Hepatic Failure/Cirrhosis
Physiology of the
Liver?
Liver disease can be categorized as:
acute, chronic and fulminant
Acute hepatitis is defined as a severe,
sudden loss of hepatocytes resulting in
failure of hepatic function, accompanied by
encephalopathy and coagulation disorder.
ALF occurs without a previous history of
liver disease
presents with: nausea, vomiting, RUP
abdominal pain ,fever, jaundice,
bilirubinuria, enlarged tender liver…..
Cont’d..
Most common causes are
viral infection
toxic ingestion(acetaminophen, mushroom
and alcohol)
autoimmune liver disease, shock
malignant infiltration
Congestive Heart failure
Chronic hepatitis
Chronic hepatitis
Evidence of long standing hepatocellular
damage.
Loss of hepatocytes, abnormal
microcirculation, and impaired hepatic
function of 6 months or longer duration are
hallmarks of chronic liver failure (CLF).
Cause of Cirrhosis
Ethanol or
Chronic viral hepatitis;
less common causes include drugs or toxins,
hemochromatosis, and primary (idiopathic)
biliary cirrhosis.
Biliary obstruction
Autoimmune disorders
Pathophysiology
alterations in the structural architecture of the
liver and function of the hepatocytes.
Slowly progressing,
Inflammation and local /widespread tissue
necrosis,
Fibrosis , liver nodule formation, and
Cirrhosis, ultimately resulting in hepatic failure
Cirrhosis results from fibrous scarring
mixed with hepatocyte regeneration
The scarring decreases both synthetic and
metabolic function
Also increases resistance to blood flow
resulting in portal hypertension and porto
- systemic shunting
Clinical Features
Edema or ascites
Fatigue, nausea, emesis, diarrhea
Low-grade intermittent or continuous fever
Jaundice , ascites, a small firm liver,
splenomegaly, pedal edema, and spider
angiomata.
Fulminant liver failure (end stage)
Fulminant liver failure (end stage)
Presented with delay in seeking medical
attention / rapid acute course
Marked by Coagulopathy, encephalopathy,
abnormal fluid shift, hepatorenal
syndrome ,hemolysis …( indicates transition
from cirrhosis)
Portal hypertension leads to splenomegaly and
varices
Ascites develops secondary to portal
hypertension
It sets the stage for spontaneous bacterial
peritonitis (survival rate 68% with one 1 month
and 31% with 6 months, GIB from varices is a
risk factor)
Spontaneous bacterial peritonitis
Is the most common complication of cirrhotic
ascites, should be suspected in any cirrhotic
patient with
fever, abdominal pain or tenderness,
worsening ascites, or encephalopathy.
Other subtle clues to SBP include
deteriorating renal function, hypothermia,
and diarrhea.
Hepatorenal syndrome
a refractory form of acute renal failure that
occurs in cirrhotic patients, may develop in
the setting of
sepsis,
acute dehydration,
overzealous diuresis, or
high-volume paracentesis.
Hepatic Encephalopathy
Is a poorly understood syndrome
Due to accumulation of nitrogeous waste
products
normally metabolized by the liver
Result in altered level of consciousness and
characteristic motor finding
Spans from chronic fatigue to acute lethargy
Asterixis
Changes in the liver metabolic capacity result
from
- Hypo/hyperglycemia
- Sepsis
- Iatrogenic interventions like TIPS (Trans
Jugular Intraheaptic Portal Shunt)
- reduces portal hypertension and
variceal
bleeding but deprives substrate to the
liver
for ammonia metabolism
Sources of nitrogenous wastes include:
- Dietary sources
- GI flora
- Protein load from occult GI bleeding
- Precipitated by infection, electrolyte
imbalance, renal failure, and
medications.
