GI & Hepatology JC056: Coffee Ground Vomitus / Tarry Stool: Upper GI Bleeding Flashcards
Upper GI bleeding definition
Bleeding from a source proximal to ***ligament of Treitz (at Duodeno-Jejunal flexure)
Ligament of Treitz:
- connect Duodeno-Jejunal flexure to Connective tissue surrounding SMA + Celiac artery
Definition of other terms
Small bowel bleeding:
- any bleeding distal to **Ampulla of Vater + proximal to **Ileocecal valve
Overt GI bleeding:
- passage of visible blood (including haematemesis, coffee ground vomiting, melena, haematochezia)
Occult GI bleeding:
- GBI with blood not detected by naked eye
- notice possibility of bleeding ∵ **Fe deficiency anaemia (FDA) / **Positive faecal occult blood test
Obscure GI bleeding:
- ***source of bleeding (either Overt / Occult) remains unknown despite
—> OGD + CLN (colonoscopy) +/- SB radiographic evaluation (traditional definition)
—> OGD + CLN + SB workup (radiographic testing, videocapsule endoscopy, enteroscopy) (stricter definition) (all need to be negative before conclude obscure GIB)
***Presentation of UGIB
Depends on **Volume + **Location of bleeding:
Small to Moderate amount (usually more Chronic course):
1. Symptoms of anaemia (fatigue, palpitation, dyspnea, dizziness, postural hypotension)
2. Asymptomatic (only incidental findings of Fe deficiency anaemia / +ve Faecal occult blood)
Larger amount (usually more Acute course):
1. Haematemesis (fresh blood / coffee-ground emesis (bleeding less severe / active: enough time for gastric acid to act on heme —> brownish))
2. Fresh blood / Coffee-ground aspirate from NG tube
3. Melena
4. Haematochezia (bright red / maroon blood: rare in UGIB unless high volume + rapid transit time)
Melena
- Black tarry stool
- Other characteristics: loose, sticky, malodourous
- Fresh (some fresh blood component suggesting **ongoing bleeding) vs Old (suggestive of **cessation of ongoing bleeding)
- Black colour: Heme oxidised by intestinal bacteria —> ***Hematin
- Usually a ***cathartic (∵ blood component stimulates gut motility) —> patients describe loose stool / diarrhoea
DDx of black stool:
1. **Fe intake (greenish / black colour)
2. **Bismuth (reddish black)
3. Beetroot (reddish black)
4. Activated charcoal
***Proximal vs Distal bleeding
Almost certain UGIB
- **Haematemesis
- **Blood in NG tube
NG tube clean:
- usually ***lower down, but can still be duodenal bleeding with competent pylorus preventing reflux of blood from duodenum into stomach
Melena:
- **Upper GI tract down to **Right / Proximal colon (enough time for bacteria to act on heme to hematin)
Haematochezia:
- ***Lower GI tract (but can still be massive bleeding from upper GI tract)
Approach to patients with suspected UGIB
- Assess severity of hypovolaemia
- mild - moderate (<15% blood volume lost): Resting tachycardia
- >=15%: Orthostatic hypotension (↓ SBP >20mmHg / ***↑ HR 20 from recumbent to standing)
- >=40%: Supine hypotension - Resuscitation
- **ABC —> secure airway if massive haematemesis with impaired consciousness
- **Large bore IV cannula —> Fluid resuscitation + Packed cell transfusion
- Monitor vital signs + ***urine output
- ICU for severe, life-threatening cases (e.g. massive bleeding requiring inotropes / intubation) - History, P/E, Investigations
- Treatment
- Replace blood lost: Blood transfusion
- Other measures
- Upper endoscopy
***History taking
記: Causes of bleeding: 潰瘍, 發炎, 嘔, 靜脈曲張, 腫瘤, 手術, 流血不止
- Usual questions on onset, duration, frequency, episode etc.
