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Surgery > Cirrhosis & Portal HTN > Flashcards

Cirrhosis & Portal HTN Flashcards

1
Q

Cirrhosis definition

A

Many definitions but common one is injury, repair, regeneration and scarring

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2
Q

Primary histological feature

A
  1. Marked fibrosis
  2. Destruction of vascular & biliary system
  3. Regeneration
  4. Nodule formation
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3
Q

causes of cirrhosis

A

Viral hepatitis: the commonest
Alcohol
Biliary obstruction
Veno-occlusive disease
Hemochromatosis
Wilson’s disease
Autoimmune
Drugs and toxins
Metabolic disease
Idiopathic

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4
Q

Classification of Cirrhosis

A

WHO divided cirrhosis into 3 categories based on morphological character
1. Micro nodular
2. Macro nodular
3. Mixed

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5
Q

Cirrhosis alcohol also know as

A

Laennec’s cirrhosis

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6
Q

NAFLD / NASH cause of cirrhosis is associated with ?

A

Obesity, Hyperlipidemia, NIDDM

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7
Q

Diagnosis? ‘

A
  • can be asymptomatic for decades
  • Hx and Physical examination
    Physical findings;
    ( Hepatomegaly, jaundice, ascites, spider
    angioma, splenomegaly, palmar erythema,
    fetor hepaticus, purpura etc.)
  • Elevated LFTs, thrombocytopenia.
  • Definitive diagnosis is by biopsy or gross
    inspection of liver.
  • Noninvasive methods include US, CT scan,
    MRI.
  • Indirect evidence - esophageal varices
    seen during endoscopy.
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8
Q

Definitive diagnosis of cirrhosis

A

Biopsy or gross inspection of liver

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9
Q

Manifestations of Cirrhosis

A

Hepatorenal syndrome
Hepatic encephalopathy
Portal hypertension
Water retention
Hematologic
Hepatocellular carcinoma

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10
Q

Patho physiology of PH

A
  • Cirrhosis results in scarring (perisinusoidal
    deposition of collagen)
  • Scarring narrows and compresses hepatic
    sinusoids (fibrosis)
  • Progressive increase in resistance to portal
    venous blood flow results in PH.
  • Portal vein thrombosis, or hepatic
    venous obstruction also cause PH by
    increasing the resistance to portal
    blood flow
  • As pressure increases, blood flow decreases
    and the pressure in the portal system is
    transmitted to its branches
  • Results in dilation of venous tributaries
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11
Q

Portal Vein Collaterals

A
  • Coronary vein and short gastric veins -> veins
    of the lesser curve of the stomach and the
    esophagus, leading to the formation of varices.
  • Inferior mesenteric vein -> rectal branches which, when distended, form hemorrhoids.
  • Umbilical vein ->epigastric venous system
    around the umbilicus (caput medusae)
  • Retroperitoneal collaterals ->gastrointestinal
    veins through the bare areas of the liver
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12
Q

Etiology of PH

A

Causes of PH can be divided into
1.Pre-hepatic
2. Intra-hepatic
3. Post-hepatic

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13
Q

Pre-hepatic PH

A

Caused by obstruction to blood flow at
the level of portal vein
Examples
- congenital atresia, extrinsic compression,
schistosomiasis, portal, superior mesenteric,
or splenic vein thrombosis

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14
Q

Post-hepatic PH

A

Caused by obstruction to blood flow at
the level of hepatic vein

Examples
- Budd-Chiari syndrome, chronic heart failure,
constrictive pericarditis, vena cava webs

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15
Q

Budd-Chiari Syndrome

A
  • Caused by hepatic venous obstruction.
  • At the level of the inferior vena cava, the
    hepatic veins, or the central veins within the
    liver itself
  • result of congenital webs (in Africa and Asia),
    acute or chronic thrombosis (in the West), and
    malignancy.
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16
Q

Acute symptoms of Budd-Chiari Syndrome

A

Acute symptoms include
- hepatomegaly, RUQ abdominal pain, nausea,
vomiting, ascites

Chronic form present with the sequelae
of cirrhosis and portal hypertension,
including
- variceal bleeding, ascites, spontaneous bacterial
peritonitis, fatigue, and encephalopathy

17
Q

Diagnosis of Budd-Chiari Syndrome

A
  • Diagnosis is most often made by US
    evaluation of the liver and its
    vasculature.
  • Cross-sectional imaging using contrast-
    enhanced CT or MRI.
18
Q

Gold standard diagnosis of Budd-Chiari Syndrome

A

Gold standard for the diagnosis has been
angiography

19
Q

Management has traditionally Budd-Chiari Syndrome

A

Management has traditionally been surgical
intervention (surgical decompression with a
side-to-side portosystemic shunt)

20
Q

First line therapy Budd-Chiari Syndrome

A

Minimally invasive treatment using TIPS may be first-line therapy now

21
Q

Portal Vein Thrombosis

A
  • Most common cause in children (fewer than
    10% of adult pts.)
  • Normal liver function and not as susceptible
    to the development of complications, such
    as encephalopathy.
22
Q

