Understanding Variceal Bleed​

Understanding Variceal Bleed

Varices are abnormal, dilated blood vessels that develop within the gastrointestinal tract due to increased pressure in the portal venous system, a condition known as portal hypertension. This elevated pressure arises from resistance to blood flow in the liver and an augmented splanchnic blood flow. As a consequence, the body forms collateral pathways, or shunts, to alleviate this pressure. These shunts, known as spontaneous portosystemic shunts (SPSS), divert blood from the portal vein to the systemic circulation. However, while these shunts serve to lower portal pressure, they can also lead to bypassing the liver’s natural filtration processes.

Variceal bleeding is a serious complication of portal hypertension. It occurs when these engorged vessels rupture, resulting in potentially life-threatening hemorrhage. Various types of varices exist, including esophageal, gastric, rectal, and paraumbilical varices, each with distinct anatomical characteristics. Understanding the anatomy and behavior of these varices is crucial for effective diagnosis and management, especially in cases where intervention is necessary to prevent or address variceal bleeding.

Variceal Anatomy:

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Variceal Type	Afferent Part	Central Part (True submucosal intragastric varices + False extra gastric varices)	Efferent Part	Other Considerations
Esophageal	Left gastric vein (aka coronary vein), posterior gastric vein	Submucosal layer of lower esophagus	Azygos and hemiazygos veins, superior vena cava	1. Main target for TIPS procedures (due to their proximity - as they are supplied predominantly by left gastric vein) 2. Ascending type - arise due to portal hypertension from portal circulation 3. Descending type - associated with tumor of thyroid and mediastinum, SVC syndrome
Gastric	Short gastric veins, left gastric vein, posterior gastric vein, gastroepiploic veins	Various locations in the stomach	Splenic vein (may connect with systemic veins)	1. Gastric varices bleeding sustained by a gastrorenal shunt. 2. Refractory HE associated with SPSS. 3. May require additional interventions such as gastric variceal embolization, BRTO, or BATO in conjunction with TIPS.
Rectal	Superior rectal vein (branch of inferior mesenteric vein)	Submucosal layer of rectal wall	Middle and inferior rectal veins (systemic circulation)	1. Ectopic Varices: Varices outside the gastroesophageal region, e.g., duodenal, rectal varices. 2. Varices located in atypical locations (e.g., duodenum, jejunum) may require specialized case based approaches.
Paraumbilical	Paraumbilical veins	Around the umbilicus (network of collateral vessels)	Portal venous system
Splenic Vein Thrombosis (Not varices, but relevant)	Drains blood from the spleen	Along superior border of pancreas, posterior to pancreas	Collateral vessels in cases of thrombosis

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Sarin's Classification of Gastric Varices (GV):

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Classification	Description
GOV1 (Gastro Oesophageal Varices Type 1) Most common type ~ 74% of the patients	Extend along lesser curvature of the stomach and reach up to the cardia
GOV2 (Gastro Oesophageal Varices Type 2)	Extends ahead of the cardia and leads towards the greater curvature of the abdomen and to the gastric fundus.
IGV1 (Isolated Gastric Varices Type 1)	Located in fundus of stomach, separate from esophageal varices
IGV2 (Isolated Gastric Varices Type 2)	Ectopic varices that occur in other parts of the stomach, without connection to esophageal varices

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Theories Related to Gastric Varices:

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Theory	Description
Hemodynamic Theory	1. Gastric varices develop due to increased portal pressure. This theory suggests that the dilation of gastric veins occurs as a compensatory mechanism to divert blood flow away from the high-pressure portal system. 2. The left gastric vein and short gastric veins are important contributors to the development of gastric varices.
Sinistral Portal Hypertension	1. This theory proposes that isolated gastric varices (IGV) can develop due to splenic vein thrombosis or obstruction. 2. This leads to increased pressure in the short gastric veins and posterior gastric veins, resulting in the formation of IGV. 3. It is associated with conditions like pancreatitis or pancreatic malignancies.
Recanalization of Obstructed Veins	According to this theory, gastric varices may develop as a result of recanalization of previously obstructed veins, such as the left gastric vein. This can occur after interventions like sclerotherapy or banding of esophageal varices. The recanalized veins can contribute to the development of gastric varices.
Growth of Pre-existing Submucosal Veins	It is suggested that pre-existing submucosal veins in the stomach may undergo hypertrophy and dilation in response to increased portal pressure. This theory emphasizes the role of anatomical variations and pre-existing vascular structures in the development of gastric varices.
Combined Mechanism	This theory proposes that gastric varices may develop as a result of a combination of factors, including increased portal pressure, altered blood flow dynamics, and anatomical variations in the gastric vasculature. It suggests that multiple mechanisms may contribute to the development and progression of gastric varices.