- Associated GI symptoms (provide hint on underlying cause):
- **Epigastric pain: Peptic ulcer, Malignancy
- **Vomiting e.g. after alcohol: Mallory-Weiss tear
- **Acid reflux / heartburn: Esophagitis, Esophageal ulcer
- **Painful dysphagia: Esophagitis, Esophageal ulcer
- **Painless dysphagia: Malignancy
- **Symptoms of cirrhosis (e.g. jaundice, leg edema, ascites): Variceal bleeding
- ***Constitutional symptoms (LOW, LOA): Malignancy
- Risk factors of DDx: H. pylori infection (treatment, follow-up test: need to confirm H. pylori eradication status), NSAIDs, HBV/HCV - Drug history / allergy
- NSAIDs (patient may not know they are taking these drugs)
—> ask IHD / chest pain, stroke, TIA, joint pain (e.g. OA, gout, recent sprain), dental extraction (from dentists)
—> analgesic together with antacid
—> given injections
- Antiplatelets, Anticoagulants
- Rate lower drugs: **β blockers, CCB —> **mask early signs of hypotension (i.e. tachycardia) - Past medical history
- Peptic ulcer disease (higher risk of recurrence)
- ***Radiation (suggest radiation enteritis) - GI surgical history
- ***Anastomotic ulcer - Social history
- Smoking (peptic ulcer disease)
- Alcohol (alcohol gastritis, Mallory-Weiss tear after repeated severe vomiting)
***Physical examination
- ***Vital signs (TURBO-P)
- Confirm the complaint
- examine vomitus
- examine material from NG tube
- ***PR exam (to confirm whether real melena / Fe-stained stool, fresh / old melena, fresh per rectal bleeding) - General examination
- **stigmata of chronic liver disease
- skin + oral mucosa (hereditary diseases e.g. **Hereditary haemorrhagic telangiectasia, **Peutz-Jeghers syndrome (hyperpigmented macules: melanin spots, high tendency to develop cancer))
- **cervical LN (malignancy) - Abdominal examination
- **epigastric tenderness (rebound, guarding —> possibility of perforation)
- abdominal mass (alcoholic cirrhosis)
- **hepatosplenomegaly (cirrhosis)
- ***PR exam - CVS exam
- **aortic stenosis (associated with bleeding from **Angiodysplasia)
- assess whether patient fit for endoscopy - Respiratory exam
- assess whether patient fit for endoscopy
***Investigations
- CBC
- ***Hb
—> may not change in initial presentation ∵ loses both RBC + plasma
—> may take a few hours for Hb to ↓ when interstitial fluid moves into vascular space / by IV infusion
- ***MCV
—> normal usually in acute bleeding
—> low in chronic Fe deficiency (small degree of chronic, intermittent, low volume bleeding), Thalassaemia
—> high (from reticulocytosis) -
**Platelet
—> normal
—> **high (∵ reactive thrombocytosis to bleeding)
—> ***low (∵ hypersplenism, consider variceal bleeding (if concomitant deranged LFT + prolonged INR))
-
**RFT
- urea high in active / recent bleeding (∵ Hb is a protein —> ↑ urea when digested in GI tract)
—> **urea abnormally higher than creatinine - LFT
- cirrhosis —> variceal bleeding - Clotting profile
- cirrhosis —> variceal bleeding - ***Type + screening, Cross matching
-
**CXR (erect)
- rule out presence of free gas (upper endoscopy **CI if presence of perforation) (sensitivity 70-80%) - ECG
- see if patient fit for urgent endoscopy - CT abdomen if suspected perforation (even if CXR does not show free gas)
- if severe epigastric tenderness / rebound / guarding
Prognostic scores of UGIB
- Predict adverse outcomes before endoscopy (e.g. further bleeding, death)
- Determine need of endoscopic intervention
- ***Pre-endoscopic Rockall score
- BP
- pulse
- age
- comorbidities - ***Glasgow-Blatchford score (GBS) (>99% sensitivity)
- BP
- pulse
- age
- comorbidities
- Hb, urea
- laboratory tests
- other markers e.g. melena, syncope
Treatment: Blood transfusion
Restrictive strategy (Hb **<7 g/dL) vs Liberal strategy (Hb **<9 g/dL)
Restrictive strategy:
- Better survival at 6 weeks
- Better rebleeding rate (esp. cirrhosis) (∵ too much blood volume ↑ portal pressure —> rebleeding of esophageal varices)
Exception of Restrictive strategy:
1. **Haemodynamically unstable
2. **Underlying CVS disease (esp. ACS)
- transfusion threshold less certain
- level >= 8/9 g/dL is recommended —> to avoid triggering acute vascular events
**Treatment: Other measures **before OGD
-
**FFP, **IV Vit K (if taking Warfarin) —> Correct coagulopathy + thrombocytopenia
- keep INR <1.5
- keep Plt >50
- Use of FFP in cirrhosis is controversial (may ↑ portal pressure) - IV PPI in **active bleeding (for **peptic ulcer)
- Esomeprazole **80mg bolus, then **8 mg/hour infusion
- ↓ bleeding stigmata of peptic ulcer + ↓ need for endoscopic haemostatic intervention - Splanchnic vasoconstrictor (**if underlying cirrhosis)
- **Terlipressin / Octreotide (in addition to PPI) —> ↓ portal pressure —> ↓ variceal bleeding
- for known cirrhosis / suspected variceal bleeding e.g. known varices, S/S, lab results - Antibiotics (if underlying cirrhosis)
- 3rd gen Cephalosporin (esp. advanced cirrhosis)
- Quinolones
—> ↓ risk of bacterial infection in cirrhosis patients with GI bleeding (lower / upper, variceal / non-variceal) —> ∵ GI bleeding lead to bacterial translocation —> ***Spontaneous bacterial peritonitis
—> ↓ other infection risk e.g. pneumonia, UTI, skin infection etc. - +/- Prokinetics (if clinically severe / ongoing active UGIB —> ↓ chance of blood / clot retained in stomach which hinders endoscopic view)
- IV Erythromycin
- IV Metoclopramide
Antibiotics in Cirrhosis with GIB
Advanced cirrhosis (Child-Pugh B / C):
- 3rd gen Cephalosporin (e.g. Ceftriaxone) (rather than Quinolone)
Upper endoscopy
Rmb: NOT first thing to do in case of UGIB!!!
