Upper GI Bleed

Question 1

Name 2 types of stress ulcers

Answer 1

1. Curling – Duodenal ulcer in Burns
2. Cushing’s – Gastric ulcer in ↑ICP

Question 2

What other causes of bleeding must you rule out in UGIB

Answer 2

• Lower GI & Ano-rectal causes
• Nasopharyngeal causes
• Haemoptysis

Question 3

How is shock classified and what are the symptoms for each class?

Answer 3

• Class 1 [<15% blood volume loss] – Compensated; asymptomatic
• Class 2 [15-30%] – Resting tachycardia, Postural hypotension, ↓Pulse pressure
• Class 3 [30-40%] – Supine hypotension, Tachypnoea, Confusion
• Class 4 [>40%] – Anuria, Lethargic

Question 4

What would you do after resuscitation in a patient with UGIB?

Answer 4

1. Monitoring for re-bleed

• Vitals – Hourly
• Hb

1. Charting

• I/O Chart [use Foley’s & Ryle’s – never in suspected varices]
• Bleeding episodes

1. Prepare for emergency/next-day OGD
2. CXR & AXR to r/o pneumoperitoneum → OGD CI-ed in perforation
   
   • Air insufflation → Abdominal compartment syndrome & Splinting of diaphragm
3. NGT & NBM – Diagnose + Decompress + OGD Prep
4. Erythromycin – Gastrokinetic properties → empties stomach
5. After OGD

• IV Omeprazole bolus 80mg + 8mg/hr continuous infusion for 3/7
  
  • ↓Recurrent bleed, ↓Hospital stay, ↓need for future endoscopy
  • Oral if not severe
• Continue monitoring for re-bleed + NBM for 1-2/7

Question 5

What are the indications of Emergency OGD in UGIB?

Answer 5

• Haemodynamic instability [stabilise BP before OGD]
• Active bleeding
• Bleeding varices

Question 6

How do PPIs reduce risk of re-bleeding in UGIB?

Answer 6

• The target for PPIs is H⁺/K⁺ ATPase responsible for acid secretion
• PPI → ↑gastric pH → ↓platelet disaggregation → ↑clot stability & ↓re-bleeding risk

Question 7

What is the pathophysiology behind NSAID-induced PUD?

Answer 7

• PUD ∵imbalance of aggressive and mucosal protective factors
• Protective factors include
• Mucous [Mucin & HCO₃^-]
• Mucosal blood flow
• Mucosal regenerative ability
• Prostaglandins [↑Mucous secretion, ↑Mucosal blood flow, ↓HCl secretion]
• NSAIDs = non-selective COX inhibition → ↓Prostaglandin production → ↓Mucosal protection

Question 8

How is gastric acid secretion regulated?

Answer 8

• Gastric HCl secreted by parietal cells in the gastric fundus & body
• Its secretion controlled by dual neurohormonal pathways which activate H⁺/K⁺ ATPase
• Hormonal – Gastrin [G-cells; antrum]; Histamine [ECL cells]
• Neural – Vagus nerve
  
  • Nerves of Latarjet – branches of CNX that relaxes the pylorus & controls gastric emptying [clinically important ∵post-vagotomy complications]
• Target of PPI is H⁺/K⁺ ATPase

Question 9

What are the typical features of peptic ulcers due to NSAIDs and HP respectively?

Answer 9

• Helicobacter pylori
• More associated with Duodenal Ulcers [which make up 75% of all PUD]
  
  • HP a/w. 85% DU; 70% GU
• Gastric ulcers ∵HP usually found in lesser curvature of stomach
• NSAIDs
• More associated with Gastric Ulcers [↑GU risk 40x; ↑DU risk 8x]
• Gastric ulcers ∵NSAIDs usually found in greater curvature of stomach
• PUD ∵NSAIDs a/w. with ↑UGIB

Question 10

What are the possible sites for peptic ulcers?

Answer 10

• Common Sites
• Duodenal Ulcers [75%] – D1
• Gastric Ulcers [20%] – Pyloric antrum; lesser curvature
• Unusual Sites
• Zollinger-Ellison Syndrome
  
  • Ulcers found in distal duodenum & jejunum in addition to common GU/DU sites
  • Cause – Gastrinoma or G-cell hyperplasia → Hypersecretion of gastrin → ↑↑ Acid → ↑Peptic ulcers
  • Suspect when
    
    • Recurrent ulcers despite adequate treatment
    • Multiple ulcers
    • Ulcers in unusual locations
    • Complicated ulcers [bleeding, perforation]
    • No Hx. of NSAID use/HP -ve
• Demonstrate by ↑Fasting Gastrin in presence of ↑Acid secretion
• Triad = Ulcer @ unusual location, Acid hypersecretion, Gastrinoma
• Stomal Ulcers – @GJ junction
  
