15.4.3 GI Bleeding Flashcards
Define haematemesis
passage of bloody or dark “coffee grounds” material from the mouth typically associated with bleeding above the ligament of Trieitz
Define Haematochezia
passage of bright red blood or maroon-coloured material from the rectum
Define malaena
passage of dark, black, tar-coloured stool usually associated with oesophageal, gastric or upper small intestinal haemorrhage
Upper GI bleeding: presentation
Remember: swallowed blood from nose, throat or coughed up from lungs and swallowed can also present with these symptoms – or mother’s cracked nipples if breastfeeding infant! (Take a good history!!)
- Hypovolaemic shock (hypotension, tachycardia, collapse)
- Vomiting fresh blood or coffee grounds (gastric acid in blood that is partially digested blood)
- Malaena
Also:
- Dizziness, weakness, syncope, heartburn, epigastric pain or tenderness
- Iron deficiency anaemia (from chronic blood loss) -> bleed very slow over long period of time
- Stool occult blood positive
-> think of breastfeeding nipples in completely well baby, vomiting blood
# Not everything that is red-coloured is blood (eg beetroot, food dyes, rifampicin) -> test if it is blood
Lower GI bleeding: presentation
- Haematochezia
- Iron deficiency anaemia (from chronic blood loss)
- Important to differentiate: is the blood mixed in with the stool? Is it fresh or altered? Is the blood on the surface of the stool? Is the blood present in the toilet bowl not the stool? Is the blood only present on toilet paper?
- Fresher the blood; the lower the bleeding in Gut
Mechanism of GIT bleeding
Mucosal injury – injury from gastric acid, infectious agents, ingestion of caustic agent, foreign body, inflammation
Blood vessel disruption - raised pressure eg chronic liver disease with cirrhosis leads to portal hypertension and bleeding from oesophageal varices
Portal hypertension
- Develops due to cirrhosis of liver or portal vein thrombosis➡️back pressure in portal vein
- Collaterals develop at anastomotic sites where portal and systemic venous systems meet ➡️development of varices = abnormal dilated veins
Slide 9 notes
Oesophageal varices
- Abnormal dilated veins at lower end of oesophagus
- Develop secondary to portal hypertension
- caused by portal hypertension and the blood trying to find varices to get back to systemic circulation
Oesophagitis
Infections:
- oesophageal candidiasis,
- herpes simplex, cytomegalovirus (pt very immunocompromised)
Noninfectious:
- reflux oesphagitis,
- pill oesophagitis (pt swallow pill and it gets stuck)
- eosinophilic oesophagitis
Gastric and duodenal bleeds
- Helicobacter pylori infection (most common cause)
- Inflammation
- Gastritis(common causes; helicobacter and PUD)
- Duodenitis
- Peptic ulcer disease
- Erosion into submucosal blood vessels or artery
Foreign body
- causes GI bleed
- common: button batteries (can go to aorta within hours), magnets (stick together in babies intestines)
- always take chest X-ray
Mallory Weiss tear
- Tear in the mucosa at the gastro-oesophageal junction
- Due to repeated forceful vomiting or retching
Other causes of upper GI bleeding
- Bleeding disorder eg haemophilia, vitamin K deficiency, stress ulcer in critically ill child
- Vascular malformation of gut
- Drug side effect eg NSAIDs inhibit prostaglandin synthesis, which is protective to the gastric lining; allows stomach acid to damage the mucosal lining
Lower GI bleeding
- Bleeding that arises beyond the ligament of Treitz
- Suspensory ligament of the duodenum – arises from right crus of diaphragm and suspends duodenojejunal flexure
Anorectal pathology
- Anal fissures/tears (enquire about sexual abuse)
- Haemorrhoids
- Fistulas
- A small tear may occur due to passing hard stool in children with constipation
- NB: always consider INFLAMMATORY BOWEL DISEASE if there is significant perianal disease
- think of chromes disease