Gurusamy KS, Kumar Y, Pamecha V et al (2009) Ischaemic preconditioning for elective liver

resections performed under vascular occlusion. Cochrane Database Syst Rev:CD007629

12. Gurusamy KS, Li J, Vaughan J, Sharma D, Davidson BR (2012) Cardiopulmonary interventions to decrease blood loss and blood transfusion requirements for liver resection. Cochrane

Database Syst Rev (5):CD007338

13. Hammond JS, Guha IN, Beckingham YJ, Lobo DN (2011) Prediction, prevention and management of postresection liver failure. Br J Surg 98:1188–1200

14. Kooby DA, Stockman J, Ben-Porat L, Gonen M, Jarnagin WR et al (2003) Influence of transfusions on perioperative and long-term outcome in patients following hepatic resection for

colorectal metastases. Ann Surg 237:860–869

15. Laurent A, Tayar C, Cherqui D (2008) Cholangiocarcinoma: preoperative biliary drainage

(Con). HPB (Oxford) 10:126–129

16. Moulton CA, Chui AKK, Mann D, Lai PB, Chui PT, Lau WY (2001) Does patient position

during liver surgery influence the risk of venous air embolism? Am J Surg 181:366–367

17. Nimura Y (2008) Preoperative biliary drainage before resection for cholangiocarcinoma (Pro).

HPB (Oxford) 10:130–133

18. Otsuka Y, Duffy JP, Saab S, Farmer DG, Ghobrial RM, Hiatt JR et al (2007) Postresection

hepatic failure: successful treatment with liver transplantation. Liver Transplant 13:672–679


Postsurgical Liver Failure


19. Paugam-Burtz C, Wendon J, Belghiti J, Mantz J (2012) Case scenario: postoperative liver

failure after liver resection in a cirrhotic patient. Anesthesiology 116:705–711

20. Picker O, Beck C, Pannen B (2008) Liver protection in the perioperative setting. Best Pract Res


21. Rahbari NN, Wente MN, Schemmer P, Diener MK, Hoffmann K, Motschall E, Schmidt J,

Weitz J, Buchler MW (2008) Systematic review and meta-analysis of the effect of portal triad

clamping on outcome after hepatic resection. Br J Surg 95:424–432

22. Rahbari NN, Garden OJ, Padbury R, Brooke-Smith M et al (2011) Posthepatectomy liver

failure: a definition and grading by the International Study Group of Liver Surgery (ISGLS).

Surgery 149:713–724

23. Reissfelder C, Rahbari NN, Koch M, Kofler B, Sutedja N, Elbers H, Buchler MW, Weitz

J (2011) Postoperative course and clinical significance of biochemical blood tests following

hepatic resection. Br J Surg 98:836–844

24. Richter B, Schmandra TC, Golling M, Bechstein WO (2006) Nutritional support for open liver

resection: a systematic review. Dig Surg 23:139–145

25. Saner F (2008) Kidney failure following liver resection. Transplant Proc 40:1221–1224

26. Serenari M, Cescon M, Cucchetti A, Pinna AD (2013) Liver function impairment in liver

transplantation and after extended hepatectomy. World J Gastroenterol 19:7922–7929

27. Shan J, Quan F, Gerile W, Tu W (2013) Management of post-hepatectomy complications.

World J Gastroenterol 19:7983–7991

28. Schreckenbach T, Wolf JL, Bechstein O, Moench C (2012) Posthepatectomy liver failure. Dig

Surg 29:79–85

29. Schroeder RA, Marroquin CE, Bute BP, Khuri S, Henderson WG, Kuo PC (2006) Predictive

indices of morbidity and mortality after liver resection. Ann Surg 243:373–379

30. Shirabe K, Shimada M, Gion T, Hasegawa H, Takenaka K, Utsunomiya T, Sugimachi K (1999)

Postoperative liver failure after major hepatic resection for hepatocellular carcinoma in the

modern era with special reference to remnant liver volume. J Am Coll Surg 188:304–309

