Upper GI Bleed

A 7-year-old boy is referred from a peripheral hospital for a 2-day history of passing black tarry stool. On the third day, he passes loose stools mixed with dark maroon blood clots. For the last week, he had been having upper respiratory tract symptoms and had daily doses of ibuprofen for his low-grade fever.

Bottom Line

Upper GI bleeds manifest as melena, haematemesis and occasionally hematochezia

In the event of an acute bleed, the patient must be resuscitated in line with first principles

An urgent GXM must be sent to prepare for blood product transfusion

Depending on the suspected aetiology, an infusion of proton pump inhibitor or octreotide may be started while awaiting endoscopic or surgical exploration

Massive bleeds warrant urgent surgical exploration, while more stable patients can be triaged for endoscopy with the paediatric gastroenterologist

What is an upper GI bleed?

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

• Hematemesis
• Melena
• Hematochezia

Are you sure it’s an upper GI bleed?

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

Red food colouring, fruit-flavoured drinks, fruit juices, and beets may colour the vomitus or stool red. They 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. 

What can cause an upper GI bleed?

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
• Haemorrhagic disease of the 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

How do we manage an acute upper GI bleed?

As in any emergency presentation, assess vital signs, level of consciousness, and perfusion (peripheral and central).

A quick physical examination may yield important clues as to the aetiology 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.

Establish an airway, supplemental O₂, establish good IV access with 2 large bore IV cannulae and depending on signs of circulatory compromise, consider fluid boluses.

Send for blood investigations, most importantly an urgent group and cross match in the event a blood transfusion is required

Keep the patient nil by mouth and pass a nasogastric tube

In large bleeds with signs of circulatory compromise, the patient will require a transfusion of blood products. If the patient continues to be unstable with continued bleeding, surgical exploration is necessary.

In the event the patient is stable but has ongoing signs of slow blood loss, semi-urgent endoscopic exploration and emergency banding and sclerotherapy are scheduled after discussion with the paediatric gastroenterologist.

Endoscopy will show if the source of bleeding is due to variceal bleeding or mucosal lesions.

Which investigations should take priority in an acute upper GI bleed?

• 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 

What if the bleeding is from a mucosal lesion?

Mucosal lesions comprise ulcerations or erosions on the oesophagus or gastric mucosa.

The aim of therapy is to neutralize or minimise the release of gastric acid with the use of proton pump inhibitor medication or H2 receptor antagonist.

How do we manage variceal bleeds?

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 temporary measure to stem the bleeding if the size of the child is appropriate. (generally > 40 kg). Complications include oesophagal perforation, aspiration, and mucosal ischaemia.

Variceal bleeds stop 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.

What is portal hypertension and how does it form varices?

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:

• oesophagal 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.

How do we investigate portal hypertension?

Via Doppler ultrasound of the liver.

Is there primary prophylaxis to prevent further variceal bleeding?

In adults, the preventative role of beta blockers is well-studied in adults and has 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, 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 haemorrhage. It is therefore not recommended in the paediatric age group.

What are the surgical options for managing oesophagogastric varices?

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

 

References

Chawla, D Seth et al. Upper gastrointestional bleeding in children. Clin Paediatrics; 6(1)2007;16-2Mileti, Ph Rosenthal. Management of Portal Hypertension in Children. Current Gastroenterol Rep (2011) 13:10-16

Chawla Y, Duseja A, Dhiman RK. The modern management of portal vein thrombosis. Aliment Pharmacol Ther 2009 30, 881-894

Molleston JP. Variceal Bleeding in Children Journal of Pediatric Gastroenterology and Nutrition 37:538–545 November 2003

Sarin SK, Agrawal SR. Extrahepatic portal vein obstruction. Semin Liver Dis. 2002;22:43-58

Schettino GCM, Fagundes EDT et al. Portal vein thrombosis in children and adolescents. J Pediatr (Rio J). 2006;82(3):178-8