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Flashcards in GI Deck (328):

Abdominal Distension DDx

1) Faeces
    - Subacute GI obstruction
    - Constipation

2) Fat
    - Obesity (slow increase, painless, weight gain)

3) Foetus
    - Pregnancy

4) Flatus
    - pseudo-obstruction or obstruction
    - Functional (usually associated with Irritable Bowel Syndrome)

5) Fluid
    - Ascites (consider DDx)
    - Tumour (esp Ovarian)
    - Distended bladder

Usually if abdominal distension with weight loss -> intra-abdominal diseases


Ascites DDx (by mechanism)

1) Fluid imbalance (peripheral arterial vasodilation; see image)

    - Hepatic cirrhosis with portal hypertension (transudate)
    - Budd-Chiari syndrome (hepatic vein occlusion; transudate)
    - Congestive heart failure, constrictive pericarditis & other right heart failure
    - Myxedema
    - Hypoproteinaemia (e.g. Nephrotic syndrome, protein-losing enteropathy)

2) Exudative

    - Intra-abdominal malignancy with peritoneal carcinomatosis
    - Infections (e.g. tuberculosis peritonitis)
    - Inflammation (e.g. SLE, pancreatitis)

3) Chylous

    - Obstruction (e.g. malignant lymphoma)
    - Iatrogenic (e.g. transection of nodes/vessels)

4) Nephrogenic

    - nephrotic syndrome
    - Haemodialysis


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Absence of bowel sounds DDx

1) Intestinal obstruction (e.g. hernia, volvulus, adhesion)

2) Paralytic ileus of any cause, e.g.

‚ÄĘ Infection (gram negs' LPS -> inflam)
‚ÄĘ Trauma (e.g. post-op -> inflam)
‚ÄĘ Bowel obstruction
‚ÄĘ Hypokalaemia (think about DDx)
‚ÄĘ Vascular ischaemia
‚ÄĘ Side effect to medications

3) Mesenteric ischaemia

4) Pseudo-obstruction (Ogilvie syndrome) 


Hyperactive Borborygmi

1) Bowel obstruction or dysmotility

2) Crohn’s disease/ulcerative colitis

3) Food hypersensitivity

4) Gastroenteritis

5) Normal 

6) Gastrointestinal haemorrhage 


Belching DDx

1) Air swallowing aka aerophagy
    - normal
    - anxiety
    - GERD
    - to relieve abdominal pain


Excessive Flatulence DDx

1) Irritable Bowel syndrome

2) Lactose intolerance

3) Intestinal Malabsorption


Caput Medusae DDx

Any condition causing portal hypertension, e.g.:

‚ÄĘ Cirrhosis of the liver
‚ÄĘ Severe heart failure
‚ÄĘ Inferior vena cava obstruction¬†

Portal hypertension causes backflow from the portal vein to the para-umbilical veins. The increased pressure and blood volume distend the veins. 


Cheilitis granulomatosa (definition and DDx)

painless enlargement of one or both lips

1)¬†Crohn‚Äôs disease ‚Äď uncommon
2) Sarcoidosis
3) Melkersson‚ÄďRosenthal syndrome ‚Äď rare¬†



aka Coffee Ground vomiting, bloody vomitus

DDx: Conditions associated with upper GI tract bleeding:

Ulcer (PUD)
AVM (vasculitis)
Mallory-Weiss tears, Malignancy
Esophagitis, erosion (stress gastritis)
Dieulafoy lesions

note: Coffee ground vomits is because blood
has been oxidised by gastric acid, hinting towards stomach or duodenum as origin



How to predict risk of mortality in upper GI bleeding

Use Rockall & Blatchford Score:

1) Older age

2) Shock

3) Comorbidity (e.g. heart failure, IHD, renal failure, malignancy)

4) Endoscopic findings (MW tear is better; malignancy is bad)

5) Stigmata of recent haemorrhage (e.g. visible bleeding vessels/clots


Courvoisier’s Law (note exception)

In (painless obstructive) jaundice, a palpable gallbladder would means it isn't gallstone:

DDx: indicates acalcuous extrahepatic obstruction, most likely a Malignant Biliary Obstruction (MBO):

1) Common bile duct obstruction
   - Cholangiosarcoma, Cholangiocarcinoma
   - CA head of pancreas
   - Biliary atresia (in infants)

2) Cystic Duct obstruction
   - mucocele

3) And many others (e.g. CA ampulla of vater, CA gallbladder, CA duodenum, rarely CA body pancreas, HCC)

*MOST UNLIKELY TO BE GALLSTONES (in which GB should be impalpable due to fibrosis as stone takes long time to develop)

1) recurrent pyogenic cholangitis in which gallbladder wall is dilatable due to lack of fibrosis (since primary pathology is not in gall bladder)

2) Double gall stones, one at the CBD (causing jaundice), the other at cystic duct (causing GB enlargement)


Cholelithiasis effects

- Asymptomatic

- Tender but impalpable gallbladder (because GB wall fibrosis)

- induce acute/chronic cholecystitis -> GB empyema

- Cystic duct/common bile duct obstruction
   -> acute biliary colic 
   -> obstructive jaundice
   -> Cholangitis
   -> (acute biliary) pancreatitis: Obstruction of pancreatic duct, thus Interstitial leak of activated enzymes, thus proteolysis and lipolysis, thus acute inflammation and destruction

- associated with GB carcinoma


Cullen's sign

Definition: Peri-umbilical ecchymoses, due to retroperitoneal bleeding. 

1) Acute Pancreatitis
2) Post-op or anticoagulation (iatrogenic)
3) Anticoagulation
4) Rectus sheath haematoma 
5) Ectopic pregnancy
6) Intrahepatic haemorrhage
7) Ischaemic bowel
8) Aortic rupture; e.g. from abdominal aortic aneurysm
9) Amoebic liver cyst
10) Perforated duodenal ulcer 

The retroperitoneum is connected to the gastro-hepatic ligament and then to the falciform ligament and finally to the round ligament. Retroperitoneal bleeding can reach umbilicus via these ligaments 

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Resonance below 5th intercostal space

1) Hyperinflation of lungs (i.e. COPD)

2) If it's decreased liver-dullness, then Fulminant hepatitis

3) Chilaiditi's sign (i.e. transverse colon is interpositioned between liver and diaphragm)

4) Chilaiditi's syndrome (if associated with abdominal pain and conditions like volvulus)


Erythema nodosum

(def, DDx & mechanism)

acute-onset eruption of red, tender nodules, predominantly over extensor surface of lower extremities 

1) Inflammatory bowel disease

2) Infections

3) Sarcoidosis

4) Rheumatological disorders

5) Drug reactions ‚Äď especially to¬†sulfonamides and the oral contraceptives

6) Malignancies

7) Pregnancy 

see image

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Grey-Turner's sign

Ecchymoses or purple discolouration of the flanks. due to retroperitoneal bleeding. 

1) Acute Pancreatitis
2) Post-op or anticoagulation (iatrogenic)
3) Anticoagulation
4) Rectus sheath haematoma 
5) Ectopic pregnancy
6) Intrahepatic haemorrhage
7) Ischaemic bowel
8) Aortic rupture; e.g. from abdominal aortic aneurysm
9) Amoebic liver cyst
10) Perforated duodenal ulcer 

associated with Cullen's sign (para-umbilical ecchymoses)

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1) Voluntary Guarding
   - anxiety, fear of pain
   - tenderness

2) Involuntary guarding
   - inflammation of parietal peritoneum (peritonism)


Board-like rigidity of abdomen when palpated

Peritonism (general peritonitis i.e. inflammation of the entire peritoneum), esp:

- due to perforated viscus, thus breathing work becomes thoracic-only with abdominal wall muscles not moving with respiration


Gynaecomastia (DDx with mechanism)

1) Physiological
   - @ puberty; because initial rise in estrogen
   - @ middle age; less testosterone production due to testicle ageing

2) Drug-induced
   - Spironolactone (a K sparring diuretics)
   - Digoxin 
   - Cimetidine
   - PPI (omeprazole)
   - Anti-androgens (flutamide)
   - Androgen
   - Ca channel Blocker (amlodipine, diltiazem, verapamil, nifedipine)

3) Hepatic Cirrhosis
   - Impaired liver reduce breakdown of androgen. The increased circulating peripheral androgen are aromatised to oestrogens 

4) Hyperthyroidism 

5) Hypogonadism
   - deficits in testosterone production 

6) Re-feeding syndrome
   - gonadal function suspended in starvation; once re-feed, estrogen rise is faster

7) Renal failure and dialysis
    - mechanism same as re-feed

8) Testicular tumours
- e.g. Benign Leydig tumours -> more estrogen produced
    - tumour increase hCG, which makes Leydig cells produce more sex hormones, with testosterone aromatised to estrogen

9) Post-radiotherapy (hypogonadism??)

10) Congenital abnormalities (e.g. Kallmann’s syndrome, Klinefelter’s syndrome) 


Hepatic venous hum DDx

Low-pitched hum heard over the liver when auscultating with the bell of the stethoscope 

1) Portal hypertension

2) Large haemangioma

3) Hepatoma 


Hepatomegaly DDx (by mechanism)

1) Neoplastic
- primary malignancy (e.g. HCC, cholangiocarcinoma)
- Metastases (usu GI tract; others are lung, kidneys, breast, gynae)
- Leukemia, lymphoma
- Benign tumours (e.g. Adenoma, Hemangioma, Focal nodular hyperplasia)

2) Metabolic
- Fatty liver
- Alcoholic liver disease
- Polycystic liver disease

3) Infective
infection & inflammation, thus enlargement
- Liver Abscess
- Liver cyst
- Acute hepatitis (acute; will be small if chronic)
- Infective mononucleosis (EBV)
- Malaria

4) Vascular
Increased back-up of venous pressure leading to vascular engorgement
- Congestive heart failure
- Hepatic venous occlusion (Budd-Chiari syndomre; primary or secondary)

5) Infiltrative
By deposition of non-liver cells/materials
- Sarcoidosis
- Amyloidosis
- Haemochromatosis
- Haemosiderosis
- Storage Disease (e.g. Gaucher disease)


Kayser‚ÄďFleischer rings DDx

Brown/blue rings at the periphery of the cornea (see pic)


1) Wilson’s disease
    - Copper accumulation leads to hepatocyte death, and Cu in circulation deposits in Descemet’s membrane

2) Chronic active liver disease

3) Primary biliary cirrhosis
    - cholestasis leads to Cu (excreted with bile) accumulation in hepatocyte, and leakage to systemic circulation after cell death

4) Multiple myeloma 

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Terry's nail DDx

A form of leuconychia, where the nail is white proximally and brown distally

1) liver disease (cirrhosis)

2) diabetes

3) congestive heart failure

**NOT with hypoalbuminaemia 

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Leuconychia DDx

1) Hereditary

2) Injury to nail base

Less common
3) Hypoalbuminaemia

4) Protein-losing enteropathies

5) Hepatic cirrhosis

6) Chronic renal failure 

7) Congestive heart failure

8) Diabetes mellitus

9) Hodgkin’s lymphoma 


Melaena definition & DDx

- Black, tarry, loose, sticky (may describe as diarrhoea)
- Malodorous
- Due to degraded blood in intestine 
- Indicative of upper GI tract bleeding:

Ulcer (PUD)
Varices (esophageal varices from portal hypertension)
AVM (vasculitis)
Mallory-Weiss tears, Malignancy
Esophagitis, erosion (stress gastritis)
Dieulafoy lesions

Note: Nonblood Causes:
- Iron
- Bismuth
- Food e.g. Licorice, rhubab


aphthous ulcer DDx

‚ÄĘ Trauma
‚ÄĘ Stress
‚ÄĘ Toothpaste

Less common
‚ÄĘ Iron deficiency
‚ÄĘ Folate deficiency
‚ÄĘ Vitamin B12 deficiency
‚ÄĘ Food hypersensitivity
‚ÄĘ Humoural/immunological
‚ÄĘ Inflammatory bowel disease
‚ÄĘ BehcŐßet‚Äôs disease
‚ÄĘ Nicorandil¬†


Muehrcke’s lines 

Two white bands that run parallel to the lunula across the width of the nail, with normal pink color in between

aka leukonychia striata:

1) Hypoalbuminaemia

2) Diseases causing serious metabolic stress

3) Chemotherapy treatment

4) Infection

5) Trauma 


Murphy’s sign (Def and DDx)

When palpating the abdomen below the right subcostal margin, the patient is asked to take a deep breath in and, on doing so, will be caught by sudden pain. 

DDx: Cholecystitis

Mechanism: On deep inspiration the lungs expand, pushing the liver downwards so the inflamed gallbladder is pushed onto the examiner’s hand, causing a sudden and unexpected sharp pain. 


obturator sign DDx (& mechanism)

Aka Cope's obturator test - Pain on internal rotation of the thigh:

DDx: Appendictitis

inflamed appendix lies in contact with the obturator internus muscle and, thus, when the leg is rotated, the appendix is stretched and irritated. 

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Psoas sign (DDx and Mech)

Pain on passive extension of thigh

1) Appendictitis
2) Psoas abscess

If the appendix is in a retro-caecal position, it may be in contact with the psoas muscle. Therefore, movement of the psoas muscle will move the inflamed appendix, causing pain, with a similar process occurring with a psoas abscess. 

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Palmar erythema 

symmetrical and slightly warm area of erythema on the thenar and hypothenar eminences of the palm, caused by increased perfusion.

