1.

LIVER CIRHOS
2. ACUTE LIVER FAILURE
3. PANCREATITIS
DR MOUNA A. ABDILLAHI BOQORE FAMILY DOCTOR
LESSON 1

•Understanding Liver
Cirrhosis:
 INTRODUCTION LIVER CIRRHOSIS

• Cirrhosis represents a late stage of progressive hepatic fibrosis

characterized by distortion of the hepatic architecture and the
formation of regenerative nodules. It is generally considered to
be irreversible in its advanced stages, at which point the only
treatment option may be liver transplantation.
INTRODUCTION LIVER CIRRHOSIS

• However, reversal of cirrhosis (in its earlier stages) has

been documented in several forms of liver disease
following treatment of the underlying cause.
• Patients with cirrhosis are susceptible to a variety of
complications, and their life expectancy is markedly
reduced.
 IN GENERAL CAUSES OF LIVER CIRRHOSIS

• Alcohol abuse: Leading cause, with prolonged heavy drinking damaging liver cells.
• Viral hepatitis: Hepatitis B and C infections can trigger inflammation and scarring.
• Fatty liver disease: Non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease
(AFLD) can progress to cirrhosis.
• Autoimmune hepatitis: Immune system attacks healthy liver cells leading to inflammation and
scarring.
• Genetic diseases: Hemochromatosis (iron overload), Alpha-1 antitrypsin deficiency, and others
can cause cirrhosis.
 CAUSES OF LIVER CIRRHOSIS

• In developed countries, common causes of cirrhosis include

●Chronic viral hepatitis (hepatitis B, C)
●Alcohol-associated liver disease
●Hemochromatosis
●Nonalcohol-associated fatty liver disease
 SOME EXAMPLES OF THE LESS COMMON
CAUSES OF LIVER CIRRHOSIS
• ●Autoimmune hepatitis
• ●Primary and secondary biliary cirrhosis
• ●Primary sclerosing cholangitis
• ●Medications (e.g, methotrexate, isoniazid)
• ●Wilson disease ( Copper build up)
• ●Alpha-1 antitrypsin deficiency
• ●Celiac disease
• ●Idiopathic adulthood
• ●Granulomatous liver disease
• ●Idiopathic portal fibrosis
• ●Polycystic liver disease
• ●Infection (eg, brucellosis, syphilis,
echinococcosis)
• ●Right-sided heart failure
CLINICAL MANIFESTATION LIVER CIRRHOSIS

• Early symptoms: Often vague and non-specific, including

fatigue, loss of appetite, nausea, and weight loss.
• Advanced symptoms: Jaundice (yellowing of skin and
eyes), ascites (fluid buildup in the abdomen), spider angiomas
(red spider-like vessels on the skin), and encephalopathy
(confusion and impaired brain function).
SPIDER ANGIOMAS ,GYNECOMASTIA & PALMER
ERYTHEMA
MAY INCLUDE NONSPECIFIC
SYMPTOMS SIGNS AND SYMPTOMS OF HEPATIC
DECOMPENSATION:-
• Anorexia, • Jaundice,
• Pruritus,
• weight loss,
• Signs of upper gastrointestinal bleeding,
• weakness,
• Abdominal distension from ascites,
• fatigue • Confusion due to hepatic encephalopathy (
Ammonia accumulation)
 PHYSICAL EXAMINATION OF LIVER
CIRRHOSIS

• findings may include

jaundice, spider angiomata,
gynecomastia, ascites , splenomegaly,
palmar erythema, digital clubbing, and
asterixis..
 LABORATORY ABNORMALITIES LIVER CIRRHOSIS

• Elevated serum bilirubin,

• Abnormal aminotransferases,
• Elevated alkaline phosphatase/gamma-glutamyl transpeptidase,
• A prolonged prothrombin time/elevated international normalized ratio (INR),
• Hyponatremia,
• Hypoalbuminemia, and
• Thrombocytopenia ( Most common finding of blood test)
 COMPLICATIONS OF LIVER CIRRHOSIS

• Portal hypertension: Increased pressure in the portal vein due to blocked blood
flow in the liver.
• Ascites: Accumulation of fluid in the abdomen due to portal hypertension.
• Esophageal varices: Enlarged veins in the esophagus prone to bleeding
• Hepatic encephalopathy: Impaired brain function due to buildup of toxins in the
blood.
• Liver failure: Complete loss of liver function, a life-threatening condition.
WHEN TO SUSPECT CIRRHOSIS — CIRRHOSIS IS
OFTEN SUSPECTED IN PATIENTS WITH

