Oesophagogastric

Question 1

What are the histological layers of the oesophagus?

Answer 1

• mucosa (non-keratinising stratified squamous epithelium, abruptly becomes glandular columnar at Z line; BM, LP; MM)
• submucosa - contains neurovascular & support tissue incl Messner neural plexus
• muscularis propria - inner circular, outer longitudinal; striated muscle in upper part (incl cricopharyngeus); smooth muscl ein lower & mixture in middle; Auerbach plexus between 2 layers of oesophagus
• NO serosa - just perioesophageal tissue/adventitia

Question 2

Describe the classification of GOJ tumours

Answer 2

The definition of adenocarcinomas of the GOJ does not allow correct comparison of diagnosis (endoscopic, radiological and pathologic), epidemiology and surgical therapy in national and international aspects, because different tumours can develope in the same area, and all called cardia tumors. Siewert and Stein recommended a classification to solve this problem.

Question 3

Describe the classification of Oesophagitis

Answer 3

Los Angeles Classification - endoscopically based

Grade A - One or more mucosal breaks, confined to the mucosal folds, each not more than 5mm in maximal length

Grade B - One or more mucosal breaks more than 5mm in length, but not continuous between mucosal folds

Grade C - Mucosal breaks that are continuous between the tops of two or more mucosal folds, but which involve less than 75% of the esophageal circumference

Grade D - Mucosal breaks which involve at least 75% of the esophageal circumference.

Question 4

Describe the classification of Gastric Ulcers

Answer 4

Historically classified using the Johnson classification, which was anatomically based and related to acidic-states:

• Type I - Lesser curve at incisura - low to normal acid state
• Type II - Two ulcers; gastric body and duodenum - high acid state
• Type III - Pre-pyloric - high acid state
• Type IV - High on lesser curve- normal acid state
• Type V - Anywhere - NSAID related

Question 5

Describe the classification of obesity

Answer 5

WHO Classification

• BMI 18.5 - 24.9 = Normal
• BMI 25 - 29.5 = Pre-obese
• BMI 30 - 34.9 = Obese class 1
• BMI 35 - 39.9 = Obese class 2
• BMI 40 - 49.9 = Obese class 3
• BMI 50+ “super obese” (non-WHO, colloquial)

Question 6

Describe the staging of gastric (MALT) lymphoma

Answer 6

Modified Blackledge system:

Stage I - Tumour confined to the GI tract without serosal penetration

Stage II - Tumour extends into abdomen nodes from the primary

II₁ - Local nodes

II₂ - Distant nodes

Stage III- Perforation of serosa with involvement of adjacent structures

Stage IV - Disseminated extra-nodal disease or supra-diaphragmatic disease.

Question 7

There is no consensus on what constitutes a safe remnant liver volume but…

Answer 7

For patients with normal livers ~20-25%

For patients following NAC ~30%

For patients with chronic liver disease ~40%

*From the companion series.

Question 8

Discuss the classification of Oesophageal Dysmotility

Answer 8

Chicago classification: a system derived from population-based high resolution manometry studies. It categorises dysmotility into 4 sub-groups:

1. Disorders with GOJ outflow obstruction: Achalasia Types I-III, Hypertensive LES.
2. Major disorders of peristalsis: Diffuse oes. spasm, Jackhammer oesophagus, absent contractility.
3. Minor disorders of peristalsis: Ineffective motility, fragmented peristalsis.
4. Normal.

Primary vs secondary:

• primary = achalasia, diffuse/distal oesophageal spasm, nutcracker/jackhammer oesophagus, hypertensive lower oesophageal sphincter, ineffective oesophageal motility
• secondary = from progressive damage induced by an underlying collagen vasuclar or neuromuscular disorder - scleroderma, dermatomyositis, polymyositis, lupus, Chagas disease

Anatomical approach based on involvement of oesophageal body or LOS - this is basis for understanding basic oesophageal manometry & often key to guide surgical therapy

• motility disorders of oesophageal body = distal oesophageal spasm (same as diffuse oesophageal spasm or corkscrew oesophagus) and hypercontractile oesophagus (same as nutcracker/jackhammer oesophagus)
• motility disorders of LOS = hypertensive LOS/GOJ outflow obstruction
• motility disorders affecting both body & LOS = achalasia, ineffective oesophageal motility

Question 9

Classify the causes of Gastric Outlet Obstruction

Answer 9

• Intraluminal
  
  • Neoplastic
    
    • Gastric cancer
    • GIST
    • Large gastric polyps
  • Foreign bodies
    
    • PEG feeding tubes
    • Bezoars
    • Gallstones (Bouveret syndrome)
• Intramural
  
  • Lymphoma
  • Diffuse gastric cancer; Linitis plastica
  • Peptic ulcer disease
  • Caustic injury
• Extramural
  
  • Pancreatitis +/- pseudocysts etc.
  • Upper abdominal malignancy
  • Retroperitoneal malignancy
  • Hepato/splenomegaly
• Neurogenic
  
  • Diabetic neuropathy
  • Infiltrative neuropathy

Question 10

Describe the classification of Hiatus Herniae

Answer 10

Anatomical classification based on the relationship of the LES to the diaphragmatic hiatus (DH):

Type 1 - “Sliding” - LES slides above DH

Type 2 - “Rolling” - Fundus rolls above DH past the LES

Type 3 - “Combined” - LES and fundus above DH

Type 4 - Stomach and other organ above DH

90% are Type 1.

Type I - asymptomatic can be mx conservatively; repair if symptomatic

Type II-IV - if asymptomatic, watchful waiting safe; if symptomatic repair (particularly if obstructive sx or have undergone volvulus)

• surgery traditionally advocated in all II-IV pts due to risk of complication, based on early series that showed much higher mortality after emergency cf elective cases (30% vs 1%); but more recent data suggests complications less common than initially thought (emergency surgery required in only 1% & operative mortality of 5.4% in this setting)

Question 11

Describe the common scoring systems used for UGI bleeding

Answer 11

• The Rockall scoring system places emphasis on a correlation between M&M and advancing age, shock, or significant co-morbidity; score <3 good prognosis, >8 poor prognosis.
  
  • derived based on 5 significant risk factors for mortality from a National UK audit
  • consists of an initial score from clinical parameters (age, shock, comorbidities) & a complete composite score after endoscopic assessment
  • initial score of zero (ie age <60, no tachycardia, no hypotension, no comorbidity): v low mortality
  • composite score, incorporating endoscopic info incl cause of bleeding & stigmata of haemorrhage has been validated in prospective studies, but more accurate in predicting mortality than risk of rebleeding
• The Glasgow-Blatchford score (Hb, urea, SBP, sex, HR, melaena, recent syncope, hepatic disease hx, heart failure), predicts the likelihood of requiring endoscopic intervention rather than risk of death
  
  • may be able to identify people who don’t need to be admitted to hospital after a UGIB (score of ≤1 are v low risk for rebleeding or mortality)
  • advantages over Rockall score, which assesses risk of death in UGIB, include a lack of subjective variables eg severity of systemic diseases and lack of a need for OGD to complete the score, so can be calculated when pt first presents
  • a simpler version of the score (modified GBS) = calculated using only the BUN, Hb, SBP and HR; score ranges from 0-16
    
    • • prospective study of modified score found it performed as well as the full GBS and outperformed Rockall score w regard to predicting need for clinical intervention, rebleeding and mortality

Question 12

Describe the classification of corrosive injury

Answer 12

Based on endoscopic findings:

1st degree - Mild erythema and oedema (superficial)

2nd degree - Ulceration and severe oedema (transmucosal w or w/o involvement of muscularis)

3rd degree - Deep ulceration, luminal obstruction, and dusky necrosis. (full thickness, w or w/o adjacent organ involvement)

Question 13

How are oesophageal varices graded?

Answer 13

• Grade 0 - absent
• Grade 1 - varices that collapse with insufflation
• Grade 2 - varices that do not collapse with insufflation
• Grade 3 - varices that occlude the lumen (large)

Question 14

Discuss the histological classification of Gastric Cancer

Answer 14

The Lauren classification remains the most useful

• Intestinal - Environmental, men>women, older age, glandular, haematogenous spread, MSI and APC mutations.
• Diffuse - Familial, women>men, younger age, poorly differentiated, trans-mural and lymphatic spread, E-cadherin mutation

The WHO classifcation recognizes four major histologic patterns of gastric cancers: tubular, papillary, mucinous and poorly cohesive (including signet ring cell carcinoma), plus uncommon histologic variants. It is less useful.

Question 15

What are the 3 distinct subgroups of patients with GORD?

How would you classify symptoms?

Answer 15

Acid reflux with oesophagitis

Volume reflux without endoscopic change

Barrett’s oesophagus

Typical symptoms - Heartburn, Acid-brash, Regurgitation

Atypical symptoms - Chest pain, Bloating

Extra-oesophageal - Globus, Cough, Dental decay, Sinus disease

Question 16

Classify the aetiological causes of dysphagia

Answer 16

• Neoplastic
  
  • Oesophageal cancer
  • Thyroid cancer
  • Pharyngeal/Oral SCC
• Mechanical
  
  • Schatzki’s ring
  • Strictures
  • Oesophageal webs
• Neurological
  
  • Parkinson’s
  • Achalasia
  • Oesophageal dysmotility
  • MS/Cerebral palsy/stroke
• Muscular
  
  • Muscular dystrophy
  • Connective tissue disease

Question 17

What are the 2011 UK National Guidance recommendations regarding resection of colorectal liver metastases?

Answer 17

Resection should be offered if a patient is fit enough, and complete resection can be achieved whilst leaving an adequate future liver remnant.

Relative contra-indications to resection include:

1. Non-treatable primary tumour
2. Loco-regional recurrence
3. Extensive nodal disease
4. Widespread pulmonary disease
5. CNS or skeletal metastases.

Question 18

Describe the classification of Barrett’s oesophagus

Answer 18

The Prague Classification is an endoscopically based system that measures the maximal longitudinal extent of Barrett’s change from the GOJ (M) and the maximal circumferential extent of Barrett’s change from the GOJ (C).

Question 19

What is the mandard score in UGI cancer?

Answer 19

Tumour regression post NAC TR 1 = complete response TR 5 = extensive cancer

Question 20

What can cause false positive Chromogranin A?

Answer 20

Liver or kidney failure, inflammatory bowel disease, atrophic gastritis or chronic use of proton-pump inhibitors

Question 21

Describe the complications of gastrectomy

Answer 21

Approximately one in four patients reports significant symptoms after gastric surgery; in 2-5%, these symptoms are disabling

• Complications relating to anastamosis
  
  • Leak
  • Stricture
  • Ulceration
  • Internal hernia
• Complications relating to motility
  
  • Rapid transit -
    
    • Dumping syndrome
      
      • Early
      • Late
    • Post vagotomy diarrhoea
  • Delayed transit
    
    • Slow transit
    • Gastric stasis
    • Afferent loop syndrome
• Complications relating to remnant stomach
  
  • Increased rates of gastric cancer after resection for benign disease
• Nutritional deficiences
  
  • Iron, the fat soluble vitamins, and B1 are all primarily absorbed in the duodenum and proximal jejunum
  • B12 levels are reduced due to reduced acidity and also reduced levels of IF.
  • Trace mineral absorption may be affected by rapid transit.

Question 22

What is Correa’s hypothesis?

Answer 22

H. pylori infection mounts a chronic inflammatory response resulting in an increased cell turnover that, over several decades, may result in an accumulation of mitotic errors. The step-wise progression of this inflammatory process was illustrated by Correa.

Question 23

How is prognosis in GIST determined?

Answer 23

• AFIP model (Armed forces institute of pathology)
  
  • uses mitotic rate, size and tumour location + completeness of resection
• NIH risk stratification scheme
  
  • uses size, mitotic counts and tumour rupture
• AJCC
  
  • uses size (T stage), mitotic rate and tumour location

Most important:

• size (T stage) - ≤2, 2-5cm, 5-10cm, >10cm (gastric >5cm, non gastric >10cm)
• mitotic rate - <5 or ≥5 per 50 HPF
• site - gastric and omentum better prognosis than other areas

Also:

• tumour rupture
• symptoms at diagnosis
• vascular invasion
• CKIT +ve or -ve

Question 24

Describe the management of bleeding and non-bleeding oesophageal varices

Answer 24

Primary prevention of variceal bleed:

• (reduce PVHTN)
• Beta-blockade with a non-selective agent such as Propanolol or Nadolol OR
• Endoscopic variceal ligation (better than sclerotherapy)

Secondary prevention of a re-bleed:

• As above
• Trans-jugular Intra-hepatic Porto-systemic shunt
• Liver transplantation

Bleeding varices are a life-threatening emergency associated with a 20% mortality and in those who make it to two weeks the 1-year survival is still only 50%.

Treatment outline:

• Haemodynamic resuscitation with blood products
• Correction of coagulopathy
• Broad spectrum antibiotics
• Vasoactive medication to reduce PHTN; Terlipressin most effective
• Intubation with balloon tamponade (Sengstaken-Blakemore tube)
• Banding of varices
• Trans-jugular Intra-hepatic Porto-systemic shunt
• Oesophageal stapling and shunt procedure; porto-caval, splenorenal, partial.

Question 25

How does Terlipressin work in bleeding oesophageal varices?

Answer 25

• Terlipressin is a Vasopressin analogue
• As a V(1) receptor agonist, it increases systemic vascular resistance, particularly in the splanchnic area, resulting in a decrease of portal pressure

Question 26

What are the parts of the oesophagus?

Answer 26

25cm long

cervical: 5cm - C6 to to T1 (thoracic inlet)
thoracic: 18cm - T1 to T10 (oesophageal hiatus)
abdominal: 1-2cm - oesophageal hiatus -> GOJ

Question 27

What is the uppper oesophageal sphincter?

Answer 27

• high pressure zone at inlet of oesophagus
• inferior pharyngeal constrictor inserts into the median raphe and is composed of the thyropharyngeus & cricopharyngeus
• cricopharyngeus muscle = responsible for generating HPZ
• Killian triangle = between oblique fibres of thyropharyngeus & transverse fibres of cricopharyngeus - site of potential weakness where Zenker diverticum forms

Question 28

What are the areas of constriction in the oesphagus?