***After stabilisation
- within 24 hours if haemodynamically stable
- within 12 hours if haemodynamically unstable
- within 12 hours if suspected variceal bleeding
Inspect:
1. Esophagus
2. Stomach
3. Duodenum (up to level of Major duodenal papilla / Ampulla of Vater / 2nd part of Duodenum D2)
—> most pathologies located within these areas
—> looping of endoscopy in stomach —> scope may not be able to advance further beyond
***Causes of Upper GI bleeding
***Common + Important (記: 潰瘍, 發炎, 嘔, 靜脈曲張, 腫瘤, 手術, 流血不止):
1. Ulcers / Erosions (duodenal, gastric, esophageal)
2. Gastritis, Duodenitis, Esophagitis
3. Gastroesophageal varices (uncommon but important)
4. Mallory-Weiss tear
5. Malignancy (gastric, esophageal)
Less common:
6. **Angiodysplasia / Telangiectasia
7. Anastomotic ulcer
8. Portal hypertensive gastropathy (only presents with occult GIB)
9. **Dieulafoy’s lesions
10. GIST with ulceration bleeding
Rare:
11. Aortoenteric fistula
12. Haemobilia, Haemosuccus pancreaticus
13. Crohn’s disease
Note:
Bleeding from Non-GI sources: ***Swallowed blood
- Epistaxis
- Haemoptysis
- Oral bleeding lesions
- Ulcers
- Duodenal, Gastric, Stomal ulcers
- 25-50% non-variceal UGIB
- ulcers high on **lesser curvature / in **postero-inferior wall of duodenal bulb (portion of duodenum closest to the stomach (5cm)) bleed more easily
—> ∵ main vessels behind (e.g. left gastric artery, gastroduodenal artery)
Causes:
1. **H. pylori
2. **NSAIDs, Aspirin
3. ***Stress (mainly in ICU patients)
***Forrest classification of UGIB
1a: Arterial jet
1b: Oozing
2a: Non-bleeding visible vessel
—> ***require endoscopic intervention
2b: Adherent clot
2c: Black spot
3: Clean base of peptic ulcer
Esophagitis / Esophageal ulcer
Causes:
1. ***Acid reflux
- obese / middle age / male
- Infection
- **Candida
- **CMV
- Herpes virus
—> esp. in immunocompromised state e.g. DM, chemotherapy, HIV - ***Pill-induced (local irritation of pills)
- elderly
- psychiatric patients esp. tetracyclines - Sclerotherapy-induced (Post-endoscopic intervention)
- ***Irradiation
- ***Caustic substance ingestion
- Gastritis, Duodenitis, Erosions
- ***H. pylori
- Drug-induced
- **NSAIDs, Aspirin (both Local + Systemic effect) —> even Enteric coated aspirin can still cause bleeding
—> almost all patients on aspirin develop mild haemorrhagic gastritis within 24 hours
—> bleeding is minimal + not clinically apparent
—> adaptation + healing occurs
- bleeding can be acute (within first few days) / chronic (after some months)
- usually **self limiting after removal of drug - Alcohol induced
- acute, chronic - ***Stress gastritis
- ICU patients (respiratory failure, hypotension, sepsis, renal failure, thermal burns, peritonitis, jaundice, neurological trauma)
—> impaired gastric / duodenal mucosal defence
- all patients with endoscopic gastritis
- 2-10% with significant bleeding
- Gastroesophageal varices
- Gastric / Esophageal varices
—> Gastric varices may accompany Esophageal varices / alone (usually in fundus) - ***very high mortality (80%)
- 5-10% of cases of UGIB
Causes:
1. **Cirrhosis
2. Non-cirrhotic portal hypertension (e.g. **Splenic vein thrombosis if isolated gastric varices)
Presentation:
1. ***Fresh large volume haematemesis
2. Coffee-ground vomiting (rare)
- Mallory-Weiss tear
- Tear near ***gastroesophageal junction in gastric / esophageal mucosa
- Repeated retching / vomiting
—> initially no blood followed by vomiting of fresh blood
—> alcohol / chemotherapy-induced - Usually ***self-limiting
- Malignancy (gastric, esophageal)
- Malignancy of stomach, esophagus are uncommon causes of UGIB
- Malignancy of duodenum is very rare
- Pay attention in elderly patients
- Bleeding usually ***self-limiting
- Angiodysplasia / Telangiectasia
- aka Vascular ectasia
