Upper GI Bleed

An UGIB is bleeding in the gastrointestinal tract proximal to the ligament of Treitz and manifests principally as

• Hemetemesis
• Melena
• Hematochezia

There are several pitfalls which may lead to misdiagnosis of melena or hematochezia.

Red food coloring, fruit-flavored drinks, fruit juices, and beets may color the vomitus or stool red.

Stools may also be black after ingestion of iron, grape juice, spinach, and blueberry.

When in doubt and in a non emergency situation – send off for a stool sample for occult blood. 

Causes can be subdivided by age group:

Neonate

            Common

• Swallowed maternal blood
• Milk protein sensitivity
• Trauma (nasogastric tube in NICU)

            Uncommon

• Stress gastritis or ulcer
• Esophagitis
• Coagulopathy associated with infection
• Congenital coagulation factor deficiency
• Vascular malformation
• Hemorrhagic disease of newborn

Infant

            Common

• Mallory-Weiss tear
• Esophagitis

            Uncommon

• Stress gastritis or ulcer
• Acid peptic disease
• Vascular malformation
• GI duplication
• Gastric/esophageal varices
• Bowel obstruction

Child-adolescent

         Common

• Esophagitis
• Esophageal varices
• Mallory-Weiss tear
• Acid-peptic disease
• Gastritis, especially H. pylori gastritis
• Caustic ingestion

           Uncommon

• Vasculitis
• Bowel obstruction
• Crohn’s disease
• Haemophilia

1. As in any emergency presentation, assess vital signs, level of consciousness, perfusion (peripheral and central).
2. A quick physical examination may yield important clues as to the etiology of the bleed and prioritize subsequent management. Look for a palpable liver and spleen (portal hypertension and hence bleeding varices) or signs of chronic liver disease. In a less acute presentation when the patient is stable, a good history will usually provide an aetiology.
3. Establish an airway, O2 supplementation, establish good IV access with 2 large bore IV cannulae and depending on signs of circulatory compromise, consider fluid boluses.
4. Send for blood investigations, most importantly an urgent group and cross match in the event a blood transfusion is required
5. Keep the patient nil by mouth and pass a nasogastric tube
6. In large bleeds with signs of circulatory compromise the patient will require transfusion of blood products. It the patient continues to be unstable with continued bleeding, surgical exploration is necessary.
7. In the event the patient is stable but has ongoing signs of slow blood loss, semi urgent endoscopic exploration and emergency banding and sclerotherapy is scheduled after discussion with the paediatric gastroenterologist.
8. Endoscopy will reveal if the source of bleeding is due to variceal bleeding or mucosal lesions.

• Complete blood count with reticulocyte count
• GXM
• Prothrombin time (PT) and partial thromboplastin time (PTT)
• Guaiac test on stool/emesis (if blood loss is not obvious)
• Alanine aminotransferase, aspartate aminotransferase, albumin, alkaline phosphatase
• Blood urea nitrogen, creatinine 

Mucosal lesions comprise of ulcerations or erosions on the esophagus or gastric mucosa.

The aim of therapy is to neutralize or minimise release of gastric acid with the use of Proton Pump Inhibitor medication or H2 receptor antagonist.

Variceal bleeding is managed with emergency banding,endoscopic sclerotherapy or injection into the varices with cyanoacrylate glue. Banding is preferred over sclerotherapy as the risk of complications is less (bleeding, perforation, pneumomediastinum).

Use of a balloon tamponade (Sengstaken-Blackmore) may also be used as a temporizing measure to stem the bleeding if the size of the child is appropriate. (generally > 40 kg). Balloon tamponade is applied for more than 24 hours and the patient’s airway is usually intubated. Complications include esophageal perforation, aspiration, mucosal ischaemia.

Variceal bleeds stops spontaneously in 50% of patients but rebleeding occurs in 40%.

Medically, intravenous octreotide is used and works by reducing splanchnic blood flow and portal pressure. The largest retrospective series in 2004 in children found octreotide stopped bleeding in 71 % of children with portal hypertension, however 52% rebled. Octreotide can be used to help with hemostasis prior to endoscopy or if endoscopy cannot be performed. 

Portal hypertension is defined as portal vein pressures exceeding 5mmHg or a portal vein to hepatic vein gradient of > 10 mmHg. Variceal bleeding is associated with a gradient of > 12 mmHg.

When the portal system becomes congested, collateral pathways develop at the junctions between the high pressure portal veins and the low pressure venous system, forming varices.

These varices are formed at:

• esophageal and gastric sub-mucosal veins which decompress the left gastric vein and the short gastric veins into the azygous vein.
• recanalization of the obliterated umbilical vein from decompression of the left portal vein to the epigastric veins resulting in the caput medusae pattern.
• inferior mesenteric vein and inferior vena cava and their tributaries (superior, middle, inferior rectal veins, common and internal iliac veins), forming anorectal varices. 

Via Doppler ultrasound of the liver.

In adults the preventative role of beta blockers is well studied in adults and have been shown to reduce portal pressure and prevent primary and secondary bleeding. (Bleeding is reduced in adults by 50%). Portal hypertension is reduced by decreasing cardiac output, and inducing splanchnic vasoconstriction through B1 and B2 blockade.

In children however limited studies suggest that bleeding rates on propanolol are not much improved compared to bleeding rates seen in the natural history of the disease. Furthermore there is a theoretical risk of harm from the B1 blockade causing decreased cardiac output, which may hinder compensatory tachycardia during acute severe hemorrhage. It is therefore not recommended in the paediatric age group. 

• Portosystemic shunts
• TIPS (transjugular intrahepatic portosystemic shunt)
• Splenectomy
• Gastrosplenic decompression