Answer 28

Measured from incisors

• 15cm - commencement - cricopharyngeal sphincter (C6) - narrowest part
• 22cm - crossed by aortic arch
• 27cm - crossed by L main bronchus
• 38cm - diaphragmatic hiatus (T10)

Question 29

Describe the antireflux mechanisms

Answer 29

• a 10mmHg protective-pressure gradient spans stomach & oesophagus; stomach and abdo oesophagus lie within 5mmHg positive intra-abdo pressure, and thoracic oesophagus is exposed to ~5mmHg -ve pressure
• reflux exception rather than rule due to:
• intrinsic oesophageal mechanisms
  
  • LOS (together w diaphragmatic sphincter/pinchcock = HPZ)
    
    • LOS not an anatomically discrete sphincter; more of a concept - HPZ of smooth muscle in distal oesophagus
    • basal tone (in state of tonic contraction)
    • adaptive pressure changes (neurotransmitters, hormones & peptides that regulate LOS = implicated in GORD)
  • intrinsic epithelial resistance
  • acid clearance (by rapid peristalsis)
• extrinsic mechanisms
  
  • diaphragmatic sphincter/R crus (together w LOC/pinchock = HPZ)
  • distal oesophageal compression (when GOJ firmly anchored in abdo cavity, increased intra-abdo pressure is transmitted to GOJ, which increases pressure on distal oesophagus & prevents spontaneous reflux of gastric contents)
  • angle of His - ‘flap valve’ - when stomach gets full, fundus pushes against oesophagus
  • mucosal rosette
  • phreno-oesophageal ligament - anchors oesophagus within +ve pressure environment
• reflux occurs when gastric pressure overwhelms the HPZ, although whether they are received as symptomatic = modulated by oesophageal sensitivity and volume, composition & clearance time of refluxate
• physiologic reflux episodes typically result from appropriate TLOSRs to vent gas - any distal oesoph exposure usu minimal, rapidly cleared & asymptomatic
• pathological reflux episodes due to 3 primary mechanisms:
• inappropriate TLOSRs
• a persistently hypotensive LOS (frequently assoc w hiatus hernia bc of displacement of GOJ into mediastinum)
• transient increases in intra-abdo pressure

Question 30

How do you identify the GOJ?

Answer 30

4 ways; 2 endoscopic, 2 external

Endoscopic

• Z line may mark GOJ as long as pt doesn’t have Barrett’s
• top of the gastric folds
• (in Asia use distal extent of pallisade vessels)

External:

• where circular muscle fibres of oesophagus join oblique fibres of stomach
• gastro-oesophageal fat pad

Question 31

What is the lower oesophageal sphincter?

Answer 31

The primary antireflux mechanism. Not an anatomically discrete sphincter; is a dynamic HPZ in distal oesophagus composed of specialised smooth msucle, arranged in eitehr clasp or sling formation, running in teh distal 2-4cm of teh oesophagus & cardia

Question 32

What are the risk factors for oesophageal foreign bodies?

Where do they impact?

Answer 32

• dentures - impair ability to judge size of food bolus
• mental/psych difficulties/substance abuse/prisoners
• oesophageal disease - eg strictures (benign/malignant), motility disorders
• eosinophilic oepsohagitis for food bolus
• most impact in cervical oesophagus but can occur at any of physiological narrowings: cricopharyngeus, aortic arch, L main bronchus, GOJ

Question 33

What is the management of oesophageal foreign bodies?

Answer 33

• FB at pharynx/cricopharyngeus (most fishbone) - direct laryngoscopy
• non-endoscopic: proteolytic agents (NOT recommended - oesophageal trauma, dangerous if aspirated); carbonated drinks or IV glucagon (no good evidence)
• 10-20% need endoscopic removal (w airway protection, GA)
• large graspers, nets, lassoes, balloon catheter
• push into stomach if <2cm - care not to perforate
• objects >5-6cm long or >2cm diameter unlikely to pass through pylorus/around duo curves
• indications for urgent removal:
• airway compromise
• absolute dysphagia w aspiration risk
• oesophageal impaction of sharp object or button battery
• oesophageal impaction of >24hrs duration
• button batteries if moving/non-impacted in stomach/SB an observe 48-72hrs - if passed into stomach & duo 80-90% will pass w/o complication
• sharp objects that enter stomach have perf risk in GIT up to 35%, usu at ICV - if retrieval safe should be attempted
• deliberate narcotic packet - don’t endoscopically remove as successful retrieval outweighed by risk of rupture; most packets will pass safely through bowel but urgent surgery if failure to progress, obstruction or rupture
• indications for surgery (1%):
• signs of obstruction, impaction, perforation or bleeding
• failed endoscopic retrieval
• failure to leave stomach
• accumulation of multiple FBs
• large >2.5cm or long sharp objects

Question 34

What are the causes of oesophageal perforation?

Answer 34

• iatrogenic most common
• usu endoscopic >50% perforations, increased risk with therapeutic interventions eg EMR, ESD, dilatation
  
  • cricopharyngeus & lower 1/3 most common
• also anterior approach spinal surgery, antireflux surgery, pulmonary resections, NGT placement, TOE, ET tube placement, POEM
• Boerhaave’s - 15%
• FB - 14% (incl stent erosion)
• Corrosive
• Penetrating > blunt trauma (blunt v rare)
• Malignancy - tumours of oesophagus & lung

Question 35

How are oesophageal perforations classified?

Answer 35

Early = presenting within 24hrs of injury vs late >24hrs

Pittsburgh Oesophageal Perforation score stratifies by morbidity, mortality and length of stay; variables are age >75, tachycardia, leukocytosis, pleural effusion, fever, noncontained leak, respiratory compromise, time to diagnosis >24hrs, presence of cancer, hypotension

Question 36

What are the clinical signs of oesphageal perforation?

Where does a thoracic perforation most commonly occur?

Answer 36

• pain most striking
• Mackler’s triad for Boerhaave’s (only 14-20% accurate): chest/lower thoracic pain ‘boring’ nature, vomiting, subcut emphysema
• cervical perf: pain in neck, torticollis, dysphagia +/ dysphonia/hoarseness, fever, surgical emphysema +/- local inflammation, systemic effects less common
• thoracic perf: chest/back/abdo pain, SOB, dysphagia & odynophagia, sometimes abdo pain/tenderness, fever +/- hypotension as chemical & microbial pleuromediastinitis develops, surgical emphysema takes time to develop (starts in mediastinum, mediastinal crunch w heartbeat heard over precordium
• thoracic perf most common site (70%) = left posterolateral oesophagus usu 3-5cm above GOJ; 2nd most common site (20%) = midthoracic, R side, at level of azygos vein; may be bilateral (10%)

Question 37

What is the pathophysiology of Boerhaave’s?

Answer 37

Boerhaave’s syndrome = effort related rupture of oesophagus in absence of pre-existing pathology - usu after forceful vomiting; other causes of barotrauma = childbirth, seizure, heavy lifting, defaecation, Heimlich manoeuvre.

Barogenic trauma -> immediate & gross gastric content contamination of mediastinum & often pleural cavity -> chemical & septic mediastinitis which can precipitate a rapid deterioration in condition. Infection usu polymicrobial: staph, strep, pseudomonas, bacteroides, ?fungi.

In cases where pleura is disrupted this can occur at time of barogenic event or subsequently as a result of gastric acid erosion, exacerbated by intrathoracic pressure; thin mediastinal pleura easily ruptured then neg intrathroacic pressure sucks gastric contents into chest.

In apparent ‘spontaneous perforation’, an underlying cause such as malignancy, peptic ulceration or infection discovered in up to 20%; eosinophilic oesophagitis can also predispose to oesophageal perf both after vomiting or after endoscopic intervention to dislodge a food bolus.

Question 38

Investigations for oesophageal perforation

Answer 38

CXR (normal in 9%)

• pleural effusion
• pneumomediastinum 40%
• widened mediastinum
• pneumothorax up to 77%
• hydroneumothorax
• collapse/consolidation
• cervical air, abdominal free air

CT w oral contrast first line

Gastrograffin swallow (avoid barium as causes inflammatory response; prefer oral water-soluble contrast which is rapidly absorbed, don’t exacerbate inflammation & have minimal tissue effects - if negative can use dilute barrium; also if high risk of aspiration might use dilute barium bc gastrograffin causes pneumonitis ++)

Endoscopy - may be useful if FB suspected or haematemesis or CT normal. Allows NG tube placement. Can convert small/partial perforation into more significant one - often safest to perform under GA w intubated so PPV decreases risk of air insufflation inot mediastinum & pleural space.

Thoracocentesis of frank gastric contents = diagnostic - pH <6, high amylase also can confirm.

Swallowed or injected oral/NG dye eg methylene blue diagnostic if comes out chest drain

Question 39

What are the criteria for non-operative management of oesophageal perforation?

Answer 39

Modified Cameron’s criteria

• early diagnosis or delayed diagnosis with contained leak
• perforation not in the abdomen
• perforation contained by mediastinal pleura
• no solid food contamination of mediastinal or pleural spaces
• drainage of contrast back into oesophagus on contrast swallow
• no symptoms of signs of mediastinitis/sepsis
• perforation does not involve neoplasm or obstruction of the oesophagus
• tolerance to pleural or mediastinal contamination w appropriate drainage
• presence of experienced thoracic surgeon and contrast imaging in the hospital

Involves ICU, NBM, NGT, enteral feeding, IV abx incl antifungals, losec, often chest drain, serial contrast studies… +/- if collection found -> perc drain; if deterioration -> surgery (20% require surgical salvage).

Also consider presence of underlying oesophageal disease.

Iatrogenic cervical perforations usu contained & thus mx can be non-op w perc drainage of collections; any resulting oesophagogastric fistulas heal rapidly in presnece of distal obstruction.

Closure with endoclips can be used to close small iatrogenic perforations immediately in the absence of significant contamination, in addition to supportive non-op tx (needs highly skilled endoscopist, ?experimental). Stents have been used but high migration rates bc not designed for normal oesophagus, need to be removed within 6-12wks to avoid complications; not standard treatment. Endoscopic lavage of contained mediastinal perfs +/- endoVAC or NG on low suction into cavity and gradually withdrawn described - not for gross contamination.

Question 40

What are the principles of surgery for oesophageal perforation?

Answer 40

Thoracic

• Debride/treat contamination - eradicate mediastinal/pleural sepsis w VATS or open throacic washout
• Source control
  
  • approach
    
    • high perforations - left neck incision
    • mid oesophagus - right thoracotomy
    • distal oesophagus - left thoracotomy +/- laparotomyh
  • identify injury, myotomy to expose full extent, debridement of devitalised tissue
  • small injury w healthy tissue, <24hrs: repair primarily in 2 layers w 2/0 or 3/0 absorbable w tissue flap coverage (intercostal muscle, pericardial fat, pleura, omentum)
  • extensive injury w devitalised areas: controlled fistulisaton by T tube
  • v large or devitalised defects: oesophageal exclusion w creation of cervical oesophagostomy & gastrostomy tube + later reconstruction
  • drain widely - eg Jackson-Pratt at perforation + 2 large bore ICDs
• if signs of obstruction (achalasia, stricture, tumour) remedy at time of initial op or repair won’t heal - eg myotomy for achalasia on opposite side to repair
• Re-expand lung
• Enteral feeding access

Cervical

• incision parallel to anteiror border of SCM, retract carotid sheath laterally & thyroid medially (finger retraction on thyroid to avoid RLN injury)
• prevertebral fascial plane entered & pus/contrast/leak identified
• suture w interrupted 3-0 prolene w ?knots inside
• if not found, place drains infeirorly into mediastinum & superiorly along postvertebral gutter -> most will close in 2-3wks if NBM

Perforation through malignancy = incurable - so any resection palliative & surgical mortality in this context high; mx non-op w sealing palliative stent. If lesion was operable before perforation & only if perf is separate to underlying malignancy consider resection to control contamination w potential cure.

Question 41

What are the causes of oesophageal strictures?

Answer 41

Fixed fibrous narrowing in oesophageal lumen

GORD/peptic strictures most common benign cause.

