FULMINANT

HEPATIC FAILURE

MS. SHALINI
M.SC. NURSING 2ND YEAR.
OBJECTIVES:
• Anatomy and physiology of liver
• Meaning of fulminant hepatic failure
• Incidence
• Etiology
• Pathophysiology
• Clinical manifestations
• Diagnostic study
• Management of FHF
ANATOMY AND PHYSIOLOGY OF LIVER:

• Liver is a reddish-brown,
wedge shaped organ.
• Liver is the heaviest
internal organ and the
largest gland in the
body. Weighing
approximately 1.5kg in
the adult.
• Located in the right
upper quadrant.
BLOOD SUPPLY
Hepatic artery: Carries oxygen- rich
blood from the aorta via celiac
plexus. One third of the blood comes
from the hepatic artery.
Portal vein: Carries blood rich in
digested nutrients from the entire
gastrointestinal tract and also from
spleen and pancreas. Two third comes
from the portal vein
• These blood vessels subdivide into
small capillaries known as sinusoids,
which then lead to lobules. The
blood in the sinusoids is a mixture of
arterial and venous blood.
• These blood vessels subdivide into small capillaries
known as liver sinusoids, which then lead to lobules.
• Lobules are the functional units of the liver.
• Lobules consists of rows of hepatic cells called
hepatocytes, which are the basic metabolic cells.
• The capillaries (sinusoids) are located between the
rows of hepatocytes and are lined with Kupffer cells,
which carry out phagocytic activity.
 BILIARY TRACT:
• Biliary tract consist of the gallbladder and
the duct system.
• Gall bladder is a pear- shaped sac located
below the liver.
• Bile is produced by the hepatic cells and
secreted into the biliary canaliculi of the
lobules.
• Bile then drains into the interlobular bile
ducts which then unite into the two main
left and right hepatic ducts. The hepatic
ducts merge with the cystic duct from the
gall bladder to form the common bile duct.
• The function of the gallbladder is to
concentrate and store bile. It can hold
approximately 45ml of bile.
• In the intestines, bilirubin is reduced
to stercobilinogen and urobilinogen
by bacterial action.
• Stercobilinogen accounts for the
brown colour stool.
• Small amount of conjugated
bilirubin is reabsorbed by the blood.
• Some urobilinogen is reabsorbed by
the blood and returned to the liver
through the portal circulation and
excreted in the bile.
• Insignificant amount of urobilinogen
is excreted in the urine.
BILIRUBIN METABOLISM :
• Bilirubin a pigment derived from the breakdown of
haemoglobin
• Bilirubin is insoluble in water it bounds to albumin for its
transport to the liver.
• This form of bilirubin is referred to as unconjugated.
• In the liver bilirubin is conjugated with glucuronic acid.
• Conjugated bilirubin is soluble and is excreted in bile.
• Bile also consist of water, cholesterol, bile salts,
electrolytes, phospholipids, bile salts are needed for fat
emulsification and digestion.
FUNCTIONS OF THE LIVER :

• Carbohydrate metabolism.
• Protein metabolism
• Fat metabolism
• Detoxification
• Steroid metabolism
• Bile synthesis
• Storage
• Mononuclear phagocyte system
INTRODUCTION:

The liver is the largest internal organ of the human

body, weighing 1200 to 1500g and performing more
than 8000 defined functions. The complexity of the
livers role means that alternations in function can
cause a myriad of multisystem problems, whether the
alteration is related to acute or chronic liver disease or
to multisystem organ dysfunction.
DEFINITION:
Acute liver failure or fulminant liver failure is defined by
the occurrence of jaundice and any degree of mental
alteration in a patient without pre-existing liver disease
who has had an illness of less than 26weeks duration.
Or
Acute liver failure refers to the development of severe
acute liver injury with encephalopathy and impaired
synthetic function (INR of ≥1.5) in a patient without
cirrhosis or pre-existing liver disease
EPIDEMIOLOGY:

There are approximately 2000 cases of ALF in the

United states each year. Although uncommon, FHF is
associated with a mortality rate as high as 80% and
generally occurs in patients without pre-existing liver
disease.
ETIOLOGY:
Infections: Drugs/ Toxins:

Hepatitis A,B,C,D,E Industrial substances

(Chlorinated hydrocarbons,
Herpes simplex virus
phosphorus)
Epstein Barr virus
Amanita phalloids
Varicella zoster
Aflatoxin (herb)
Dengue fever virus
Medications (isoniazid,
Rift valley fever virus rifampicin, halothane,
methyldopa, tetracycline etc.)
Acetaminophen toxicity
Cocaine
 CONT..