1) Pregnancy (raised estrogen -> vascular changes)

2) Chronic Liver Disease (raised estrogen)

3) Autoimmune (e.g. RA)

4) Hyperthyroid (raised oestradiol-17-beta)

4) Neoplasm (increased angiogenic factors and estrogen from tumour)


Pyoderma gangrenosum 

Chronic inflammatory skin disease in which a painful nodule/ pustule breaks down to form a progressively enlarging ulcer with a raised, tender, undermined border

1) Idiopathic (50%)

2) IBS esp Ulcerative colitis (50%)

3) Rheumatological disease

4) Paraproteinaemia/ monoclonal gammopathy

5) Haematological malignancy 

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Rebound tenderness 

DDx: any cause of peritonitis 


Rovsing’s sign 

Definition: When the left lower quadrant is palpated, pain is felt over the right lower quadrant 



Sialadenosis Ôľądef and DDx)

Definition: persistent enlargement of usu parotid gland (neither inflammatory or neoplastic) - palpable as a soft, bilateral, symmetrical and non-tender enlargement of the parotid glands 

1) Indicative of chronic liver disease, as it's associated with chronic alcoholism

2) Diabetes mellitus

3) Malnutrition


Sister Mary Joseph nodule 

A hard, metastatic tumour nodule located at the umbilicus. 

1) Metastatic cancer (usually adenocarcinoma)
   [source is often abdominal organs:]
     - stomach
     - pancreas
     - Colorectal
     - ovary
     - etc


Spider naevus DDx

1) Alcoholic liver disease 
2) Hep B, C
3) Pregnancy
4) Oral contraceptives or hormone replacement
5) Thyrotoxicosis

Increased plasma oestrogen and substance P have been implicated in vasodilatation and neovascularisation to form spider naevi 


Splenomegaly DDx (by mech)

1) excessive immunological response 
    - infectious mononucleosis (EBV)
    - bacterial endocarditis
    - CMV
    - HIV

2) Increased RBC destruction
    - haemolytic diseases, e.g.:
    - hereditary spherocytosis
    - G6PD deficiency
    - beta-thalassaemia  

3) Congestive engorgement 
    - Portal hypertension (think about causes)

4) Myeloproliferative disorders 
    - PV, CLL
    - myelofibrosis
    - hairy cell leukaemia 

5) Infiltrative disorders (depositing non-splenic material within the spleen)
    -  Sarcoidosis
    - Amyloidosis

6) Neoplastic


Steatorrhoea DDx (by mechanism)

Caused by malabsorption syndromes (esp fat) such as:

1) Luminal cause (fat not broke down):
    - Pancreatic insufficiency (no lipase)
    - Cirrhosis and biliary obstruction (no bile salt)
    - Biliary tree disease
    - Drugs (e.g. lipase inhibitors) 
    - Giardia lamblia infection 

2) Mucosal cause (fat not absorbed)
    - Coeliac disease 
    - Inflammatory bowel disease

3) Lymphatic cause (fat not transported)
    - trauma to lymphatic system
    - congenital intestinal lymphaniectasia
    - Lymph obstruction


Abdominal Striae DDx

‚ÄĘ Obesity and weight gain

‚ÄĘ Cushing‚Äôs syndrome

‚ÄĘ Pregnancy

‚ÄĘ Puberty

‚ÄĘ Steroid therapy¬†


Uveitis/iritis DDx

1) Eye trauma

2) Infection

3) Inflammatory bowel disease (IBD)

4) Vasculitis 


Hematochezia DDx

Fresh bright red bloof per rectum, indicative of LGI bleeding, or massive UGIB

DDx: NADIR (plus massive UGIB i.e. UVA MED)
Inflammatory Bowel Disease, Infectious colitis, Ischemia
'Rhoids (Haemorrhoids)

Massive UGIB:
Aortoenteric fistula
Dieulafoy's lesion

Full version below:

N) Neoplasm
- Colorectal cancer

- aka angiodysplasia, vascular ectasia
- common in 60+

D) Diverticulosis
- note LGIB is rare in diverticulitis

I) Inflammatory Bowel Disease

I) (Infective) colitis
- infective colitis
- radiation colitis

I) Ischemia
- Acute mesenteric ischemia
- Chronic mesenteric ischemia

R) 'Rhoids (Anorectal sources)
- haemorrhoids
- rectal ulcer
- rectal varices
- anorectal fissures

beware that massive UGIB might mimic LGIB:
1) Duodenal or gastric ulcer
2) Esophageal or gastric varices
3) Aortoduodenal fistula
4) Dieulafoy's lesion


Image modalities for gastrointestinal 

1) Plain film (AXR)

2) Barium & contrast studies
    - swallow
    - meal
    - follow-through
    - enema

3) CT

4) angiography
5) US
6) MRI


How to determine position of patient in AXR

If erect -> fluid level in GI tract, stomach etc

if supine -> no Fluid level


Bowel gas pattern in AXR

- Stomach is always present (large gas bubble)

- Small bowel: 2-3 loops of non distended bowel 

- Large bowel: rectum and sigmoid gas almost always present 


How to determine bowel dilatation on AXR

‚Äú3, 6, 9‚ÄĚ rule to look for bowel dilation

-> 3cm+ small bowel
-> 6cm+ large bowel
-> 9cm+ caecum


When to use water soluble dye instead of Ba

- Suspected partial SBO (as barium might cause complete obstruction)

- Suspected perforation or anastamotic leak (Barium peritonitis ‚Äď 50% mortality if both barium and feces were released into the peritoneal cavity)

note: however, Inferior image quality and unable to perform double contrast studies 


Double contrast used in barium study

barium, methycellulose 


GI Angiography investigation (types, and indications)

1) DSA Digital subtraction Angiography
   - gold standard
   - allow intervention e.g. coil anf drain

2) Mesenteric CTA 

when suspecting:

‚ÄĘ Acute or chronic mesenteric ischemia
‚ÄĘ Aneurysm
‚ÄĘ Crohn‚Äôs disease
‚ÄĘ GI bleeding


Apple Core Sign (def & DDx)

Definition: A stricture can be seen. Possibly malignant due to mucosal irregularity and shouldering formed from soft tissue  

- colorectal cancer (if large bowel)


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Rat-tail sign (aka Bird beak sign); definition & DDx

DDx: Achalasia 

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Coffee bean sign (DDx)

- Most likely volulus, either sigmoid or caecal

Caecal volvulus
- younger patient 30-50yo
- LUQ to RLQ
- dilated small bowel

Sigmoid volvulus
- Elderly
- Right abdomen up to diaphragm 
- Dilated small & large bowel
- Head characteristically point to RUQ

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multiple air-fluid levels in AXR (DDx) 

aka "string of beads/pearls", along with
- Dilated small bowel
- Paucity of large bowel gas

==> Small bowel obstruction


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Pneumoperitoneum AXR signs

- Free gas collection under diaphragm

- Air outlining Gall bladder, liver edge, falciform ligaments and other organs

- Rigler's sign/ Double wall sign -> when gas on both sides of bowel wall


Ulcerative colitis AXR signs

ONLY AT COLON, Mucosal or submucosal 

1)¬†Low density around colon wall¬†‚ÄĒ> pneumotosis

2) Thumbprinting (indicate edematous bowel wall thickening)

3) Featureless colon (no haustra)

4) Continuous lesion

5) Rarely causes fistulas, abscesses or strictures 

6) Look for polyps due to relevance of colon cancer


Crohn's disease AXR signs

Any part of GI tract, transmural:

1) Skip lesions (patchy inflammation)

2) Strictures, fistula, and abscesses


excoriation marks DDx

- Indicates pruritus from:

1) Chronic renal failure (mainly from uraemia and accumulation of pruritogenic factors)

2) Hepatobiliary causes
   - Biliary obstruction
   - Viral hepatitis
   - Primary biliary cirrhosis (AMA)
   - Primary sclerosing colangitis (IBD)
   - Drug induced cholestasis

3) Hematological
   - polycythaemia vera
   - leukemia
   - lymphoma
   - rarely in iron deficiency anaemia

4) Endocrine
   - Hyper/hypo -thyroidism
   - DM
   - MEN II
   - Carcinoid

5) Neurological (very rarely)
   - MS
   - stroke
   - cerebral tumour


Dysphagia definition and classification

Definition: sensation of difficulty of swallowing, classified into:

1) Oropharyngeal dysphagia
   - cannot perform oro-pharyngeal transfer
   - feels difficulty initiating swallowing, or chew
   - cannot chew
   - may cough, choke, tracheal aspirate, nasal regurgitation, drooling
   - swallowing with gurgling noise
   - regurgitation (within 1 second!)
   - associated with dysphonia or dysarthria

2) Esophageal dysphagia
   - cannot pass bolus from upper esophagus to stomach
   - feels food "sticks" after swallowing
   - Substernal or epigastric region, sometimes chest pain
   - delayed regurgitate

we can also classify it based on nature:

1) Mechanical dysphagia (due to obstruction)
   - swallowing of fluid is better than solid

2) Functional dysphagia (due to poor coordination)
   - both fluid and solid cannot swallow

3) Psychogenic
   - e.g. Globus hystericus


Differentiating mechanical and functional esophageal dysphagia (by history)

Mechanical VS functional:

1) Onset: gradual or sudden VS gradual

2) Progression: often VS variable

3) Food texture: fluid okay VS cannot fluid

4) Food temp: Not related VS affected by temp

5) Response to bolus: regurgitate VS regurgitate, sometimes passes with water


Dysphagia DDx

A) Oropharyngeal
- Oropharyngeal cancer
- Hypopharyngeal cancer

- Stroke
- Parkinson's
- Myasthenia Gravis
- Bulbar or Pseudobulbar palsy (esp pharyngeal plexus CN IX, X; and also CN V3 and XII of tongue)

B) Esophageal
(mechanical; extraluminal)
- Neck mass e.g. Goitre
- Mediastinal tumour e.g. lung, germ cell
- Esophageal hiatal hernia

(mechanical; intramural)
- Esophageal cancer
- CA Cardia
- Esophagitis (peptic, eosinophilic, candidiasis)
- Strictures (e.g. peptic, drugs, eosinophilic esophagitis)

(mechanical; intraluminal)
- Foreign body (i.e. steakhouse syndrome)
- Plummer-Vinson syndrome (upper esophageal web)
- Schatzki Ring (lower esophageal web)
- Esophageal Diverticulum

- Achalasia
- Diffuse Esophageal Splasm
- Secondary motility disorder from e.g. Diabetes, scleroderma

C) Psychogenic
- Globus hystericus


Muscle types in upper alimentary canal

Tongue, oropharynx, UES, upper 5% of esophagus: striated muscles

Mid 35%-40% of esophagus: mixed striated and smooth muscles 

Distal 50-60% of esophagus: smooth muscle 


Phases of swallowing

1) Oral
   - voluntary
   - mastication
   - rolling food into bolus by tongue movements

2) Pharyngeal
   - involuntary
   - oro-pharyngeal transfer
   - laryngeal elevation (so epiglottis covers glottis)
   - elevation of soft palate

3) Esophageal
   - Involuntary
   - peristalsis


Nerves involved in swallowing action


Mastication = V3

Buccinator to contain food inside of teeth = VII

Salivary production:
VII‚ÄĒchorda tympani¬†
IX‚ÄĒlesser petrosal

Tongue movement:
mylohyoid (V3 - mylohyoid nerve)
genioglossus, styloglossus, hyoglossus (the rest XII)

Oro-pharyngeal transfer reflex:
afferent limb of reflex is IX and efferent limb is the pharyngeal plexus (IX and X)

soft palate is tensed by tensor palatini (Vc), and then elevated by levator palatini (pharyngeal plexus‚ÄĒIX, X)¬†





Investigations in dysphagia

1) Endoscopy and biopsy (sometimes interventional too e.g. dilatation of strictures); biopsy and brush cytology esp important in suspected esophageal cancer

2) Neurological examination

3) VFSS, with barium swallow

4) High resolution manometry (pressure sensor), with esophageal manometric tomography

5) Trans-esophageal ultrasound helps to determine depth of penetration of tumours and used for stageing


Esophageal cancer types (site, risk factors)

1) Sqaumous cell carcinoma
Site: mainly upper and middle esophagus; 1/3 in lower
- Predominant form in HK, high prevalence in Hebei, Henan, Beijing
- Smoking
- Alcohol
- Nitrosamine, NPC, mediastinal radiation
- Aflatoxin (mouldy food), no fruits and veggies, micronutrient deficiency (selenium)
- achalasia, Plummer-Vinson
- caustic ingestion, hot beverage

2) Adenocarcinoma
: distal third of esophagus or gastroesophageal junction
- Predominant form in caucasians and men
- GERD, Barrett esophagus
- Smoking
- Obesity
- alcohol


Esophageal cancer stageing

Starts with TNM Staging

Then staged together in different combination of TNM status.


I - lamina propria or submucosa; nodes negative

IIa - muscularis propria or adventitia; nodes negative

IIb - muscularis propria; positive regional nodes

III - adventitia; positive regional nodes OR adjacent structure invasion (with or w/o nodes)

IV - distant metastasis


Barrett esophagus

Complication of longstanding acid reflux disease (GERD):

- salmon-red in endoscopy

- lower esophageal squamous epithelium replaced by columnar mucosa (intestinal metaplasia with goblet cells)

- risk of developing esophageal adenocarcinoma

- require routine endoscopic surveillance



Clinical features of esophageal cancer

- progressive dysphagia (esp solid foods)

- weight loss 

- anorexia

- cervical lymphadenopathy

- odynophagia, chest pain, haematemesis, hoarseness (suggests mediastinal invasion; recurrent laryngeal nerve in the latter)

- Tracheo-esophageal or broncho-esophageal fistula (--> cough when swallowing, aspiration pneumonia, pleural effusion)


Esophageal cancer treatment

1) Palliative care (as most presents at advance stage)
- endoscopic stenting (self expanding)

2) Esophagectomy if stage I, IIa:
i) Two-stage Lewis-Tanner operation (laparatomy plus right thoracotomy for gastroesophageal anastomosis

ii) Three-stage McKeown approach (same as above plus third incision in the neck to complete the cervical anastomosis)

iii) Laparascopic plus Transhiatal (?)