Diagnosis Portal Vein Thrombosis

A

Diagnosis by sonography, CT and MRI

23
Q

Initial manifestations of portal vein thrombosis

A

variceal bleeding in a noncirrhotic patient
with normal liver function

24
Q

Portal Vein Thrombosis - Causes

A
  • Umbilical vein infection (the most common cause
    in children).
  • Coagulopathies (protein C and antithrombin III
    deficiency).
  • Hepatic malignancy, myeloproliferative disorders.
  • Inflammatory bowel disease.
  • pancreatitis.
  • trauma.
  • Most cases in adults are idiopathic.
25
Q

Portal Vein Thrombosis - Therapeutic options

A
  • Therapeutic options are esophageal variceal ligation and sclerotherapy.
  • Distal splenorenal shunt.
  • Rex shunt in patients whose intrahepatic
    portal vein is patent (most commonly
    children).
26
Q

Splenic Vein Thrombosis - cause

A

Most often caused by disorders of the
pancreas
- acute and chronic pancreatitis, trauma, pancreatic
malignancy, and pseudocysts

Related to the location of the splenic vein

27
Q

The common variceal in Splenic Vein Thrombosis + management

A
  • Gastric varices are present in 80% of patients
  • Occurs in the setting of normal liver function
  • Readily cured with splenectomy (variceal
    hemorrhage), although observation for
    asymptomatic patients is acceptable.
28
Q

Complications of PH

A
  • GI bleeding due to gastric and
    - esophageal varices
  • Ascites
  • Hepatic encephalopathy
29
Q

Varices - Most life threatening complication is

A
  • bleeding from esophageal varices
  • Distal 5 cm of esophagus
  • Usually the portal vein-hepatic vein
    pressure gradient >12 mm Hg
  • Bleeding occurs in 25-35% of pts. With
    varices and risk is highest in 1st yr
30
Q

Prevention of Varices

A
  • Primary prophylaxis: prevent 1st
    episode of bleeding.
  • Secondary prophylaxis: prevent recurrent episodes of bleeding
    Include control of underlying cause of
    cirrhosis and pharmacological and surgical
    interventions to lower portal pressure.

Beta blockade: Beta blockade (Nadolol,
Propranolol)

Nitrates:Organic nitrates

Endoscopy: Sclerotherapy (no longer used) and
variceal ligation

Surgery: No longer performed

31
Q

Treatment of Varices

A

Initial Management:

Airway control
2. Hemodynamic monitoring
3. Placement of large bore IV lines
4. Full lab investigation (Hct, Coags, LFTs,)
5. Administration of blood products
6. ICU monitoring

Pharmacologic Treatment of Varices

Endoscopic Therapy for Varices

Balloon Tamponade

TIPS

Surgical Intervention

Surgical Shunts

32
Q

Pharmacologic Treatment of Varices

A
  • Decreases the rate of bleeding.
  • Enhances the endoscopic ability to visualize
    the site of bleeding.
  • Vasopressin - potent splanchnic
    vasoconstrictor; decreases portal venous
    blood flow and pressure.
  • Somatostatin: decrease splanchnic
    blood flow indirectly; fewer side
    effects.
  • Octreotide: Initial drug of choice for
    acute variceal bleeding.
33
Q

Endoscopic Therapy for Varices

A
  • Endoscopic Sclerotherapy: complications
    occur in 10-30% and include fever,
    retrosternal chest pain, dysphagia,
    perforation.
  • Endoscopic variceal ligation: becoming the initial intervention of
    choice; success rates range from 80-100%
34
Q

Balloon Tamponade

A
  • Sengstaken-Blakemore tube
  • Minnesota tube
  • Alternative therapy for pts. who fail
    pharmacologic or endoscopic therapy
35
Q

TIPS

A

Transjugular inrahepatic portasystemic shunt

1st line treatment for bleeding esophageal
varices when earlier-mentioned methods fail

Success rates 90-100%

Significant complication is hepatic
encephalopathy

36
Q

Surgical Intervention

A
  • Liver transplantation
    only definitive procedure for PH caused by cirrhosis
  • Shunts
  • Totally diverting (end-side portacaval)
  • Partially diverting (side-side portacaval)
  • Selective (distal splenorenal shunt

Devascularization

37
Q

 Surgical Shunts - Non Selective Shunts

A

1) End-to-side Portocaval Shunt.
2)-Side-to-side Portocaval Shunt.
3)-Large diameter Interposition Shunt (e.g.
Mesocaval Shunt).
4)-Central Splenorenal Shunt.

38
Q

Surgical Shunts - Selective Shunts

A

1)-Distal Splenorenal Shunt ( Warren
Shunt)

2)-Small diameter Portocaval H-graft
Shunt.

39
Q

Portosystemic Shunt:

A

Whipple introduced portocaval shunt in
1945 —- Reduce the variceal bleeding
& ascites

In non selective PS-shunt, post shunt
encephalopathy is common

Encephalopathy is higher
if (1)-Pt. Age >50Y
2)-Poor liver function(G-C)
3)-Previous history of encephalopathy

Surgery (14 decks)

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