  • Presents as epigastric pain in post-gastrectomy patients
  • OGD required to determine if it is on the stomach or jejunal side
  • ∵↑Acid content in jejunal mucosa [X resistant to acid] ∵
    
    • Incomplete vagotomy
    • Incomplete gastrectomy → e.g. retained antrum syndrome [rare; acid content directly → jejunum bypassing residual antral tissue left behind by surgery → retained tissue stimulated by ↓acid content → ↑gastrin secretion]
    • Underlying ZES
• Meckel’s diverticulum – 2ft from ileocecal valve
  
  • In those that possess ectopic gastric mucosa

Question 11

What specific drug history should you enquire about in PUD?

Answer 11

• NSAIDs + whether H₂ blocker was given in conjunction
• Corticosteroids – chronic use can lead to poor ulcer healing
• Anticoagulants – ↑risk of bleeding PUD

Question 12

How can PUD present?

Answer 12

1. Incidental finding on OGD
2. Dyspepsia

• Ulcer-like = Burning, intermittent epigastric pain
  
  • DU – Relieved by food; Worsened by hunger
  • GU – Worsened by food
• Dysmotility-like = N&V, Bloating, Belching
• Mixed

1. Complicated PUD [4Bs]

• Bleed [Haemorrhage]
• Burst [Perforation]
• Block [GOO]
• Burrow [Erosion → surrounding structures]

Question 13

What are the risk factors for Gastric CA?

Answer 13

• H. pylori → chronic gastritis & intestinal metaplasia [2x risk]
• Ask for previous OGD, triple therapy, urease breath test
• Smoking – 2x risk
• Diet – ↑nitrosamine or smoked foods
• Family history
• 1.5x risk if +ve FH in 1^o relative [parents & siblings]
• Hereditary diffuse gastric CA [CDH1 mutation → e-cadherin]
• Specific hx
• Polyp found on previous OGD
• Barrett’s oesophagus
• Post-gastrectomy with Bilroth >7yrs ago for benign disease [bile reflux induce intestinal metaplasia]
• Chronic atrophic gastritis – Menetrier’s or Pernicious anaemia

Question 14

What are the histological subtypes of Gastric CA?

Answer 14

• 95% = Adenocarcinoma [Lauren classification]
• Intestinal type – ↑common in elderly male smokers; distal stomach
  
  • Histology – Papillary, Tubular, Mucinous
  • Haematogenous spread
• Diffuse type – ↑common in young female, proximal stomach; poor prognosis
  
  • Histology – Signet Ring cells; Linitis plastic [type 4 Borrmann’s]
  • Associated with CDH1 mutation for e-cadherin
  • Transmural & Lymphatic spread
• 5% = Non-adenocarcinoma

Question 15

What are the possible diagnoses if a gastric tumour was non-adenocarcinoma?

Answer 15

Carcinoid tumour – ∵hypergastrinaemia → stimulate ECL cells [histamine]

• Presents as carcinoid syndrome [vasoactive substances in systemic circulation]
• → Sweating, Flushing, Diarrhoea, Abdominal colicky pain, Bronchoospasm
• This presentation indicates malignant disease [localised = X carcinoid syndrome ∵first-pass effect]

Lymphoma – Gastric MALT tissue

• RFs – H. pylori, Trisomy 3

GIST

• Derived from interstitial cells of Cajal [myenteric pacemaker cells]
• 75% benign; Malignant features = Size >10cm; Extra-gastric site; ↑Mitotic index
• Associated with c-KIT & PDGFRA mutations
• Most found incidentally; may → bleed [anaemia, melena]; obstruction [LOW, early satiety]; mass effect [vague abdominal pain]

Question 16

CLCPM for Gastric CA

Answer 16

• Complications [4]
• Bleeding [anaemic sx., haematemesis, melena]
• Perforation [sudden severe abdominal pain, fever, shock]
• Malnutrition [LOA, LOW]
• Obstruction
  
  • GOO – N&V, electrolyte imbalance, shock, +succussion splash
  • Cardia tumour – Dysphagia, early satiety
• Local Sx – Dyspepsia [N&V, Bloating]
• Constitutional Sx – LOA, LOW, Night Sweats, Fatigue
• Paraneoplastic
• Seborrhoeic keratosis
• Thrombophlebitis & DVT [Trousseau’s Sign]
• Metastatic [below]

Question 17

How does Gastric CA spread?