3) Chemotherapy plus RT before surgery might help

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Name some esophageal motility disorders 

1) Achalasia
- incomplete relaxation of LES with aperistalsis 
- rat tail sign

2) Diffuse esophageal spasm
- simultaneous contraction with no peristalsis
- corkscrew sign

3) Nutcracker esophagus
- aka jackhammer esophagus, hypertensive peristalsis
- Peristalsis but extremely forceful and strong contractions

4) Nonspecific esophageal dysmotility
- weak peristalsis


Achalasia definition and causes

Definition: an acquired esophageal motility disorder, criteria being:

   - incomplete relaxation of LES when swallowing
   - Aperistalsis of esophagus

In barium swallow, typically shows "bird-beak" or "rat-tail" sign

- Mostly idiopathic (selective degeneration of inhibitory NO neurons of LES muscles)
- adenocarcinoma of proximal stomach in Caucasian
- Chagas disease


Achalasia Treatment

No cure; all palliative management:

1) Medical therapy
   - antimuscarinics (dicyclomine)
   - sublingual nitroglycerin or Calcium channel blocker

2) Adaptive measures
   - chew food well before swallow
   - sleep with trunk elevated
   - avoid eating before sleep

3) Botox injection to LES during endoscopy

4) Forceful dilatation
   - pneumatic balloon dilatation
   - alternatives e.g. mechanical, hydrostatic

5) Surgical
   - Heller myotomy (remove circular muscles of LES)
   - POEM (per-oral endoscopic myotomy)


Diffuse esophageal spasm diagnosis

1) Esophageal manometry
   - simultaneous, multiphasic, repetitive, non-peristaltic contractions that occur after a swallowing
   - LES sphincter function is normal (i.e. normal LES pressure)

2) Barium swallow
   - "corkscrew esophagus"

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DES clinical features

Diffuse esophageal spasm present as:

1) Chest pain (mimics angina), radiate to jaw, shoulder, arms, and back

2) Dysphagia, with uncommon regurgitation


DES defintion and management

Diffuse esophageal spasm

Non-peristaltic spontaneous contraction of esophageal body (several segments contract simultaneously)

- No completely effective therapy

- sublingual nitroglycerin or Calcium channel blocker (decreases amplitude of contractions)

- Tricyclic antidepressants for symptomatic relief

- Some suggests esophagomyotomy if patient is incapacitated by symptoms


Plummer-vinson syndrome (clinical signs)

A triad of:
- iron deficiency anemia
- Dysphagia
- Cervical esophageal webbing

other signs are:
- glossitis (beefy red, smooth tongue)
- angular stomatitis
- koilonychia
- splenomegaly
- thyroid enlargement
- fatigue and weakness from anaemia

10% will develop squamous cell carcinoma of oral cavity, hypopharynx, or esophagus


Schatzki Ring (definition, cause, symptoms, complications)

Circumferential ring in the lower esophagus (i.e. distal esophageal web) that is accompanied by a hiatal hernia

- GERD, caustic ingestion, pill-induced esophagitis
- e.g. ingestion of acid, alkali, bleach, detergents (usu due to suicide attempts)
- Alkali ingestion is more dangerous than acid due to esophageal liquefactive necrosis, with full-thickness perforation (not seen is acid)

- Usually asymptomatic
- Mild to moderate dysphagia
- May present with reflux

- Dysphagia
- Reflux
- Full-thickness necrosis and perforation
- Stricture formation
- Risk of esophageal cancer


Schatzki Ring management

- Avoid vomiting, gastric lavage, and oral intake (as it can compound to original injury)

- Steroids and antibiotics

- Bougienage for esophageal dilatation if stricture

- Antireflux surgery if reflux is present

- Esophagectomy if full thickness necrosis occured


Commonest esophageal diverticulum (& pathogenesis)

Zenker's diverticulum

Found in the upper third of the esophagus. A sac-like outpouching of the mucosa and submucosa through Killian's triangle, an area of muscular weakness between the transverse fibers of the cricopharyngeus and the oblique fibers of the lower inferior constrictor. Often causes by a failure of cricopharyngeal muscle to relax during swallowing, which increases intraluminal pressure.


Zenker's diverticulosis clinical features

Seen in >50yo patients:

- Dysphagia, regurgitation, vomiting
- Halitosis
- Weightloss
- Chronic cough


Some types of esophageal diverticulum

- Zenker diverticulum (upper 1/3)

- Traction diverticulum (midpoint)

- Epiphrenic diverticulum (lower 1/3)


Traction diverticulum (location, pathogenesis, symptoms)

Midpoint of esophagus near the tracheal bifurcation

Traction from contiguous mediastinal inflammation and adenopathy (commonly due to pulmonary TB), in which the hilar node scarring retracts the esophagus, forming diverticula

Usually asymptomatic and does not require treatment


Epiphrenic diverticulum (location, pathogenesis, symptoms)

Lower third of esophagus

Due to spastic esophageal dysmotility, or achalasia

Dysphagia, more related to the underlying motility disorder


Management of esophageal diverticula

Investigate with barium swallow, followed by:

Zenker diverticula:
- cricopharyngeal myotomy
- Diverticulectomy is secondary

Traction diverticula:
- Treat TB
- Diverticulectomy is usually unnecessary

Epiphrenic diverticula:
- Esophagomyotomy (myotomy of lower sphincter)
- Diverticulectomy is secondary


Types of hiatal hernia

1) Sliding hiatal hernia
- i.e. Type 1
- >90% of cases
- Progressive disruption of gastroesophageal junction leads to upward herniation of cardia via esophageal hiatus
- No hernia sac
- associated with GERD

2) Paraesophageal hiatal hernia (aka rolling)
- - Type 2: Stomach herniates into thorax via esophageal hiatus, but GEJ does not and remain below the diaphragm
- Type 3: a mix of 2 and 3, with both GEJ and stomach herniating into thorax via esophageal hiatus; GEJ is intact
- Type 4: when type 3 is associated herniation of other viscera e.g. intestines

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Clinical features of esophageal hiatal hernia

- majority are asymptomatic

- Heartburn, chest pain, dysphagia


Complications of esophageal hiatal hernia

Sliding hiatal hernia:
- Reflux esophagitis (barrett esophagus, esophageal cancer)

Paraesophageal hiatal hernia
- GI obstruction (organoaxial volvulus, mesenteroaxial volvulus -> see pic)
- hemorrhage
- incarceration
- Strangulation

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Diagnosis and management of hiatal hernia

- Barium swallow

Management of Type 1
- Medical treatment (antacids)
- Lifestyle modification (small meal, elevation of head after meal)
- Nissen fundoplication if no response to medical therapy or with esophagitis

Management of Type 2
- Elective surgery due to serious complications e.g. obstruction, incarceration, strangulation


Esophageal perforation causes

- Forceful vomiting (boerhaave syndrome)

- blunt trauma

- Iatrogenic (e.g. EGD, NG tube, other instrumentation)

- (rare) esophageal pathology e.g. cancer, ulcer


Esophageal perforation presentation

"Mackler triad"
- history of dietary overindulgence and overconsumption of alcohol
- chest pain and subcutaneous emphysema
- after recent vomiting

other signs:
- pain (retrosternal, chest, shoulder, neck)
- dysphagia
- dyspnoea
- hemetemesis, melena
- dysnpoea, tachypnoea
- fever
- Hamman sign (i.e. mediastinal crunch produced by heart beating against air filled tissues)
- pneumothorax, pleural effusion (high amylase in pleural tap)


Ix and Mx of esophageal perforation

- CXR: pleural effusion, pneumothorax, pneumomediastinum, hydrothorax or hydromediastinum
- Contrast esophagram (soluble Gastrografin swallow)
- Pleural fluid analysis: amylase rich
- don't do EGD!!

- If stable (medical): IV fluids, parenteral nutrients, NPO, antibiotics, H2 blocker
- If unstable (surgical): Tube thoracostomy for drainage, and primary repair of perforation


Etiology of esophageal ulcers

1) Esophageal cancer

2) Gastric acid (GERD, Zollinger-ellison syndrome)

3) Infection (Candida, TB, EBV, CMV, HSV, HIV)

4) Pill induced

5) Irradiation (malignancy)

6) Sclerotherapy induced (usu post endoscopy)

7) Caustic ingestion (suicide)

8) Alcohol, smoking



Pill induced esophagitis (location, demographics)

- mid esophagus
- ulcers are usually opposite to one another

presented usu in elderly patient with slight motility problems


Causes of medication induced esophagitis

1) Antibiotics¬†‚ÄĒ¬†Tetracycline,¬†doxycycline, and¬†clindamycin

2) Anti-inflammatory medications - aspirin and NSAIDs

3) Bisphosphonates - for osteoporosis


Dyspepsia definition

A spectrum of epigastric symptoms, e.g. heartburn, indigestion, bloating, epigastric discomfort, and epigastric pain


Dyspepsia DDx

1) Functional Dyspepsia (60%) aka Non-ulcer dyspepsia

2) Gastroduodenal
   - Peptic ulcer disease (10%)
   - GERD
   - Gastritis
   - Gastric cancer (rare)
   - DM gastroparesis
   - lactose introlerance

3) Esophageal
   - Esophageal cancer
   - Diffuse esophageal spasm
   - Hiatal hernia

4) Hepatobiliary
   - Gallstone (biliary colic)
   - cholecystitis

5) Pancreatic
   - Pancreatitis
   - CA pancreas

6) Drug-induced
   - NSAID, aspirin, aledronate

7) Atypical IBS

6) Cardiovascular
   - Dissected aortic aneurysm
   - MI, myocarditis 

7) Chest
   - Pneumothorax, PE

8) O&G
   - PID, ectopic pregnancy

and many more....


What to ask in history of pain?






Associated symptoms

Time course

Exacerbating and relieving factors

Severity (out of 10 marks)


Red flags of Dyspepsia (require endoscopy!)

1) Onset age >55
- increased Gastric cancer incidence

2) family hx of GI cancer

3) Weight loss (>10%)

4) Vomiting

5) Dysphagia, Odynophagia

6) GI bleeding


What are the pain severity in:

1) Peptic ulcer

2) Appendicitis, diverticulitis 

3) Biliary Colic, pancreatic disease

4) Renal colic, intestinal disease

5) Ruptured aortic aneurysm 

1) Peptic ulcer
- Constant, especially post-prandial

2) Appendicitis, diverticulitis 
- Progressively increasing

3) Biliary Colic, pancreatic disease
- Increases, plateaus, then drops

4) Renal colic, intestinal disease
- Up & down, cyclical on & off pattern

5) Ruptured aortic aneurysm 
- Catastrophic onset of extreme pain


DDx for Acute epigastric pain with back radiation 

-ÔĀģ Posteriorly penetrating peptic ulcer

-ÔĀģ Biliary colic

-ÔĀģ Acute pancreatitis

-ÔĀģ Dissecting aneurysm¬†


DDx for (Epigastric pain + repeated vomiting)

- Gastroenteritis (food poisoning)

- Acute pancreatitis

- GI obstruction


Peptic Ulcer disease causes

1) H Pylori infection

2) NSAID & aspirin (by inhibiting prostaglandin production, thus impaired mucosal protection from acids)

3) Gastric acid hypersecretory states e.g. Zollinger Ellison syndrome (gastrinoma)

4) Emotional stress, personality type (Type A)

5) Crohn's disease

6?) Alcohol, coffee and smoking might be related


Sites of peptic ulcers

1)ÔĀģ Gastric ulcer
Type I: on lesser curvature
Type II: gastric and duodenal
Type III: Prepyloric (within 2cm proximal to pylorus)
Type IV: Near esophagogastric junction

2)ÔĀģ Duodenal ulcer

3)ÔĀģ Esophageal ulcer

4)ÔĀģ Meckel‚Äôs diverticulum¬†
as it is often formed by gastric mucosa/cells that produces gastric acid

5)ÔĀģ Anastomotic ulcer (after surgery e.g. gastrojejunal anastomosis, Roux-en-Y, etc)


Clinical features of peptic ulcer disease

1) Epigastric pain & dyspepsia
- "Aching or gnawing" in nature
- Nocturnal pain (more common in DU)
- Hunger pain (if DU, eating will relieve pain)

2) Upper GI bleeding

3) Vomiting, nausea, early satiety, weight loss


Complications of Peptic ulcer disease (and diagnosis)

1) Chronic GI bleeding, thus iron deficiency anaemia
- stool guaiac

2) Perforation (DU perforate more due to thinner wall)
- Upright CXR shows free air under diaphragm
- CT scan to detect free abdominal air

3) Gastric outlet obstruction (due to massive ulcer at the pylorus, or ulcer stricture; common in DU or Type III GU) 
- Barium swallow
- Saline load test (empty stomach with NG tube, add 750mL saline, aspirate back 400+mL after 30 min means positive)



Differentiation between DU and GU

DU vs GU:

Increased offensive factors VS decreased mucosal defensive factors

Younger (40yo)

Associated factors
Type O blood, NSAID, more associated with H Pylori VS Type A blood, Smoking

Nocturnal pain & hunger pain (relieved by food) VS not relieved by food

1-2 cm distal to pylorus VS stomach


ESRH classfication

"Endoscopic stigmata of Recurrent Haemorrhage" aka Forrest classification to look for chance of re-bleeding of ulcers:

Ia = spurting (80-90% rebleeding)

Ib = oozing (30% rebleeding)

IIa = non bleeding with visible vessels (20-50% rebleeding)

IIb = adherent clot (20-30% rebleeding)

III = clean base (0-2% rebleeding)


Risk factors for recurrent ulcer bleeding

‚ÄĘ Age >60yrs
‚ÄĘ Comorbidity, or hospitalised for other conditions
‚ÄĘ Coagulopathy¬†