Hypo perfusion: Metabolic disorders:

Venous obstructions Wilsons disease
Budd-Chiari syndrome Tyrosinemia
Veno-occlusive disease Heat stroke
Ischemia Galactosemia
 CONT..
Surgery: Other:

Jejunoileal bypass Reyes syndrome

Partial hepatectomy Acute fatty liver of
pregnancy
Liver transplant failure
Massive malignant
infiltration
Autoimmune hepatitis
PATHOPHYSIOLOGY:
Etiology

Loss of normal function of hepatic tissue which occurs over a short period of
time

Loss of metabolic, secretory, and regulatory effects of the liver cells

Rapid accumulations of toxic substances

Massive necrosis of the hepatocytes

Impaired bilirubin conjugation, decreased production of clotting factors,

depressed glucose synthesis, decreased lactate clearance

Clinical manifestations
MECHANISMS OF ACUTE LIVER FAILURE (ALF):
PERSPECTIVES FROM LIVER INJURY.
Pathogen or toxic substance directly damages cellular
organelles or triggers the cellular cascade pathway.

Disturbing intracellular homeostasis.

Immune responses (including innate and adaptive),

eventually converge on liver cell death pathways
including apoptosis, autophagy, necrosis and necroptosis.

Immune‐mediated liver injury.

CLINICAL MANIFESTATIONS:

• Headache
• Hyperventilation
• Palmer erythema
• Spider nevi
• Bruises
• Edema
• Asterixis
 CONT..

• Jaundice
• Coagulopathies
• Hypoglycaemia
• Metabolic acidosis
• Risk of infection
• Ascites
 CONT..

• Altered carbohydrate, protein, and glucose

metabolism.
• Hypoalbuminemia
• Fluid and electrolyte imbalance
• Acute portal hypertension
DIAGNOSIS:

History and physical examination:

Timing of symptom onset
 History of alcohol use.
 History of prior episodes of jaundice.
Medication use
 Risk factors for intentional drug overdose, such as a
history of depression or prior suicide attempts.
Toxin exposure
 Risk factors for acute viral hepatitis
 Family history of liver disease such as Wilson disease
HEPATIC ENCEPHALOPATHY IS ASSESSED BY USING
A GRADING SYSTEM:
Grade I: Changes in behavior, mild confusion, slurred
speech, disordered sleep, Slight asterixis and normal
EEG.
Grade II: Lethargy, moderate confusion, marked
asterixis and abnormal EEG.
Grade III: Marked confusion (stupor), incoherent
speech, sleeping but wakes with stimulation, asterixis
present and abnormal EEG.
Grade IV: Coma, initially responsive to noxious stimuli,
later unresponsive, asterixis absent and abnormal EEG.
LABORATORY TESTS:

• Hepatic function panel ( bilirubin, AST, ALT, ALP,

albumin)
• PT, INR, APTT
• Aminotransferase levels
• Serum ammonia
• CBC
• Electrolytes
 CONT..

• ABG
• Fctors I (fibrinogen), II (prothrombin), V,VII,IX,X
• Autoimmune screen
• Ceruloplasmin, alpha-1-antrypsin.
 CONT..

• Ultrasound of abdomen with Doppler

• Abdominal computed tomography (CT)
• X-ray and ECG as baseline
• MRI of the brain
• Ct head
• Liver biopsy
MANAGEMENT:
Ammonia level: Neomycin or lactulose is administered
to remove or decrease production of nitrogenous
wastes in the large intestine.
Lactulose is a synthetic keto analog of lactose split
into lactic acid and acetic acid in the intestine, is
given orally or as enema.
Vitamin K
 Fresh-frozen plasma (to maintain reasonable prom
thrombin time)
 Platelet transfusions
Guidelines from the American Association for the Study
of Liver Diseases (AASLD) suggest that all patients
(including those without signs of infection) should have
routine (eg, daily) urine, sputum, and blood cultures, as
well as chest radiographs to detect bacterial or fungal
infection. Antibiotic can be started if the patient shows
any signs of infection.
CEREBRAL EDEMA

It can be managed by administration of Injection Mannitol.

Other intervention to control intracranial hypertension
include elevating the head of the bed to 30 degrees.
 Treating fever and hypertension,
Minimizing noxious stimulation, and correcting hypercapnia
and hypoxemia.
If renal failure develops continuous CRRT should be
initiated.
• Intubation and mechanical ventilation may be needed
as hypoxemia persists.
• Administration of IV fluids and vasoactive medications
are required to prevent prolonged episodes of
hypotension.
• FHF continues and the patient’s shows no immediate
signs of improvement or reversal, the patient should
be considered for a liver transplant.
NUTRITION