Precipitating factors
GI bleeding
Infection
Hypokalemia
Hypolemia and/ hypoxia
Large protein meal
Constipation
Drugs (sedatives )
Hypoglycemia
Staging of Hepatic Encephalopathy
STAGES Features
I General apathy
II Lethargy, drowsiness, variable
orientation, Asterixis
III Stupor with hyperreflexia,
extensor plantar reflexes
IV coma
DDX
Hepatic Encephalopathy is a Dx of
exclusion
In a cirrhotic patient with altered mental
status the following should be ruled out
- Hypoglycemia
- SDH
- Electrolyte imbalance
- Wernicke- korsakoff syndrome
- Drugs like benzodiazepines
- Sepsis, Renal failure…
Diagnosis
Serum transaminases (ALT and AST),
serum alkaline phosphatase,
Total and direct bilirubin,
Serum albumin,
Serum glucose and electrolytes,
Viral hepatitis studies
ammonia, BUN and creatinine, CBC, and
PT/INR
Cont’d..
Elevated serum ammonia suggests hepatic
encephalopathy.
Ultrasound guided paracentesis to check for
bacterial peritonitis.
A total WBC greater than 1000/mm 3 is diagnostic
for SBP
Ultrasound can also identify infectious or mass
lesions, and hepatic and portal thrombosis.
Abdominal CT and head CT in patients with mental
Emergency Department Care and
Disposition
1. Patients with abdominal pain, fever,
acidosis, leukocytosis, significant hypo or
hypervolemia, new onset or worsening
encephalopathy, coagulopathy with
bleeding, or significant electrolyte
abnormalities should be admitted to the
hospital. Hepatorenal syndrome warrants
nephrology consultation.
2. Management of ascites include
spironolactone , 50 to 200 milligrams/d, and
amiloride, 5 to 10 milligrams/d.
Abstinence from alcohol and other
hepatotoxins is essential for outpatient
management.
A protein-restricted diet helps prevent the
complication of hepatic encephalopathy.
Paracentesis is necessary for symptomatic
relief of ascites or to diagnose SBP.
Administer albumin , 1.5 grams/kilogram IV
before paracentesis, to guard against
complications related to fluid shifts.
Removal of more than 1L of ascitic fluid can
lead to hypotension, so careful monitoring is
required.
Initiate antibiotics in patients with SBP.
Cefotaxime 2 grams IV every 8 hours or
ceftriaxone 2 grams IV every 24 hours
Suspect gastroesophageal variceal bleeding
in patients with hematemesis, melena, or
hematochezia
Correct coagulopathy in patients who are
bleeding or are scheduled for a procedure:
give vitamin K, 10 milligrams PO or IV. FFP
Admit all patients with acute hepatic failure
(prolonged PT, hypoglycemia, coagulopathy,
encephalopathy, marked jaundice) to the
intensive care unit.
Treatment(Hepatic Encephalopathy )
Aimed at reducing the production of nitrogenous
waste products and intestinal bacteria
- Reducing protein intake
- Lactulose is the main stay of treatment
lactulose, 20 grams PO
*Neomycin po
( Metronidazole as alternative in patients
with
hearing impairment/acute renal failure)
MOA of lactulose
In the colon, lactulose (beta-
galactosidofructose) and lactitol (beta-
galactosidosorbitol) are catabolized by the
bacterial flora, resulting in an acidic pH. The
reduction in pH favors the formation of the
nonabsorbable NH4+ from NH3, trapping
NH4+ in the colon and thus reducing plasma
ammonia concentrations.
Additional effect of lactulose
1. Increased incorporation of ammonia by bacteria
for synthesis of nitrogenous compounds.
2. Modification of colonic flora, resulting in
displacement of urease-producing bacteria with
non-urease-producing Lactobacillus .
3. Cathartic effects of a hyperosmolar load in the
colon that improves gastrointestinal transit,
allowing less time for ammonia absorption.
4. Increased fecal nitrogen excretion (up to
fourfold) due to the increase in stool volume
Supportive care
- judious fluid, vitamins, correct
electrolyte
Liver transplantation ( last option)
COLLABORATIVE CARE
Oxygenation/Ventilation
Circulation/Perfusion
Fluids/Electrolytes
Mobility/Safety
Skin Integrity
Comfort/Pain Control
References
Tintinallis emergency medicine manuals 7th
edition
Critical care nursing 11th edition
Manuals of critical care nursing 7th edition