‚ÄĘ Shock on presentation
‚ÄĘ Hb ‚ÄĘ Need Blood Transfusion

‚ÄĘ Large ulcer
‚ÄĘ Ulcer on higher posterior lesser curve¬†
‚ÄĘ Ulcer on inferior posterior wall of¬†D1 (duodenal bulb)


Management of PUD

1) Resuscitation if active bleeding and shock

2) EGD to verify bleeding, and stratify patients according to "Endoscopic Stigmata of Recent Hemorrhage" ESRH aka Forrest's classification

->) therapeutic endoscopy if ESRH IIb or above

->) Surgery (plication, highly selective vagotomy, truncal vagotomy, pyloroplasty, Billroth I gastectomy; see pic)

->) Discharge with medical therapy if ESRH III (see next card)

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Medical therapy for ESRH III PUD

1) Supportive
- stop NSAID, aspirin; 
- Switch to less ulcerogenic NSAID or COX-2 inhibitor 
- Restrict smoking, alcohol, coffee
- Control emotional stress
- Avoid eating before bedtime (which stimulates nocturnal gastric acid level)

2) Anti-secretory agents
- H2 receptor blocker e.g. Cometidine, ranitidine
- PPIs e.g. Omeprazole, Iansoprazole
- Antacids e.g. aluminium hydroxide, calcium carbonate, bismuth subsalicylate

3) H Pylori eradication
- Start with Triple therapy with PPI, Clarithromycin, Amoxicillin

4) Cytoprotection
- Sucralfate (facilitates ulcer healing)
- Misoprostol (esp for NSAID using patients)

5) Surgery (usu for complications)
- Close perforation and perform plication, highly selective vagotomy, truncal vagotomy, pyloroplasty, Billroth I gastectomy 
- Surgically correct gastric outlet obstruction

- In NSAID cases, start by stopping NSAID, and give PPI or misoprostol
- In H Pylori cases, start with triple therapy, and give PPI or H2 receptor blocker or antacids


Indication of surgery for PUD

- therapeutic endoscopist not available

- massive bleeding

- failed endoscopic therapy

- rebleed after endoscopic therapy 

- Complications of PUD e.g. gastric outlet obstruction, perforation


Pathogenesis of NSAID induced peptic ulcers

1) NSAIDs itseld irritates and damages the GI mucosa, thus increasing offensive factor

2) NSAID inhibits prostaglandin, bicarbonate, and mucus production of gastric mucosa, thus reducing defensive factors


Risk factors for upper GI complications occurring with NSAIDs 

Patient-related factors:
- age >60 years
- history of PUD or upper GI complications.

Drug-related factors
- relatively toxic NSAID
- high dose of NSAID (or two NSAIDs used concurrently)
- concurrent use of an anticoagulant
- concurrent use of a corticosteroid. 


H pylori prevalence

- Afflicts about 50% of population in HK & China, lower in developed worlds

- 50-80% in developing countries and 10-40% in developed countries

- Increased with age, poor hygiene, poor scio-economic status, overcrowding


H pylori transmission

- Mostly transmitted in childhood

- Possibly transmitted by oral-oral or faecal-oral route with humans as the only reservoir

- Associated with bad water supply, poor sanitory condition, crowded environment, low socio-economic status 


how to diagnose H pylori (with pros & cons)

1) Urea breath test (by ingestion of C-13-labelled urea)
- commonly used for acute infection, & monitoring

2) Stool antigen ELISA test
- commonly used for acute infection, & monitoring

3) Serum, or whole blood, or urine antibody ELISA test (to test for IgG, as it is a chronic infection)
- not affected by recent intake of drugs (e.g. PPI, antibiotics, bismuth)
- cannot be used for post treatment testing as Ab level remain high for 6-12 months
- whole blood is near patient test, while serum is lab test
- urine is good for epidemiological studies

4) PCR

Invasive (based on gastric antral biopsy specimens during upper endoscopy):
5) Rapid urease test
- Easy, simple, fast (24hr), highly accurate, CHEAP (cos home made)

6) CLO test (i.e. Campylobacter like organism)
- Easy, simple, fast (24hr), highly accurate
- expensive

6) Histology with H&E, warthin-starry silver, modified Giemsa

7) Bacterial culture
- less sensitive
- only test that allows antibiotics sensitivity testing
- useful in triple therapy failure


Urea breath test procedures

1) Fasting for 4 hours

2) Get Baseline sample at Time 0
[Test meal: Fatty meal / citrate solution]

3) Give 13C urea powder / tablet 50mg to 200mg

4) Time 30: second sample, which is analysed with Mass spectrometer / infra-red machine 


Post-treatment H pylori test (choice and precautions)

(side question: what drugs will affect post treatment H pylori test)

- Use Urea breath test, Stool antigen, histology, or culture

- NEVER use antibody test (serum, whole blood, urine) as antobidy will remain high for 6-12 months

- Avoid false negative by waiting at least 4 weeks after stopping all drugs, as "PPI, Antibiotics, and Bismuth" will prevent regrowth of any remnant H pylori, the longer the better

- H2 blocker and antacids will not affect results, but will still be prudent to stop it 2-3 days before test


Microbiological facts about H pylori

- Gram negative

- Rod,spiral shape

- with unipolar flagella

- can be stained with H&E, modified Giemsa, Warthin-Starry silver, etc

- Strong urease activity, which converts urea into ammounium and bicarbonate

- positive urease, oxidase, and catalase tests

- Columbia agar with 7% horseblood and H pylori selective supplement under microaerophilic conditions produced by gas generating system


H. pylori associated diseases 

- non-ulcer dyspepsia (i.e. functional dyspepsia)

- Acute and chronic gastritis (antral-predominant & pan-)

- duodenal ulcer (from antral predominant), gastric ulcer (from pan-gastritis)

- gastric cancer (more so in pangastritis)

- GALT lymphoma

Extra-GI system:
- Anemia (B12 and Fe deficiency from atrophic gastritis) 

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H pylori Eradication regimen

Based on Asia Pacific Consensus:

1. TRIPLE THERAPY (twice daily b.i.d. for 7 days) of:

1) PPI standard dose

2) Clarithromycin 500mg 

3) Amoxicillin 1000mg (or consider Metronidazole 400mg if penicillin allergic, note 50% Mitronidazole resistance in HK)

^ note: Masstricht I Consensus suggested PPI + Amoxicillin + Metronidazole as an alternative but it is at least 10% inferior and no longer used

2. RESCUE THERAPY (quadriple therapy for 7 days) of:

1) PPI standard dose b.i.d.

2) Metronidazole 400mg t.i.d.

3) Tetracycline 500 mg q.i.d.

4) Colloidal Bismuth Subcitrate 120 mg q.i.d. 

^ note: minimal resistance, but a lot more side effects e.g. Bismuth causing lax stool & metallic taste, tetracycline staining teeth

i) Fluoroquinolone containing regimen

ii) Sequential therapy (b.i.d. for 10 days)
- not routinely used in HK
- see pic

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Why won't triple therapy improve some patient's dyspepsia?

Firstly, about 7% of H pylori in HK are dual-resistant against clarithromycin, and metronidazole, making triple therapy increasingly less effective

Secondly, H pylori infection is associated with many diseases that cause dyspepsia, such as FD, PUD, gastric cancer, MALT lymphoma, which cannot be relieved simply by H pylori eradication - the symptomatic response rate is only about 20-40%

Thirdly FD is multi-factorial and can be caused by other issues apart from H pylori.


Triple therapy side effects

PPI: osteoporosis and infection risk

Amoxicillin: Rash 

Antibiotics: Pseudomembranous colitis 
- profuse watery diarrhoea
- more associated with fluoroquinolones, clindamycin, cephalosporin
- Normal gut flora disturbed, thus clostridium difficile overgrowth


Mx and Ix when suspecting pseudomembraneous colitis

1) Fresh stool for Clostridium difficiles toxins

2) Fresh stool sample for viruses (if Norwalk viruses suspected)

3) Stool cultures should be sent

4) Stop previous antibiotics (don't give empirical antibiotics either!)

5) Arrange early sigmoidoscopy +/- biopsy (esp when uncertain)

6) Consider urgent CT abdomen to exclude ischaemic colitis and consult surgery, if suspect ischemic colitis


Mechanism of GERD

1. Ineffective clearance of esophagus and gastric dysmotility

2. Defective ‚ÄúLower Esophageal Sphincter‚ÄĚ (LES)¬†


GERD categories

1) Non-erosive reflux disease (NERD; main group)
- reflux symptoms
- normal esophageal mucosa by EGD

2) Erosive esophagitis
- reflux symptoms
- mucosal lesions by EGD
- with or without local complications (e.g. strictures, Barrett's, adenocarcinoma)

3) Extra-esophagea disease
- reflux symptoms
- plus asthma, chronic cough, globus sensation, posterior laryngitis (hoarseness), sleep disorders, bronchiectasis, non-cardiac chest pain, dental erosion


LA classification of esophageal ulcers

LA classification (e.g. in GERD with erosive esophagitis):

A =mucosal break shorter than 5mm

B =mucosal break longer than 5mm, doesn't cross mucosal folds

C =crosses mucosal folds,

D =more than 75% of circumference


Risk factors for GERD

- obesity, high BMI
- smoking, alcohol, caffeine
- diet e.g. chocolate, high-fat food (which decreases LES pressure)
- family history

- Genetics of upper GI physiology
- Decreased esophageal motility
- Gastric outlet obstruction
- Type I Hiatal hernia
Note that H pylori infection is protective!


Clinical features of GERD

1) Heartburn, dyspepsia, chest pain
- post prandial retrosternal pain (non-cardiac chest pain)
- Acid feeling in stomach
- exacerbated by lying down, esp after meal
- mimic angina 

2) Dysphagia, Regurgitation

3) Waterbrash (reflex saliva hypersecretion)

4) Early satiety

5) Post prandial nausea, vomiting

6) Cough (from aspiration or cough reflex triggered by acid reflux in lower esophagus)

7) Hoarseness, sore throat, globus sensation


Complications of GERD

1) Erosive esophagitis

2) Peptic strictures
- causing upper GI obstruction, dysphagia
- (some say GERD causes Schatzki rings)

3) Esophageal ulcers, leading to upper GI bleeding
- may cause iron deficiency anemia

4) Barrett esophagus, Adenocarcinoma of esophagus

5) Recurrent pneumonia (due to repeated aspiration)
- Cytology of bronchoscopic aspirates will show "lipid-laden macrophages" 

6) Extraesophageal symptoms
- asthma, bronchiectasis, chronic cough, globus sensation, posterior laryngitis (hoarseness), sleep disorders, non-cardiac chest pain, dental erosion


Diagnosing GERD

1) Symptomatic questionnaire (accuracy around 90%)
- Chinese GERDQ (7-item)

2) PPI testing
- conducted over 1-4 weeks

3) Ambulatory 24 hour esophageal pH monitoring
- Gold standard
- inconveient, uncomfortable

3.5) Catheter-Free pH System with a pH capsule clipped to distal esophagus via endoscopy (i.e.  BRAVO system)
- 48 hours, up to 98 hours, thus more sensitive
- wireless

4) EGD with biopsy
- detects erosive esophagitis & other macroscopic complications
- useless in NERD (majority)
- useful in dysphagia, odynophagia, GI bleeding

5) Multichannel Intraluminal Impedance (MII)
- Measurement of resistance of electric conductivity during swallowing and reflux
- Determine the nature of reflux material (acid, vs bile, food, air) 

6) Esophageal manometry (if suspect motility disorder)

7) Barium swallow to assess complications


Pros and Cons of various GERD diagnostic methods

1) GERD questionnaire
+ non-invasive
‚Äč+ sensitive, cost-effective
- recall bias

2) PPI test
+ non-invasive
+ sensitive, cost-effective
- might be placebo effect
- no RCT done on Asians, whom has higher prevalence of H pylori

3) 24-hr pH monitoring
+ Gold standard with high sensitivity
- might easily miss NERD
- not widely available
- unpleasant, expensive, inconvenient, uncomfortable

4) BRAVO system
+ convenient as it is wireless
+ 48-94 hours placement, thus very high sensitivity
+ Very specific
- Very expensive
- Inavailability

5) EGD
+ can visualise reflux esophagitis
+ can get biopsy for H pylori test or Ix for malignancy
- cannot visualise NERD
- invasive, expensive, uncomfortable

6) Multichannel Intraluminal Impedance 
+ allow differentiation of different reflux content (acid vs air, bile, food)
+ Visualise direction of movement


Treating GERD

1) Lifestyle modification
- low fat diet
- quit alcohol, smoking, caffeine, chocolate, spicy food
- weight reduction
- avoid tight belts and corsets
- elevate head when lying
- avoid eating 2-3 hours before bed

2) Medical therapy (high level step down therapy)
- PPI before meal (omeprazole, lansoprazole) -> p.r.n. if non-erosive (LA class grade A, B); life long maintenance if erosive esophagitis (LA classification grade C, D; due to high relapse)

- Antacids (aluminium hydroxide, Ca carbonate) after meals & at bedtime
- H2 receptor blocker (cometidine, ranitidine)
- add a Prokinetics: metoclopramide, domperidone, cisapride (to prevent non-acid reflux in LES motility problem)

3) Antireflux surgery
- Nissen fundoplication (open or laparascopic), for patient with normal esophageal motility
- Partial fundoplication, when esophageal motility is poor
4) Treat complications


Compare the initial medical therapy options for GERD

1) High level step down regimen
- Start with daily PPI
- q.d. 30 min before breakfast
- b.i.d. 30 min before breakfast & 120 min before last meal
- gradually step down if symptomatic control

2) Traditional step up regimen
- Antacids -> H2 blocker -> PPI 

PPI therapy is better than traditional step up regimen because:
- Lower total drug and consultation cost 
- Faster symptom control (within 1 week cf. weeks)
- Rapid oesophagitis healing
- Can be used for diagnosis too (i.e. PPI test)


Diagnostic criteria of Functional dyspepsia

It is a diagnosis by exclusion!

