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A LIFE-THREATENING condition,liver failure results from liver dam-age. In many cases, the damage isgradual and silent, causing fewsymptoms until the organ loses allof its functions.Liver failure can be acute or take

the form of chronic liver disease(CLD), which leads to irreversibleend-stage liver disease (ESLD).• CLD typically stems from alcoholabuse, hepatitis or, less often,hemochromatosis (excess ironstores) and malnutrition.

• Acute liver failure (ALF) is lesscommon than CLD. In the devel-oping world, it usually resultsfrom hepatitis B or E; in Europeand the United States, from acet-aminophen overdose. Othercauses include illicit drug use,herpes simplex virus, cyto meg a -lovirus, Epstein-Barr virus, aden-ovirus, and parvovirus. ALF is a medical emergency

when it occurs in someone withno history of liver disease. Al-though sometimes reversible, it

may warrant a liver transplant. In a patient who does have a history of liver disease, ALF iscalled acute-on-chronic liver fail-ure. Nonalcoholic steatohepatitisis a form of CLD caused by fatbuildup in the liver; its exactcause is unknown. ALF can be classified as hypera-

cute, acute, or subacute based onthe patient’s prognosis and timefrom onset of jaundice to enceph a -lopathy. (See Classifying ALF.)Both ALF and CLD can lead to

multisystem organ failure—quicklywith ALF and gradually with CLD.To understand the effects of a fail-ing liver, you need to comprehendthe mechanisms involved. (See Un-derstanding liver functions.)

AssessmentALF and CLD share many signs andsymptoms, including:• decreased appetite• nausea• jaundice• fatigue

• asterixis (flapping tremor)• peripheral edema• coagulopathy• dark urine• muscle wasting• bleeding esophageal varices• cerebral edema• sepsis• hepatic encephalopathy.Abnormal liver function test re-

sults include an increased serumalanine level and an aminotrans-ferase level that’s 10 to 100 timesthe upper limit of normal. Typical-ly, serum bilirubin and prothrombintimes are increased and the albu-min level is decreased. Make sure to assess patients for

signs and symptoms of hepatic en-cephalopathy and note their pro-gression. Keep in mind that in-creased confusion suggests hepaticencephalopathy and cerebral ede-ma. (See Grading hepatic en-cephalopathy).

TreatmentInterventions depend on whether

How to help patients with liver failure

Your astute assessment and management can help patients survive this life-threatening condition.

By Shari J. Lynn, MSN, RN

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the patient has ALF or CLD, aswell as the specific dysfunctionspresent. (See Common dysfunc-tions in ALF.)

ALF treatment Treatment of ALF focuses on cor-recting the cause. Patients requireurgent treatment and monitoring,including serial blood and coagu-lation tests. Specific measures mayvary with the systemic dysfunc-tions present. Expect invasivemonitoring for patients with car-diovascular problems, such as hy-potension and intravascular vol-ume depletion, along with volumedepletion correction, vasopressors,and inotropic support, if needed.Patients who’ve ingested acetamin-ophen require I.V. acetylcysteine. To reduce the risk of aspiration

pneumonitis, patients with a de-creased level of consciousness arelikely to be intubated. Those withmetabolic and renal dysfunctionsrequire fluid management andblood glucose normalization, inaddition to possible renal replace-ment therapy (such as dialysis).Encephalopathy necessitates

treatment of fever and hypona-tremia, as well as sepsis screening.Some patients may require tran-scranial ultrasonography and in-tracranial pressure (ICP) monitor-

ing. High-grade encephalopathywarrants endotracheal intubation,with partial pressure of carbondioxide maintained between 31and 44 mm Hg and serum sodiumbetween 145 and 150 mmol/L. In-tracranial hypertension calls forosmotherapy, temperature control,and rescue therapy (such as in-domethacin and thiopentone). An-tibiotic prophylaxis may be givento patients at high sepsis risk.

CLD treatment Treatment focuses on stopping ad-ditional liver damage and slowingdisease progression, as well asmanaging symptoms. It includes ahealthy, low-sodium diet; abstainingfrom alcohol and illicit drugs; andaddressing medical problems asthey occur. Ultimately, patients mayneed a liver transplant.