Aetiology

• congenital
  
  • webs
  • epidermolysis bullosa - AR, blistering of skin & oral mucosa +/- oesophageal web formation
• inflammatory
  
  • GORD -> Schatski ring
  • Crohns, Sarcoid
  • eosinophilic oesophagitis - causes concentric ridges/furrows
  • infective - candida, CMV, herpes, TB - usu in immunosuppressed
• neoplastic
• iatrogenic
  
  • post scleortherpay fibrosis
  • after radiation
  • after prolonged NGT
• tablets/drugs, poisons, toxins incl corrosive
• structural: webs eg Plummer Vinson syndrome

Question 42

Aetiology and pathophys of corrosive oesophageal injuries

Answer 42

• usu from alkaline ingestion
  
  • readily available strong alkalis = cleaners & bleachers
• readily available acids = toilet cleaner (HCl acid), battery fluid (sulphuric acid), metal-working agents (phosphoric acid, hydrofluoric acids)
• severity of any injury = related to corrosive properties, conc, amount, viscosity & duration of contact w mucosa
  
  • intentional ingestions = larger quantities of agent (accidental by children usu small)
• type of injury depends on pH
  
  • alkaline -> liquefaction necrosis of several layers of oesohpageal mucosa - involves dissolution of proteins & collagen, thrombosis of bld vessels
  • acids -> coagulation necrosis -> formation of protective escar; however ingestion of any strong caustic agent in sufficient quantity will inflic potenitally fatal oesophageal injury & acid assoc w greater systemic effects, a higher perf rate & higher mortality than alkali
• commonly said that acid causes more gastric damage whereas alkali ingestion causes oesophageal injury but no evidence to support this
• results in stricture development if injury involves submucosa/deeper layers

Question 43

Investigation and management of corrosive/caustic oesophageal injuries

Answer 43

• assess initially for upper airway compromise - dyspnoea, drooling, stridor, hoarseness, inflammatory oedema of lips/mouth/tongue/oropharynx +/- intubation/cricothyroidotomy
• endoscopy & CT both have roles in determining optimum mx, predicting complications; in practice these in combo w pt’s clinical status will dictate mx
  
  • endoscopy = gold-standard for staging; should have within 24hrs (unless obviously perforated) as risk of perforation increases after 48hrs; can also place nasoenteral tube which can also act as partial stent to prevent strictures (may benefit from repeat scope 48-72hrs after admission)
  • CT w IV & oral contrast - grading system proposed
• Management
  
  • Analgesia
  • NG under fluoroscopic or endoscopic guidance
  • antisecretory agents
  • grade 1 and 2a burns: admit & observe for 5-7days, w diet reintroduced after 24-48hrs; endoscopy or contrast rad 6-8wks after d/c to assess for strictures
  • grade 2b & 3 burns: observe, NJ feed & if no evidence of progression to perf then COFs from 48hrs but be aware perf risk present for ≥7 days
  • if present w perf or deteriorate - emergency oesophagogastrectomy (stomach almost always injured) - usu oesophagostomy & delayed recon 6-8wks later
  • some advocate for laparoscopy to asses gastric viability; controversial
  • abx only if infection, perf or aspiration
• up to 50% get strictures
  
  • most can be mx w bougie dilatation but wait 6wks; may require multiple dilatations
  • young pts w long, grade 3/4 strictures likely to need lifetime repeated dilatations w cumulative risk of iatrogenic perf & ca - consider surgery; bypass or stricturoplasty w vascularised graft of colon (but retains long-term cancer risk) or thoractomy, resection, colonic recon
  • squamous malignant transformation in 16% - 1000x risk; latent period 15-40yrs

Question 44

Discuss oesophageal webs and rings

Answer 44

• web - thin extension of normal oesophageal tissue composed of mucosa & submucosa only
  
  • nb Schatzki ring should really be called web
  • Schatzki ring = concentric, nonmalignant, fibrous thickening & narrowing of GOJ w squamous epithelium above & columnar cells below
• rings - concentric smooth, thin extension of normal tissue into oesophagus, that consists of all 3 layers: mucosa, submucosa & muscle
• aetiology
  
  • congenital - failure of normal canalisation of oesophagus -> typically mid or lower oesophagus
    
    • epidermolysis bullosa
  • Plummer Vinson syndrome: postcricoid webs & iron deficiency
  • Schatzki ring - unknown, correlations to reflux disease & hiatal hernia
• clinical
  
  • many asymptomatic
  • dysphagia espec if lumen ≤13mm
  • meat impaction
  • presence of Schatzki ring not pathological but can be seen in pts suffering from dysphagia or obstruction
• mx
  
  • lifestyle changes - cut food smaller
  • PPIs
  • dilatation - r/o malignancy w biopsy first
    
    • Schatzki ring often needs repeat dilatations
  • endoscopic electrocautery
  • occasionally resection

Question 45

What is the classification and aetiology of diverticular disorders of the oesophagus?

Answer 45

• focal pouches of oesophageal wall consisting of mucosa, submucosa +/- muscularis
• classification
  
  • by location
    
    • pharyngoesophageal (Zenker)
    • parabronchial (midoesophageal)
    • epiphrenic (supradiaphragmatic)
  • traction vs pulsion
  • false (involve mucosa & submucosa only, Zenker & epiphrenic (pulsion)) vs true (involve all 3 layers, midoesophageal (traction))
• aetiology
  
  • traction diverticula = from external inflammatory mediastinal lymph nodes adhering to oesphagus as they heal & contract, pulling oesophagus during process so overtime wall herniates; more common in midoesophageal region round carinal nodes
  • pulsion diverticula = occur bc of increased intraluminal pressure generated from abnormal motility disorders

Question 46

Zenker’s diverticulum

Answer 46

• a form of false, pulsion diverticula of posterior mucosa between the 2 parts of the inferior constrictor - thyropharyngeus above & cricopharyngeus below (Killian’s dehiscence/triangle which is devoid of muscle in posterior wall)
• aetiology: ?result of loss of tissue elasticity & muscle tone w age, along w abnormal motility which increases intraluminal pressures, as well as the sphincter muscle becoming non-compliant & fibrotic w age
  
  • as diverticulum enlarges, mucosal & submucosal layers dissect down left side of oesophagus into superior mediastinum, posteriorly along prevertebral space
• clinical
  
  • small - asymptomatic
  • sticking in throat, nagging cough, excessive salivation, intermittent dysphagia
  • as increases - regurgitation of foul-smelling, undigested material, gurgling in neck during swallowing, halitosis, voice change from pressure on RLN, resp infections
• diagnosis - barium swallow; manometry & endoscopy not needed
• mx - treat ?regardless of size or if large enough to be symptomatic
  
  • treat underlying GORD
  • principles = excise or plicate pouch and divide hypertensive cricopharyngeus (myotomy)
  • surgical: incision in left side of neck
    
    • myotomy of prox & distal thyropharyngeus & cricopharyngeus muscles
    • diverticulum <2cm - myotomy alone sufficient
    • >5cm sac, excise
    • or diverticulopexy - secure diverticulum to posterior pharynx which allows free vertical movement on deglutination (suspends diverticulum upside down to prevent refilling)
  • endoscopic exclusion: Dohlman procedure
    
    • for 2-5cm sacs
    • endoscopic division of common wall between oesophagus & diverticulum w laser, electrocautery or stapler device similarly successful (placed via oropharynx) - so oesophagus & diverticulum form common channel
    • postop course slightly shorter - overnight stay, take liquids next day
• outcomes of repair: >90% asymptomatic, 5% complications incl RLN palsy & cutaneous fistula, 1.2% mortality

Question 47

Midoesophageal diverticula

Answer 47

• form of true diverticulum which involves all layers of oesophageal wall, occurring in mid-oesophagus as a result of traction
• aetiology - result from external inflammation adhering to oesophagus pulling oesophagus over time
  
  • historically inflamed mediastinal nodes from TB; now histoplasmosis & resulting fibrosing mediastinitis more common
• clinical
  
  • most asymptomatic
  • often found incidentally
  • dysphagia, chest pain, regurg usu indicative of underlying primary motility disorder
  • chronic cough - suspect bronchoesophageal fistula
• ix
  
  • barium swallow dx, typically on right bc of overabundance of structures in mid-thoracic region on left
  • CT helpful to identify any mediastinal lymphadenopathy
  • endoscopy to r/o mucosal abnormalities incl cancer hidden in sac
  • manometry - in all, to identify primary motor disorder
• mx
  
  • guided by results of manometry
  • asymptomatic w underlying mediastinal LNs - treat underlying cause
  • diverticulum <2cm - observe
  • if progresses to sx or diverticulum ≥2cm - surgery
    
    • usu have wide mouth & rest close to spine so diverticulopexy can be done - suspended from thoracic vertebral fascia
    • if severe chest pain or dysphagia & documented motor abnormality, long oesophagomyotomy also indicated

Question 48

Epiphrenic diverticula

Answer 48

• false/pulsion diverticula of oeosphagus found adjacent to diaphragm in distal third of oeosphagus, within 10cm of GOJ
• aetiology: most often related to thickened oeosphageal musculature or increased intraluminal pressure
  
  • often assoc w DES, achalasia or IEM disorders
  • or congenital (Ehlers Dalnlos) or traumatic
• clinical
  
  • most asymptomatic - dx often made during workup for motility disorder
  • sx usu related to motility disturbance
• ix
  
  • barium swallow - delineates diverticulum & underlying motility disorder
  • manometry to ix motility
  • endoscopy - to evaluate for mucosal lesions
• mx
  
  • similar to mid oesophageal diverticulum, tend to wide-mouthed & rest close to spine
  • small <2cm - suspend from vertebral fascia with diverticulopexy + myotomy begun at neck of diverticulum and extended onto LOS
  • if diverticulectomy: vertical stapling device placed across neck & diverticulum excised, with bougie in to avoid narrowing; muscle closed over excision site & long myotomy on opposite wall extending from level of diverticulum onto LOS
  • if large hiatal hernia also present, diverticulum is excised, a myotomy performed & hiatal hernia repaired - otherwise high incidence post-op reflux

Question 49

Discuss the pathophysiology of acid production in the stomach

Answer 49

Parietal cells in the gastric antrum and cardia express a proton pump on their luminal surface. This H+/K+ ATPase secretes H+ into the lumen of the stomach, reducing the pH. Insertion and activity of H+/K+ ATPase is under neurohumoral control via the vagus nerve, acetylcholine and gastrin. PPIs remain the optimum medical therapy as they reduce expression of the final common pathway of all three variables in acid production.

Question 50

What are the risk factors for oesophageal adenocarcinoma and SCC

Answer 50

Adenocarcinoma (include) - central obesity, GORD, Barrett’s, smoking, male

SCC (include) - smoking, nitrosamine-containing compounds, achalasia, chronic dysplasia from strictures or erosive injuries

Question 51

What is the classification of bleeding upper GI ulcers?

Answer 51

Forrest classification - predicts rate of re-bleed

Ia - actively bleeding

Ib - oozing

IIa - visible vessel

IIb - adherent clot

IIc - pigmented base

III - clean ulcer base

Question 52

What are the virulence factors of H pylori?

Answer 52

Include flagella, urease, phospholipase, Cag-A, Vac-A toxins

Question 53

Slipped gastric band

Answer 53

• vomiting and intractable epigastric pain
• abnormal angle of band against spine, often referred to as Phi angle (usu 4-60 degrees)
• slipped band may cause symmetrical, anterior or posterior prolapse
• posterior prolapses are caused by counter-clockwise slippage & a vertical position of the band
• anterior prolapses are caused by clockwise slippage & the lie of the band if often horizontal
• immediate mx: decompression of band via port; ideally a Huber needle is used but any needle can be used in an emergency
• subsequent mx: depends on pt’s condition - if acutely unwell w physiology suggestive of ischaemia in a strangulated stomach, need acute laparotomy & removal of band; if well then need inpatient removal or adjustment of band by bariatric surgeons

Question 54

What is GORD? How is it classified?

Answer 54

GORD = troublesome symptoms or complications caused by reflux of gastric contents into oesophagus

Montreal classification

• subdivides GORD into oesophageal & extra-oesophageal syndromes
• oesophageal syndromes are subdivided into symptomatic syndromes vs syndromes with oesophageal injury
  
  • symptomatic syndromes include
    
    • typical reflux syndrome and reflux chest pain syndrome
      
      • typical reflux syndrome = acid reflux, volume reflux, dysphagia (espec if large hiatus hernia but also concern for cancer)
      • reflux chest pain syndrome
      • these can manifest as NERD (non-erosive reflux disease - those w increased levels of acid reflux) or oesophageal hypersensitivity (those without acid reflux)
  • syndromes with oesophageal injury include those with oesophagitis, stricture, Barrett’s or adenocarcinoma
• extraoesophageal syndromes are those with either established associations or proposed associations
  
  • established associations = reflux cough, reflux laryngitis, reflux asthma, reflux dental erosions
  • proposed associations = pharyngitis, sinusitis, idiopathic pulmonary fibrosis, recurrent otitis media

2/3 of pts w symptom-defined GORD have apparently normal endoscopy (NERD); 2/3 of pts w reflux oesophagitis are symptomatic

Question 55

What are the risk factors for GORD?

Question 56

What are the mechanisms for extraoesophageal symptoms in GORD?

Answer 56

1. Proximal oesophageal reflux & microaspiration of gastroduodenal contents -> direct caustic injury to larynx & lower resp tract (most common mechanism)
2. Distal oesophageal acid exposure triggers vagal nerve reflex -> bronchospasm & cough (due to common vagal innervation of trachea & oesophagus)

Question 57

Discuss your investigations for GORD

Answer 57

• PPI trial - if no alarm sx; symptomatic response suggestive of GORD; if good response & happy on PI no further ix indicated
• endoscopy - if suspected cancer, pts at high risk of BO & those w insufficient response to PPI trial; looking for
  
  • hiatus hernia
  • oesophagitis
  • Barretts
  • worse case exclude cancer, achalasia (though can be missed on endoscopy), GOO
• consider referral to another specialty if atypical sx only
• consider specialised tests (all 3 together)
  
  • oesophageal manometry
  • 24hr pH testing
  • impedance study
• who needs more tests:
  
  • typical sx & abnormal endoscopy = can go straight to surgery
  • atypical sx & abnormal endoscopy = cautiously could go straight to surgery, but low threshold for further testing to check their sx do correlate w the acid reflux
  • typical sx + normal endoscopy = further tests mandatory
  • atypical sx + normal endoscopy = definitely further tests + be v careful about how you consent them later
• barium swallow not used routinely - limited role in dx of GORD

Question 58

What are the indications for antireflux surgery?

Answer 58

1. Pts whose sx aren’t adequately controlled by lifestyle measures/PPI
2. Pts whose sx are controlled but have side effects or don’t want to be on long-term PPI

• immediate side effects (generally mild): headache, abdominal pain, flatulence, constipation, diarrhoea
• long term: small risk bone fractures, malabsorption of Ca/B12/mag/iron, increased susceptibility to some bacterial infections (C diff, pneumonia)

NB: has never been proven that surgery stops Barretts progressing to cancer (only one trial that has shown surgery is superior to medical tx in causing regression of Barrett’s but some methodological issues); so not enough evidence to say BO is an indication for surgery on its own - should be selected for surgery on basis of sx & response to meds.

Question 59

What are the principles of antireflux surgery?

Answer 59

Overall, prevent reflux but preserve pt’s ability to swallow normally.

• restore normal pressure at LOS
• correct H/H but w normal angle of His and ≥1.5cm of abdominal LOS length
• avoid too tight a wrap

Surgical steps:

• expose oesophageal hiatus
• reduction of any HH
• complete mobilisation of GOJ, lower oesophagus
• ensure adequate lenght of intra-abdo oesophagus
• repair oesophageal hiatus w sutures to crura (‘cruroplasty’)
• wrap fundus of stomach around oesophagus
  
  • surgeon’s preference; 360 degree total good durability but more side effects; partial wraps slightly less side effects but also slightly higher risk of recurrent reflux
  • Nissen 360 degree complete wrap
  • Toupet 270 degree posteiror fundo
  • Dor 180 degree anterior fundoplication
    *

Question 60

What is a hiatus hernia? What is gastric volvulus?

