Varices

Question 1

45-year-old man admitted to SAU with history of hematemesis. O/E Jaundice and ascites PMH: ETOH abuse After a 2 nd episode of hematemesis he becomes

confused. ↓BP, ↑ HR (shock)

Differentials?
What are your concerns regarding this patient

Management

Answer 1

• Bleeding esophageal varices due to portal HTN caused by cirrhotic liver
• Mallory-Weiss tear
• Boerhaave’s syndrome
• Bleeding peptic ulcer

1.Another attack of haematemsis.
2.Heamodynamically unstable and might require blood transfusion.
3.Risk of shock and AKI
4.Higher risk of bleeding from somewhere else due to chronic liver disease and disturbed coagulation.
5.Concerned about aspiration pneumonia and will need prophylactic antibiotic.

Decompensated liver disease related:
1.Hepatic encephalopathy.
2.Hepatorenal syndrome.
3.SBP

My first priority is resuscitation:

Give high-flow oxygen.
Establish two large-bore IV lines.
Send blood urgently for cross-matching, coagulation profile (PT, INR), platelet count, and baseline investigations.
Begin fluid resuscitation and transfuse 2–4 units of fresh whole blood as required, in consultation with hematology.
If coagulopathy is present, give FFP and platelets.
Monitor closely: pulse, BP, hourly urine output, and CVP if available.

Next, I would start pharmacological therapy to reduce portal hypertension: vasopressin or octreotide infusion.

Definitive control is by urgent endoscopy:

Endoscopic band ligation (not more than 6 bands per session) is the preferred option.
If not possible, sclerotherapy may be performed.

If bleeding remains uncontrolled despite endoscopy, I would consider balloon tamponade with a Minnesota tube as a temporary salvage measure.

At the same time, I would take measures to prevent hepatic encephalopathy by maintaining fluid/electrolyte balance, giving lactulose, and avoiding protein overload.”

Question 2

Cause of thrombocytopenia in this case?

What are the indications for platelet transfusion?

Blood findings in alcoholic patients? Features of FBC to suggest ETOH abuse?

Sites of portosystemic shunt

Answer 2

• Hypersplenism • DIC • Hemodilution • Chronic low platelet production

Ongoing coagulopathy with continued bleeding
or as a part of massive blood transfusion protocol.

•	Platelet dysfunction (e.g., antiplatelet drugs, congenital disorders) with bleeding
•	Massive transfusion protocol – to maintain platelets > 50 ×10⁹/L
•	Disseminated intravascular coagulation (DIC) with active bleeding

• Low platelets due to toxic effect on bone marrow, impaired hematopoiesis (also affecting RBCs and WBCs)
• Raised mean corpuscular volume (MCV), anemia (megaloblastic and hemolytic)
• Elevated liver enzymes (serum GGT, AST, ALT and ferritin)

1. Lower end of oesophagus — between oesophageal branches of the left gastric vein (portal) and azygos vein (systemic).
   
   2. Upper part of anal canal — between superior rectal vein (portal) and middle and inferior rectal veins (systemic).
   3. Umbilicus — between veins of ligamentum teres (portal) and superior and inferior epigastric veins (systemic).
   4. Bare area of liver — between hepatic/portal veins (portal) and inferior phrenic veins (systemic).
   5. Retroperitoneal region — between colic veins (portal) and body wall veins (systemic).
   6. (Rare) — Patent ductus venosus connecting left branch of portal vein and IVC.

Question 3

Which varices are usually bleeding?

Pathogenesis of portal HTN in chronic alcoholism:

Surgical treatment options / Therapeutic maneuvers to reduce portal venous pressure apart from drugs?

Answer 3

Varices in the submucosa of the lower esophagus are the common source of major bleeding

• Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular regeneration. The fibrosis obstructs portal venous return and portal hypertension develops.
• Arteriovenous shunts within the liver also contribute to the hypertension.

• Portosystemic shunts (splenorenal shunts - TIPSS: a metal stent is inserted via the transjugular route using a guidewire passed through the hepatic vein to the intrahepatic branches of the portal vein.)

• Stapled esophageal transection: The gastric vein and short gastric veins are ligated, and the distal esophagus is transected and re-anastomose just above the cardia using a stapling gun

• Orthotopic liver transplantation (OLT) - Treatment of choice in patients with advanced liver disease

Question 4

How alcohol causes cirrhosis?

What are the hepatic changes as a consequence of excessive alcohol consumption?

How is alcohol metabolized by the liver?

Mechanism of ascites?

Cause of confusion in this patient

Patient with macrocytic anemia, what could be the cause?

How vitamin B12 deficiency causes macrocytic anemia

If the patient is to go for liver transplant, what will you tell his family?

Answer 4

• Changes in lipid metabolism
• Decreased export of lipoproteins
• Cell injury caused by reactive oxygen species and cytokines

• Fatty change
• Alcoholic hepatitis with liver cell damage
• Cirrhosis
• Hepatocellular carcinoma

Alcohol is metabolized in the liver mainly by three pathways.
The major one is alcohol dehydrogenase in the cytosol, which converts ethanol to acetaldehyde.
Secondly, the microsomal ethanol oxidizing system (CYP2E1 in the smooth ER) is induced in chronic alcohol use.
Thirdly, a minor pathway is catalase in peroxisomes.
All produce acetaldehyde, which is then converted by aldehyde dehydrogenase in mitochondria to acetic acid.”

• Increased formation of hepatic and splanchnic lymph
• Hypoalbuminemia
• Retention of salt and water due to increased aldosterone and antidiuretic hormone levels

Hepatic encephalopathy

Nutrition deficiency (vitamin B12 deficiency) with chronic alcoholism

Vitamin B12 is important in DNA synthesis. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis

• Counseling regarding patient condition, proposed treatment options, outcome of treatment,

• Lifestyle modifications, abstinence from alcohol 6 months later

• ABO matching

• Immunosuppression

Question 5

Sengstaken Blakemore tube?

Ports?

Modification

If there is no modification?

Indications for Sengstaken tube placement?

Technique?

Answer 5

Double balloon tamponade

• Port for gastric ballon
• Port for esophageal ballon
• Port for gastric suction

:

Esophageal suction port to help suction of esophageal contents (Minnesota tube) Sengstaken-Blakemore tube (3 lumen) replaced by Minnesota tube (4 lumen) as allows aspiration of both gastric and esophageal contents, not just gastric contents

Insert NG tube

Acute life-threatening bleeding from esophageal or gastric varices…
• that does not respond to medical therapy (including endoscopic hemostasis and vasoconstrictor therapy)
• when endoscopic hemostasis and vasoconstrictor therapy are unavailable

• Position the patient and elevate the head of the bed to 45
• Anesthetize the posterior pharynx and nostrils with topical anesthetic
• Coat the balloons with lubricating jelly
• Pass the tube from the nostrils to at least 50 cm mark
• Suction from the gastric and esophageal ports
• When the gastric ballon is correctly positioned in the stomach, inflate the ballon with 500 ml of air and clamp, the port, pull the tube back until resistance is felt against diaphragm
• Inflate the esophageal ballon by the sphygmomanometer to 30-45 mmHg and clamp the port
• When bleeding is controlled, reduce the esophageal ballon by 5 mmHg every 3 hours until 25mmHg is reached without bleeding then keep the tube for 12-24 hours
• Deflate the esophageal ballon for 5 min/6 hours to prevent esophageal necrosis

Question 6

What is massive transfusion protocol

Answer 6

Massive transfusion is defined as replacement of one blood volume within 24 hours, or >10 units of packed red cells in 24 hours, or >4 units in 1 hour with ongoing bleeding.