Rome III criteria for functional dyspepsia:

1) 1 or more of:
- Bothersome postprandial fullness
- Early satiety
- Epigastric pain
- Epigastric burning 

2) With no evidence of structural disease (during upper endoscopy) and normal baseline blood test

3) In last 3 months with an onset at least 6 months before diagnosis


Subtypes of functional dyspepsia

1) Postprandial distress syndrome:
- Bothersome postprandial fullness, early satiety, with abdominal bloating and belching
- aka dysmotility-like

2) epigastric pain syndrome:
- epigastric pain and burning
- aka ulcer-like



Etiology of FD

Functional dyspepsia's etiology is poorly understood, with the following correlations:

1. Gastric motor dysfunction
- Delayed or accelerated gastric emptying
- Antral hypo-motility, Stiff gastric fundus

2. Visceral hypersensitivity and altered brain processing 
- Gastric or duodenal hypersensitivity
- Psychological disturbances

3. Mucosal inflammation
- H pylori infection
- Gut microbiota disturbance (e.g. after GE)

4. Diet (e.g. dairy)

5. Genetics
GNb3, TRPV1 polymorphism 


Functional dyspepsia management

1) Anti-secretory agents
- Antacids (aluminium hydroxide, Ca carbonate)
- H2 receptor blocker (cimetidine, ranitidine)
- usually use PPI (omeprazole)
-> these are more helpful for epigastric pain syndrome FD
-> some argue PPI use in Asians are not useful

2) H pylori eradication (if positive)
- Triple therapy with PPI, clarithromycin 500mg, amoxicillin 1000mg (b.i.d. 7 days)

3) Low lactose diet, low FODMAP Diet

4) Novel agents
- Prokinetics (D2 antagonists) e.g. metoclopramide, domperidone
- Antidepressant (tricyclics, SSRI, peripheral opioid agonist) e.g. Fluoxetine
- 5-HT3 antagonist, e.g. Memantine, odansetron
- Partial 5-HT4 antagonist, e.g. Tegaserod
- Sumatriptan (for migraine)

5) Alternative therapy (limited success)
- psychological therapy
- herbal, acupuncture
- probiotics


Definition of upper GI bleeding (& DDx)

Bleeding in the GI tract proximal to ligament of Treitz (suspensory ligament of duodenum)

1) Ulcer
- peptic ulcer disease (DU or GU, from H pylori or NSAID mainly)
- Esophageal ulcer (pill induced, GERD, ZES, infection etc)

2) Varices
- gastric or esophageal varices from portal hypertension

3) Arterial venous malformation
- Telangiectasia or Angiodysplasia
- Gastric Antral Vascular Ectasia (watermelon stomach)
- Aortoenteric fistula (if aortic stenting)

4) Mallory-Weiss tears, Malignancy
- Mallory-weiss tears (alcohol, chemotherapy)
- Gastric tumour
- Esophageal tumour
- gastrointestinal stromal tumor (GIST)

5) Erosion, esophagitis
- esophagitis (e.g. reflux esophagitis)
- Acute or chronic gastritis (H pylori or NSAID)
- Stress gastritis
- Duodenitis

6) Dieulafoy lesions (submucosal layer of stomach)

7) plus some rare ones like
- Hemobilia (e.g. trauma, ERCP, PTBD, gallstone)
- haemosuccus pancreaticus (e.g. haemorrhagic pancreatitis, pancreatic duct, splenic artery etc)
- Duodenal or jejunal diverticulum
- Crohn’ s disease 

[8) fastitious bleeding from other sources]
- haemoptysis
- swallowed blood from epistaxis or oral bleeding lesions


DDx of sever upper GI Bleeding

1) Duodenal or gastric ulcers

2) Esophageal or gastric varices

3) Aortoduodenal fistula

4) Dieulafoy's lesion


Role of EGD in upper GI bleeding

Rapid assessment in massive upper GI bleeding (i.e. surgery) for:

‚ÄĘ Verify bleeding source

‚ÄĘ Stratify patients according to risk of rebleeding

‚ÄĘ Therapeutic endoscopy can stop bleeding e.g. clerotherapy, heat coagulation, adrenaline injection

‚ÄĘ as¬†definitive surgery, or¬†temporizing means before definitive surgery¬†


Important history in upper GI bleeding

1) Onset and time course, duration

2) Blood in forms of: Haematemesis, coffee ground vomitus, melena, haematochezia 

3) Anaemia symptoms (postural hypotension, confusion, lethargy, dizziness, LOC, palpitation, angina, dyspnoea)

4) Associated symptoms:
- pain (esp epigastric)
- early satiety (cancer, PUD)
- chronic liver disorder (pain, jaundice etc)
- vomiting, alcohol, chemotherapy (MW tears)
- anorexia, cachexia, fever (malignancy)
- painful dysphagia (esophagitis, EU)
- painless dysphagia (cancer)
- increased bleeding (e.g. petechiae, nose bleeding)

5) Past Medical Hx
- PUD, bleeding tendency, H pylori infection
- GERD symptoms
- Liver disease e.g. cirrhosis, HB
- Coagulopathy
- Previous irradiation (enteritis)
- Conditions that need NSAID (e.g. joint pain, MI, stroke)
- Previous aortic aneurysm

6) Surgical Hx
- Previous GI surgery
- Previous aortic stenting or surgery

7) Drug Hx
- Aspirin, NSAID
- anticoagulant, antiplatelet

8) Social Hx
- Alcohol, smoking, caustic substance, suicidality


Physical examination in upper GI bleeding

1) Generation examination
- pallor, hydration status
- examine the vomitus, NG tube aspirates, and stool (look for blood)
- tachycardia (maybe bradycardia from vagal slowing of heart)
- BP (orthostatic hypotension or hypotension)
- Capillary refill prolonged
- hemocue for Hb level
- (if cirrhosis): finger clubbing, stigmata of chronic liver disease, edema
- (if cancer): cachexia, fever, lymph nodes

2) GI examination
- epigastric tenderness
- hepatomegaly, splenomegaly, ascites?
- abdominal mass

3) PR exam
- Fresh blood or melena?


Presentation of on-going upper GI bleeding

- Coffee ground vomiting (due to methaemoglobin)

- Haematemesis

- Coffee ground or fresh blood from nasogastric tube

- Tarry stool /melaena (due to haematin)

- Haematochezia (aka fresh melena)

- Tachycardia (note in severe GI bleeding, vagal slowing of heart will lead to bradycardia)

- (orthostatic) hypotension

- Drop in haemoglobin level (hemocue)


Investigations in upper GI bleeding

1) Simple tests
- Hemocue
- CBC (low Hb, normal MCV if acute bleeding, low MCV if chronic bleeding, platelet can be high or low)
- Clotting profile (platelet, PT, aPTT)
- RFT (urea abnormally higher than creatinine, due to blood absorption & hypovolemia -> high BUN: creatinine ratio)
- Type and screen (to prepare transfusion)
- Haemodynamic status (blood pressure, pulse, respiratory rate, capillary refill) 

2) Cause investigation
- Oesaphago gastro duodenoscopy is FIRST LINE (barium meal used to be first line)
- Second line Ix are: NG tube, angiography, Radioisotope bleeding scans, colonoscopy, capsule endoscopy, single balloon enteroscopy, Double balloon enteroscopy 
- Last resort: Exploratory laparotomy

3) Specific tests
- e.g. CT or PET when suspecting malignancy
- biopsy from EGD
- H pylori tests (e.g. urea breath test, rapid urease test)
- etc.


Why hematocrit is not used to assess blood loss?

Hematocrit is not able to reflect the degree of blood loss, as it means to erythrocyte volume as a percent of total blood volume. Therefore it will remain normal with blood loss, until after 24-48 hours the blood volume is restored, only then will it drop.


Resuscitation and monitoring in Massive upper GI bleeding patient

- secure ABC
- NG tube placement
- Central venous line
- fluid resuscitation with transfusion (after type & screen), or colloids
- Oxygen

- Vitals (BP, pulse rate, respiratory rate, core temp)
- Hourly shock chart
- Urine output (via Foley catheter)
- PCWP via CV line (Swan-Ganz catheter)
- Cardiac monitor
- Pulse oximetry


Emergency bleeding control in upper GI bleeding

(just general principles)

1) Therapeutic EGD
mostly for ulcers:
- epinephrine injection
- sclerotherapy
- Thermal methods, Argon plasma coagulation 
- Band ligation
- Endoloops

2) Sengstaken Blakemore tube 
- for esophageal varices

3) Medical therapy
- Empirical IV PPI infusion until diagnosis
- Octreotide, terlipressin for esophageal varices by splanchnic vasoconstriction, which reduces portal hypertension)

4) Emergency surgery
- depending on what the cause is


Mallory-Weiss tear site and pathogenesis

- Gastroesophageal junction
- Mucosal tear (not transmural, which is Boerhaave syndrome)

- Repeated retching and vomiting due to binge drinking, chemotherapy, bulimia, or other causes


Mallory-Weiss tear management

- 90% stop bleeding without treatment

- Surgical management: oversewing of tear

- Angiographic embolisation

- Acid suppression to promote healing

- Manage vomiting if correctable


Angiodysplasia site and associations

(basically telangiectasia in the GI tract)

Most common in colon, but can be found in stomach and duodenum

- elderly
- Aortic stenosis (causing GI hypo-perfusion?)
- Chronic renal failure
- hereditary hemorrhagic telangiectasia 
- prior radiation therapy 


Etiology of gastritis or duodenitis

1) Drug induced
- aspirin, NSAIDs
- most common cause of acute gastritis
- Almost all patient on aspirin develop mild hemorrhagic gastritis within 24 hours 

2) H Pylori infection
- most common cause of chronic gastritis (leading to Type B atrophic gastritis)

3) Alcohol-induced, heavy smoking, caffeine

4) Physiological Stress (aka Stress gastritis)
- usu ICU patients
- respiratory failure, renal failure, shock, sepsis, peritonitis, burns
- 2-10% with significant bleeding

5) Autoimmune Metaplastic Atrophic Gastritis (AMAG)
- aka Type A gastritis, in cases of pernicious anemia
- Serum anriparietal antibody, anti-intrinsic factor antibodies

6) Surgical causes
e.g. Alkaline reflux gastritis due to bile reflux in Billroth II procedure


Vomiting DDx (basic categories)

1) GI & abdomen
- mechanical obstruction (tumours of GI tract)
- pseudo obstruction, small bowel dysmotility (trauma, serious infectin, MI, post operative)
- Gastroparesis (DM, scleroderma, metabolic, idiopathic)
- gastroenteritis or food poisoning from toxins (B cereus)
- peritonitis (acute pancreatitis, acute cholecystitis)
- radiotherapy

2) Neurological & psychiatric
- increased ICP
- vertigo (BPPV, meniere etc)
- otitis media
- anorexia nervosa, bulimia nervosa

3) Endocrine & metabolic
- hyperemesis gravidarum 
- electrolyte imbalance (hyponatremia)
- hyperthyroidism
- DKA in DM
- Addison's disease
- uraemia from renal failure

4) Drugs and chemical
- Alcoholism
- Chemotherapy
- Antibiotics (metronidazole)
- Digitalis
- Narcotics

5) Others
- Cyclic vomiting syndrome (by exclusion)


What is the difference between vomiting, regurgitation, and rumination

Vomiting: Involves vomiting centre; with forceful abdominal and thoracic muscle contraction associated with retching; distinctive feature is prominent autonomic features, e.g. nausea, sweating, waterbrash

Regurgitation: sudden, effortless return of small amount of gastric contents into pharynx/mouth 

Rumination: repeated, effortless regurgitation followed by re-chewing, re-swallowing or expulsion; associated with psychiatric or behavioural disorders


Investigations in vomiting

1) Suspects GI problems:
- Erect and supine AXR (look for obstruction by 3-6-9 rule, coiled spring sign, string-of-pearl sign, haustra pattern, apple core etc)
- CT or MRI
- Ultrasound for cholecystitis
- Serum amylase for pancreatitis
- Surgical Hx
- Stool culture esp if fever

2) Drug review

3) CNS review
- CT brain
- vestibular system review (Hallpike maneuvre if vertigo)

4) Blood test
- Blood culture
- Electrolyte panel


Name me some antiemetics

1) Antihistamine (H1 receptor antagonist)
- dimenhydrinate, promethazine
- esp for vestibular causes e.g. motion sickness

2) Anticholinergics (muscarinic receptor antagonist)
- Hyoscine (aka scopolamine)
- esp for vestibular causes

3) 5HT3 receptor antagonist
- Ondansetron
- effective against vomiting caused by endogenous toxins, drugs & chemicals

4) D2 receptor antagonist
- Metoclopamide, Domperidone
- effective against vomiting caused by endogenous toxins, drugs & chemicals

Some other agents not routinely used:
+) 5HT4 antagonist e.g. cisapride
+) Erythromycin
+) Prednisolone


Complications of vomiting

1) Dehydration

2) Hypokalemia, hyponatremia, hypernatremia, metabolic alkalosis

3) Mallory Weiss tear

4) Boerhaave syndrome


Gastric tumour with high obstruction (Symptoms and sign)

Symptoms from History:
1) Constitutional symptoms e.g. cachexia, anorexia
2) Dysphagia, Vomiting
3) Epigastric pain, Dyspepsia, early satiety
4) Hematemesis, melena
5) Anemia symptoms e.g. nausea, dizziness, weakness, LOC
6)¬†Paraneoplastic ‚Äď nephrotic syndrome¬†

Physical signs from PE:
- Vomitus (not bile stained, might be blood)
- Distension in epigastrium
- Succussion splash
- Abdominal mass (omental met, bulky tumour)
- Ascites if peritoneal met
- Lymph nodes (Virchow, Irish)
- PR exam with melena, might feel Blumer's shelf
- Pale
- Acanthosis nigricans


Name some gastric tumours

1) Gastric adenocarcinoma

2) Benign gastric tumour (less than 2%, rare)
- Hyperplastic polyps
- Adenomatous polyps

3) Non-Hodgkin Lymphoma
- Primary gastric lymphoma (PGL)
- MALT lymphoma

- i.e. gastrointestinal stromal tumour

5) Gastric carcinoid


Epidemiology of gastric adenocarcinoma

4th leading cause of cancer deaths in Hong Kong:

Location: High prevalence in Asia (HK, Jp, Kor, China), East europe, South America

Sex: Male

Age: around 60



Classification of Gastric adenocarcinoma

Lauren classification:

1) Intestinal type cancers (30%)
- from gastric mucosa; glandular
- hematogenous spread to distant organs

2) Diffuse type cancers (70%)
- from lamina propria
- transmural local invasion, and lymphatic spread with early metastasis
- worse prognosis


Risk factors for gastric adenocarcinoma (name some protective factors too!)