Answer 60

Hiatus hernia = an extension of the peritoneal cavity into the thoracic cavity through the oesophageal hiatus of the diaphragm

Gastric volvulus = rotation of the stomach >180 degrees around a fixed axis of rotation

• organoaxial = most common, accounts for almost all - stomach rotated around anatomical (longitudinal) axis, represented as a line drawn from cardia to pylorus, frequently resulting in gastric strangulation
• mesentericoaxial = antrum of stomach rotates anteriorly & superiorly around a transverse axis that extends from mid-lesser curvature to mid-greater curvature
  
  • typically incomplete & results in intermittent gastric obstruction rather than acute strangulation

Question 61

Describe the presentation of gastric volvulus

Question 62

What is Barrett’s Oesophagus?

Answer 62

• the metaplastic replacement of stratified squamous epithelium of the oesophagus by columnar epithelium +/- presence of intestinal metaplasia proven histologically
  
  • Aus guidelines, AGA, ACG & ESGE all believe IM necessary for dx of BO; BSG, Asia Pacific Working Group & BOBCAT group feel IM not needed for dx of BO
  • supporting IM being mandatory = risk of oesophageal adenocarcinoma much lower in pts w columnar metaplasia w/o intestinal metaplasia cf those with
  • also debate about whether you need ≥1cm of IM - but most guidelines (not Aus) recommend 1cm at least

Question 63

What should be done when Barrett’s oesophagus is suspected while performing a gastroscopy?

Answer 63

Biopsies assessing for intestinal metaplasia (columnar epithelium w goblet cells) should be performed when any length of salmon pink mucosa is seen extending above the GOJ into the tubular oesophagus for a confirmed dx of BO (ie suspect BO in these pts)

Checklist for endoscopic exam of BO:

• level of GOJ, SCJ and diaphragmatic indentation
• describe BO using Prague C & M criteria
  
  • C = max circumferential extent; depth of endoscope insertion at GOJ minus depth of endosopic insertion from circumferential extent of suspected columnar epithelium
  • M = max extent; depth of endoscope insertion at GOJ minus depth of endoscopic insertion from max extent of columnar junction
  • (previously arbitrary classification of long-segment & short-segment Barrett’s ≥3cm & <3cm)
• describe lesions within a segment of BO according to distance from incisors, clock-face position & Paris endoscopic classification system (protruding, excavated or flat)
• mapping biopsies using Seattle protocol
  
  • 4 quadrant biopsies at 2cm intervals
  • • separate biopsies from anatomic cardia
  • for dysplastic segments, biopsies should be taken at 1cm intervals
  • • targeted biopsies from any lesions & the immediately surrounding epithelium

Question 64

What is the Z line?

How do you identify the GOJ endoscopically?

How do you identify a hiatus hernia endoscopically?

Answer 64

• Z-line = squamocolumnar junction - where squamous epithelium turns into columnar epithelium
• GOJ = imaginary level at which oesophagus ends & stomach begins
  
  • endoscopists in West: most proximal extent of gastric folds
  • in East: distal extent of lower oesophageal palisade vessels (longitudinally-oriented blood vessels in lower oesoph)
• in absence of squamous intestinal metaplasia, Z line & GOJ coincide
• diaphragmatic indentation can be used to identify presence of a hiatus hernia where GOJ lies above DI

Question 65

What is the management of Barrett’s Oesophagus?

Answer 65

Risk of progression from BO to adenocarcinoma

• general population of pts w BO: 0.25% per year
• LGD: risk poorly defined bc of differences in how pathologists dx LGD; roughly 0.54% per year
• HGD: 4-8% per year
• overall risk of developing oesophageal ca 30x higher than general population

Management

• non-dysplastic BO - surveillance
  
  • <1cm: discharge from f/u (most guidelines say not actual BO)
  • if 1-3cm repeat scope 3-5yrs; if no IM on repeat biopsies d/c
  • if ≥3cm, may have intensive surveillance, possibly q2-3yrs
• indefinite, low and high grade dysplasia should be confirmed by a 2nd pathologist
• indefinite for dysplasia - 2nd pathologist rv + repeat endoscopy 3-6mo; if concern for dysplasia remain then surveillance at 12mo or back to usual screening if repeat biopsies show no dysplasia
• LGD - confirm by expert pathologist, repeat OGD w Seattle protocol biopsies if not done, then either
  
  • endoscopic eradication preferred (RFA, endoscopic resection of entire segment, photodynamic therapy or spray cryotherapy) - tx of choice based on SURF trial
  • or endoscopic surveillance valid alternative; q6mo for 1yr then annually til reversion to non-dysplastic BO; if 2 consecutive endoscopies find no dysplasia then surveillance can be downgraded to that of non-dysplastic BO)
• HGD or intramucosal carcinoma - confirm by expert pathologist, repeat OGD w Seattle protocol biopsies if not done, then
  
  • usually endoscopic eradication w endoscopic resection (EMR/ESD) of any visible mucosal irregularities then, if no submucosal invasion on histo, ablation usu w RFA to flat segments
    
    • post treatment 12wk high dose PPI then re-scope - initially after eradication 3monthly for 1yr then annually thereafter
  • oesophagectomy only in special circumstances eg pts unwilling to undergo surveillance (occult LNs only in 1-2% of pts w HGD or IMC in BO)
• oesophagectomy if T1b disease except with: sm1, well differentiated, no LVI or poor surgical candidate

Question 66

What is the definition and classification of a gastric bezoar?

Answer 66

• foreign body resulting from accumulation of ingested material, most commonly found as a hard mass or concretion in the stomach (rare)
• Classification
  
  • phytobezoars: composed of vegetable matter
    
    • most common
    • persimmon accounts for majority
    • male predominance, 40s to 50s
  • trichobezoars: composed of hair
    
    • gastric trichobezoars w long tailes that extend through small bowel = rapunzel syndrome
    • female predominance, 20s
  • pharmacobezoars: ingested medications
    
    • ER nifediipine, theophylline, enteric-coated aspirin, sodium alginate, sucralfate
  • other: tissue paper, shellac, fungus, Styrofoam cups, cement, vinyl gloves, milk curd etc

Question 67

What is the pathogenesis of and risk factors for gastric bezoars?

Answer 67

• usually result from ingestion of indigestible material in pts w impaired grinding mechanism of stomach & interdigestive migrating motor complex
  
  • initially thought delayed gastric emptying was underlying cause of all bezoars but studies found mots pts have normal or accelerated gastric emptying & composiiton of ingested material plays important role
• disopyrobezoars (from persimmon) form as they contain high concs of an insoluble tannin called shibuol which forms a coagulum when mixed with gastric acid
  
  • proline-rich secretions from parotid & subclavian glands have high affinity for binding tannins & promote formation
• trichobezoars form in those w trichotilomania & tricophagia
  
  • begin as retained hair in gastric folds, denatured by gastric acid, become black due to oxidation & combine w food to become enmeshed mass
  • colonised by bacteria giving halitosis
• once formed, bezoars grow by continued ingestion of food rich in cellulose & other indigestible material, matted together by protein, mucous & pectin
• complications: GI perforation, peritonitis, protein-losing enteropathy, steatorrhoea, pancreatitis, intussusception, obstructive jaundice, appendicitis, constitpation, pneumatosis intestinalis

Risk factors

• gastric dysmotility - many have had gastric surgery incl vagotomy & pyloroplasty; gastroparesis impairs grinding mechanism & IMC
• GOO
• dehydration
• anticholinergic agents
• opiates
• diverticulum
• medications w insoluble carrying vehicle

Question 68

What are the clinical manifestations and options for management of gastric bezoars?

Answer 68

• clinical
  
  • may remain asymptomatic for yrs
  • insidious onset
  • pain, N&V, early satiety, anorexia, weight loss
  • bleeding secondary to concurrent gastric ulcers/PUD/pressure necrosis
• management
  
  • lifestyle prevention - increase water intake, modify diet, chew food, psych evaluation, assess for motility disorder
  • medical
  • chemical dissolution w adjuvant prokinetic metoclopramide
    
    • preferred if mild symptoms
    • noninvasive, inexpensive
    • risk of partial dissolution & subsequent SBO
    • coca-cola via gastric lavage
    • cellulose
    • papin
    • N-acetylcysteine
  • adult prokinetics eg metoclopramide
• endoscopic removal w fragmentation - if fail to dissolve or are resistant to chemical dissolution (trichobezoars)
  
  • or if mod/severe sx due to large bezoars
  • involves fragmenting w a water jet, direct suction through large channel endoscopy, forceps or shares; fragments can then be cleared w endosscope or by using a large bore NGT, or allowing to pass thorugh GI tract
• operative:
  
  • reserved for failed dissolution & endoscopy but signif complications incl bleeding & obstruction
  • if pharmacobezoar treat as for GI decontamination; principle not to disrupt bezoar as can release copious active medication
  • if gastrostomy or enterotomy performed to remove bezoars, check remainder of SB & stomach to exclude other retained bezoars

Question 69

Discuss the phases of nutrient absorption and conditions causing malabsorption

How else can malabsorption be classified

Answer 69

• 3 steps required for normal nutrient absorption:
  
  • luminal processing
  • absorption into intestinal mucosa
  • transport into circulation

1. Luminal phase
   
   • substrate hydrolysis
     
     • digestive enzyme deficiency eg chronic panc
     • digestive enzyme inactivation eg ZES
     • dyssynchrony of enzyme release, inadequate mixing eg post Bilroth II procedure
   • fat solubilisation
     
     • diminished bile salt synthesis eg cirrhosis
     • impaired bile salt secretion eg chronic cholestasis
     • bile salt de-conjugation eg bacterial overgrowth
     • increased bile salt loss eg ileal disease or resection
   • luminal availability of specific nutrients
     
     • diminished gastric acid eg atrophic gastritis - vit B12
     • diminished intrinsic factor eg pernicious anaemia - vitB12
     • bacterial consumption of nutrients - eg bacterial overgrowth - vit B12
2. Mucosal (absorptive) phase
   
   • brush border hydrolysis
     
     • congenital disaccharidase defect eg sucrase-isomaltase deficiency
     • acquired disaccaridase defect eg lactase deficiency
   • epithelial transport
     
     • nutrient-specific defects in transport eg Hartnup’s disease
     • global defects in transport eg Celiac sprue
3. Postabsorptive, processing phase
   
   • enterocyte processing e.g. abetalipoproteinaemia
   • lymphatic eg intestinal lymphangiectasia

Other Classifications:

• global vs selective
  
  • global = from diseases assoc w either widespread mucosal involvement or reduced absorptive surface
    
    • typically broad array of nutrients not adequately absorbed eg celiac sprue
  • selective = from diseases that interfere w absorption of a single nutrient or limited array of nutrients, eg pernicious anaemia
• primary/congenital vs acquired
  
  • congenital = from congenital defects in membrane transport systems of intestinal epithelium
  • acquired = from acquired defects in epithelial absorptive surface eg Crohn’s, celiac or after extensive surgical resection or intestinal bypass

Question 70

What is the role of non-operative management in oesophageal perforation?

Answer 70

• ~60% of oesophageal perforations are iatrogenic
• Some of these may be suitable for non-operative management if they fulfill Cameron’s criteria
  
  • Minimal symptoms
  • No evidence of sepsis
  • Oral contrast restricted to mediastinum and flows back into oesophagus.
• Non-operative management consists of NPO, endoscopic NGT, IV ABx and AFx, TPN or distal enteral feeding, PPI, and serial review and imaging.

Question 71

What is diffuse/distal oesophageal spasm?

Answer 71

- aka Corkscrew oesophagus

• a motility disorder of oesphageal body; Chicago classification: a major disorder of peristalsis
• involves uncoordinated contractions of oesophageal body, worse in lower 2/3 oesophagus
• dysphagia & sometimes chest pain which may be related to eating
• HRM: normal mean IRP, ≥20% premature contractions w DCI >450mmHg.s.cm; some normal peristalsis may be present
• barium swallow: ~30% corkscrew oesophagus, may have epiphrenic diverticulum +/- bird beak narrowing
• 24hr pH monitoring important bc GOR may be trigger of sx
• management: rx of reflux if secondary to GORD; reassurance; avoid trigger food; medical therapy eg nitrates CCBs, and bougie dilatation may help dysphagia, botox some effect but not sustainable. Surgery may be indicated if incapacitating symptoms failed to resolve, or if pulsion diverticulum - long oesophagomyotomy through left thoracotomy with extent guided by manometry + fundoplication for reflux protection

Question 72

What is Nutcracker/Jackhammer/Hypercontractile oesophagus?

Answer 72

• oesphageal motility disorder of oesophageal body; Chicago classification ‘major disorders of peristalsis’
• characterised by excessive contractility in which peristaltic contractions are coordinated, but significantly elevated in amplitude
• can be primary or secondary to GORD
• symptoms: chest pain & dysphagia +/- odynophagia (regurg & reflux uncommon)
• HRM: at least 2 swallows with DCI >8000mmHg.s.cm. Hypercontractility may be localised to LES & may be missed using DCI criteria.
• 24hr pH monitoring useful to differentiate from dysmotility secondary to GORD
• Ba swallow usu normal
• Mx: if secondary to GORD, reflux mx; nitrates/CCBs may help. ?Heller myotomy & partial fund -> chest pain persists in 50%; but dysphagia improves in 80%

Question 73

What is hypertensive lower oesophageal sphincter/GOJ outflow obstruction?