- **small bowel / **colon > stomach / duodenum
- unusual variant: Gastric antral vascular ectasia (GAVE) / Watermelon stomach (red stripes radiating from pylorus to antrum)
Associated conditions:
- **Elderly
- Cirrhosis
- Chronic renal failure
- Radiation
- Scleroderma
- **Hereditary haemorrhagic telangiectasia
- Aortic stenosis (Heyde’s syndrome), Left ventricular assisted device
Hedye’s syndrome (triad):
1. Aortic stenosis
2. Anaemia
3. Acquired coagulopathy (∵ high shear stress on blood through narrowed aortic valve —> conformational change of vWF —> early degradation of vWF —> making pre-existing angiodysplastic lesions easier to bleed)
***Endoscopic intervention to stop bleeding
3 main modalities:
1. Injection with **adrenaline
2. **Heater probe
3. ***Hemoclips (for Mallory-Weiss tear, Angiodysplasia, Dieulafoy’s lesions)
Others:
4. **Argon plasma coagulation (for Angiodysplasia)
5. **Band variceal ligation / ***Sclerotherapy (for Esophageal varices) (rare, ∵ high risk of perforation / stricture)
6. n-butyl-2-cyanoacrylate (tissue adhesive) (for Gastric varices)
***Things to do after OGD
Peptic ulcer as an example:
1. ***Continue PPI (infusion / oral depending on severity based on Forrest classification)
- ***Resume Aspirin ASAP in those with high cardiothrombotic risk once endoscopic haemostasis has been achieved
- early resumption of Aspirin does NOT ↑ rebleeding rate with PPI coverage but ↓ mortality due to ACS / stroke
- 1-3 days, certainly within 7 days
- thrombotic events: 7-30 days, usually between 7-10 days - ***Eradicate H. pylori
- prevent recurrent peptic ulcer - Long term PPI if concomitant Aspirin use
If OGD negative but ongoing ***massive bleeding
Usually in setting of **Fresh melena (indicate bleeding not from upper GI but from small bowel / colon)
∵ if haematemesis, usually indicate missed pathology —> **2nd OGD preferred
if fresh PR bleeding —> usually ***Colonoscopy done first instead of OGD
Colonoscopy (+ Intubation of terminal ileum)
—> Brisk / Massive suspected small bowel bleeding
—> Stabilise patient haemodynamically
If patient stable
—> **Red cell scan / **CT angiography
—> Angiography if positive
—> Embolisation if positive
If patient unstable
—> ***Angiography directly (∵ can do Embolisation at the same time)
If Red cell scan / CT angiography / Angiography negative —> Specific management:
- **Enteroscopy vs **Surgery vs ***Intraoperative enteroscopy
Angiography
- Detects bleeding at **0.5-1 ml/min (require **higher rate of bleeding)
—> if CTA / RBC scan negative —> Angiography likely negative
—> Localise a site of bleeding in 50-72% of patients with massive haemorrhage but only 25-50% of patients when active bleeding has slowed / stopped -
**Contrast extravasation
—> can only be detected at time of **active bleeding
Advantage:
- ***Therapeutic also (embolisation at the Same time)
Complications:
- Catheter site infection
- **Thromboembolism (e.g. ischaemic bowel)
- Contrast (allergy, **nephropathy)
CT Angiography
- Detects bleeding at ***0.3 ml/min (can detect much lower rate)
-
**Contrast extravasation
—> can only be detected at time of **active bleeding
Disadvantage:
- ***NO therapeutic interventions (vs Usual angiography)
Complications:
- Contrast (allergy / nephropathy)
RBC scan
- a Radionuclide scan
- Technetium (99mTc) sulphur colloid + 99mTc pertechnetate-labelled autologous RBC
- Detect **Slow / Intermittent bleeding which is not shown by angiography
—> minimum rate of **0.1-0.5 ml/min
—> as little as ***5ml of intra-luminal blood will give +ve scan
—> allow sequential scans + ↑ probability of bleeding site identification
Disadvantage:
- Delayed scan may identify site of blood ***pooling only but not site of bleeding
If OGD negative but ongoing ***subacute bleeding