●Stigmata of chronic liver disease discovered on physical

examination
●Evidence of cirrhosis on laboratory or radiologic testing or by
direct visualization while undergoing a surgical procedure
●Evidence of decompensated cirrhosis, which is characterized by
the presence of dramatic and life-threatening complications,
such as variceal hemorrhage, ascites, spontaneous bacterial
peritonitis, or hepatic encephalopathy
 IMAGING STUDIES FOR LIVER CIRRHOSIS

• Abdominal Ultrasound should be first choice.The findings must be

viewed in light of other signs of cirrhosis, such as physical
examination or laboratory test findings. In addition to evaluating the
liver, abdominal imaging may reveal hepatocellular carcinoma or
extrahepatic findings suggestive of cirrhosis, such as ascites, varices,
splenomegaly, and hepatic or portal vein thrombosis.
• In advanced cirrhosis, the liver may appear small and nodular
 LIVER BIOPSY FOR LIVER CIRRHOSIS

• The gold standard for diagnosing cirrhosis is

examination of an explanted liver, either at autopsy or
following liver transplantation, because the
architecture of the entire liver can be appreciated. In
clinical practice, cirrhosis is diagnosed with a liver
biopsy
PROGNOSIS AND PREVENTION OF LIVER CIRRHOSIS

• Prognosis: Depends on the severity of cirrhosis and timely diagnosis and

treatment. Early intervention can improve the outcome.

• Prevention: Avoiding risk factors like heavy alcohol

consumption, unprotected sex, and exposure to toxins. Early diagnosis and
treatment of contributing conditions like viral hepatitis and fatty liver disease.
LESSON 2

•Acute Liver Failure

 ACUTE LIVER FAILURE

• Definitions –
• Acute liver failure refers to the development of severe acute liver injury with
encephalopathy (altered mental status) and impaired synthetic function (international
normalized ratio [INR] of ≥1.5) in a patient without cirrhosis or preexisting liver disease.

• While the time course that differentiates acute liver failure from chronic liver failure
varies between reports, a commonly used cutoff is an illness duration of <26 weeks.
 TIMING OF ACUTE LIVER FAILURE

• Hyper Acute ------------------------------- < 7days

• Acute………………………………. 7-21 days
• Subacute …………….> 21days but <26 weeks
 ETIOLOGY OF ACUTE LIVER FAILURE

• Acetaminophen (paracetamol)
• •Idiosyncratic drug reactions
• •Viral hepatitis
• •Autoimmune hepatitis
ETIOLOGY OF ACUTE LIVER FAILURE

• Wilson disease
• •Ischemic hepatopathy
• •Budd-Chiari syndrome
• •Veno-occlusive disease
ETIOLOGY OF ACUTE LIVER FAILURE

• Acute fatty liver of pregnancy/HELLP (hemolysis,

elevated liver enzymes, low platelets) syndrome
• •Malignant infiltration
• •Partial hepatectomy
• •Mushroom poisoning
ETIOLOGY OF ACUTE LIVER FAILURE

• •Sepsis
• •Heat stroke
• Viral and drug-induced hepatitis are the
most common causes of acute liver failure
in adults.
 CLINICAL MANIFESTATIONS – ACUTE LIVER
FAILURE

• Clinical manifestations of acute liver failure include hepatic

encephalopathy and an INR ≥1.5 (all of which are required
for the diagnosis), and may include jaundice, hepatomegaly,
right upper quadrant tenderness, elevated liver enzymes,
and thrombocytopenia
DIAGNOSTIC EVALUATION – ACUTE
LIVER FAILURE
• Determining the etiology of acute liver failure requires a combination of history-taking,
laboratory tests, and imaging studies. If the initial evaluation fails to identify an etiology, a
liver biopsy may be required.
• Because patients may decompensate rapidly, the initial evaluation should be broad, even in
patients with a presumed cause for their acute liver failure. A broad evaluation is required to
identify a cause of the acute liver failure and to prepare for possible liver transplantation.
LABORATORY TESTING – ACUTE LIVER FAILURE

should be obtained at presentation include

• Prothrombin time/INR.
• Serum chemistries (sodium, potassium, chloride, bicarbonate,
blood urea nitrogen, creatinine, glucose, calcium,
magnesium, phosphate, lactate dehydrogenase).
 LABORATORY TESTING – ACUTE LIVER
FAILURE

• Liver blood tests (AST, ALT, alkaline phosphatase, GGT,

total and direct bilirubin, albumin).
• -Complete blood count with differential.
• -Acetaminophen level.
• -Blood and urine toxicology screen
including phosphatidyl ethanol testing.
 LABORATORY TESTING – ACUTE LIVER
FAILURE

• Viral hepatitis
• -Serum pregnancy test in females of childbearing potential
who are not already known to be pregnant.
• -Autoimmune markers (antinuclear antibody, anti smooth
muscle antibody, anti-liver/kidney microsomal antibody type
1, anti-liver soluble antigen, immunoglobulin levels).
 LABORATORY TESTING

• -Arterial blood gas.