Answer 73

• dysmotility disorder characterised by an elevated basal pressure of LOS with normal relaxation, and normal peristalsis in oesophagus; similar to achalasia, but hypertensive sphincter DOES relax in response to swallowing & normal oesophageal peristalsis
• disorder of LOS
• Chicago classification ‘disorders with GOJ outflow obstruction’
• clinical: chest pain, dysphagia
• HRM: (>15mmHg), sufficient evidence of peristalsis such that criteria for types I-III achalasia not met
• Ba swallow may show narrowing at GOJ w delayed flow & abnormalities of oesophageal contraction but these are nonspecific findings
• Mx: botox temporary, balloon dilatation may give long-term relief, surgery if don’t respond - lap modified Heller oesophagomyotomy & in pts w normal oesophageal motility, a partial antireflux procedure added

Question 74

What is achalasia?

Answer 74

• literal meaning = failure to relax
• an oesophageal dysmotility disorder characterised by
• impaired/absent relaxation of LOS w
• decreased/absent peristalsis of body and
• increased pressure of oesophagus
• Chicago classification: disorders with GOJ outflow obstruction
• type I achalasia (classic) - incomplete LES relaxation, aperistalsis and absence of oesophageal pressurisation
  
  • increased median IRP (>15mmHg), 100% failed peristalsis (DCI >100mmHg); premature contractions w DCI values <450mmHg.s.cm meet criteria for failed peristalsis
• type II achalasia (with oesophageal compression) - incomplete LES relaxation, aperistalsis and panoesophageal pressurisation in ≥20% swallows
  
  • increased median IRP (>15mmHg), 100% failed peristalsis, panoesohpageal pressurisation w ≥20% of swallows; contractions may be masked by oesophageal pressurisation & DCI shouldn’t be calculated
• type III achalasia (spastic achalasia) - incomplete LES relaxation and premature contractions (DL >4.5 seconds) in ≥20% swallows
  
  • increased median IRP (>15mmHg), no normal peristalsis, premature (spastic) contractions w DLI >450mmHg.s.cm with ≥20% of swallows; may be mixed w panoesophageal pressurisation
• pathophys remains unclear but inflammatory infiltrate at level of myenteric plexus -> progressive neuronal loss & subsequent loss of peristalsis & appropriate LOS relaxation - ?idiopathic/infectious/autoimmune

- primary vs secondary

• primary = due to loss of gangion cells in myenteric (Auerbach) plexus - more common
• secondary may be due to
  
  • pseudoachalasia = rare presentation of Ca and GOJ
  • Chagas’ disease - South America, Trypanosoma cruzi (bite from infected bug) - initially viral type illness then long-term neurological disorders w diffuse ganglion cell involvement (incl destruction of myenteric plexus) -> cardiomyopathy, megacolon, megaureter, megaoesophageus
• clinical: classic triad = dysphagia, regurg, of undigested food, weight loss; also chest pain
• aspiration pneumonias/lung abscess/bronchiectasis from longstanding achalasia - resp complications 10%
• premalignant condition - up to 8% in 20yrs; mucosa develops changes of chronic stasis; oesophagitis & ulcer -> dysplasia -> SCC most commonly (from long-standing retained undigested fermenting food in body of oesoph causing mucosal irritation)
• investigations
• CXR - homogeneous, usu R-sided paramediastinal soft tissue opacity +/- mediastinal widening, air-fluid levels, absence of gastric bubble, resp complications
• endoscopy - exclude malignancy/oesophagitis; LOS closed & subtle ‘tightness’ but not like malignant stricture; oesophageal dilatation/fluid & food debris but in earlier stages this isn’t present
• barium swallow - bird-beak, various degrees prox dilatation (mild <4cm, severe >6cm), delayed emptying through LOS, lack of peristaltic waves in body&failure of relaxation of LOS, lack of gastric bubble (tight LOS not allowing air to pass into stomach)
• manometry

Question 75

What is the management of achalasia?

Answer 75

• palliative treatment - directed toward relieving functional obstruction caused at LOS (while minimising risk of reflux) but none able to address decreased motility in oesophagal body
• medical rx: effective in a few - SL GTN, CCBs, nitrates (SM relaxation at LOS)
• endoscopic:
• balloon dilatation = most effective non-surgical mx; stretch cardia w 30-40mmHg balloon initially to disrupt muscle at LOS
  
  • 70% effective; 50% symptomatic again after 1-20yrs; disadvantages 20-30% GORD, 2-5% perf rate
• botox = less effective than dilatation; directly into LOS which blocks acetylcholine release, prevents SM contraction, relaxes LOS
  
  • effective in 85% but 40-50% have recurrent sx by 6mths; causes inflammation at GOJ which makes subsequent myotomy more difficult so used mostly in elderly/poor surgical candidates who are also not fit for pneumatic dilatation & risk of perforation
• POEM (peroral endoscopic myotomy) = division of LOS - mucosal incision at a point prox to where myotomy planned to commence, develop submucosal tunnel, then divide circular muscle fibres in distal oesoph down to stomach, mucosa closed at end. Disadvantage = not combined w antireflux procedure & signif reflux rate
• surgery:
• Modified Heller myotomy +/- partial fundoplication
  
  • divide phrenooesophageal ligament to expose lower oesophagus
  • divide all circular fibres of lower oesphagus (usu 6-8cm) & 1-2cm on stomach/cardia
  • routine loose fundo; 20% reflux if no fundo - but controversial & avoid 350 degree bc inc risk dysphagia
  • complications: mucosal perf - recognise & repair intraop, paraoesophageal hernia, subphrenic abscess, pneumonia, pleural effusion
  • good result in 80-90%, mortality <1%; cancer risk persists - consider surveillance endoscopy
• oesophagectomy occasionally required for end-stage disease

Question 76

What is ineffective oeosphageal motility?

Answer 76

• dysmotility disorder of distal oesophagus, usu associated w GORD
• minor disorder of peristalsis (Chicago classification)
• may be secondary to inflammatory injury of oesophageal body due to increased exposure to gstric contents; once altered motility present, appears irreversible
• dx by manometry: >50% infective swallows, ineffective swallows can be failed or weak
• mx = prevention w tx of GORD best; once occurs irreversible

Question 77

Describe the classification + treatment of Gastric Carcinoid

Answer 77

Gastric carcinoid is now classified as a subgroup of gastropancreatic NETs:

Type 1 (75%) - Usually rise in patient with atrophic gastritis. More common in women. Small. Well differentiated. 90% 5-yr-OS.

• <1cm observe <1cm EMR. Consider antrectomy to remove G cells.

Type 2 (5%) - Occur in those with gastrinoma with MEN-1. Require WLE and removal of gastrinoma. 70% 5-yr-OS.

• Resection

Type 3 (20%) - Very aggressive. Require gastrectomy and D2 resection. 50% 5-yr-OS.

• Likely gastrectomy +/- LN dissection

Question 78

How can the causes of portal hypertension be categorised?

Answer 78

Pre-hepatic

• PV thrombosis
• SV thrombosis
• Schistosomiasis (intrahepatic)
• Sarcoidosis (intrahepatic)

Intrahepatic

• Cirrhosis - any cause
• Cytotoxic drugs
• Acute EtOH hepatitis

Post-hepatic

• Budd-Chiari
• Veno-occlusive disease
• Constrictive pericarditis

Question 79

What are the criteria for transplant in patients with cirrhosis and HCC?

Answer 79

The Milan and UCSF criteria.

Question 80

What is the aetiology of peptic ulcer disease?

Question 81

Gastric cancer staging

Answer 81

• Tis - carcinoma in situ (intraepithelial tumour w/o invasion of lamina propria, high-grade dysplasia
• T1 - invades lamina propria, muscularis mucosae or submucosa
  
  • T1a - invades lamina propria or muscularis mucosae
  • T1b - invades submucosa
• T2 - invades muscularis propria
• T3 - invades subserosal connective tissue w/o invasion of visceral peritoneum or adjacent structures
• T4 - invades serosa (visceral peritoneum) or adjacent structures
  
  • T4a - invades serosa (visceral peritoneum)
  • T4b - invades adjacent structures/organs (spleen, T colon, liver, diaphragm, panc, abdo wall, adrenal gland, kidney, SB, retroperitoneum)
• N1 - 1-2 regional nodes
• N2 - 3-6 regional nodes
• N3 - ≥7 regional nodes
  
  • N3a - 7-15 regional nodes
  • N3b - ≥16 regional nodes
• M0 or M1

Question 82

Define:

gastric adenocarcinoma

gastric dysplasia

early gastric carcinoma

advanced gastric adenocarcinoma

Answer 82

gastric adenocarcinoma = a primary malignancy that arises from gastri epithelium

gastric dysplasia = synonymous with intra-epithelial neoplasia, stratified into low and high grade

early gastric carcinoma = limited to mucosa or submucosa w or w/o regional LN mets (T1 regardless of LN status)

advanced gastric adenocarcinoma = infiltrates into muscularis propria & beyond

Question 83

How are junctional tumours managed?

Answer 83

tumours arising at GOJ or in cardia of stomach within 5cm of GOJ that extend into GOJ = staged and treated as oesophageal rather than stomach cancers

tumours that arise beyond 5cm distal to GOJ, or are within 5cm of GOJ but w/o extension to junction = gastric cancers

Question 84

Discuss the epidemiology of gastric cancer

Answer 84

overall decreasing in incidence - thought to be due to decreased smoking and increased identification & treatment of H pylori

certain countries eg Japan and Korea have high rates

distal cancers more common in Asian populations; more proximal lesions seen more frequently in Western pouplations

M>F, particularly for gastric cardia cancers

Question 85

Risk factors for gastric cancer

Answer 85

• environmental
  
  • prominent geographic variation
  • low SES
  • smoking
  • obesity
  • evidence for diet conflicting ?diet low in F&V w high salted, smoked, preserved foods or nitrate composition
• medical
  
  • H pylori infection - 6x increased risk
    
    • most H pylori will remain asymptomatic but small proportion will develop gastric carcinoma attributed to diff bacterial strains, host-inflam genetic susceptibility and in particular H pylori virulence factors eg vacA and CagA toxins
  • prior gastric surgery eg distal gastrectomy espec Bilroth II
  • EBV - 10% gastric ca assoc w EBV
  • chronic atrophic gastritis
  • pernicious anaemia
  • gastric adenomatous polyps
• genetic - 10% familial clustering but only 1-3% related to identified inherited gastric carcinoma predisposition syndrome
  
  • hereditary diffuse gastric cancer - CDH1 gene- 70-80% lifetime risk
  • FAP - dysplastic fundic gland polyps
  • Li Fraumeni
  • Lynch syndrome
  • Peutz-Jeghers

Question 86

What is atrophic gastritis?

Answer 86

Aka metaplastic atrophic gastritis or gastric atrophy - used to describe a form of chronic gastritis that, in addition to inflammation, is associated w mucosal thinning, loss of specialised cells in gastric glands, and changes in epithelial cell types (ie metaplasia)

Includes 2 main subtypes: autoimmune and environmental metaplastic atrophic gastritis

Autoimmune = a form that results in the replacement of the normal oxyntic mucosa in teh gastric body by atrophic & metaplastic mucosa –> corpus predominant atrophic gastritis, reduced or absent acid and pepsin production & loss of intrinsic factor –> may progress to severe form of VitB12 deficiency anaemia known as pernicious anaemia

Environmental = due to things like H pylori +/- diet

Question 87

What is the pathogenesis of gastric adenocarcinoma?

Answer 87

• Main hypothesis = Correa hypothesis - multistep process
  
  • pathway of transformation from normal mucosa to gastritis to chronic atrophic gastritis –> metaplasia –> dysplasia –> cancer
    
    • recently been expanded with stepwise molecular alterations
  • several of the risk factors have a pathway that leads to either gastritis or atrophic gastritis
    
    • H pylori causes chronic gastritis –> eventually loss of gastric glands and replacement of nomral mucosa by intestinal metaplasia, which then predisposes to malignant transformation
    • inflammation of gastric mucosa can also be due to chemical agents (NSAIDs, alcohol, bile reflux) or the consequence of an autoimmune process (eg pernicious anaemia w parietal cell autoantibodies)
  • chronic inflammation can either result in shrinkage or complete disappearance of typical gastric glands followed by replacement fibrosis of the lamina propria or the replacement of the native glands by metaplastic glands (ie intestinal metaplasia); both conditions involve ‘atrophy’ but only the prsence of metaplastic glands = considered a condition w increased risk of carcinoma development
  • genetic changes thought to occur during this pathway:
    
    • association between overexpression of COX2 and cyclin D2
    • p53 mutations
    • gastric ca been found to have MSI
    • can have alteration in transcription factors eg CDX1 and CDX2
  • chronic gastric ulcer
    
    • typically located at edge of atrophic mucosa
    • if found on endoscopy, malignant til histo proven otherwise
    • pts w gastric ulcer have increased risk for gastric carcinoma as gastric ulcer & gastric carcinoma have same risk factors, but overall <1% of all gastric carcinoma develop in pre-existing peptic ulcers

Question 88

What are the following which may be found on biopsy at time of gastroscopy:

Chronic atrophic gastritis

Intestinal metaplasia

Gastric dysplasia

Answer 88

• chronic atrophic gastritis = not itself pre-malignant; usu a response to chronic inflammation which may be from H pylori, NSAIDs, chronic alcohol use, bile reflux or autoimmune gastritis
  
  • results in shrinkage/disappearance of typical gastric galnds
  • can be followed by fibrosis of lamina propria OR intestinal metaplasia
  • chronic atrophic gastritis w/o intestinal metaplasia: treat cause - eradicate H pylori, PPI, repeat gastroscopy in 3yrs
• intestinal metaplasia - involves replacement of native glands by metaplastic glands - can be intestinal type or pseudopyloric type
  
  • is assoc w increased risk of carcinoma development
  • H pylori eradication, use of PPI, repeat gastroscopy & mapping biopsies q3yrs
• gastric dysplasia
  
  • synonymous with intra-epithelial neoplasia
  • usu would see at endoscopy espec if high grade dysplastic lesion - w flat or depressed or polypoid growth pattern (polypoid dysplasia = adenoma, flat lesion dysplasia)
  • low grade - 25% risk of adenocarcinoma development within 10mo-4yrs
    
    • eradicate H pylori, treat w PPI, ensure good mapping biopsies, repeat gastroscopy within 12mo
  • high grade - 60-80% risk over 1-5yrs
    
    • classified as carcinoma in situ so should be managed as gastric cancer

Question 89

What is the incidence of lymph node mets in early gastric cancer and what are the risk factors for these?