Liver transplantation Patients ages 12 and older whoprogress to the point of needing aliver transplant are assessed usingthe Model for End-Stage Liver Dis-ease (MELD) scoring system; thoseyounger than age 12 are assessedusing the Pediatric End-Stage LiverDisease (PELD) system. Blood testsused to determine MELD scores areserum bilirubin, serum creatinine,serum sodium, and internationalnormalized ratio (INR). Blood testsused to determine PELD scores arebilirubin, albumin, and INR. TheMELD score also considers the pa-tient’s renal function and whetherhe or she is on dialysis; the PELDtakes into account the child’s ageand degree of failure to grow.

Acute liver failure (ALF) can be classified as shown below. Keep in mind, though, thatthese classifications have limited usefulness in clinical practice because they don’tnecessarily indicate prognosis.

Time from jaundice to Classification encephalopathy Risk of cerebral edema

Hyperacute Less than 7 days Common (occurs in more than 70% of patients)

Acute 8-28 days Common (occurs in more than 55% of patients)

Subacute 5-12 weeks Low (occurs in fewer than 15% of patients))

Classifying ALF

A highly vascular organ, the liver is perfused by 1,500 mL of blood per minute.About 75% of its blood supply comes from the portal vein and 25% from the he-patic artery. Portal-vein blood is rich in nutrients and toxins, as it comes from theGI tract and spleen. The liver detoxifies substances in the body and produces endothelin and nitric

oxide. Endothelin causes vasoconstriction; nitric oxide induces vasodilation.Working together, these two mediators regulate hepatic blood flow. In liver disease, portal-vein pressure rises, resulting in portal hypertension and

an imbalance of endothelin and nitric oxide. Excessive nitric oxide productionleads to splanchnic blood-vessel dilation, causing blood to shunt away from ma-jor organs and increasing blood flow to the liver—in particular, the portal vein.This shunting reduces kidney perfusion, in turn activating the renin-angiotensin-aldosterone system (which regulates blood pressure) as the kidneys try to in-crease their own blood volume. Aldosterone activation increases sodium absorption in the loop of Henle, caus-

ing water retention and increased blood volume. Excess nitric oxide leads to dila-tion of abdominal vessels; at the same time, blood pressure in the kidneys de-creases. Sodium and water continue to be reabsorbed, causing circulatory volumeto rise—to the point that fluid leaks from the intravascular space and overloadsthe lymphatic system. Eventually, this fluid leaks into the peritoneal cavity, result-ing in ascites, a hallmark of liver failure. In chronic liver disease, cirrhosis occurs as fibrotic tissue develops. The liver at-

rophies and shrinks as more scar tissue forms. These effects are irreversible.

Understanding liver functions

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The patient’s results are enteredinto a formula that yields a score.MELD scores range from 6 (less ill)to 40 (gravely ill); PELD scores,from negative numbers to 99. A pa-tient’s MELD or PELD score canchange as his or her conditionworsens. Besides reflecting the pa-tient’s disease severity, the MELD orPELD score determines how urgent-ly he or she will need a liver trans-plant in the next 3 months. Thus, itdetermines the patient’s placementon the liver-transplant waiting list.

Nursing careNursing care for patients with liverfailure focuses on supporting bodysystems, managing signs and symp-toms of decreased liver function,and avoiding worsening cerebraledema. • Monitor level of consciousness,blood pressure, volume status,blood and coagulation tests, andsigns and symptoms.

• Keep the head of the bed elevat-ed 30 degrees, with the patient’shead in the neutral position.

• Decrease stimulation, such asfrequent suctioning.

• Stay alert for hypercapnia andhypoxia; correct these conditionsas indicated and ordered.

• Manage fever aggressively with afan, cooling blanket, or both.

• Watch for signs and symptoms ofinfection and possible sepsis; ad-minister antibiotics, as neededand ordered.

• Maintain strict glucose monitor-ing for possible hypoglycemia orhyperglycemia.

• Provide nutritional support as or-dered.Patients who reach an acuity

level that warrants close monitor-ing (such as those in an intensivecare unit with grade 3 or 4 hepaticencephalopathy) require ICP mon-itoring.