• -Arterial lactate.
• -Arterial ammonia.
• -Blood type and screen.
• -Serologic testing for HIV.
• -Amylase and lipase.
 ADDITIONAL LABORATORY TESTS THAT ARE INDICATED
IN SPECIFIC CIRCUMSTANCES INCLUDE:

• Ceruloplasmin level or Biopsy if high suspicion for Wilson disease, may

be required.
• -Anti-hepatitis D virus antibodies in patients with acute or chronic
hepatitis B and Anti-hepatitis E virus
• -Urinalysis to look for proteinuria in females who are pregnant.
•IMAGING – LABORATORY TESTING – ACUTE LIVER
FAILURE

• Imaging with abdominal Doppler ultrasonography, CT scanning,

venography, or MRI and magnetic resonance venography (MRV)
should be obtained to look for evidence of Budd-Chiari syndrome.
• Imaging is also used to asses for malignancy
•IMAGING – LABORATORY TESTING – ACUTE LIVER
FAILURE

• However these imaging be used with caution because the

contrast agents used are associated with renal injury.
Additionally, the patient should be hemodynamically stable
prior to obtaining imaging.
 MANAGEMENT OF ACUTE LIVER
FAILURE
General principles of management :-includes
• Ensuring the patient is being cared for in the proper setting,
Patients with acute liver failure should be managed at a liver
transplant center in the intensive care unit (ICU
• Monitoring for worsening liver failure,
• Treating complications, and
• Providing nutritional support
 LABORATORY MONITORING OF ACUTE LIVER
FAILURE

• Serial laboratory tests are used to follow the course of a patient's liver
failure and to monitor for complications.
• Serum aminotransferases and bilirubin should be monitored daily.
• More frequent monitoring (three to four times daily) should be performed
for coagulation parameters, complete blood counts, metabolic panels,
and arterial blood gasses.
• perform finger sticks to monitor blood glucose levels every six hours
MANAGEMENT OF COMPLICATIONS OF ACUTE LIVER
FAILURE

1. Hepatic encephalopathy – Lactulose has not been shown to improve overall

outcomes, and it may lead to bowel distension that could result in technical difficulties
during liver transplantation.
However, if lactulose is used, endotracheal intubation should be performed prior to its
administration in patients with advanced (grade III or IV) encephalopathy.

Continuous renal replacement therapy (CRRT) is also an option for removing ammonia in
addition to managing other metabolic disturbances and fluid balance
MANAGEMENT OF COMPLICATIONS ACUTE LIVER
FAILURE

2. Cerebral edema –

Complications of cerebral edema include ICP elevation and brainstem

herniation.

intracranial pressure (ICP) monitoring to guide treatment for cerebral edema,

rather than basing treatment decisions on the clinical signs of cerebral edema.
However, ICP monitoring has not been shown to increase overall survival and is
associated with complications such as infection and bleeding
 MANAGEMENT OF CEREBRAL EDEMA IN
ACUTE LIVER FAILURE

• Minimizing stimulation,
• Maintaining appropriate fluid balance, and
• Elevating the head of the patient's bed.

• For patients who are at high risk of developing cerebral edema, we also suggest
prophylactic treatment with hypertonic saline
PROGNOSIS – ACUTE LIVER FAILURE

• Approximately 40 percent of patients with

acute liver failure will recover spontaneously
with supportive care.
• For the rest who receive a transplantation, one-
year survival rates are greater than 80 percent
LESSON 3

•Acute pancreatitis
ACUTE PANCREATITIS

• Acute pancreatitis is an inflammatory condition

of the pancreas characterized clinically by
abdominal pain and elevated levels of pancreatic
enzymes in the blood.
 ETIOLOGY –ACUTE PANCREATITIS

• A number of conditions are known to cause acute pancreatitis. Of

these,
(Gallstones and chronic alcohol use disorder )
account for approximately two-thirds of cases.
Gallstones (including microlithiasis) are the most common cause of
acute pancreatitis, however, only 3 to 7 percent of patients with
gallstones develop pancreatitis.
 ADDITIONAL EVALUATION IN PATIENTS WITH ACUTE
PANCREATITIS WITHOUT A CLEAR ETIOLOGY

