Page 1487 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1026 PART 9: Gastrointestinal Disorders

TABLE 106-3 Typical Timelines for Various Types of Liver Failure • Lee WM, Stravitz RT, Larson AM. Introduction to the revised
Acetaminophen Toxicity American Association for the Study of Liver Diseases Position
Paper on acute liver failure 2011. Hepatology. 2012;55:965-967.
Day 2 Day 3 Day 4
• Lescot T, Karvellas C, Beaussier M, Magder S. Acquired liver
Arterial pH <7.3 Arterial pH <7.3 PT >100 s (INR >6.0) injury in the intensive care unit. Anesthesiology. 2012;117:898-904.
PT >50 s (INR >3.0) PT >75 s (INR >4.4) Progressive rise in PT • Reuben A, Koch DG, Lee WM, Acute Liver Failure Study G. Drug-
Oliguria Oliguria Creatinine >300 µmol/L induced acute liver failure: results of a U.S. multicenter, prospec-
Creatinine >200 µmol/L Creatinine >200 µmol/L (3.4 mg/dL) tive study. Hepatology. 2010;52:2065-2076.
(2.26 mg/dL) (2.26 mg/dL) Encephalopathy
Hypoglycemia Encephalopathy Severe thrombocytopenia • Rutherford A, King LY, Hynan LS, et al. Development of an accu-
Severe thrombocytopenia rate index for predicting outcomes of patients with acute liver
failure. Gastroenterology. 2012;143:1237-1243.
All Other Etiologies
• Torres HA, Davila M. Reactivation of hepatitis B virus and hepatitis
Hyperacute Acute Subacute C virus in patients with cancer. Nat Rev Clin Oncol. 2012;9:156-166.
Encephalopathy Encephalopathy Encephalopathy • Wlodzimirow KA, Eslami S, Abu-Hanna A, Nieuwoudt M,
Hypoglycemia Hypoglycemia Hypoglycemia Chamuleau RA. Systematic review: acute liver failure—one dis-
PT >30 s (INR >2.0) PT >30 s (INR >2.0) PT >20 s (INR >1.5) ease, more than 40 definitions. Alimentary Pharmacol Therapeut.
Renal failure Renal failure Renal failure 2012;35:1245-1256.
Hyperpyrexia Hyponatremia
Shrinking liver volume on CT
REFERENCES
TABLE 106-4 Guidance Regarding Liver Transplantation Referral
Complete references available online at www.mhprofessional.com/hall
Acetaminophen-Induced ALF All Other Etiologies
pH <7.3 after fluid resuscitation PT >100 (INR >6.5)
OR all of the following: OR any three of the following:
PT >100 or INR >6.5 Seronegative hepatitis or DILI CHAPTER Management of the Patient
Serum creatinine >300 µmol/L (3.4 mg/dL) Age <10 or >40
Grade III or IV encephalopathy Jaundice to encephalopathy time 107 With Cirrhosis
OR >7 days
Serum lactate >3.5 mmol/L at 4 hours or Bilirubin >300 µmol/L (17.5 mg/dL) Sonali Sakaria
>3.0 mmol/L at 12 hours PT >50 (INR >3.5) Ram M. Subramanian

capacity. For example, a recent model proposed by the Acute Liver Failure
Study Group (ALFSG) includes such a measure—cytokeratin 18. 26 KEY POINTS
Decision to proceed to transplantation should not just consider pre- • Portal hypertension, resulting from increased intrahepatic resis-
diction of mortality without transplantation, but also address likelihood tance to portal flow and increased portal inflow, marks the transi-
of survival with transplantation. This has been addressed in several tion from compensated to decompensated cirrhosis.
papers and it seems likely that age (>45 years) and need for other organ • The sequelae of portal hypertension affect each organ system,
support (vasopressors, renal, and ventilator support), especially when requiring multi-disciplinary management.
using a less than optimal graft, have a poor survival. Equally with the
opportunity to consider living-related transplantation, it may be that • Grades III and IV hepatic encephalopathy require immediate ICU
organs can be obtained before there is severe physiological disturbance; transfer and elective intubation for airway protection.
the balance to this however requires the clinician to be sure the patient • Pulmonary derangements resulting from portal hypertension may
will not survive without transplantation as the risks to the donor and to be severe and include hepatopulmonary syndrome, portopulmo-
the recipient need to be considered. Table 106-4 outlines the approach nary hypertension, and hepatic hydrothorax.
to liver transplantation referral. • Hepatorenal syndrome is a diagnosis of exclusion and is character-
ized by renal impairment in the setting of advanced liver disease,
KEY REFERENCES circulatory dysfunction, and increased activity of the renin-angio-
tensin system.
• Bernal W, Hyyrylainen A, Gera A, et al. Lessons from look-back • SBP is a known precipitant of HRS, which is a cause of increased
in acute liver failure? A single centre experience of 3300 patients. mortality in cirrhotic patients; therefore empiric antibiotic treatment
J Hepatol. 2013;59:74-80. is warranted in patients in whom the suspicion for SBP is high.
• Craig DG, Bates CM, Davidson JS, Martin KG, Hayes PC, Simpson • Aggressive intravenous resuscitation, airway protection, and early
KJ. Staggered overdose pattern and delay to hospital presentation endoscopic management of cirrhotic patients presenting with sus-
are associated with adverse outcomes following paracetamol- pected variceal bleed is critical.
induced hepatotoxicity. Br J Clin Pharmacol. 2012;73:285-294.
• Hsu C, Hsiung CA, Su IJ, et al. A revisit of prophylactic lamivudine for
chemotherapy-associated hepatitis B reactivation in non- Hodgkin’s INTRODUCTION
lymphoma: a randomized trial. Hepatology. 2008;47:844-853.
• Lee WM, Hynan LS, Rossaro L, et al. Intravenous N-acetylcysteine Hepatic decompensation in the critical care setting can present in two
improves transplant-free survival in early stage non-acetaminophen distinct contexts, which include acute liver failure and acute on chronic
acute liver failure. Gastroenterology. 2009;137:856-864, 64 e1. liver failure. In this chapter, we discuss the critical care approach to acute
on chronic liver failure. In the intensive care setting, severe cases of acute

section09.indd 1026 1/14/2015 9:27:18 AM