Answer 89

• incidence of LN mets = 2-3% for intramucosal carcinomas, 20-30% for submucosal carcinomas
• risk factors for LN mets in early gastric ca = younger age at time of dx, size >20mm, depressed macroscopic type, undifferentiated, presence of an ulcer or scar, lymphatic invasion, submucosal invasion by >500um

Question 90

What targeted therapies are available for use in metastatic gastric cancer?

Answer 90

Trastuzumab - targets HER2 (commonly amplified and overexpressed in intestinal-type carcinoma, rarely in diffuse)

Ramucirumab - targets VEGFR

Question 91

Genes implicated in gastric cancer

Answer 91

• p53 mutations in 60%, equal in the different histo subtypes - so most frequently mutated gene in gastric cancer
• APC mutations - in 30-40% of well & mod differentiated intestinal-type gastric carcinoma
• MMR genes - MSI in 15-40% gastric cancers, more common in intestinal type and in older women
• CDH1 - hereditary diffuse gastric cancer - 70-80% lifetime risk

Yasui proposed a multistep model of molecular alterations, refining the multistep model of histo changes proposed by Correa - at least 4 different molecular pathways to develop differentiated & undifferentiated types of gastric cancer

Question 92

How is gastric cancer classified?

Answer 92

• type of cancer
  
  • adenocarcinoma 95% vs others (SCC, adenosquamous, carcinoid, GIST, lymphoma)
• early vs advanced
• TNM staging system
• macroscopic appearance: Borrman classification (advanced ca), Paris classification (early ca)
• histologic subtypes of gastric carcinoma - Lauren, WHO
• molecular subtypes
• grading - well diff, moderately diff, poorly diff

Question 93

How is the macroscopic appearance of gastric carcinoma classified?

Answer 93

• Early gastric cancers: Paris system
  
  • type 0-I = polypoid (protruded or pedunculated)
  • type 0-II = nonpolypoid
    
    • type 0-IIa - slightly elevated
    • type 0-IIb - flat
    • type 0-IIc - slightly depressed
  • type 0-III = excavated
• Advanced gastric cancers: Borrman classification
  
  • type 1 = protruded
  • type 2 = ulcerated w elevated borders
  • type 3 = ulcerated w infiltrative margins
  • type 4 = diffusely infiltrating
  • type 5 = not fitting other types (unclassifiable)

Question 94

Discuss the histologic classification systems of gastric cancer

Answer 94

Lauren classification - adenocarcinoma (considered pathologically different but treated similarly)

• intestinal type gastric cancers (60-70%)
  
  • well, mod or poorly diff but usu well
  • usu mass-forming type; sharply demarcated & have a pushing margin
  • occur in setting of atrophic gastritis - assoc w Correa hypothesis
  • gland forming
  • M>F
  • older age
  • sporadic, in high risk countries
  • often located in antrum
  • liver mets
  • Borrman type II pattern
• diffuse type gastric cancers
  
  • undifferentiated, w or w/o signet ring cells
  • composed of scattered, poorly cohesive cells or small clusters of cells & diffusely infiltrative
  • more ulcerating, diffuse lesion & rather than ofrming a mass the cells infiltrate through wall of stomach; can get Linitis plastica if extensive infiltration (rigid, non-expandable stomach)
    
    • cells have lost E-cadherin which is why cells don’t stick together & are diffusely infiltrating
  • more likley to be assoc w familial type of gastric ca - assoc w CDH1 mutation
  • F>M
  • younger age
  • similar incidence in most countries
  • worse prognosis
  • often in prox body of stomach
  • more prone to peritoneal disease
• mixed type

WHO classification - histopathological subtypes of adenoca - tubular, papillary, mucinous, signet ring, mixed

Question 95

Discuss the molecular classification of gastric adenocarcinoma

Answer 95

• genomically stable tumours (GS; diffuse histology)
• tumours w chromosomal instability (CSI; intestinal histology)
• EBV positive (EBV, w marked DNA hypermethylation)
• microsatellite unstable tumours (MSI, w elevated mutation rates)

Question 96

What are the criteria for genetic testing for a CDH-1 mutation?

What is the management in a carrier?

Answer 96

• testing criteria = 1 of:
  
  • 1 diffuse gastric cancer in family dx before 40
  • 2 gastric cancers in the family, 1 of which was diffuse gastric cancer diagnosed at <50yrs
  • 3 confirmed diffuse gastric cancers in 1st or 2nd degree relatives, regardless of age
  • personal or family history of diffuse gastric cancer and lobular breast ca with at least one case dx before age 50

Question 97

What should you note on gastroscopy if you find a gastric cancer

Answer 97

• macroscopic classification (Paris or Borrman)
• location & extent of lesion, relationship to anatomical landmarks
• any other abnormal findings
• prox & distal extent of tumours
• biopsy to diagnose - at least 6-8 biopsies

Question 98

Gastrin

Answer 98

Secreted by G cells in gastric antrum

Acts to increase gastric motility and gastric acid production

Question 99

Gastrin levels in Zollinger-Ellison syndrome

Answer 99

• diagnostic
  
  • >10x upper limit of normal (1000pg/mL), and
  • pH <2
  • –> no further testing required
• equivocal
  
  • 1-20x upper limit of normal
    
    • may be pathologic or related to PPI
    • confirmatory testing off PPI
    • if remains equivocal - secretin stimulation test
      
      • normal G cells are inhibited but gastrinoma cells are stimulated

Question 100

What impact can scleroderma have on the oesophagus?

Answer 100

Smooth muscle atrophy

Functional oesophageal disorder with weak peristalsis

Also prone to severe reflux which may be refractory to medical management and require partial fundoplication

Question 101

Eosinophilic oesophagitis:

epidemiology

pathogenesis

presentation

investigation

management

Answer 101

• uncommon 1:1000
• pathogenesis
  
  • likely allergic
    
    • possibly food intolerance vs peptic
• presents as dysphagia or stuck food bolus
• diagnosis
  
  • endoscopy: friable, ringed oesophagus
  • histo: >15 eosinophils per HPF
• management:
  
  • PPI
  • dietary elimination
  • steroid (topical)
  • dilatation for strictures

Question 102

Routine staging investigations in gastric cancer

Answer 102

• gastroscopy and biopsy
• EUS and biopsy if linitis plastica suspected?? can be used if clarification needed on possible LN involvement which may alter management
• CT CAP
  
  • sensitivity of 33% for peritoneal disease
  • also poor at detecting organ invasion
  • but good at distant mets
• staging laparoscopy and cytologic lavage (T2 and above)
  
  • also gives info re location of tumour & whether involving adjacent organs
• MDM
• role of PET scan not well established, PET avid 60-90% of time (diffuse, mucinous, signet cell ones often not PET avid, also only detects peritoneal disease in ~50%)

Also consider: nutrition, comorbidities, fitness for surgery

Question 103

Management of early gastric cancer

Answer 103

• T1a - endoscopic resection if clearly confined to mucosa, well-differentiated, ≤2cm and non-ulcerated
  
  • EMR is acceptable for lesions <10-15mm with v low probability of advanced histo (Paris 0-IIa), but ESD is treatment of choice
  • if final histo T1a, no further treatment
  • if final histo T1b, resection (as 5-11% risk of LN involvement) but adjuvant therapy not required
• cT1b - straight to surgery if medically fit

Question 104

Management of advanced gastric cancer

Answer 104

ie T2 and above

• medically fit and surgically resectable
  
  • 4 rounds pre-op FLOT (flurouracil, leucovorin, oxaliplatin, docetaxel)
  • then restage with CT, (PET scan if had one before and tumour was avid)
  • if pre chemo had +ve cytology or large bulky tumour consider repeat laparoscopy but not routine
  • if no progression of disease, undergo resection then do 4 postop rounds
• medically fit but surgically unresectable
  
  • palliative chemo
    
    • HER2 negative: platinum + fluoropyrimidine-based doublet or triplet regimen
    • HER2 positive: trastuzumab +/- CF/CX (cisplatin/5FU or cisplatin/capecitabine)
    • or clinlical trials
• if not surgical candidate: best supportive cares

Question 105

Discuss the role of neoadjuvant/adjuvant chemo/chemorad in gastric cancer

Answer 105

• for patients with potenitally resectable gastric cancer, randomised trials ane meta-analyses indicate a significant survival benefit over surgery alone for a number of approaches, including:
  
  • adjuvant chemoradiotherapy (2 US trials, INT 0116 (Macdonald protocol) & CALGB 80101)
  • periop (preop and postop) chemo (MAGIC and FLOT
  • adjuvant chemo alone (used in East Asia)
• few trials have directly compared these approaches and optimal way to integrate combined modality therapy not been definitively established (in general European practice favours purely chemo approach whilst chemorad favoured in US?)
• although no randomised trials demonstrating overall survival benefit from neoadj therapy vs upfront surgery followed by adjuvant therapy, neoadjuvant approach is favoured given greater chance of deliveirng therapy in preop setting (also note in MAGIC only 55% got post-op chemo)
• radiotherapy not generally part of routine management given toxicity
• best chemo regimen for neoadj not established but FLOT4-AIO tiral demonstrated survival benefit of FLOT over ECF
  
  • if lower performance status or thought unlikely to tolerate FLOT, can use FOLFOX or CAPOX
• if have upfront surgery with potentially curative gastric resection, recommend adjuvant chemorad or chemo if positive nodes or T3/4 (favour chemorad if not had adequate D2 lymphadenectomy or have node-positive or incompletely resected (R1 or R2) disease

Question 106

MAGIC trial

Answer 106

NEJM 2006 (UK)

• a sentinel study in the treatment of gastric, GOJ and lower oesophageal cancer
  
  • surgery and ECF (epirubicin, cisplatin and 5-FU) - 3 cycles of both neoadjuvant and adjuvant therapy
  • vs surgery alone
• T2+ or greater, N0 or N+
• significant 5 year survival benefit to perioperative therapy - 36% vs 23%
• 55% completed post-op chemo
• criticisms: included GOJ tumours which we now treat as oesophageal and there were a number of pts in neoadj group that had R2 resection, thought to be due to inadeqaute staging; pts didn’t have dx lap pre-op

Question 107

FLOT4 trial

Answer 107

Journal of clinical oncology 2017 (German)

• adenocarcinoma of the stomach and GOJ (not distal oesophagus)
• T2+, N0 or N+
• 4x 2week cycles of FLOT both pre and post surgery (fluorouracil, leucovorin, oxaliplatin, docetaxel)
• vs ECF (MAGIC) or ECX (capecitabine)
• surgery 4wks later
• FLOT superior to MAGIC - 50 vs 35 months median survival
• 95% vs 97% proceeded to surgery
• 37% MAGIC completed all chemo, 46% FLOT completed all chemo
• but criticism that this high tolerance of FLOT hasn’t been replicated clinically
• (survival outcome similar to that seen in CROSS trial with combined neoadj chemorad - 48mo)

Question 108

MacDonald study

Answer 108

NEJM 2001 (US)

• found postop CRT gave significant survival benefit for gastric cancer & has become standard of care in US?
• 5FU given in first and last weeks of rad (45Gy) and 2x 5-day courses of 5-FU-leucovorin given monthly
• DFSS 49% vs 32%, OS 52% vs 41%
• but significant proportion of pts (54%) had only a D0 resection & survival in surgery-alone arm was relatively poor (42% 3yr survival)
• possible that CRT was making up for less than adequate surgery, since survival outcomes in combined modality arm of Macdonald study equivalent to European surgical-only studies where D1 and/or D2 dissection been performed

Question 109

Surgical principles in oncologic gastric surgery

Answer 109

• total or subtotal are the only appropriate operations
• at least 5cm margin
• left gastric pedicle should be taken with any operation
• D2 lymph node resection is superior (spleen and pancreas preserving resection of nodal basins 1-12)
• at least 16 lymph nodes (30 is desirable)
• cardia or prox stomach - total gastrectomy and roux en Y oesophagojejunostomy
• tumours in distal stomach - where you think you can get 5-6cm above, consideer subtotal gastrectomy + gastrojejunostomy (still take greater omentum)
  
  • subtotal gastrectomy = oncological operation (taking left gstric artery and all lymph nodes; which is different to distal gastrectomy which is done for non-oncological reasons)

Question 110

What is a D1 vs D2 lymphadenectomy in gastric cancer? Which is preferred?