• In patients with acute pancreatitis at a young

age (<35 years) or a family history of
pancreatitis, genetic testing should be
performed for hereditary pancreatitis.
• endoscopic ultrasonography (EUS)
• (MRCP) following secretin administration.
HISTORY FINDINGS IN ACUTE PANCREATITIS

Prior symptoms of gallstone disease (eg, biliary colic) or documentation of gallstones on

prior imaging.
●Systemic symptoms including unexplained weight loss or new onset of diabetes.
●Amount and pattern of alcohol use. Alcoholic pancreatitis is unlikely to be the underlying
etiology in the absence of a history of over five years of heavy alcohol consumption (>50 g
per day).
 HISTORY FINDINGS IN ACUTE PANCREATITIS

• Medication use
• Prior surgery, endoscopic retrograde cholangiopancreatography
(ERCP), or trauma.
• History of hypertriglyceridemia or hypercalcemia.
• Concomitant autoimmune diseases suggestive of autoimmune
pancreatitis.
• Family history
 CLINICAL FEATURES –ACUTE PANCREATITIS

• The majority have acute onset of severe upper abdominal pain.

• Patients may have associated nausea and vomiting.
• On physical examination, patients have;
• abdominal tenderness to palpation.
• Patients with severe acute pancreatitis may have fever,
tachypnea, tachycardia, hypoxemia, and hypotension.
 LABORATORY FINDINGS –ACUTE PANCREATITIS

• Early in the course, pancreatic enzymes leak out of

acinar cells to the interstitial space and then the systemic
circulation.
• Patients with acute pancreatitis may therefore have acute
elevations in serum amylase and lipase in addition to
other pancreatic enzymes, breakdown products, and
inflammatory mediators.
LABORATORY FINDINGS – ACUTE PANCREATITIS

• Serum lipase has a slightly higher sensitivity for acute

pancreatitis, and elevations occur earlier and last longer
compared with elevations in amylase. Serum lipase is
therefore especially useful in patients who present late to the
clinician. Serum lipase is also more sensitive compared with
amylase in patients with pancreatitis secondary to alcohol
ABDOMINAL CT SCAN FINDINGS –ACUTE
PANCREATITIS

• Approximately 85 percent of patients with acute pancreatitis have acute

interstitial edematous pancreatitis characterized by an enlargement of the
pancreas on contrast-enhanced abdominal computed tomography (CT) scan.

• Approximately 15 percent of patients have necrotizing pancreatitis with

necrosis of the pancreatic parenchyma, the peripancreatic tissue, or both.
DIAGNOSIS –ACUTE PANCREATITIS

• The diagnosis of acute pancreatitis is defined by the presence of two of the following:
1. Acute onset of persistent, severe, epigastric pain often radiating to the back,
2. Elevation in serum lipase or amylase to three times or greater than the upper limit of normal,
3. characteristic findings of acute pancreatitis on imaging (contrast-enhanced computed
tomography, magnetic resonance imaging, or transabdominal ultrasonography)
 DIAGNOSIS –ACUTE PANCREATITIS

In patients with characteristic abdominal pain and

elevation in serum lipase or amylase to three
times or greater than the upper limit of normal,
no imaging is required to establish the diagnosis
of acute pancreatitis.
WHAT IF????????????

• In patients with abdominal pain that is not

characteristic for acute pancreatitis????? or a serum
amylase and/or lipase activity that is less than three
times the upper limit of normal???
A contrast-enhanced abdominal CT scan is needed to
establish the diagnosis of acute pancreatitis and to
exclude other causes of acute abdominal pain.
NATURAL HISTORY AND DISEASE –ACUTE
PANCREATITIS –

• In most patients with acute pancreatitis, the disease is

mild in severity and patients recover in three to five
days without complications or organ failure.
However, 20 percent of patients have moderately severe
or severe acute pancreatitis with local or systemic
complications or organ failure.
HIGHER SCORES INDICATE GREATER ILLNESS
SEVERITY AND WORSE PROGNOSIS
• The APACHE (Acute Physiology and Chronic Health Evaluation)
 MANAGEMENT: ACUTE PANCREATITIS

• can be divided into two broad categories:

Edematous, interstitial acute pancreatitis and Necrotizing acute pancreatitis.
Mild acute pancreatitis is characterized by the absence of organ failure and
local or systemic complications.
Moderately severe acute pancreatitis is characterized by no organ failure or
transient organ failure (<48 hours) and/or local complications.
Severe acute pancreatitis is characterized by persistent organ failure (>48
hours) that may involve one or multiple organs.
1. SUPPORTIVE CARE

• Including:-
• pain control,
• goal-directed intravenous fluids especially during the first 24 hours, and
• correction of electrolyte and metabolic abnormalities.