Postoperative care After liver transplantation, assessthe patient for such complications

Hepatic encephalopathy occurs when an impaired liver can no longer remove toxinsfrom the blood, which causes serum ammonia levels to rise. Osmotic disturbancesthen occur in the brain, along with inflammation and increased cerebral blood flow. Patients with hepatic encephalopathy exhibit confusion, hyperthermia, respira-

tory and circulatory problems, and increased intracranial pressure (ICP). Treatmentmay include lactulose given by mouth or as an enema to remove ammonia throughthe GI tract, titrated to three to four soft stools in 24 hours. Rifaximin, an antibiotic,may be used to treat infection; sodium benzoate, to decrease ammonia production;and hypertonic saline solution, to decrease elevated ICP. Various scales have been developed to diagnose and classify hepatic encepha -

lopathy. The table below shows a system with four grades of increasing severity.

Grade Signs and symptoms

Grade 1 • Mild lack of awareness • Euphoria or anxiety • Shortened attention span • Impaired performance of addition or subtraction

Grade 2 • Lethargy or apathy • Minimal disorientation of time or place • Subtle personality changes • Inappropriate behavior • Impaired performance of addition or subtraction

Grade 3 • Somnolence to semi-stupor but responsive to verbal stimuli • Confusion • Gross disorientation

Grade 4 • Coma (unresponsive to verbal or noxious stimuli)

Grading hepatic encephalopathy

Acute liver failure (ALF) leads to alterations in many body systems, as shown below.

Body system Common dysfunctions

Cardiovascular • Hypotension • Intravascular volume depletion • Low cardiac output • Right ventricular failure • Vasodilation

Central nervous system • Intracranial hypertension • Progressive encephalopathy

Hematologic • Coagulopathy

Immunologic • Increased risk of sepsis

Metabolic • Hyperammonemia • Hypoglycemia • Hyponatremia • Impaired drug metabolism • Lactic acidosis

Renal • Renal dysfunction

Respiratory • Increased risk of aspiration pneumonitis

Common dysfunctions in ALF

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as bleeding, infection, and rejec-tion. Monitor the patient’s tempera-ture, urine output, neurologic statusand hemodynamic pressures. Alsoprovide education about immuno-suppressive drugs.

Managing ascitesLiver failure commonly causes as-cites—fluid buildup in the peri-toneal cavity. As indicated, take ap-propriate steps to manage ascites,which can affect multiple body sys-tems. The physician may order di-uretics and a low-sodium diet. Al-dosterone antagonists (such asspironolactone) may be used totreat ascites instead of loop diuret-ics (such as furosemide) becausethey spare potassium and addressascites pathophysiology. Althoughpatients with ascites may be placedon fluid restrictions, studies fail toshow this intervention is effective.Be aware that patients who under-go paracentesis to treat ascites may

need follow-up fluid replacementand albumin administration.

Rising to the challenge With continuing medical advancesand more patients waiting for liverdonors, you’re likely to encountermore patients with liver failure. Tooptimize outcomes, make sureyou’re familiar with the signs andsymptoms of liver failure, ascites,and hepatic encephalopathy. Final-ly, be sure to provide emotionalsupport to patients and families.

Shari J. Lynn in an instructor at the Johns HopkinsUniversity School of Nursing in Baltimore,Maryland.

Selected referencesBernal W, Wendon J. Acute liver failure. NEngl J Med. 2013;369(26):2525-34.

Blackmore L, Bernal W. Acute liver failure.Clin Med (Lond.) 2015;15(5):468-72.

Clements A, Greenslade L. Nursing care forend-stage liver disease. Nurs Times. 2014;110(29):16-9.

Fullwood D, Purushothaman A. Managingascites in patients with chronic liver disease.Nurs Stand. 2014;28(23):51-8.

Fullwood D, Sargent S. Complications inacute liver failure: managing hepatic en-cephalopathy and cerebral oedema. Gas-trointest Nurs. 2014;12(3):27-34.

Larsen FS, Bjerring PN. Acute liver failure.Curr Opin Crit Care. 2011;17(2):160-4.

National Institute of Diabetes and Digestiveand Kidney Diseases. Liver transplantation.2012. niddk.nih.gov/health-information/health-topics/liver-disease/liver-transplant/Pages/facts.aspx

National Library of Medicine. Acute liver fail-ure. Updated June 28, 2016. livertox.nih.gov/Phenotypes_fail.html

Patton H, Misel M, Gish RG. Acute liver fail-ure: an evidence-based management proto-col for clinicians. Gastroenterol Hepatol (NY).2012;8(3):161-212.

Take steps tomanage ascites,which can affectmultiple body

systems.