Answer 110

• D1 -= nodal stations 1-7 (perigastric only)
• D1+ = D1 plus 8a, 9, 11p
• D2 = nodal stations 1-12a (nodes along hepatic, left gastric, celiac and splenic arteries + splenic hilum)
• D3 = some use it to describe a D2 + porta hepatis and periaortic nodes (1-16); others use it to describe a D2 + periaortic nodal dissection alone
  
  • most Western surgeons & AJCC consider these distant mets & don’t recommend removing these nodes during potentially curable gastrectomy
• Sydney RPA group retrospective analysis suggests better outcomes in spleen and panc preserving D2 resection (2018 WJO)
• UTD: given the apparent impact of D2 lymphadenectomy on disease-specific survival, most major centres are performing this. NCCN guidelines recommend gastric cancer resection includes regional lymphatics, includign perigastric (D1) nodes as well as those along the left gastric artery, common hepatic artery, celiac artery, splenic hilum, and splenic artery (D2 lymph nodes), with the goal of examining 15 or more lymph nodes
  
  • no evidence that a D3 (paraaortic) lymphadenectomy confers a survival benefit over a D2 dissection & is associated w greater periop moertality
  • routine splenectomy or pancreatectomy discouraged - also increases m&m w/o survival; only if direct tumour extension to panc or spleen
• arguments in favour of extended lymphadenectomy (D2 or D3 vs D1):
  
  • removing larger number of nodes more accurately stages disease extent
  • failure to remove these nodes leaves behind disease in as many as 1/3 of pts
  • a consequence of more accurate staging = to minimise stage migration - the resulting improvement in stage-specific survival may explain the better results in Asian pts
• the evidence supporting D2 dissection in potentially curable gastric cancer when it can be done without increasing operative mortality is based on the most recent analysis of the Dutch trial and the 2015 Cochrane review
  
  • no significant advantage in OS or DFS but significant diference in disease specific survival
  • higher postop morbidity and mortality with D2 (mortality in Cochrane = RR 2.02)
• prior to these trials, no randomised trial had demonstrated any initial survival advantage with D2 resection, though many consider the 2 larger trials (Dutch trial and MRC trial) underpowered

Question 111

What are the lymph node stations in gastric cancer

Answer 111

• lesser curve = 1, 3, 5
• greater curve = 2, 4, 6
• left gastric = 7
• CHA = 8
• coeliac trunk = 9
• splenic hilum = 10
• splenic artery = 11
• hepaticoduodenal ligament/along free edge of lesser omentum = 12

Question 112

Early complications following gastrectomy

Answer 112

• anastomotic leak
  
  • most at oesophagojejunostomy
  • contrast swallow if suspected
  • if drain already in place & minor leak, fasting & alternative nutrition
  • no drain or septic signs = reoperate - sometimes repair join or drain and either way feeding jej
  • similar for early and delayed but unlikely to repair join if delayed
• duodenal stump leak
  
  • prophylactic drain near stump
  • options if leak are foley/T tube into stump or if pinhole, suction drain close to it and retrograde inserion of duodenal compresion tub efrom jejunum
  • feeding jej for feeding & for returning suctioned duo content into intestine; w good duo decompression, enteral feeding doesn’t need to be stopped or reduced
• pancreatic fistula
  
  • after D2 lymphadenectomy even w/o pancreatectomy
  • prophylacctic suction drain along upper border of panc
  • increased amylase in drain fluid on day1 or 2 postop = useufl marker
• bleeding
  
  • first few hours - early reop
  • secondary due to intra-abdo infection after leak/fistula = dangerous - pseudo-aneurysm, can have herald bleed; angioembolisation
• postsplenectomy infections

Question 113

Early dumping syndrome

Answer 113

• occurs within 30min after a meal, or even during a meal
• rapid filling of prox SB w hyperosmolic content –> large fluid shifts (rapid movement of fluid from extracellular compartment into gut) –> hypovolaemia
• secondary neurohumoral/sympathetic response
  
  • palpitations
  • abdo pain
  • diarrhoea
  • nausea
• management - avoid simple carbs, increase complex carbs/protein/fibre, small frequent meals, separate food and fluid by 30mins
• 68%

Question 114

Late dumping syndrome

Answer 114

• secondary to hypoglycaemia after ingestion of food, likely hormonally mediated
  
  • rapid inflow of carbs into jejunum –> oxyhyperglycaemia –> hyperinsulinaemia followed by hypoglycaemia
  • GLP-1 secreted from prox jej mucosa thought to play some role in this hypersecretion of insulin
• symptoms of hpoglycaemia: dereased LOC, confusion, abdo pain, diarrhea, nausea, tachycardia
• management: behavioural modifications - avoid simple carbs, increase complex carbs/protein/fibre, small frequent meals, separate food and fluids by 30mins
• unlike early dumping, mediations may be necessary (and may be effective)
  
  • Nifedipine
  • Acarbose
  • Octreotide
• 38%

Question 115

Nutritional problems following gastrectomy

Answer 115

• decreased fat absorption = main major nutrient affected bc mixing of bile acid & panc lipase becomes insufficient –> c/o steatorrhoea
• vit B12
  
  • binds to IF secreted by parietal cells of stomach & is absorbed in ileum
  • after total gastrectomy, pts absorb no B12 & body stores gradually depleted –> megaloblastic anaemia, though may take up to 24mo to become clinically apparent
    
    • 1g vit B12 IM q3/12 for life
  • distal gastrectomy: B12 deficiency can develop even after distal gastrectomy leaving a small atrophic remnant
    
    • monitor MCV
• vit D
  
  • absorption of fat-soluble vitamines (ADEK) may decrease in pts w fat malabsorption
    
    • of these, vit D clinically important espec in post-menopausal women
    • combined with decreased Ca absorption after gastrectomy, leads to metabolic bone disorders from 2yrs after surgery
    • postmenopausal women & all pts >70 should take oral ca & vit D supplement for life after total gastrectomy
• iron
  
  • ​absorption mainly occurs in duo & upper jej
  • in presence of gastric acid, ferric iron (Fe3+) in foodstuffs is deoxidised to easily absorbable ferrous iron (Fe2+)
  • iron absorption may be decreased after gastric resection due to decreased acid & rapid food passage in intestine
  • IDA common & oral iron supplement useful

Question 116

What are some factors predictive of a gastric lesion having submucosal or deeper invasion?

Answer 116

• Paris classification
  
  • protruding lesions - 57% submucosal invasion
  • slightly elevated - 29%
  • completely flat - 20%, slightly elevated - 40%
  • excavated often proper muscle layer already involved
• tumour size >30mm
• remarkable redness
• ulceration
• if lesion confined to mucosa it tends to move over the peristaltic waves; whereas peristaltic waves seem to curve around tumours that have invaded proper muscle layer (avoid endoscopic resection)
• mucosal or submucosal lesions (m-sm1) usually completely lift whereas deeper (sm2-sm3) incompletely lift and non-ligting usually invasion deeper than sm3

Question 117

Define oesophageal squmaous cell dysplasia and SCC

Answer 117

• dysplasia = presence of unequivocal neoplastic cells within epithelium
  
  • squamous cell dysplasia = ‘low grade’ when architectural & cytological abnormalities are seen in basal half of squamous epithelium w preserved maturation in upper half
  • ‘high grade’ when more than basal half show architectural & cytological abnormalities
  • ‘full thickness dysplasia’ = carcinoma in situ/non-invasive carcinoma (but these words discouraged to celary separate HGD from invasive ca
• SCC = a neoplasm that at least penetrates the epithelial BM into lamina propria

Question 118

Define early oesophageal cancer

Answer 118

Contained within superficial components of the epithelial lining with no LN involvement (so differs from gastric ca which is irrespective of LNs)

• stages 0 or Ia
• stage 0 = Tis or HGD of epithelium
• stage I = T1a or T1b w/o LNs involved
  
  • T1a = intramucosal carcinoma, can be subclassified according to level of invasion
    
    • confined to epithelium (m1), lamina propria (m2), muscularis mucosa (m3)
  • T1b can be subclassified into
    
    • Sm1 (inner third), sm2 (middle third), sm3 (outer third)
  • relevant bc relates to risk of lymphatic invasion (lymph network in oesoph is concentrated in submucsoa but there are lymphatic channels in lamina propria)

Question 119

What are the parts of the oesophagus?

Answer 119

Cervical oesophagus = hypopharynx to thoracic inlet/sternal notch (15-20cm from incisors on endoscopy)

• upper thoracic oesophagus = thoracic inlet to azygos vein (20-25cm from incisors)
• midthoracic = azygos vein to inferior pulmonary vein (25-30cm from incisors)
• lower thoracic = lower border inf pulmonary vein to GOJ

Question 120

Epidemiology of oesophageal cancer

Answer 120

• SCC & adno make up >90%
• other rarer types: NETs, melanoma, leiomyosarcoma, oesophageal lymphomas
• geographic variation
  
  • adeno most comon in developed world (60% vs 40%) & vice versa
• changes in incidence
  
  • adenoca increasing in incidence dramatically in recent decades but stabilised/decreased in last 10-15 years; within subpop of younger whites, incidence increasing
  • SCC decreasing in incidence in last few decades both worldwide & in West, but still most common worldwide
  • these changes thought to reflect increasing obesity & GORD (adenoca risk factors) & decreased smoking (SCC risk factor)
• differences in location
  
  • adeno more likely to occur in distal oesophagus (75%); more proximally 25%
  • SCCmore common in middle (50%); distal 35%, prox 15%?
• M>F, age 50-70
• at time of dx >50% will have unresectable or metastatic disease

Question 121

Risk factors for oesophageal cancer

Answer 121

• Adeno:
  
  • Barrett’s (95% assoc w this)
  • GORD - frequency & duration
  • obesity
  • smoking
  • M>F
  • H pylori protective
  • no clear assoc w ETOH
• SCC
  
  • smoking
  • alcohol
  • hot beverages, high intake BBQ meat, pickled veges, low F&V
  • HPV 16,18 (small subset)
  • previous corrosive injury
  • achalasia, Zenker’s diverticulum, Plummer-Vinson syndrome = all associated with retained food; thought that decomposing bacterial release various chemicals that irritate mucosal lining

Question 122

Pathogenesis of oesophageal ca

Answer 122

• GORD to adenocarcinoma sequence
  
  • chronic exposure of squamous epithelium to gastric contents & reflux –> inflammation –> metaplasia of oesophageal lining into Barrett’s (gastric columnar epithelium) –> increasing dysplasia –> adenocarcinoma
  • involves stepwise accumulation of genetic mutations
  • p53 gene has been implicated in this as a signif gene
  • other changes include: HER2, ERBB2, cyclin-D1, cyclin-E, retinoblastoma protein, p16
• SCC
  
  • multistep process; precursor lesions similar to dysplastic Barrett’s
    
    • normal squamous epithelium –> dysplasia –> invasive carcinoma
    • squamous cell dysplasia (predates ca y 5yrs) - low grade or high grade
  • genes involved: p53, retinoblastoma gene, p16, cyclin D1

Question 123

Pathology of oesophageal cancer:

Answer 123

• ADENOCARCINOMA:
  
  • invasive clusters or glands w evidence of nuclear atypia with size and shape variation and potentially mitoses
  • well, mod or poorly differentiated
  • papillary and/or tubular (intestinal type according to Laurenclassification)
  • 10% mucinous or signet ring cell type
  • variants:
    
    • non-Barrett’s oesophagus-assoc adenoca = rare & may arise either from heterotopic gastric mucosa or from epithelium of submucosal oesophageal glands
    • adenoid cystic carcinoma = v rare; identical to salivary gland-type adenoid cystic carcinoma, thought to arise from submucosal oesophageal glands
• SCC:
  
  • keratinisation w keratin whorls adn cytological atypia
  • well, mod or poorly differentiated
  • 3 main variants
    
    • verrucous carcinoma - v rare & locally aggressive
    • spindle cell carcinoma - highly aggressive w evidence of squmaous & spindle cells on histopath
    • basaloid - anothr rare variatn w poor prognosis
• tumours in upper third more likely to spread to cervical & upper mediastinal nodes but signif proportion will also spread to perigastric nodes
• tumours in middle and lower oeosph: upper mediastinal & perigastric nodes
• SCC mets due to haematogeonous spread go to liver, lung, adrenal, kidney

Question 124

Staging work-up for oeosphageal ca

Answer 124

• bloods
• endoscopy and biopsy
• staging CT CAP - will upstage 15% of pts
• EUS
  
  • not routinely used; can be adjunct to assess and allow FNA of suspicious nodes; if suspicion for non-regional nodes, may biopsy using EUS or bronchosocpy bc would change mx approach
  • can help differentiate depth of tumour (not good for T1a vs T1b but ok for T2/3/4)
  • ie some controversy but may be used if trying to differentiate early oesophageal cancer that could go straight to surgery, or in working out nodal disease - institution dependent
• consider EMR
• staging laparoscopy for lower third espec in T3/4 disease
  
  • looks for peritoneal disease, occult liver mets, gives idea re local extent of tumour & whether there is any obvious involvement of surrounding nodes + extent of cancer down the stomach, + washings for peritoneal disease
• routine PET in preop staging (1% not PET avid)
• restage with CT after neoadj therapy
• frailty assessment
• CPEX or lung function studies
• consider ECHO
• nutritional assessment

Question 125

Oesophageal cancer staging

Answer 125

• Normal oesophagus
  
  • mucosa - epithelial layer, lamina propria, muscularis mucosa
  • submucosa
  • muscularis propria
    
    • inner circular
    • outer longitudinal
  • adventitial tissue (no serosa)
• Tis = carcinoma in situ/HGD
• T1
  
  • T1a = invades just lamina propria or MM
  • T1b = invades into submucosa
• T2 = into muscularis propria
• T3 = into adventitia
• T4 = invades into adjacent structures
  
  • T4a: pleura, pericardium, azygos vein, diaphragm, peritoneum
  • T4b: aorta, vertebral body, trachea
• N1 = 1-2 regional nodes
• N2 = 3-6 regional nodes
• N3 = ≥7 nodes
• M1 = any distant mets incl LNs outside regional nodes (regional nodes = celiac axis, para-oesophageal nodes, cervical lymph nodes but NOT supraclavicular)
• Stage 1 & 2 = no lymph nodes (except T1N1 = IIB); stage 3 = nodes

Question 126

Management of oesophageal cancer

Answer 126

• selected T1a lesions: EMR (+/- ablation in ACA)
  
  • HGD or intramucosal ACA (T1a)
    
    • early sm1 (T1b) have higher rate of LN involvement so take into consideration along w pt factors - if low risk featrues, LN involvement <10%
  • squamous HGD & SCC w invasion to m1 & m2
    
    • m3 and sm1 have higher rate of LN involvement which must be taken into account but an option if pt unwilling/unfit for resection (w/o LVI)
  • less likely to be successful for long segment barretts >8cm, poorly differentiated ACA, lesions >2cm, large hiatus hernia & if poorly controlled GORD
  • high dose PPI to help EMR & ablation sites to heal
• upfront surgery:
  
  • high risk T1a lesions that can’t be treated endoscopically (LVI or larger lesions)
  • most T1b tumours (except some sm1 in ACA) can’t be treated endoscopically
  • extensive, multifocal lesions & ulcerated tumours may be difficult to eradicate endoscopically - includes +ve margins after EMR/ESD for T1a IMC
  • also poor oesophageal body function eg achalasia
  • pt who isn’t committeed to long-term surveillance w repeated endoscopy w or w/o further endoscopic treatment
  • clinical T2N0 controversial - surgery alone expected to give overall 5yr survival 40-65% for pathological T2N0 ca, but clinical stage of T2N0 = inaccurate in majority of cases & many found to have node-pos disease on final path after oesophagectomy
    
