Ruptur Varises Esofagus

01Pathophysiology

The root cause of esophageal varices is portal hypertension, which in most clinical scenarios arises from hepatic cirrhosis. Chronic liver injury, whether from alcohol, viral hepatitis, or other insults, leads to progressive fibrosis and architectural distortion of the hepatic parenchyma. This fibrosis increases intrahepatic vascular resistance, which raises pressure within the portal venous system. Normal portal pressure is approximately $5-10mmHg5\{-\}10\backslash \; mmHg$. When the hepatic venous pressure gradient (HVPG) exceeds $10mmHg10\backslash \; mmHg$, varices begin to form. When HVPG reaches $\ge 12mmHg\backslash geq\; 12\backslash \; mmHg$, the risk of variceal hemorrhage becomes clinically significant.

As portal pressure rises, blood seeks alternative low-resistance pathways to return to the systemic circulation. These portosystemic collaterals develop at several anatomical sites, but the most clinically dangerous are the submucosal veins of the distal esophagus and gastric fundus. These veins were never designed to handle high-pressure, high-volume flow. They become progressively dilated, tortuous, and thin-walled. The critical concept here is wall tension: according to the Law of Laplace ($T=P\times rT\; =\; P\; \backslash times\; r$), as the transmural pressure ($PP$) increases and the vessel radius ($rr$) enlarges, wall tension ($TT$) rises dramatically. Once wall tension exceeds the tensile strength of the vessel wall, rupture occurs.

This is why the vignette patient presents with painless, large-volume hematemesis. The bleeding is painless because the esophageal mucosa overlying the varix erodes passively under pressure rather than through an inflammatory or ulcerative process. The volume of hemorrhage can be profound because these collateral channels carry a substantial fraction of portal blood flow, and the bleeding is arterial-equivalent in pressure. Patients rapidly develop signs of hypovolemic shock: tachycardia, hypotension, pallor, and altered mental status.

The connection between pathophysiology and physical exam findings is direct. Spider angiomata reflect hyperestrogenism due to impaired hepatic estrogen metabolism. Ascites results from portal hypertension combined with decreased albumin synthesis and sodium retention via the renin-angiotensin-aldosterone system. Splenomegaly is caused by congestion from portal venous back-pressure. Jaundice reflects the liver's inability to conjugate and excrete bilirubin. All of these signs point back to the cirrhotic liver that caused the portal hypertension in the first place.

02Classification and Clinical Manifestation

Variceal Size Classification

High-Risk Stigmata on Endoscopy

Child-Pugh Classification (Severity of Underlying Cirrhosis)

03Diagnostic Workup

Upper endoscopy is both the best initial diagnostic test and the most accurate confirmatory test. This is a critical point for exam purposes. Unlike many diseases where the screening test and gold standard differ, variceal hemorrhage is a situation where a single procedure serves as both the diagnostic and the therapeutic intervention.

The workup begins at the bedside. When a patient with known or suspected liver disease presents with hematemesis, you should immediately draw a complete blood count to quantify blood loss (keeping in mind that hemoglobin may not yet reflect the full severity of acute hemorrhage due to hemoconcentration), coagulation studies (PT/INR will often be elevated due to impaired hepatic synthesis of clotting factors), and a comprehensive metabolic panel to assess renal function and hepatic markers. A type and crossmatch is ordered early because transfusion is almost always necessary.

The pivotal step is urgent upper endoscopy, which should be performed within 12 hours of presentation, ideally after the patient has been hemodynamically stabilized. Endoscopy will directly visualize the esophageal varices and identify whether they are the source of bleeding. It also distinguishes variceal bleeding from other causes of upper GI hemorrhage (peptic ulcer, Mallory-Weiss tear, gastric malignancy). Once varices are identified as the source, endoscopic band ligation is performed during the same procedure, making it simultaneously diagnostic and therapeutic.

An important nuance: do not delay endoscopy for "perfect" resuscitation. Prolonged aggressive fluid resuscitation can paradoxically worsen portal hypertension and rebleeding. The goal is hemodynamic stability sufficient for safe sedation, not normalization of all parameters.

04Management and Treatment

Step 1: Acute Resuscitation. The immediate priority is hemodynamic stabilization. Establish two large-bore IV lines (16-gauge or larger). Begin volume resuscitation with isotonic crystalloid. Transfuse packed red blood cells using a restrictive transfusion strategy with a target hemoglobin of $7-8g\mathrm{/}dL7\{-\}8\backslash \; g/dL$. This threshold is deliberately conservative because over-transfusion increases portal pressure and raises the risk of rebleeding. This is one of the most commonly tested concepts. Fresh frozen plasma and platelets should be given for clinically significant coagulopathy, but routine correction of INR in a cirrhotic patient is not standard practice because the INR does not accurately reflect bleeding risk in cirrhosis.

Step 2: Pharmacologic Therapy (Start Before Endoscopy). Begin octreotide as soon as variceal hemorrhage is suspected, even before endoscopy. Octreotide causes splanchnic vasoconstriction, reducing portal blood flow and portal pressure. The dose is a 50 mcg IV bolus followed by a 50 mcg/hr continuous infusion for 3 to 5 days. Where available, terlipressin (a vasopressin analogue) is an alternative, dosed at 2 mg IV every 4 hours initially, then reduced to 1 mg IV every 4 hours after bleeding is controlled, continued for up to 5 days.

Step 3: Prophylactic Antibiotics. This is a frequently tested and commonly missed step. Patients with cirrhosis who present with upper GI bleeding have a very high rate of bacterial infections (spontaneous bacterial peritonitis, urinary tract infections, pneumonia), and these infections worsen outcomes. Ceftriaxone 1 g IV once daily for 7 days is the recommended regimen. Antibiotic prophylaxis has been shown to reduce mortality, not just infection rates. An alternative in patients without advanced liver disease is oral norfloxacin 400 mg twice daily.

Step 4: Urgent Endoscopy with Band Ligation. Perform upper endoscopy within 12 hours. Administer IV erythromycin (250 mg) approximately 30-120 minutes before endoscopy as a prokinetic to clear blood from the stomach and improve visualization. Endoscopic band ligation (EBL) is the procedure of choice. Bands are placed on the varices starting at the gastroesophageal junction and working proximally. EBL is preferred over endoscopic sclerotherapy because it has fewer complications (fewer strictures, fewer ulcerations, lower rebleeding rates).

Step 5: Rescue Therapy for Refractory Bleeding. If bleeding persists despite two sessions of endoscopic therapy plus vasoactive drugs, the next step is TIPS (transjugular intrahepatic portosystemic shunt). TIPS creates a shunt between the portal vein and the hepatic vein within the liver parenchyma, directly lowering portal pressure. The primary complication of TIPS is hepatic encephalopathy, because portal blood now bypasses the liver. Balloon tamponade with a Sengstaken-Blakemore tube or Minnesota tube is used only as a temporary bridge (less than 24 hours) to TIPS or repeat endoscopy, due to the risk of esophageal rupture and aspiration.

Step 6: Long-Term Secondary Prophylaxis. After the acute episode resolves, patients require combination therapy to prevent rebleeding: a non-selective beta-blocker (nadolol or propranolol, titrated to a resting heart rate of $55-60bpm55\{-\}60\backslash \; bpm$) combined with serial endoscopic band ligation sessions every 2 to 4 weeks until the varices are obliterated. Non-selective beta-blockers work by reducing cardiac output (beta-1 blockade) and causing splanchnic vasoconstriction (beta-2 blockade), both of which lower portal pressure. Carvedilol is an emerging option with additional alpha-1 blocking properties that further reduce portal resistance.

Contraindications to note: Non-selective beta-blockers are contraindicated in patients with refractory ascites, spontaneous bacterial peritonitis, or a systolic blood pressure below 90 mmHg, as they can worsen hemodynamics in these decompensated patients.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common trap with variceal hemorrhage questions is forgetting the antibiotics. Students correctly identify the need for resuscitation, octreotide, and urgent endoscopy, but omit prophylactic ceftriaxone. On the exam, when the question asks for the "next best step" in a patient who has already been started on octreotide and is awaiting endoscopy, the answer is often the antibiotic, not another intervention.

A second frequent error is over-transfusion. A vignette may describe a hemoglobin of 6 g/dL and offer answer choices that include "transfuse to hemoglobin of 10 g/dL." This is a deliberate distractor. The correct target is $7-8g\mathrm{/}dL7\{-\}8\backslash \; g/dL$. Transfusing beyond this threshold raises portal venous pressure and increases the likelihood of rebleeding. This restrictive strategy is counterintuitive for students trained to "correct the number," and test-writers exploit that instinct.

A third pitfall involves confusing primary versus secondary prophylaxis. A patient with known cirrhosis who has varices on screening endoscopy but has never bled is managed with either a non-selective beta-blocker or band ligation (not both). A patient who has already had a variceal bleed requires both a non-selective beta-blocker and serial band ligation. Mixing up these regimens is a common source of wrong answers.

Watch for vignettes that present a patient with portal hypertension and upper GI bleeding but try to trick you into selecting a peptic ulcer diagnosis. The giveaway for varices is the constellation of painless hematemesis combined with physical exam findings of chronic liver disease (ascites, splenomegaly, spider angiomata, jaundice). If the stem mentions epigastric pain, NSAID use, or H. pylori, it is steering you toward peptic ulcer disease instead.

Finally, remember the sequencing of interventions. Pharmacotherapy (octreotide) and antibiotics are started before endoscopy. Band ligation is preferred over sclerotherapy. TIPS is used only after endoscopic therapy has failed. Balloon tamponade is a bridge, not a definitive treatment. The exam tests whether you understand this hierarchy, not just whether you can name the correct treatments.