The majority of patients with mild pancreatitis require no further therapy, and recover
within three to seven days.
Patients with moderately severe and severe pancreatitis require more intensive
monitoring as they have transient (<48 hours) or persistent (>48 hours) organ failure
and local or systemic complications.
2. PAIN CONTROL

• Abdominal pain is often the predominant symptom in patients with acute

pancreatitis.

• Adequate pain control requires the use of intravenous opiates, such

as morphine and fentanyl, usually in the form of a patient-controlled
analgesia pump.
3. NUTRITION – 1

• Mild pancreatitis, recovery generally occurs quickly, making it unnecessary

to initiate supplemental nutrition.
• A soft diet can be started early (within 24 hours) as tolerated if the pain is
decreasing and inflammatory markers are improving.
• We usually start with a low-residue, low-fat, and soft diet, provided there is
no evidence of ileus or significant nausea and/or vomiting.
3. NUTRITION – 2

• severe pancreatitis, we recommend enteral nutrition through a naso-

jejunal tube placed endoscopically or radiologically rather than
initiating parenteral nutrition .

• If the target rate is not achieved within 48 to 72 hours and if severe acute
pancreatitis is not resolved, supplemental parenteral nutrition should be
provided.
●INDICATIONS FOR FOLLOW-UP IMAGING –

• Patients with :
1. Moderately severe or severe acute pancreatitis,
2. signs of sepsis, or
3. clinical deterioration 72 hours after initial presentation,
should undergo a contrast-enhanced CT scan to assess the presence of
pancreatic or extra-pancreatic necrosis and local complications
COMPLICATIONS OF ACUTE PANCREATITIS

1. Acute peripancreatic fluid collection,

2. pancreatic pseudocyst,
3. Acute necrotic collection (ANC), and
4. walled-off necrosis (WON)
 PATIENTS WITH GALLSTONE PANCREATITIS

• In patients with gallstone pancreatitis, we recommend urgent (<24 hours)

endoscopic retrograde cholangiopancreatography and sphincterotomy for patients
with cholangitis .

• Cholecystectomy should be performed after recovery from acute pancreatitis in all

operable patients with gallstone pancreatitis or biliary sludge
 CHRONIC PANCREATITIS

• Is an ongoing process of pathologic response to pancreatic

injury.
• Abdominal pain is the most common clinical symptom.

• As chronic pancreatitis progresses, patients may develop

exocrine pancreatic insufficiency (steatorrhea, maldigestion)
and diabetes.
 COMPLICATIONS OF CHRONIC PANCREATITIS

• Include
1. pancreatic pseudocyst,
2. bile duct or duodenal obstruction,
3. visceral artery pseudoaneurysm,
4. pancreatic ascites and pancreatic pleural effusions,
5. gastric varices due to thrombosis of the splenic vein, and
6. pancreatic malignancy.
 CHRONIC PANCREATITIS MANAGEMENT

• screen patients with chronic pancreatitis for smoking and

alcohol use and encourage vigorous efforts at cessation.
• In addition, patients with chronic pancreatitis are advised to
consume low-fat meals, small meals, and avoid dehydration
 CHRONIC PANCREATITIS MANAGEMENT

• Look for alternative diagnosis at presentation

• Initial evaluation should include a detailed history to assess for the presence of
abdominal pain at baseline, the character of pain, severity, and impact on quality o
life.
• To identify alternative reversible causes of abdominal pain, we perform high-
quality computed tomography (CT) or magnetic resonance imaging (MRI).
CHRONIC PANCREATITIS MANAGEMENT

• The majority of patients with pain due to

chronic pancreatitis require analgesics.
Use a stepwise approach to treatment with the
goal of avoiding high-dose opioids for pain
control.
 CHRONIC PANCREATITIS MANAGEMENT

• Begin with acetaminophen ( Paracetamol) and/or nonsteroidal

anti-inflammatory drugs (NSAIDs) for initial management of
abdominal pain due to chronic pancreatitis.
• In patients with refractory pain due to chronic pancreatitis and an
obstructed, dilated pancreatic duct, we suggest initial endoscopic
drainage rather than surgical therapy