31. Thomas M, Weninger E, Angele M, Bösch F, Pratschke S, Andrassy J, Rentsch M, Stangl M,

Hartwig W, Werner J, Guba J (2015) Intraoperative simulation of remnant liver function during

anatomic liver resection with indocyanine green clearance (LiMON) measurements. HPB


32. Tympa A, Theodoraki K, Tsaroucha A, Arkadopoulos N, Vassiliou I, Smyrniotis V (2012)

Anesthetic considerations in hepatectomies under hepatic vascular control. HPB Surg: ID


33. Van den Broek MAJ, Olde SWM, Dejong CHC, Lang H, Malagó M, Jalan R, Saner FH (2008)

Liver failure after partial hepatic resection: definition, pathophysiology, risk factors and treatment. Liver Int 26:767–780

34. Vos JJ, Wietasch JK, Absalom AR, Hendriks HG, Scheeren TW (2014) Anaesthesia


35. Yang LQ, Tao KM, Liu YT, Cheung CW, Irwin MG, Wong GT, Lv H, Song JG, Wu FX, Yu

WF (2011) Remifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats

via inducible nitric oxide synthase expression. Anesthesiology 114:1036–1047

Postoperative Delirium


Franco Cavaliere


What Is Delirium?

Delirium or acute confusional state is a syndrome characterized by the depression

of the highest mental functions and by a typical time course [2, 17]. Symptoms

occur acutely, manifest a fluctuating trend, especially in relation to night and day

alternation, and in most cases resolve without leaving sequelae. Condition for diagnosis is that such symptoms cannot be explained with a state of preexisting dementia, in accordance with the definition given by the Diagnostic and Statistical Manual

of Mental Disorders (DMS-IV): “The essential feature of a delirium is a disturbance

in consciousness that is accompanied by a change in cognition that cannot be better

accounted for by a pre-existing or evolving dementia.”

Alterations of consciousness do not reach the severity of stupor or coma; rather,

patients do not pay attention to the surrounding environment and in certain phases

may have a more or less marked drowsiness. The attention span is reduced, and they

are easily distracted during the interaction with doctors and family members.

Among cognitive processes, memory of recent events and orientation in space and

time are particularly compromised. Often, patients do not know where they are (in

the hospital, in the orthopedic ward, etc.) nor have the correct time references

(which day and time are now, it is day or night, how old they are, etc.). There may

also be language disorders, such as an inability to speak or write object names.

Disorders of emotions manifest themselves from time to time with anxiety, fear,

depression, irritability, anger, or euphoria. Diagnosis is often suspected when the

patient reports altered perceptions, spontaneously or at the request of the doctor.

Altered perceptions are classified into misinterpretations, delusions, and hallucinations. An example of misinterpretation of a real situation is to believe that the

F. Cavaliere

Department of Cardiovascular Sciences, Catholic University of the Sacred Heart,

Largo Francesco Vito 1, Rome 00168, Italy

e-mail: franco.cavaliere@policlinicogemelli.it

© Springer International Publishing Switzerland 2016

D. Chiumello (ed.), Topical Issues in Anesthesia and Intensive Care,

DOI 10.1007/978-3-319-31398-6_10


F. Cavaliere


administration of a drug is an attempt to poison or that hospitalization is a kidnapping. An illusion is an erroneous perception of a sensation, often visual; for example, an infusion line or a fold of the sheet may look like a snake or a worm. A

hallucination is a perception that does not match any real sense; particularly frequent is watching insects on the walls or persons in the vicinity of the bed.

Psychomotor activity is also affected by delirium. There are two distinct forms,

the overactive one, characterized by hyperactivity, restlessness, and insomnia, and

the underactive one, characterized by hypoactivity, drowsiness, and detachment

from the environment. Mixed forms are also possible, alternating hypo- and hyperactive phases. Hyperactive forms are often easier to diagnose because patient management becomes problematic. Delirium is classified as prevalent when it is already

present at the admission to the hospital, incident when it occurs during hospital stay,

and subsyndromic when it does not match all the criteria needed for diagnosis [7].

Finally, delirium may overlap to a preexisting dementia [10].