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Classification of Spontaneous Porto-Systemic Shunts (SPSS):

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SPSS Type	Frequency	Variceal Bleeding	Hepatic Encephalopathy (can be associated with Cirrhosis-Related Parkinsonism)	Portal vein Thrombosis (Occur in large shunts)	Laterality and venous component
Gastrorenal shunt	80%-85% of patients with gastric varices	+	+	+	Left (Short gastric vein and Posterior gastric vein)
Gastrocaval shunt	Less frequent than gastrorenal shunt	+	-	-	Left (Short gastric vein and Posterior gastric vein)
Splenorenal shunt	14%-21% of patients with cirrhosis	-	+	+	Left (Short gastric vein and Posterior gastric vein)
Mesorenal shunt	Uncommon	-	+	-	Central
Paraumbilical shunt	6%-30% of patients with portal hypertension	-	+	+	Right (Left gastric vein)
Rectal varices	Rare	+ (Lower gastro-intestinal bleeding)	-	-	Right (Left gastric vein)
Esophageal varices	40%-80% of patients with cirrhosis	+ (Hematemesis or melena)	-	-	Right (Left gastric vein)

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Key Considerations for Intervention in variceal bleed:

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Aspect	Information
Red Signs in EV	- Red wale marks, hematocystic spots, cherry-red spots indicate high-risk for bleeding.
Size of GV	- Larger GV are more likely to bleed.
Portal Hypertension Severity	- Degree of portal hypertension influences intervention decisions. - TIPS not effective in gastric varices with low portosystemic gradient of < 12 mmHg
Previous Bleeding Episodes	- History of bleeding increases the likelihood of future bleeding and may warrant intervention.
Underlying Liver Disease	- Severity of liver disease and presence of cirrhosis influence the approach to treatment.
Patient's Overall Health Status	- Consider comorbidities, performance status, and life expectancy when deciding on intervention.

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Management of Gastric Varices:

Clinical Presentation	Initial Management	TIPSS Consideration	High Risk Patients
Acute VH	Endoscopic Therapy (Band Ligation, Sclerotherapy)	Consider	1. CTP > 13, Rescue TIPSS futile 2. CTP C with baseline S. Creat ≥ 1 mg/dl (Child C-C1 criteria) 3. HVPG > 20 mmHg 4. MELD score ≥ 19
Recurrent VH	Endoscopic Band ligation and Non-selective beta-blockers	For non-responders
High-Risk VH (Active Bleeding)	Early TIPS Placement (Within 72 Hours)	First-line Option	1. Child B with active bleed

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Treatment Option	Description
Initial Management of Variceal Hemorrhage	1. Resuscitation - Focus on circulatory and respiratory status - Early esophagogastroduodenoscopy (EGD) within 12-24 hours 2. Transfusion Strategy - Restrictive packed red blood cell transfusion - Maintain Hb level of 7-9 g/dL 3. Platelets Transfusion - Target platelet count > 50 x 10^9/L 4. Cryoprecipitate Transfusion - Target fibrinogen level 100-120 mg/dL 5. Coagulopathy Correction - PT and INR not reliable indicators - Avoid fresh frozen plasma 6. Antibiotic Prophylaxis - Ceftriaxone 1g IV daily for 7 days 7. Alternative Antibiotic (if discharged early) - Ciprofloxacin 500mg orally twice daily for 7 days
Primary Prophylaxis of Gastric Varices	β-Blocker: Starting Dose and Maximum Dose 1. Nadolol: 20-40 mg daily and - 160 mg/day (patients without ascites), - 80 mg/day (patients with ascites) 2. Propranolol: 20-40 mg twice daily and - 320 mg/day (patients without ascites), - 160 mg/day (patients with ascites) 3. Carvedilol: 3.125 mg twice daily and - 6.25 mg twice daily
Vasoactive Agents Used in Acute Variceal Hemorrhage	1. Octreotide: - 50 µg IV bolus, followed by 50 µg/hour IV infusion - A second 50 µg IV bolus may be given after 1 hour if bleeding is ongoing 2. Somatostatin: - 250 µg IV bolus, followed by 250-500 µg/hour IV infusion - A second 250 µg IV bolus may be given after 1 hour if bleeding is ongoing 3. Terlipressin: - 2 mg IV every 4 hours for 48 hours or until bleeding cessation, followed by 1 mg IV every 4 hours
Endoscopic Variceal Ligation (EVL)	Effective for primary prophylaxis of bleeding in GOV1, as well as treatment of bleeding GV
Endoscopic Cyanoacrylate Injection (ECI)	Effective for treating bleeding from both GOV1 and GOV2
Balloon-Occluded Retrograde Transvenous Obliteration (BRTO)	1. Considered for Posterior and Short gastric vein predominant varices. 2. Effective for treatment of bleeding GOV1 and IGV1
Transjugular Intrahepatic Portosystemic Shunt (TIPS)	1. Considered for Left gastric vein predominant varices. 2. Considered in refractory cases, especially when other treatments fail
Plug Assisted Retrograde Transvenous Obliteration (PARTO)	Alternative to BRTO; uses a vascular plug instead of a balloon catheter.
Coil Assisted Retrograde Transvenous Obliteration (CARTO)	Alternative to BRTO; uses large-sized coils instead of a plug.

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References