    • but may not be survival advantage for neoadj in this group
    • NCCN guidelines - selectively offer neoadj therpay based on pretest prob of upstaging - recent study found long tumours (>3cm), presence of LVI & high grade as clinical factors have risk of upstaging of >48.1%
• surgical principles
  
  • many favour subtotal oesophagectomy bc of longitudinal spread in submucosal lymphatics for both squamous & adeno
  • ideally 10cm mragin, otherwise 5cm
  • need to consider cervical phase if only a short prox resection margin can be obtained through thoracic exposure (near total oesophagectomy)
  • distally for adeno may require sleeve resection of lesser curve & fundus espec for Siewert type 2
  • clear CRM is important prognostic factor - radical en bloc resection techniques
  • radical lymphadenectomy
    
    • one field - upper abdominal lymphadenectomy incl removal of diaphragmatic, R & L paracardial, lesser curvature, left gastric, coeliac, common hepatic & splenic artery nodes
    • two field - above + removal or paraoeosphageal nodes, para-aortic nodes (together w thoracic duct), R & L pulmonary hilar, subcarinal & R paratracheal nodes
    • three field - above + neck dissection clearing brachiocephalic, deep lateral & ext cervical nodes + R&L recurrent nerve lymphatic chains (deep anterior cervical nodes)
  • nonradical lymphadenectomy
    
    • only the nodes in direct proximity to the tumour, the oesophagus and upper stomach are removed
  • operation of course for mid and lower htird oesophageal ca + type 1 and 2 tumours of GOJ: subtotal oesophagectomy w 2-field lymphadenectomy, aiming at least 15-18 nodes
  • thoracic two-stage oesophagectomy (Ivor Lewis) for mid and distal oeosphageal tumours wtih anastomosis in upper chest between upper oesophagus & usu a gastric conduit
  • three-stage oesophagectomy (McKeown) - abdo, thoracic and neck incision - anastomosis made in neck through cervical incision - for prox/mid oesophageal tumours where won’t get adewquate prox clearance with 2-stage procedure
  • pharyngolaryngo-oeosphagectomy for carcinoma of hypopharynx & cervical oesophagus - SCC in this region needs resection of larynx, lower pharynx, cervical trachea, thyroid gland & cervical oesophagus - often primary tx for pts who have had radical rad for other malignancies in the region and salvage therapy following relapse after chemorad
    
    • if tumour has extended to lower part of cervical oesophagus, total pharyngolaryngo-ogesophaectomy & gastric transposition, w pharyngogastric recon required
  • minimally invasive oesophagectomy - thoracoscopic mob of oesoph & lap mob of stomach - promising data from high-volume centres
  • recon of stomach
    
    • stomach w gastric tube - relies on right gastroepiploic arcade, also preserve right gastric (L gastric taken)
    • colonic or jejunal conduit
    • route: posterior mediastinum >retrosternal >presternal
• oesophageal SCC
  
  • neoadjuvant CRT followed by surgery vs definitive CRT
    
    • OS equivalent but non-op strategy has higher local tumour recurrence; can do definitive CRT with close surveillance & salvage surgery on demand
    • no data comparing the two but PCR rate with definitive chemorads only ~50% therefore remains a role particularly in young & fit patients for surgery
  • for cervical SCC, use definitive CRT (surgery morbid & good evidence for definitive chemorad in laryngeal SCC & cervical oesophageal SCC)

SO SCC

• Tis and T1a - endoscopic therapy (preferred) or oesophagectomy
• T1b-T2N0 low risk lesions (<3cm, well differentiated) - oesophagectomy
• T2N0 high risk lesions (LVI, ≥4cm, poorly differentiated) + T3/T4 + nodal involvement
  
  • preop chemorad
  • or definitive chemorad (for cervical oesophagus)
• T4b = definitive chemorad or consider chemo alone in setting of invasion of tachea, great vessels, vertebra or heart

ACA

• Tis, T1a: endoscopic therapy (preferred) or surgery
• some sm1 T1b: endoscopic therapy or surgery
• T1b not superficial and low-risk T2N0 (<3cm, well differentiated: surgery
• T2N0 (high risk: LVI, ≥3cm, poorly differentiated), T3/4 or nodal involvement: preop chemorad (preferred) or definitive chemorad (only if decline surgery) or periop chemo (?MMH uses FLOT for junctional ACA?) or preop chemo
• T4b - definitive chemorad; consider chemo alone in setting of invasion of trachea, great vessels, vertebral body or heart
• postop rad only used for pts w microscopic evidence of residual disease after R1 resection (irradiates gastric pull-up)
• definitiv e(radical) single agent rad is an option in elderly pt w localised disease (espec SCC) who is clearly not candidate for operation & may not tolerate chemo component of CRT

Question 127

Complications of oesophagectomy

Answer 127

• anasotmotic leak 5-10%
• conduit necrosis
• pneumonia
• cardiac complications
• AF
• chyle leaks
• RLN palsies
• tracheo-oesophageal fistulas

Question 128

Oesophageal stenting considerations in adenocarcinoma

Answer 128

not before RTX - stent will migrate

position of tumour - too close to cricopharyngeus will not be tolerable

type - partially covered is preferable

use fluoroscopy in its placement

Question 129

CROSS trial and FLOT trial for oesophageal cancer

Answer 129

• (original trial = MAGIC - in both gastric and lower oesophageal adenocarcinomas)
• CROSS 2012
  
  • neoadjuvant chemorad and surgery vs surgery alone for oesophageal & junctional cancers
  • 75% adenocarcinoma and 23% SCC - T1N1 or T2-3N0-1
  • carboplatin and paclitaxel for 5wks and concurrent radiotherapy (41.4Gy in 23 fractions, 5 days per week), followed by surgery 4-6wks later
  • significant survival advantage to neoadjuvant therapy with mean survival of 48 vs 24mo
  • greater R0 resection, similar periop morbidity, greatest benefit in SCC but present for both
• FLOT
  
  • GOJ (and stomach) adenocarcinoma
  • FLOT was better than MAGIC

Clear survival benefit of neoadj CRT or chemo over surgery alone in pts w oesophageal ca but clear advantage of CRT over chemo not been established

MMH uses FLOT for junctional adenocarcinomas and CROSS for oesophageal SCC?

Question 130

Options for symptom control in unresectable or metastatic oeosphageal cancer

Answer 130

• chemo, radiation, local radiation w brachytherapy, local therapies eg laser ablation, photodynamic therapy, balloon dilatation, stents
• palliative chemo benefits largely confined to pts w good performance status
• stents endosocpically or fluoroscopically
  
  • across GOJ give bad reflux & don’t place within 5cm of cricopharyngeus (risks prox migration, laryngeal compression, intractable pain, globus sensation; stents acn move or erode or hav eingrowth
  • SEMS (metal stents) have better improvement in dysphagia * less adverse events

Question 131

What is the frequency of malignancy in gastric ulcers?

Answer 131

4%. 30% for ulcers >3cm

Question 132

Discuss the aetiology of gastric ulcers

Answer 132

2 predominant causes + H pylori and NSAIDs

others = smoking, marginal ulcer after bariatric surgery, fasting, crack cocaine/cocaine/meth, gastrinoma/ZES, critical illness, steroids, high salt diets, alcohol, chemo with bevacizumab, radiation, low SES

• H pylori infects half of world’s population
  
  • H pylori in 70% of pts w peptic ulceration treated surgically - previously 80-95% of duo and 75% of gastric but prevalence decreased
  • pts w ulcer perforation & confirmed H pylori infection have 5% ulcer recurrence at 1yr if eradicated vs 35% if not
• Nsaids
  
  • selective COX2 inhibitors developed to try reduce GI side-effects of NSAID use; reduced annual risk from 1.27 to 0.44%

Question 133

Discuss the pathogenesis of peptic ulcers

Answer 133

• caused by decreased defensive factors, increased aggressive factors or both
  
  • protective factors include: mucosal bicarb secretion, mucus production, adequate blood flow, growth factors, cell renewal, endogenous prostaglandins
  • damaging/aggressive factors include: excess HCl acid secretion, pepsins, ethanol ingestion, smoking, duo reflux of bile, ischaemia, NSAIDs, hypoxia, H pylori
  • although now clear most ulcers are caused by H pylori or NSAIDs, still important to understand all other protective & causative factors to optimise tx & ulcer healing and prevent disease recurrence
    *

Question 134

Discuss H pylori and its role in the pathogenesis of peptic ulcers

What other complications is it associated with?

Answer 134

• spiral or helical gram-negative rod with 4-6 flagella that resides in gastric-type epithelium within or beneath the mucous layer
  
  • this location protects the bacteria from acid & antibiotics
  • its shape and flagella aid its movement through the mucous layer towards a less acid environment
• produces enzymes that help it adapt to this hostile environment
  
  • mainly urease - capable of splitting urea into ammonia and bicarb, creating an alkaline microenvironment in the setting of an acidic gastric milieu
  • but secretion of this enzyme facilitates detection of the organsim
• microaerophilic, can only live in gastric epithelium - can also be found in heterotopic gastric mucosa (prox oesophagus in Barrett’s, gastric metaplasia in duo and within a Meckel’s or in the rectum)
• mechanisms responsible for H pylori injury - 4 proposed:
  
  • production of toxic products that cause local injury
    
    • breakdown products from urease activity (eg ammonia)
    • cytotoxins
      
      • VacA (not all strains) - induces vacuolation and cell death
      • CagA (cytotoxin-associated gene) - improves adherence
    • a mucinase that degrades mucus & glycoproteins
    • phospholipases that damage epithelial cells & mucous cells
    • platelet-activating factor - known to cause mucosal injury & thrombosis in the microcirculation
  • induction of a local mucosal immune response
    
    • attract neutrophils & monocytes, which then produce numerous proinflam cytokines & reactive oxygen species
  • increased gastrin levels with increase in acid secretion
    
    • basal & stimulated gastrin levels significantly increased presumably secondary to decrease in somatostatin release from antral D cells bc of infection w H pylori
    • during acute pahse of H pylori infection, acid secretion is decreased; with chronic infection, H pylori has trophic effects on ECL & G cells which can result in acid hypersecretion
    • but if oxyntic glands destroyed by chronic infection, hypoacidity will result
  • gastric metaplasia occurring in duodenum
    
    • likely a protective response to reuced duo pH, resulting from acid hypersecretion; this allows H pylori to colonise these areas of duodenum which causes duodenitis & likely predisposes to duo ulcer formation
• complications of H pylori infection:
  
  • gastritis
  • PUD
  • MALT lymphoma
  • gastric adenocarcinoma
  • (H pylori may actually be protective against oesophageal cancer)

Question 135

How do NSAIDs cause peptic ulcers?

Answer 135

• NSAIDs are absorbed through the stomach and small bowel and act as systemic inhibitors of the cyclooxygenase enzymes
• these enzymes form a rate-limiting step of prostaglandin synthesis in the GI tract
• prostaglandins promote gastric and duodenal mucosal protection via numerous mechanisms, including increasing mucin and bicarb secretion adn increasing blood flow to mucosal endothelium
• presence of NSAIDs disrupts these naturally protective mechanisms, increasing risk of peptic ulcer formation in the stomach and duo
• NSAID users have 1-4% risk per yr of clinically significant GI event incl bleeding, pyloric obstruction and perforation
• H pylori ulcers more frequently found in duo; NSAIDs in stomach
• H pylori ulcers almost always assoc w chronic active gastritis; not frequently found w NSAID-induced ulcers

Question 136

How do you test for H pylori?

Answer 136

gold standard = mucosal biopsy (either urease assay or histo exam of biopsy samples)

if endoscopy not required, evaluation of serum antibodies (IgG) = test of choice for initial dx but drawback is that it remains positive after treatment and eradication

to monitor treatment efficacy: stool antigen (uses monoclonal antibodies to H pylori antigens) or urea breath test (carbon-labelled urea breath test, based on ability of H pylori to hydrolyse urea)

H pylori eradication helps with initial healing but primary efficacy is in preventing recurrence. 20% of pts fail initial therapy (can be from antibiotic-resistant strain) so need to check for eradication with one of above at 4-6wks after therapy

Question 137

What is the management of gastric NETs?

Answer 137

• type I (75%)
  
  • in pts w chronic atrophic gastritis, F>M, mean age 63
  • often small, polypoid, multicentric tumours, usu behave in benign fashion but when larger (1-2cm) can metastasise to nodes
  • 7-12% have local nodes at presentation
  • <2cm - remove endosocpically
  • if >2cm, >6polyps at presentation or recurrence = resect
  • if antrectomy performed, ECL hyperplasia will regree due to decreased gastrin production
  • endoscopic surveillance, ex prognosis w >90% 5yr survival
• type II (8%, rare)
  
  • occur in pts w gastrinoma/ZES as part of MEN1
  • intermediate behaviour between type I & typ eII carcinoids w 10-30% risk of metastasising
  • same management as type I + remove gastrinoma whenever possible
  • 70% 5yr survival but MEN1 syndrome dictates outcomes more than carcinoid tumour
• type III (21%)
  
  • sporadic NETs, actually NECs
  • much more aggressive, usu high Ki67 index & mitotic rate
  • usu present w large ulcerating solitary mass, sometimes w liver mets
  • more common in middle-age men
  • gastrectomy, usu total, w clearance of local LNs (D2 resection); local resection not recommended
  • 50% 5yr survival

Question 138

Specific risks of fundoplication

Answer 138

inability to burp and vomit

slipped wrap - stomach above wrap

recurrent HH - stomach and wrap in chest

dysphagia

redo

vagus injury

injury to accessory left hepatic artery

Question 139

How is acid reflux diagnosed and scored objectively

Answer 139

DeMeester score

• a composite score of the acid exposure during 24 or 48 hour ambulatory pH monitoring
• 6 parameters
  
  • percent total time pH<4
  • percent upright time pH <4
  • percent supine time <4
  • number of reflux episodes
  • number of reflux episodes lasting ≥5mins
  • longest reflux episode (minutes)
• composite score >14.72 indicates reflux