Incidence of Delirium in the Perioperative Period

Postoperative delirium typically occurs in the first 48 h after surgery. It must be

distinguished from the transient phenomena of agitation that may be observed during recovery from anesthesia and from postoperative cognitive dysfunction which,

likewise delirium, affects superior brain functions, first of all the memory, but has

different characteristics (Table 10.1).

Incidence of delirium varies in different series, but is anyway high, especially in

the elderly. After elective surgery, delirium affects between 10 and 75 % of patients

older than 65 years [6]. This percentage is heavily influenced by the type of surgery.

For example, delirium occurs more frequently after vascular surgery and oral surgery of long duration (36 and 42 %, respectively) than after ophthalmologic procedures, such as extraction of the lens (4.4 %). Hip surgery is also characterized by a

high incidence of postoperative delirium (5–30 %), which increases if the intervention is associated with prolonged bed rest as in traumatic fractures.

Influence of surgery can be explained in part by the characteristics of interventions (duration, amount of postoperative pain, risk of hypotension, hypoxia, and

anemia) and in part by patient features. For example, vascular surgery is often

Table 10.1 Differential

diagnosis between delirium

and postoperative cognitive

dysfunction (POCD)

Clinical features

Delay after




















Sometimes after months

Modified from Krenk and Rasmussen [5]


Postoperative Delirium


performed on elderly patients, affected by arterial hypertension and suffering from

an advanced degree of atherosclerosis. Of note, the incidence of postoperative delirium is positively correlated with the number of hypotensive episodes, of arterial

desaturations, and of blood transfusions that occur during the surgical procedure.


Etiology and Pathogenesis

The etiology of postoperative delirium is complex and multifactorial. Causes and

contributing factors can be divided in five groups:

(a) Factors that alter brain metabolism. These include hypoperfusion, hypoxia,

anemia, hyperthermia, fluid and electrolyte abnormalities, liver and kidney failure, some endocrine disorders, and deficiency of vitamin B1 and B12.

(b) Abnormal and annoying stimuli and, in general, all that can alter perceptions.

Pain caused by inadequate analgesia facilitates the onset of delirium (although

opioid administration can be a facilitating factor). This is particularly relevant

for the elderly or for patients suffering from dementia who are very susceptible

to the onset of delirium and often receive inadequate doses of analgesics.

Endogenous stimuli, e.g., relating to constipation or bladder distension, may

also induce the occurrence of delirium. Finally, inadequate ambient lighting or

removal of hearing aids or glasses may alter patient perceptions, favoring the

isolation of the patient himself and the appearance of altered perceptions.

(c) Some drugs, often having anticholinergic activity. They include some analgesics (codeine, meperidine, morphine), antibiotics, antifungals and antivirals

(acyclovir, amphotericin B, cephalosporins, ciprofloxacin, imipenem-cilastatin,





trimethoprimsulfamethoxazole), antiepileptic drugs (phenobarbital, phenytoin), cardioactive

drugs (captopril, clonidine, digoxin, dopamine, labetalol, lidocaine, nifedipine,

nitroprusside, procainamide, propanolol), drugs of abuse (alcohol, sedatives,

hypnotics, hallucinogens, amphetamine, cannabis, cocaine, phencyclidine), and

others (hydroxyzine, ketamine, metoclopramide, theophylline, atropine, scopolamine, nonsteroidal anti-inflammatory agents).

(d) Acute suspension of certain drugs and substances that are active on the nervous

system, such as sedatives, opioids, alcohol, and nicotine.

(e) Environmental factors. Sometimes, delirium occurrence is simply caused by

partying from home and relatives, admission to the hospital, and prolonged bedding. In intensive care units, environmental noise and night lighting worsen the

quality of sleep and alter circadian rhythm. Absence of time references, such as

calendars and clocks, and the lack of information and entertainment tools, such

as books, newspapers, radio, and television, favor patient disorientation in time

and space and, ultimately, cause delirium occurrence.

The pathogenesis of delirium is also complex and still not fully cleared. It

has been hypothesized that a role is played by an imbalance in the brain

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