- Diet (e.g. nitrosamine, preserved, smoked, salted food)
- Smoking
- EBV, H pylori (thus type B atrophic gastritis)
- Pernicious anemia (thus type A atrophic gastritis)
- Atrophic gastritis (EMAG & AMAG)
- Adenomatous polyps
- Menetrier disease
- Hereditary (E-cadherin mutation)

Protective factors:
- Fresh fruit and vegetables
- Vit C, trace elements, selenium 


What is "Correa's theory"

Acute gastritis
Chronic gastritis
Atrophic gastritis
Intestinal metaplasia
Gastric adenocarcinoma


Mode of Spread of gastric adenocarcinoma

1) Direct invasion
- e.g. pancreas, colon

2) Lymphatic spread (more in diffuse type)
- Virchow's
- Irish's

3) Transcoelomic spread (aka peritoneal seeding)
- 1/3 may cause ascites
- Omental metastasis
- Krukenberg tumour
- Sister Mary Joseph nodule
- Blumer's shelf (in pouch of Douglas)
- Malignant ureteric obstruction (-> hydronephrosis, acute renal failure)

4) Hematogenous spread (more in intestinal type)
- Liver met (hepatomegaly, jaundice)
- Lung met (dyspnoea, pleural effusion, lymphangitis carcinomatosis, canon ball lesions in CXR)


Morphology of gastric adenocarcinoma


Linitis plastica
-¬†‚ÄėLeather bottle‚Äô stomach
- diffuse submucosal infiltration, leading to a rigid and thickened stomach wall
- mucosa might be normal
- confirmed by endoscopic ultrasound or CT scan 


Investigations in suspected gastric adenocarcinoma

Screening Ix

Routine checks
- CBC (anemia)
- LFT, RFT (baseline, as well as to assess met)

Diagnostic Ix
- EGD, with biopsy
- Double contrast barium meal will help to (note if linitis plastica, the stomach might not be distended by effervescence)

Genetic Ix
- Genetic testing for HER-2 mutation to consider targeted therapy with herceptin

Stageing Ix
- CXR, CT scan, PET/CT
- Endoscopic ultrasound (can note linitis plastica, for T, N stage)
- Abdominal USG
- Laparascopic staging (e.g. peritoneal washing with cytology; for peritoneal spread)
- Peritoneal tap with cytology (if ascites)
- FNA or excisional biopsy of LN for cytology

Follow-up Ix
Serum tumour markers e.g. CEA, CA 19-9 


Staging of gastric adenocarcinoma

TNM staging

T (depth of invasion)
Tis = in situ
T1 = submucosa
T2 = muscularis propria
T3 = Subserosa
T4 = perforates serosa

N (number of regional LN)

M (Distant metastasis)


Management of Gastric adenocarcinoma

1) Surgical resection is the only definitive treatment:
- Endoscopic mucosal resection (EMR) for early gastric cancer (i.e. T1)
- Endoscopic submucosal dissection (ESD) is even newer
- Laparoscopic gastric resection can be considered
- Proximal and middle tumour: total gastrectomy with Roux-en-Y esophago- jejunostomy
- Distal tumour: subtotal gastrectomy with Billroth II gastro- jejunostomy

2) Lymphadenectomy to remove 15 LN

3) Adjuvant Therapy
- pre-op neoadjuvant chemotherapy
- post-op adjuvant chemoradiotherapy (5-FU based)
- add Herceptin if HER2 positive
4) Palliative Therapy for patients with peritoneal, hepatic, or nodal metastasis:
- Supportive care with pain control
- Palliative resection for bleeding
- Palliative bypass (GJ) for outlet obstruction
- Endoscopic stenting (for outlet obstruction)
- Systemic chemotherapy
- Regional intra-arterial chemotherapy 


In Billroth II procedure, why is stomach connected to jejunum but not duodenum?

Because duodenum is attached to the retroperitonium while jejenum is freely intra-peritoneal. If a gastro- duodenostomy is performed, the tension between the retroperitoneal duodenum and stomach will be too large, causing anastomosis leak, or even dehiscence.


What are some of the post-gastrectomy complications?

1) Nutritional disturbances
- Iron, folate, Vit B12, Calcium, Vit D deficiency
- causes anaemia, neuropathy, dementai, osteomalacia

2) Dumping syndrome (common in Billroth II)
- Nausea, epigastric distress, explosive diarrhoea due to rapid emptying of high-osmolar carbohydrate load to small intestine

3) Alkaline reflux gastritis (common in Billroth II)
- due to bile reflux back to stomach
- epigastric pain, nausea, bilious emesis

4) Loop syndrome (Billroth II)
- due to mechanical obstruction of afferent of efferent limbs

5) Roux stasis syndrome (in Roux-en-Y)
- functional obstruction due to lack of pacesetter potential in roux limb from proximal duodenum, thus no peristalsis


Differentiating intestinal obstruction and ileus

1) Different mechanism: mechanical obstruction implies a physical barrier to the progress of intestinal contents, while a paralytic ileus implies failure of peristalsis to propel the intestinal contents with no mechanical barrier 

2) Bowel sounds are usually hyperactive in mechanical obstruction of intestines (note it can be reduced in severe case) while paralytic ileus is presented with sluggish and absent bowel sounds

3) Colicky pain is more likely to present in bowel obstruction.

4) Looking at AXR, gas distribution should be proximal to site of obstruction in mechanical obstruction, while uniformly diffuse in distribution (in small bowel, colon, rectum) in paralytic ileus


Etiology of paralytic ileus

1) Intra-peritoneal
- Post-operative (abdominal surgery)
- Peritonitis
- Intra-abdominal abscess
- Inflammatory/ infective conditions
- Intestinal ischaemia 

2) Retroperitoneal
- Retroperitoneal haematoma/infection
- Aortic, spinal, urological operations
- Pancreatitis

3) Metabolic abnormalities
- hypokalemia (and other electrolyte imbalance)
- sepsis
- uraemia
- hypothyroidism
- lead poisoning, porphyria 

4) Medication
- opiates
- anticholinergics
- antihistamines
- catecholamines 

Spinal cord injury




Clinical presentation of paralytic ileus

- Abdominal distention

- Constipation

- Vomiting

- Abdominal pain: diffuse, constant and less severe

- Sluggish or absent bowel sounds 

- (and features suggestive of underlying etiology)


Ix and Mx of paralytic ileus

- Confirms by AXR, physical exmaination
- Contrast medium will fail to pass beyonf a fixed point

- NPO (Nil by mouth); Always fast after operation; Resume feeding after bowel movement 
- Intravenous fluid, parenteral nutrition
- Nasogastric tube for decompression
- Identify and treat the predisposing cause
- Monitor and assessment by daily abdominal X-rays and physical examination


Natural history and pathogenesis of post-operative ileus

Natural History:
It is the period of inhibition of activity after abdominal or retroperitoneal operations; the bowel activity will return in the order of small intestines > stomach > colon

- Reflex inhibition
- Stress, leading to Cytokines and other serum factors
- Opiates 



What are the negative impact of post-operative ileus

- Delays feeding

- Causes nausea and vomiting

- Decreases mobility

- Increases hospital stay 


How to shorten duration of post operative ileus?

1) Use laparascopic approach
- less manipulation
- less pain, less stress
- Maintenance of peritoneal milieu 

2) Epidural anaesthesia

3) Early feeding

4) Routine NG tube for decompression (usually not necessary)


Important characters to differentiate in Small Bowel Obstruction (SBO)

1) Partial vs Complete obstruction
- partial obstruction: passing gas and bowel movement is possible, constipation (might be seen in adhesion, Crohn disease, radiation stricture, disseminated malignant disease)
- complete obstruction: obstipation (not even gas)

2) Closed loop vs Open loop obstruction
- closed loop: occluded at at least two points, which compromises blood supply making it very emergent

3) Is it strangulated?

4) Proximal vs Distal obstruction
- can be differentiated by site of distention in AXR
- proximal: early, bilious emesis
- distal: late, thicker feculent emesis

5) Acute vs Chronic


Etiology of SBO

1) Adhesions & bands (most common)
- from previous intraperitoneal operations (thus not related in Caesarian section, hernia repair, which are all extraperitoneal)
- congenital, post-inflammatory

2) Incarcerated Hernias (second common)

3) Volvulus
- caused by adhesions, or congenital anomaly e.g. intestinal malrotation

4) External compression
- intraperitoneal tumours e.g. head of pancreas, pelvic met
- intraperitoneal abscesses
- hematomas
- Superior mesenteric artery (SMA) syndrome (in which D3 is compressed by the angle between descending aorta and SMA)

5) GI tract tumour
- e.g. stomach adenocarcinoma, small intestine tumour

6) Strictures
- secondary to ischemia, inflammation (Crohn disease), radiation, drug or previous surgery

7) Intussusception
- due to e.g. Tumours, polyps, enlarged mesenteric LN, Meckel diverticulum

8) Gallstone ileus
- as a complcation of cholecystitis, where a cholecystoduodenal or choledochoduodenal distula allows gallstones to enter GI tract and lodge at ileocecal valve

9) Foreign body

10) Bezoars
- often in toothless elderly
- orange, ŚÜ¨ŤŹá

11) Parasitic worms


Hx and PE in SBO

1) History & symptoms
- Hx of bowel obstruction
- Surgical Hx of abdominal or pelvic operation
- Hx of cancer
- Hx of abdominal/pelvic radiation
- Hx of abdominal inflammatory condition (e.g. Crohn's)
- Colicky abdominal pain 
- Abdominal distention
- Nausea and vomiting (if early bilious -> proximal; if late thick feculent -> distal)
- Constipation (might still be some bowels from colon or distal SB), followed by Obstipation

2) PE
- Vitals (might enter shock)
- Examine the vomitus (bilious or feculent)
- Hydration status

abdominal exam:
- Surgical scars
- Distended abdomen with colicky pain
- Examine for masses, hernias, peritonitis
- Hyperactive bowel sounds (might become absent at late stage)
- PR exam might find an empty rectum, look for blood



Features suggestive of strangulated SBO

1) Increased, severe, continuous abdominal pain and tenderness

2) Hematemesis (blood in the vomitus)

3) Fever

4) Tachycardia, leucocytosis, lactic acidosis

5) Peritonitis signs (guarding, rebound tenderness)

6) Imaging:
- Thumbprinting
- loss of mucosal pattern
- Pneumoperitoneum (gas within the bowel wall; football sign, double wall sign)
- Gas within intrahepatic branches of the portal vein


Pathophysiology in SBO patients

1) Dehydration
- intestinal distention causes reflex vomiting, hypersecretion proximal to obstruction point, and decreases absorption
- thus loss of fluid to extracellular space and peritoneal cavity 
- therefore dehydration, hypovolemia, hypokalemia, hypochloremia, and metabolic alkalosis
- hypovolemia will then cause tachycardia, hypotension, tachypnoea, confusion, oliguria

2) Bacterial overgrowth
- bacterial overgrowth in obstruction portion, which then translocate and causes sepsis

3) Increased peristalsis to over the obstruction

4) Lymphatic or venous congestion , causing edema

5) Compromise blood supply
- in close loop or strangulate SBO
- leading to necrosis and perforation of bowel, causing peritonitis



Investigations and results in SBO

Bedside tests:
1) CBC (look for leucocytosis if sepsis or peritonitis)

2) Dehydration status
- Urine output (Foley catheter to assess dehydration status)
- BP, pulse rate, respiratory rate
- BUN:Creatinine ratio

3) ABG (volume contraction -> metabolic alkalosis; if with necrotic bowels, there might be metabolic acidosis)

4) LFT, RFT (for baseline; electrolyte for hypokalemia, hypochloremia)

5) Serum amylase (if pancreatitis) or lactate (increased if strangulated)

6) Type and Screen (to prepare for surgery)

Imaging studies
1) CXR: exclude perforation and pneumoperitoneum

2) AXR (supine & erect)
- coiled spring sign (esp in jejunum due to tight valvulae conniventes)
- string-of-pearl sign
- strangulation (thumb printing, pneumatosis cystoides intestinalis, free peritoneal gas)
- football sign (if pneumoperitoneum)
- Toxic megacolon
- cut off of gas collection (indicative of site of obstruction)
- air in biliary tree (suggestive of cholechododuodenal fistula in gallstone ileus)

3) CT scan with contrast
- IV contrast to note viability of bowel 

4) Water soluble contrast study
- use Gastrografin  (NOT barium!!)
- small bowel follow-through
- Differentiates complete and partial obstruction 
- Therapeutic effect (as it is hyperosmolar so shift water to lumen) and shortens hospital stay


Why don't we use barium contrast study in Intestinal obstruction?