**Colonoscopy
—> Subacute ongoing small bowel bleeding
—> Stabilise patient
—> **Video capsule endoscopy (VCE) / **CT enterography (CTE)
—> proceed to **Deep endoscopy (i.e. SB endoscopy) if positive
—> Treat accordingly
If Video capsule endoscopy (VCE) / CT enterography / Deep endoscopy negative:
—> RBC scan / Angiography / Surgery / Intraoperative endoscopy
—> young patients: ***Meckel’s scan
Video capsule endoscopy (VCE)
記: for ***Vascular + Inflammatory lesions
Setup:
- Capsule + Transmitter
- Receiver + Recorder
- Workstation
Use:
- Examine **entire small bowel
- Diagnostic only
- Complications —> **Capsule retention
Indications:
- Obscure GI bleeding
- Non-stricturing small bowel Crohn’s disease
- Celiac disease
- ***Hereditary polyposis syndromes (e.g. Peutz-Jeghers syndrome, Familial adenomatous polyposis with duodenal polyps)
Contraindications:
- **Known / suspected GI obstruction / strictures (e.g. Crohn’s)
- **Swallowing disorders
- ***Severe motility problems
- Uncooperative / Unreliable
Disadvantage:
- Take 1-2 hours to review footage
CT enterography (CTE)
記: for ***Small bowel masses
Ingest neutral contrast
—> ***distend bowel lumen (vs Normal CT: bowel lumen collapsed)
—> detect subtle bowel lesions
Video capsule endoscopy (VCE) vs CT enterography (CTE)
Similar yields
- VCE has higher yields for **vascular + inflammatory lesions
- CTE better at detecting **SB masses
- negative CTE —> positive VCE in 57%
- negative VCE —> positive CTE in 50%
—> VCE and CTE are ***complementary examinations
Deep endoscopy / Double-balloon enteroscopy (DBE)
- Working length 2m, overtube 1.4m
- 240-360cm distal to pylorus
- 102-140cm proximal to ICV
- Reason for difficulty is elastic nature of looped intestine
- Role of flexible overtube with a balloon
—> prevent stretching of shortened intestine to allow advancement of scope
—> intubated intestine is shortened by gentle withdrawal of endoscope while both balloons at the tip are inflated to grip the intestine
Targeted DBE:
- Oral route (Antegrade approach)
- Anal route (Retrograde approach)
—> depends on suspected site of lesion from VCE / CTE
Advantages:
- **Biopsy + **Therapeutic interventions possible (∵ with accessory channel + tip deflection capability)
- Medical conditions can be treated with non-surgical endoscopic treatments:
—> **Bleeding
—> **Mucosal neoplastic lesions
Single balloon enteroscopy
- Balloon attached to overtube only
- Up + Down adulation of scope
- Low chance of examining whole bowel
DBE vs SBE
- Operator
- DBE: 2
- SBE: 1/2 - Time
- DBE: Slower intubation
- SBE: Faster intubation - User friendly
- DBE: ++
- SBE: +++ - Depth
- DBE: ++++
- SBE: ++ - Holding in ICV
- DBE: +++
- SBE: ++ - Total enteroscopy (chance of examining whole SB)
- DBE: 78%
- SBE: 25%
Meckel’s diverticulum
- Remnant of omphalomesenteric duct, arising from antimesenteric surface of middle-to-distal ileum
-
**Rule of 2:
—> 2% of population
—> M:F = 2:1
—> **within 2 feet from ICV
—> 2 inches in length
—> 2% develop complications (usually before age of 2)
—> a bleeding diverticulum usually lined by 2 different types of mucosa: Intestinal mucosa + Heterotopic mucosa (gastric, duodenal, ***pancreatic, colonic) - ***Ectopic gastric mucosa
—> acid secretion
—> ulcer / bleeding adjacent to / just downstream from diverticulum
Meckel’s scan
- IV 99mTc pertechnetate (affinity for **gastric mucosa) —> Scintigraphy to identify diverticula containing **ectopic gastric mucosa (<25% of cases)
—> Meckel’s diverticula lacking gastric mucosa will NOT be seen - Does NOT detect active bleeding (i.e. Presence of Meckel’s diverticulum does not mean it is the bleeding source)
- May reveal a ***potential bleeding source if other tests unrevealing (esp. children / young adults)