Answer 17

1. Local invasion to surrounding organs – Duodenum, Pancreas, Transverse colon
2. Lymphatic spread

• 1) Peri-gastric LNs → 2) Along arterial supply [coeliac branches] → 3) para-aortic LNs
• 4) LSCLN [Virchow’s; Troisier’s Sign]

1. Haematogenous spread [venous → poral system]
   * Liver mainly [jaundice, ascites, hepatosplenomegaly]; rarely Lung, Brain, Bone
2. Trans-coelomic spread

• Peritoneal seedling → Carcinomatosis → SBO [malignant adhesion/direct extraluminal compression] + Ascites
• Sister-Mary-Joseph nodule – umbilical nodule [spread along umbilical vein]
• Krukenberg tumour – enlarged ovaries
• Blumer’s tumour – ant. rectal wall spread [Pouch of Douglas]

Question 18

What are the aims of investigation in suspected gastric CA?

Answer 18

1. Identify complications + Pre-operative assessment

• CBC, LFT [albumin used as marker for nutritional status], RFT, PT/aPTT
• T&S
• • CXR, ECG

1. Confirm the diagnosis – OGD + Biopsy
2. Staging – TMN

• T & N stage → Endoscopic US
  
  • T – visualise the depth of tumour infiltration [best prognostic indicator]
  • N – can identify para-gastric LNs + guide FNAC of suspicious nodes
• M stage → PET-CT
  
  • Can visualise distant mets; esp. the liver
  • CT thorax for cardia CA; CT abdomen/pelvis for M staging if patient cannot afford PET
• Laparoscopic staging – can identify micro-metastasis in peritoneum in patients with previous lower staging
• Screening using OGD + biopsy may be indicated in high-risk patients
• >20yrs since partial gastrectomy [for benign disease]
• +ve family history
• Patients with atrophic gastritis/pernicious anaemia

Question 19

What are the treatment modalities for gastric CA?

Answer 19

1. Therapeutic endoscopy – mucosal resection/submucosal dissection
   * For early stage disease [X invasion of muscularis externa]
2. CURATIVE → Radical gastrectomy – involves
3. Gastrectomy – Wide resection with proven [>6cm negative resection margin on intra-op frozen section]
   
   • Subtotal preferred in distal tumours∵O-J stomy more difficult ∵O does not have serosa
   • Total used for proximal/diffuse tumour
4. Lymph Node Dissection** – **D2 extended dissection [para-epigastric + LNs accompanying arteries supplying stomach]
5. Reconstruction – Bilroth I [G→D]; Bilroth II [G→J]; Roux-en-Y [O→J]
   
   • Subtotal usually + Bilroth II; Total usually + Roux-en-Y
6. Neo-/Adjuvant ChemoRT
   
   • 6x courses of chemo [epirubicin + 5FU + cisplatin]; 3x pre-op; 3x post-op
7. PALLIATIVE → Management of complications

• Bone Pain – EBRT
• Bleeding – TAE; EBRT
• Obstruction – Stenting, Bypass [GJ], Gastrectomy
• Perforation – surgery

Question 20

Outline the post-gastrectomy complications

Answer 20

• Early Complications
• General Surgical – Bleeding, Infection, Damage to surrounding tissue
• Anastomotic Leak
• Duodenal Stump Rupture – ∵Afferent limb dilatation in volvulus/kinking
• Late Complications – relates to functions of the stomach

1. Storage Related
   
   • Early Satiety – advise frequent small meals
   • Early Dumping Syndrome – Hypovolaemic shock due to rapid transit of hyperosmotic chyme [esp. carbohydrates] → small intestines → drawing fluid → lumen
   • Late Dumping Syndrome – Hypoglycaemia due to reactive hyperinsulinaemia stimulated by rapid passage of ↑↑carbohydrates → small intestines
2. Nutrition Related
   
   • Fe deficiency anaemia – ↑common
     
     • Duodenum [site of Fe absorption] bypassed in Bilroth II and Roux-en-Y
     • ↓Gastric transit time → ↓Fe3+ → 2+ conversion by gastric acid

• Vitamin B12 deficiency → pernicious anaemia [only in total gastrectomy]
  
  • Fundus & prox. body preserved in subtotal gastrectomy → parietal cells & intrinsic factor still released

1. Afferent Loop
   
   • Afferent loop can become obstructed ∵kinking/volvulus/adhesions → Post-prandial epigastric pain with non-billous vomiting
   • ↑Pressure in afferent loop can be transmitted back to biliary system → Obstructive jaundice [ascending cholangitis], Pancreatitis
2. Acid/Bile Related
   
   • Stomal ulcer can form on jejunal side of anastomosis ∵↑acid content
   • Chronic bile reflux → stomach can → chronic gastritis → CA recurrence
   • Retained antrum syndrome
3. Bezoar