1) Barium precipitates complete obstruction

2) Barium peritonitis 


Management of SBO (name the indications too)

Non-operative management 
For non-strangulated, open loop SBO (no fever, tachycardia, peritonitis), mainly "Drip and Suck":

- IV fluid resuscitation & electrolyte (add K to counter hypokalemia)
- NG tube decompression
- NPO with parenteral nutrients
- Early evaluation with Gastrografin follow through
- antibiotics
- Treat underlying cause (e.g. reduce the hernia)

Operative Intervention
For close loop, strangulated obstruction, volvulus, peritonitis, Pneumoperitoneum, Pneumatosis cystoides intestinalis, or when conservative therapy does not resolve SBO after 48 hours:

- Pre-operative preparation with fluid/electrolyte resuscitation and NG tube decompression
- Midline incision for access
- Enterolysis and adhesiolysis for adhesions
- Hernia repair via standard groin incision
- Derotation, resection and fixation for volvulus
- Enterotomy and removal for foreign body
- Resection of necrotic bowels
- Enteroenteric or enterocolic anastomosis to bypass unresectable obstructions
- Gastrostomy tube


How to prevent adhesion from surgery

- Gentle handling of bowel during surgery

- Laparascopic approach results in fewer adhesions than open techniques (except acute appendictitis)

- Removal of powder from gloves

- Use saline lavage

- Use bioabsorbable antiadhesion barriers, e.g. Seprafilm (hyaluronic acid) or Adept (icodextrin 4% solution)


Meckel diverticulum pathogenesis

Most common congenital anomaly of GI tract due to:

- failure of the vitelline (omphalo-mesenteric) duct to obliterate by the 6th week of fetal development

- Apex or fibrous cord adherent to the umbilicus 

- Thus a true diverticulum with all layers of bowel wall is formed on the antimesenteric border of ileum, 2 feet from ileocecal valve



Meckel diverticulum, Rule of 2

On antimesenteric border of ileum, 2 feet from ileocecal valve


Male: female ratio = 2:1

usually before 2yo

Contains 2 types of mucosa namely intestinal and heterotopic (gastric or pancreatic)



Meckel diverticulum presentation (& complications)

- mostly asymptomatic

- may show painless, episodic bleeding (due to peptic ulcer formed due to acid production from the gastric mucosa of Meckel diverticulum)

- Intussusception or Littre hernia might cause intesetinal obstruction (or due to volvulus of small bowel around the fibrous band that connects diverticulum and anterior abdominal wall)

- may cause perforation

- Meckel diverticulitis (which resembles appendictitis with peritoneal signs)


Diagnosis and management of Meckel Diverticulum

1) Meckel scan (radionucleotide study based on Tc-99m uptake by ectopic gastric mucosa)

2) Tagged red blood cell scan (when bleeding)

3) Contrast studies with SBFT or enteroclysis

1) Resection by simple diverticulectomy when SBO is present

2) Segmental small bowel resection required for acute diverticulitis, vovulus, or bleeding

3) Incidental diverticulectomy during other abdominal surgery is not indicated


Etiology of colonic mechanical obstruction

Usually at sigmoid colon:

1) Volvulus
- caecal volvulus (in young)
- sigmoid volvulus (in old)

2) External compression
- extraperitoneal tumours e.g. pelvic met

1) GI tract tumour
- Colorectal carcinoma
- Hematoma

2) Strictures
- secondary to anastomotic, radiation, ischaemic, endometriotic 

3) Intussusception

4) Diverticular disease

Also consider "Pseudo-obstruction"
i.e. Ogilvie Syndrome


Ogilvie Syndrome (definition, presentation, etiology)

Signs, symptoms, and radiographic evidence of large bowel obstruction are present, but there is no mechanical obstruction 

- Massive colon dilatation in the absence of mechanical obstruction 
- No colicky pain
- Hypoactive bowel sounds

1) recent surgery or trauma 

2) severe extracolonic medical illnesses (e.g., sepsis, malignancy) 

3) medications (e.g., narcotics, psychotropic drugs, anticholinergics) 


Diagnosis and management of Ogilvie Syndrome

By exclusion (until mechanical obstruction and volvulus are ruled out)
- Hypaque enema (both diagnostic and therapeutic)

1) Stop offending agents (narcotics, other drugs)

2) NPO, fluid/electrolyte resuscitation, NG tube or parenteral nutrition

3) Decompression with nasogastric suction, rectal tube, aggressive enema regimen (cottonseed and docusate sodium enema); consider colonoscopic decompression lastly

4) IV Neostigmine infusion

5) Surgical decompression with cecostomy or colostomy

6) Total colectomy with end ileostomy (EI) as the last resort


To screen and diagnose Colorectal cancer

Screening tests:

2) PR exam (look for blood, Blumer's shelf)

3) Colonoscopy
- most sensitive and specific
- take biopsy for diagnosis

4) Flexible sigmoidoscopy
- can reach area where 50-70% of polyps occur

5) Barium enema

6) AXR, supine and erect
- fluid level from obstruction
- Haustra pattern

6) Serum tumour marker
- CEA (carcinoembryonic antigen)
- used as baseline to monitor treatment efficacy and recurrence surveillance
- prognostic significance (worse prognosis if >5ng/mL)

Clinical Stageing
1) CT scan
- with IV contrast or rectal contrast

2) PET-CT scan


Clinical presentation of colorectal cancer

1) Constitutional symptoms
- weight loss, anorexia, cachexia

2) Abdominal pain

3) Large bowel obstruction
- distention
- hyperactive borborygmi
- Constipation or obstipation
- (is uncommon in right sided tumours)

4) Peritonitis due to colonic perforation
- guarding, tenderness, rebound tenderness

5) Blood in stool and Anemic symptoms
- melena, hematochezia
- malaise, LOC, pallor

6) Change in bowel habits
- tenesmus
- pencil stool


Specific presentation of CRC in different sites

Right sided tumours
- occult blood in stool, melena more common
- triad of anemia, weakness, RLQ mass
- uncommon obstruction due to larger luminal diameter in caecum
- uncommon change in bowel habits

Left sided tumours
- Hematochezia more common
- common present with obstruction (due to small luminal diameter), thus distention, obstipation
- common present with change in bowel habits, i.e. alternating diarrhoea and constipation
- common with narrowing of stool ("pencil stool")

Rectal cancer
- Hematochezia more common
- Tenesmus
- Rectal mass


What kind of tumour are colorectal cancer?

Majority are endoluminal adenocarcinoma arising from mucosa.

Sometimes carcinoid tumours, lymphomas (MALT lymphoma), and Kaposi sarcoma (in HIV)


How does CRC spread?

Colorectal cancer spread by:

1) Direct extension
- first circumferentially
- then through the bowel wall
- later invade adjacent peritoneal organs

2) Hematogenous
- most common via portal circulation to liver 
- via lumbar or vertebral veins to lungs

3) Lymphatics
- regional LN
- Virchow's node

4) Transperitoneal and intraluminal


Risk factors of CRC

1) Age >50yo (thus start screening)

2) Adenomatous polyps
- villous adenoma has the greatest malignant potential
- higher risk if polyps are large and plenty

3) Past history of CRC or adenomatous polyps

4) IBD
- Ulcerative colitis poses more risk than Crohn Disease

5) Family History
- Multiple first degree relatives with CRC
- esp any firsst degree relatives with CRC under 60yo

6) Diet
- high fat, low fibre

7) Major polyposis syndromes
- Gardner syndrome
- Turcot syndrome
- Peutz-Jeghers
- Familial juvenile polyposis coli

8) Hereditary nonpolyposis CRC
(i.e. Lynch syndrome I & II)


Name of polyposis syndrome and explain

1) Familial adenomatous polyposis (FAP)
- hereditary APC gene mutation (AD)
- hundreds of polups in colon, duodenum is also involved in 90%
- risk of CRC is 100% around 40yo
- Prophylactic colectomy is required

2) Gardner syndrome
- variant of FAP (AD)
- with extra symptoms i.e. osteomas, dental abnormalities, benign soft tissue tumours, desmoid tumours, sebaceous cysts
- risk of CRC is 100% around 40yo
- Prophylactic colectomy is required

3) Turcot syndrome
- AD or AR
- polyps
- plus cerebellar medulloblastoma or glioblastoma multiforme

4) Peutz-Jeghers syndrome
- AD
- Single of multiple harmatomas scattered through GI tract mainly in small bowels (80%), but also colon (60%) and some in stomach (30%)
- harmatomas have very low malignant potential
- hyperpigmentation spots around lips, oral mucosa, face, genitals, palmar surface
- Slight increased incidence in other carcinomas (stomach, ovary, breast, cervix, testicle, lungs)
- causes intussusception or GI bleeding

5) Family juvenile polyposis coli
- rare, presents in childhood
- small risk of CRC
- present with 10-hundreds of colon harmatomatous polyps

6) PTEN  harmatoma tumour syndrome (PHTS)

7) MEN 2b

8) NF1


Tell me about HNPCC

Hereditary nonpolyposis colorectal cancer, is an autosomal dominant condition:

Also known as Lynch syndrome:

1) Lynch syndrome I (i.e. site specific CRC)
- early onset CRC
- no antecedent adenomatous polyposis

2) Lynch syndrome II (i.e. cancer family syndrome)
- same as Lynch syndrome I, but with:
- increased number and early onset of other cancers (i.e. brain, skin, stomach, pancreas, biliary tract, breast, female genital tract)


Treatment scheme of CRC in general

1) Staging via colonscopy, biopsy, CXR, AXR, PET/CT
- also do genetic testing for VEGF and EGFR mutation

2) Serum CEA level used to establish baseline

3) Pre-operative preparation
- Oral antibiotic
- bowel preparation (NPO) to reduce stool volume and facilitate colonic manipulation 
- Type and screen

4) Specific surgical resection depending on the lesion
- Different between right and left sided CRC
- Adequate LN retrieval (at least 12)
- cut out any previously unrecognised suspected met and do a frozen section

5) Post surgical routine management
- epidural placement for pain management
- SC enoxaparin

6) Adjuvant therapy
- Chemotherapy via FOL-FIRI (5-FU and irinotecan) or FOLFOX (5-FU and oxaliplatin)
- Radiotherapy
- Targeted therapy with VEGF inhibitor (bevacizumab) an EGFR inhibitor (cetuximab)


Surgical treatment of right sided and tranverse CRC (i.e. caecum to splenic flexure)

1) Right or extended right colectomy, with anastomosis
- if patient is stable
- resection includes the distal 10 cm of terminal ileum to the transverse colon, taking the ileocolic, right colic, and right branch of the middle colic vessels 

2) Resection without anastomosis 
- if the patient or the bowel condition is not favourable (i.e. emergency operation)

3) Palliative procedure by stoma, bypass, or stenting
- in advanced tumour
In transverse CRC, a tranverse colectomy or extended right colectomy can be done, with or without anastomosis depending on bowel preparation


Surgical resection of left sided CRC

Left-colon lesions require dividing the IMA at its origin

1) 3-stage operation (not common today)
i) transverse colostomy
ii) Resection and anastomosis 
iii) Closure of colostomy 
- used in an unstable patient with markedly dilated colon  

2) Hartmann’s operation
- resection with colostomy and either mucous fistula or Hartmann pouch
- No anastomosis, and the stoma will be left there forever
- if inadequate bowel preparation

3) Segmental resection with primary anastomosis
- Use on-table lavage if inadequate bowel preparation

4) Segmental resection with primary anastomosis and proximal diverting ileostomy

5) Subtotal colectomy and ileosigmoidostomy
- short tract lead to frequent bowels


Use of metallic stent in colorectal cancer

Inserted under endoscope (sometimes with fluoroscopic guidance), for:

1) Definitive palliation in unresectable CRC
- thus avoid surgery
- avoid stoma

2) As a bridge to surgery
- Avoids emergency surgery with insufficient bowel preparation
- Buys time for Elective operation with bowel preparation 
- More time to stage the disease
- Lower operative mortality and mortality
- Avoids stoma


Why is primary anastomosis not preferable in emergency management of righ sided CRC?

When we decide to do an emergency surgery on right sided CRC:

1) Patient is usually weak, malnourished, and dehydrated

2) Proximal colon is usually edematous and unhealthy, with its blood supplt easily obliterated

3) Heavy bacterial and faecal load in proximal colon due to obstruction. Without proper bowel preparation, easily cause post-op infection

4) The ileocaecal valve remain competence, thus a close loop obstruction might be formed after surgery, causing perforation of large bowel

-> all these make an anastomosis very risky


What are the main types of colonic polyps?

A. non-adenomatous polyps
1) Hyperplastic polyps
- most common, 90%
- remain small and asymptomatic

2) Inflammatory polyps
- aka pseudopolyps
- associated with ulcerative colitis

3) Hamartomatous polyps 
- rare, - some polyposis syndrome e.g. Peutz Jehgers, Familial juvenile polyposis coli, PHTS, NF1, MEN2b

B. Adenomatous Polyps
1) Villous adenoma
- greatest risk of malignancy

2) Tubulovillous adenoma
- intermediate risk of malignancy

3) Tubular adenoma
- low risk of malignancy
- most common of adenomatous polyps

C. Malignant polyps
aka T1 colorectal cancer



What types of colonic volvulus are there? What are their pathogenesis?

