Liver Failure

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

Liver Failure

Uploaded by

Copyright:

Available Formats

Liver Failure

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Liver Failure

Uploaded by

Copyright:

Available Formats

Hepatic Failure/Cirrhosis

 toxic ingestion(acetaminophen, mushroom

 Congestive Heart failure

Chronic viral hepatitis;

less common causes include drugs or toxins,

hemochromatosis, and primary (idiopathic)

liver and function of the hepatocytes.

Inflammation and local /widespread tissue

Cirrhosis, ultimately resulting in hepatic failure

mixed with hepatocyte regeneration

resulting in portal hypertension and porto

Fatigue, nausea, emesis, diarrhea

Low-grade intermittent or continuous fever

Jaundice , ascites, a small firm liver,

splenomegaly, pedal edema, and spider

 Presented with delay in seeking medical

attention / rapid acute course

abnormal fluid shift, hepatorenal

peritonitis (survival rate 68% with one 1 month

ascites, should be suspected in any cirrhotic

worsening ascites, or encephalopathy.

deteriorating renal function, hypothermia,

 Is a poorly understood syndrome

II Lethargy, drowsiness, variable

serum alkaline phosphatase,

Total and direct bilirubin,

Serum glucose and electrolytes,

 Viral hepatitis studies

ammonia, BUN and creatinine, CBC, and

lesions, and hepatic and portal thrombosis.

Cefotaxime 2 grams IV every 8 hours or

Suspect gastroesophageal variceal bleeding

in patients with hematemesis, melena, or

bleeding or are scheduled for a procedure:

(prolonged PT, hypoglycemia, coagulopathy,

You might also like

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.