• It is required to prevent catabolism of body stores of

proteins.
• To prevent protein catabolism, severe protein
restrictions should be avoided; a daily intake of 60
grams of protein is reasonable for most patients with
acute liver failure.
• In patients with grade I or II encephalopathy, oral or
enteral feeding is usually sufficient to meet metabolic
requirements. If adequate enteral feeding cannot be
provided, parenteral nutrition should be initiated
MEDICATIONS TO AVOID :

• In general, sedation should be avoided and the effects of

sedation may mask the signs of worsening encephalopathy or
cerebral edema.
• However, in patients with severe agitation that cannot be
managed in any other way, short-acting benzodiazepines in
low doses may be given.
• In patients who require sedative medications,
benzodiazepines, barbiturates, and propofol, are preferable to
opioids because opioids can decrease the seizure threshold.
• Nephrotoxic drugs should be avoided. In addition, intravenous
contrast agents should be used with caution.
TREATMENT OF THE UNDERLYING
CAUSE:
Acetaminophen toxicity:
N-acetylcysteine can dramatically improve the prognosis in
patients with acetaminophen toxicity.
N-acetylcysteine is administered within eight hours following
acetaminophen overdose.

Hepatitis B infection:
Antiviral therapy with a nucleos(t)ide analogue may be
beneficial in patients with acute liver failure from acute
hepatitis B virus infection.:
MUSHROOM POISONING
• In patients with Amanita phalloides ingestion, early
administration of activated charcoal is recommended.
• Additional therapies include administration of silibinin
and penicillin G

Herpes simplex virus infection:

Patients with suspected or documented herpes simplex
virus infection should receive acyclovir (5 to 10 mg/kg
every eight hours with adjustment as needed based on
the patient's renal function) for at least seven days or
until herpes simplex virus infection has been excluded.
WILSON DISEASE

Patients with acute liver failure due to Wilson disease

typically require liver transplantation, though plasma
exchange to remove copper may act as a temporizing
measure. Although hemodialysis, peritoneal dialysis, and
hemofiltration have also been used, plasma exchange with
fresh frozen plasma replacement is often preferred since it
can remove relatively large amounts of copper in a short
period of time. There is no role for chelation therapy in the
management of acute liver failure due to Wilson disease.
ACUTE FATTY LIVER OF PREGNANCY

There is no specific medical treatment for acute

fatty liver of pregnancy. As a result, the primary
treatment is prompt (usually emergent) delivery
once the mother has been stabilized
NURSING MANAGEMENT:
Nursing diagnosis:
Ineffective breathing pattern related to decreased lung
expansion.
Impaired gas exchange related to ventilation/ perfusion
mismatching or intrapulmonary shunting.
Decreased cardiac output related to alterations in
preload.
Ineffective renal tissue perfusion related to decreased
renal blood flow.
Risk for infection.
• Imbalanced nutrition less than body requirements
related to lack of exogenous nutrients or increased
metabolic demands.
• Disturbed body image related to actual change in
body structure, function, or appearance.
• Compromised family coping related to critically ill
family member.
NURSING INTERVENTION

Maintaining surveillance for complications: As the

neurologic condition worsens, respiratory depression
and arrest can occur quickly. Continuous pulse oximetry
monitoring and ABG analysis are helpful in assessing
adequacy of respiratory efforts. A thorough neurologic
assessment should be performed at least every hour.
PATIENT AND FAMILY EDUCATION:

Teaching should be based on the interventions

necessary for preventing the recurrence of the
precipitating etiology. If the patient is considered a
liver transplant candidate, the patient and family will
need specific information regarding the procedure and
care.
COMPLICATIONS:

• Cardiac dysrhythmias
• Acute respiratory failure
• Sepsis
• MODS
• Acute renal failure
• Cerebral edema
RESEARCH ARTICLE

Incidence and prognosis of early hepatic dysfunction in

critically ill patients- A prospective multicentre study
Ludwig Kramer, Barbara Jordan, Wilfired Drummi, Peter
Bauer, Philipp G.H,
The research provides strong evidence that early
hepatic dysfunction occurring in 11% of critically ill
patients, presents a specific and independent risk
factor for poor prognosis.
CONCLUSION:

FHF is potentially reversible. The FHF patient’s outcome

depends on the balance between liver injury on the one end and
liver regeneration and repair on the other. If the liver injury can
be attenuated, or the liver repair and regenerative responses
can be enhanced, then recovery is likely. Recent advances in
molecular and cell biology have resulted in the identification of
molecular targets that might soon be purposefully manipulated
to tip the balance and achieve this goal.
BIBLIOGRAPHY:

I. Carlson, K. K. (2009). Advanced critical care nursing.

Saunders Elsevier.
II. Linda D.U, Kathleen M.S, Mary E.L. Thelans critical
care nurisng.fifth edition.
II. Uptodate.com
III. WWW. dynamed.com