1) Sigmoid volvulus
- 60%
- common in elderly
- acquired due to sigmoid redundancy with narrowing of mesenteric pedicle

2) Caecal volvulus
- 30%
- common in younger population
- due to congenital failure of appropriate cecal tethering

3) Transverse volvulus, splenic flexure volvulus
- very rare
- presentation similar to sigmoid volvulus


Risk factors for volvulus

1) Old age, chronic illness, institutionalisation, CNS disease (sigmoid volvulus)

2) Sigmoid redundancy with narrowing of mesenteric pedicle (sigmoid volvulus)

3) Congenital lack of caecal tethering (caecal volvulus)

4) Chronic consripation, antimotility drugs, laxative abuse

5) Previous abdominal surgery


Diagnosis and findings in volvulus

1) Sigmoid volvulus
AXR will show:
- Omega loop sign (inverted U)
- "Bent inner tube sign" which points towards RUQ
- Gas bubbles along the large intestines before sigmoid colon

Water soluble contrast enema show:
- "bird's beak sign" at the obstructed junction
- aka "ace of spade sign"

CT will show:
- "Swirl sign"

2) Caecal volvulus
AXR will show:
- "Coffee bean sign"
- extends to LUQ

Water soluble contrast enema show:
- "bird's beak sign" at the obstructed junction
- aka "ace of spade sign"



Treatment of volvulus

1) Sigmoid Volvulus
- Sigmoidoscopy decompression
- Placement of rectal tube for decompression

- Elective sigmoid colectomy with anastomosis if uncomplicated
- emergency Hartmann procedure (sigmoid colectomy, end descending colostomy, blind rectal stump) if complicated with peritonitis

2) Caecal Volvulus
- Emergency surgery required:
- Laparatomy and ileocolectomy with primary anastomosis or ileostomy


How to differentiate GI tract bleeding and anorectal bleeding by stool examination?

Lower GI tract bleeding:
Hematochezia with blood mixed with stool

Anorectal bleeding:
Hematochezia with blood separated from stool


Investigations in lower GI tract bleeding

1) Simple tests
- Hemocue 
- CBC (Hb is usually not as low as in UGIB)
- Clotting profile (platelet, PT, aPTT)
- RFT (BUN: creatinine ratio might not be raised, unlike UGIB)
- Type and screen (to prepare transfusion)
- Haemodynamic status (blood pressure, pulse, respiratory rate, capillary refill) 

2) Cause investigation
- Proctoscopy, Sigmoidoscopy, PR exam (rule out anorectal cause)
- EGD, NG tube to rule out upper GI bleeding
- Colonoscopy & Enteroscopy to confirm lower GI source
- Second line Ix are: Angiography, radionucleotide bleeding scan, push enteroscopy, capsule endoscopy, single balloon enteroscopy, Double balloon enteroscopy
- Last resort: Exploratory laparotomy

3) Specific tests
- e.g. CT or PET when suspecting malignancy
- biopsy from endoscopy
- serum tumour markers
- etc.


Common causes of Lower GI tract bleeding

N) Neoplasm
- Colorectal cancer
- post polypectomy 

- aka angiodysplasia, vascular ectasia
- common in 60+

D) Diverticulosis
- note LGIB is rare in diverticulitis

I) Inflammatory Bowel Disease

I) (Infective) colitis
- infective colitis
- Radiation proctocolitis
- from IBD
- idiopathic

I) Ischemia
- Acute mesenteric ischemia
- Chronic mesenteric ischemia

R) 'Rhoids (Anorectal sources)
- haemorrhoids
- rectal varices (related to portal hypertension)
- anal or rectal ulcer
- fissure-in-ano

beware that massive UGIB might mimic LGIB:
1) Duodenal or gastric ulcer
2) Esophageal or gastric varices
3) Aortoduodenal fistula
4) Dieulafoy's lesion


Pathogenesis and risk factors of Diverticulosis

- Increased intraluminal pressure cause inner layer of colon bulge through focal area of weakness in colon wall (usu blood vessel penetration)

Risk factors:
- Low-fiber diet
- Constipation (which increases intraluminal pressure)
- Positive family history
- Old age


Common site of diverticulosis in HK

Most common location is Sigmoid colon

Righ sided diverticulosis is also common in Asians (therefore colonoscopy is better than sigmoidoscopy to visualise diverticulosis in HK)


Complications of diverticulosis (& diverticulitis)

1) Painless lower GI Bleeding
- due to rupture of vasa rectum
- usually clinical insignificant and stops spontaneously

2) Diverticulitis
- when faeces are impacted in diverticulum, causing inflammation and bacterial overgrowth

3) Complications of diverticulitis:
i) Abscess formation

ii) Fistulization
- Colovescial fistula most common
- Colovaginal fistula in women
- Rarely, colocutaneous fistula, coloenteric fistula

iii) Obstruction
- due to chronic inflammation and thickening of bowel wall

iv) Free colonic perforation
- leads to peritonitis


Diverticulosis diagnosis and management

- Colonscopy (better as right sided diverticulosis is common in Asian)
- Angiography

- Endoscopy therapy to stop bleeding (e.g. sclerotherapy, adrenaline injection, endoclip)
- Percutaneous drainage if abscess
- Hartmann procedure if perforation and peritonitis (full colonoscopy might be better in Asian due to prevalence of righ sided disease)

- antibiotics if diverticulitis
- High fiber diet (e.g. bran, psyllium)


Angiodysplasia of colon (pathogenesis, site, correlation)

A degenerative process with aging, in which ectasia of vessels lying in the submucosa of colon

Anywhere in colon, but commonly right sided

- Osler-Weber-Rendu disease 
- Aortic stenosis (seen in 25% of AVM patients)


Diagnosis and management of colon angiodysplasia


- in 90% of patient bleeding stops spontaneously
- manage by colonoscopic coagulation (sclerotherapy, adrenaline, etc)
- Consider right hemicolectomy if recurrent and persistent bleeding


Name me the colitides

1) Inflammatory Bowel Diseases
- Ulcerative colitis
- Crohn's disease
- Indeterminate colitis

2) Ischemic colitis
- acute mesenteric ischemia
- iatrogenic IMA ligation after AAA repair

3) Infectious colitis
- Pseudomembranous colitie
- Bacterial (E coli, shigella)
- CMV colitis
- Amoebic colitis
- Neutropenic enterocolitis (usually after chemotherapy in AML)

4) Radiation proctocolitis


Radiation proctocolitis pathogenesis (& risk factors)

Pelvic radiotherapy for malignancy might dmage the rectal mucosa, leading to formation of vascular telengiectasis

Risk factors:
- high dose irradiation to pelvis
- vascular diseasse
- old age
- previous low anterior resection


Radiation proctocolitis management

1) Endoscopic treatment 
- Infrared coagulation
- Argon beam coagulation
- Laser

2) Stool softeners, steroid enemas, topical 5-aminosalicylic acid

3) Transanal 4% formalin when (2) fails

4) Surgery if bleeding is unstoppable
- Diverting colostomy
- Proctectomy 
- Endoscopic dilation for str


Types of acute mesenteric ischemia

1) Arterial embolism (50%)
- usually cardioembolism
- AF, MI, valvular disorder

2) Arterial thrombosis (25%)
- Acute occlusion from plaque rupture over pre-exusting atherosclerotic disease
- Concurrent atherosclerotic disease in other site (e.g. CAD, stroke, PVD)

3) Non-occlusive mesenteric ischemia (20%)
- Splanchnic vasocontriction due to low cardiac output
- often seen in critically ill elderly patients

4) Venous thrombosis (less than 10%)
- thrombophilia, COC, malignancy, infection



Clinical presentation of acute mesenteric ischemia

Acute presentation of:

1) Severe abdominal pain
- aka "abdominal angina"
- often post-prandial due to increased blood demand

2) Anorexia, vomiting

3) GI bleeding

4) If intestinal infarction occured:
- peritoneal signs (rebound tenderness, guarding)
- shock (hypotension, tachycardia)
- Sepsis (lactic acidosis, fever, confusion)


Diagnosis of acute mesenteric ischemia

1) Mesenteric angiography for definitive diagnosis

2) AXR (to look for other causes of abdominal pain)

3) Barium edema ("thumbprinting" due to thickened edematous mucosal folds)

Othe Ix:
- CBC (shows leucocytosis)

- ABG (shows metabolic acidosis)


Management of acute mesenteric ischemia

1) Supportive therapy
- IV resuscitation, electrolyte resuscitation
- broad spectrum antibiotics

2) Direct intra-arterial infusion of Papaverine (vasodilator) into mesenteric system during arteriography
- relieves occlusion and vasospasm

3) Embolectomy or Direct intra-arterial infusion of thrombolytics
- if due to venous thrombosus

4) Surgery
- Resection of infarcted bowel is required if bowel infarction occured


Chronic mesenteric ischemia causes

Chronic mesenteric ischemia is caused by atherosclerotic occlusion of main mesenteric vessels (celiac, SMA, IMA)


How to localise the bleeding site in a destabilised patient with massive GI bleeding that required emergency surgery?

Intraoperative endoscopy:

- Peroral (too long)
- Through enterotomy
- Laparoscopic assisted 

Supportive procedures:
- Foley catheter inserted through appendicotomy or enterotomy
- Bowel preparation by on table antegrade irrigation
- Effluent from anus 


Use of Angiography in GI system (procedure and function)

Selective catheterization of coeliac, SMA, IMA by Seldinger technique, with injection of contrast dye. It is quite hard to intrepret however.

- Detect bleeding sites along GI tract (extravasation of contrast; not too sensitive for slow or stopped bleeding)
- Detect angiodysplasia
- Detect vascular tumours
- Detect acute and chronic mesenteric ischemia
- Therapeutic function for injection of drugs (e.g. vasopressin to decrease bleeding; papaverine to increase blood supply for ischemia)
- Therapeutic function by Transcatheter arterial chemoembolization (TACE, thus reduce the blood supply to tumours)


What are the complications of angiography in GI system

1) Due to contrast
- Contrast allergy (anaphylaxis)
- Contrast nephritis -> renal failure (prophylaxis by N-acetylcysteine)

2) Bleeding from puncture site 

3) Due to drug injection
- Vasopressin would affects heart, and worsen mesenteric ischemia
- Papaverine would worsen bleeding

4) Due to TACE
- May cause mesenteric ischemia, and bowel infarction


Explain function and procedure of radioisotope bleeding scan

Sulphur colloid and tagged RBC are labelled with Technetium (Tc 99m). When in blood stream, these tagged RBC will not be cleared quickly and will not be taken up by liver & spleen. Thus site of bleeding can be identified (if scan is delayed, maybe only site of blood pooling can be identified)

- Very sensitive - thus detect intermittent or slow bleeding, which is not shown by angiography
- A screening tool to look for bleeding if bleeding site is obscure 
- Specificity not high


Therapeutic modalities of endoscope

1) Removal of tissue
- plication of ulcers
- polypectomy

2) Hemostasis
- Sclerotherapy by injection of sclerosants
- Adrenaline injection
- Thermal (heat probe, BICAP probe, Laser, Argon plasma coagulation)
- Electrocoagulation
- Haemoclips, endoloops

3) Dilatation of strictures
- Stenting


What is a Push enteroscopy

Upper endoscopy "pushed" beyond the DJ flexure, usually using Long endoscope with overtube

- allow examination of jejunum too


Indications and contraindications of capsule endoscopy

- Obscure GI bleeding/Iron deficiency anemia
- Abnormal imaging of the small bowel
- Recurrent abdominal pain
- Chronic diarrhea
- Follow up of Celiac disease, Crohn’s disease, Small bowel tumours, NSAID induced GI damage, Polyposis syndromes 

- known or suspected gastrointestinal obstruction or strictures
-¬†‚ÄčSwallowing disorders¬†
- Severe motility problems 
- Pacemakers or other implantable electromedical devices 


Pros and cons of capsule endoscopy

+ Non invasive
+ Great for small bowel
+ color video image

- Expensive
- No exact in localisation (cannot to-and-fro examination, thus missing lesions)
- Cannot take biopsy 
- No therapeutic value
- Sub-optimal visual clarity 
- Long viewing time of video, up to 2 hrs 



Procedure of double ballon enteroscopy

DB enteroscopy allows visualisation of the entire small bowels despite the elastic nature of the looped intestines which makes scope pushing difficult:

- The long enteroscope is either inserted per-oral or per-anal ro reach small bowels

- The intubated intestine is shortened by gentle withdrawal of the endoscope while the balloon at its tip is inflated to grip the intestine 

- A flexible overtube with a balloon prevents stretching of the shortened intestine 


SB enteroscopy VS DB enteroscopy

- SB enteroscopy needs fewer operator (1) than DB (2)

- SB enteroscopy has a faster intubation time

- SBE is more user friendly

- However, DB enteroscopy can reach greater depth and visualise the entire small bowel more readily

- DBE can also hold in ileocecal valve 


Definition of diarrhoea (and chronic diarrhoea definition)

Must first evaluate the normal bowel pattern of the patient, usually defined by:

- increase in daily stool volume, frequency and fluidity

- Stool weight > 250g/24h

- ‚Č•3 times/day

- liquidity 

Chronic diarrhoea
is defined by diarrhoea for more than 4 weeks (‚Č•3 loose stools/day)


DDx of diarrhoea

1) Exudative (blood, pus, PMN in faeces)
- Crohn's disease
- Ulcerative colitis
- Gastroenteritis (E coli)
- Pseudomembraneous colitis

2) Motility
- Irritable bowel syndrome
- hypermotility in thyrotoxicosis

3) Secretory (persist despite fasting)
- Cholera
- VIPoma
- bile salt malabsorption
- Laxative abuse

4) Osmotic (disappear with fasting)
- indigestion (lactose intolerance)
- Sorbitol and mannitol related osmotic diarrhea 
- caffeine or methyxanthine-induced diarrhea 
- Malabsorption, e.g:
. small bowel diseases 
. Short gut syndrome (after resection)
. bacterial overgrowth 
. pancreatic diseases 

5) Dysentery
- Shigella, Entamoeba histolytica, and Salmonella



Investigations in chronic diarrhoea

1) Blood test
- CBC (anemia? leucocytosis? eosinophilia? neutrophilia for infection?)
- ESR, CRP (CRP higher in inflammatory diarrhoea)
- Serum electrolyte panel (Na, K, Ca, albumin)
- Thyroid function test (TSH) 
- RFT (baseline for contrast, sometimes ARF causes vomiting, also for electrolytes)
- ANF, ASCA, p-ANCA (for Crohn's disease, ulcerative colitis)

2) