Acute Upper Gastrointestinal Bleed

Welcome to Today’s Episode!

In this episode, we’re diving into Acute Upper GI Bleeding—exploring the common causes, including peptic ulcers, esophageal varices, and portal hypertension. We’ll cover how to assess and stabilize patients, key diagnostic tools, and the latest treatment strategies to manage this life-threatening condition effectively.

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Transcript

Welcome to today’s episode of AudioBoards. In this session, we’re discussing Acute Upper Gastrointestinal Bleeding, a life-threatening condition that can stem from several causes, including peptic ulcers and esophageal varices. Timely diagnosis and intervention are crucial for managing these patients effectively. Let’s dive in.

Patients with Acute Upper GI bleed commonly present with hematemesis or melena. So, what causes these bleeds? The most common causes include peptic ulcers, portal hypertension, and bleeding that usually arises from esophageal varices. Lacerations of the gastroesophageal junction, particularly with a history of heavy alcohol use or retching, can also be a culprit. Vascular anomalies are another common cause, with the most frequent being angioectasias or telangiectasias. Additionally, the Dieulafoy lesion involves an aberrant, large-caliber submucosal artery, most commonly found in the proximal stomach, which causes recurrent, intermittent bleeding.

Other causes include gastric neoplasms, gastric mucosal erosions due to NSAIDs, alcohol, or severe medical or surgical illness (stress-related mucosal disease). Unusual causes of upper GI bleeding include hemobilia—often associated with hepatic tumors, angiomas, or penetrating trauma—and pancreatic malignancy or pseudoaneurysm.

Now, let's discuss how we assess the hemodynamic status of patients with suspected upper GI bleeding. A systolic blood pressure lower than 100 mm Hg identifies a high-risk patient with severe acute bleeding. If the heart rate is over 100 beats per minute with a systolic blood pressure over 100 mm Hg, this suggests moderate acute blood loss. A normal systolic blood pressure and heart rate indicate a relatively minor hemorrhage.

For patients with significant bleeding, it’s crucial to start two 18-gauge or larger intravenous lines before proceeding with diagnostic tests. Blood should be sent for a CBC, prothrombin time with INR, serum creatinine, liver enzymes, and blood typing and screening. In patients showing signs of hemodynamic compromise, 0.9% saline or lactated Ringer's infusion should be administered, and they should be crossmatched for 2 to 4 units of packed RBCs.

To assist with the diagnostic process, erythromycin (250 mg) should be given intravenously 30 minutes before upper endoscopy to promote gastric emptying and potentially improve the quality of the endoscopic evaluation.

For hemodynamically stable patients, RBC transfusion is recommended when the hemoglobin level falls below 7 g per dL, maintaining a hemoglobin level between 7 to 9 g/dL. In the absence of ongoing bleeding, the hemoglobin should rise approximately 1 gm per dL for each unit of transfused packed RBCs. However, in patients with severe GI bleeding, it’s essential to transfuse blood before the hemoglobin level reaches 7 grams per dL. Blood transfusion should not be withheld in patients with massive active bleeding, regardless of the hemoglobin value.

For patients with platelet counts under 50,000 per mcL, platelets should be transfused. If the patient is uremic and actively bleeding, three doses of desmopressin should be administered at 12-hour intervals. If the patient is on anticoagulation therapy, the decision to reverse anticoagulation must carefully weigh the benefits against the risks.

Virtually all patients with upper GI bleeding should undergo upper endoscopy within 24 hours of arriving in the emergency department. This allows for identifying the bleeding source, assessing the risk of rebleeding, and performing endoscopic therapy as needed.

For patients with peptic ulcers and high-risk features, such as active bleeding, a visible vessel, or an adherent clot, intravenous proton pump inhibitors reduce the risk of rebleeding after endoscopic treatment. For lesions at low risk for rebleeding—such as esophagitis, gastritis, clean-based ulcers, or Mallory-Weiss tears—oral PPIs once or twice daily are sufficient.

In cases of persistent bleeding from ulcers, angiomas, or Mallory-Weiss tears that have failed endoscopic therapy, intra-arterial embolization is an option, especially in patients who are poor surgical candidates.

Now let’s talk more about esophageal varices, a major cause of upper gastrointestinal bleeding in patients with underlying liver disease.  Esophageal varices are dilated submucosal veins that form as a result of portal hypertension, which most commonly arises due to cirrhosis. As liver function declines and portal venous pressure increases, blood flow is diverted into smaller veins within the esophagus, causing them to dilate. While many patients may have esophageal varices without any symptoms, the real danger lies in the risk of bleeding, which can become life-threatening.

Several key factors influence the likelihood of variceal bleeding:

1. The size of the varices: Larger varices have a much higher risk of rupture.
2. Red wale markings: These are longitudinal dilated venules on the surface of varices, observed during an endoscopy. Their presence signals an elevated risk of bleeding.
3. The severity of liver disease, assessed by the Child-Pugh score, which evaluates factors like bilirubin, albumin levels, and ascites.
4. Active alcohol use or abuse, which further exacerbates liver damage and increases the risk of bleeding.

So, how do these patients typically present? Upper GI bleeding is the hallmark symptom, often preceded by retching or dyspepsia, which could be linked to alcoholic gastritis or alcohol withdrawal. If the bleeding becomes severe, it can result in hypovolemia or even shock, accompanied by postural hypotension and other signs of circulatory collapse.
When dealing with an upper GI bleed caused by esophageal varices, initial management focuses on rapid stabilization. Intravenous fluids or blood products are essential to restore circulatory volume. But it’s critical to avoid overtransfusion, as that could increase portal venous pressure, thus raising the risk of rebleeding.

One of the challenges in managing variceal bleeding is the coagulopathy that often accompanies advanced liver disease. This includes thrombocytopenia, deficiencies in clotting factors (such as 1, 2, 7, 9, and 10), and a heightened state of fibrinolysis. Interestingly, the INR, which measures clotting, does not provide an accurate reflection of coagulopathy in cirrhotic patients, making its routine use somewhat unreliable. Fresh frozen plasma should not be administered routinely in stable patients with an elevated INR, as it has no proven benefit and may actually increase the risk of complications, including increased portal pressures and deep vein thrombosis.

To control bleeding, octreotide and somatostatin infusions are administered, which reduce portal pressures by decreasing splanchnic blood flow. These medications should be administered immediately upon admission and continued for 3 to 5 days if varices are confirmed by endoscopy or else discontinued.

Terlipressin, another medication, is a synthetic vasopressin analog that helps reduce variceal pressures while preserving renal perfusion. However, it’s important to note that terlipressin is contraindicated in patients with significant cardiovascular or vascular disease.

And when it comes to coagulopathy, if the patient has a prolonged prothrombin time, vitamin K should be considered. In addition, for patients with cirrhosis and signs of encephalopathy, lactulose is administered every 8–12 hours as needed to promote two or three bowel movements daily.

Once the patient’s hemodynamics are stabilized, endoscopy is essential to confirm the diagnosis of varices and to rule out other causes of bleeding, such as Mallory-Weiss tears or peptic ulcer disease. If varices are found, the main therapeutic approach is band ligation—a procedure in which rubber bands are placed around the varices to stop the bleeding. This procedure is typically followed up every 2 to 4 weeks until the varices are either eliminated or reduced to a minimal size. For patients with very low platelet counts—below 50,000 per mcL, avatrombopag, an oral thrombopoietin receptor agonist  should be considered , to help raise platelet levels before endoscopic procedures.

In cases where massive variceal bleeding occurs, a temporary measure such as mechanical tamponade with a specialized nasogastric tube may be used. The Minnesota or Sengstaken-Blakemore tubes, which contain large balloons, can help control hemorrhage temporarily until more definitive therapies, such as TIPS, are available.

TIPS—Transjugular Intrahepatic Portosystemic Shunt—creates a shunt between the portal vein and the hepatic vein, effectively bypassing the liver’s high-pressure system. At centers where TIPS are available, emergency portosystemic shunts are no longer performed as it is associated with a high mortality rate. 

Once the bleeding has been controlled, preventing rebleeding is the next goal. The use of nonselective beta-blockers, such as propranolol or nadolol, in conjunction with variceal band ligation, reduces the risk of recurrent bleeding. TIPS can also be highly effective in preventing rebleeding, but it’s associated with a higher risk of encephalopathy and complications such as stenosis or thrombosis in the stent.

Given these complications, TIPS should be reserved for patients with two or more episodes of variceal bleeding that haven’t responded to other treatments.

Finally, liver transplantation remains the ultimate solution for patients with chronic liver disease and bleeding esophageal varices. Orthotopic liver transplantation should be considered in all such patients, with band ligation or TIPS used to control the bleeding until they are transplanted.

In summary, managing esophageal varices requires a multi-step approach: stabilizing the patient, controlling bleeding, addressing underlying coagulopathy, and preventing rebleeding. Given the complexity of the condition, particularly in patients with advanced liver disease, a multidisciplinary approach is crucial for improving outcomes. 

That’s all for today’s episode. Thanks for listening to AudioBoards. Stay tuned for more educational content in our next episode! The views and opinions expressed on the AudioBoards Podcast do not necessarily reflect those of our employers. This podcast is for educational purposes only and should not be used to diagnose or treat any medical conditions. It is not a substitute for professional medical advice. Always consult a qualified, board-certified healthcare provider for any medical concerns.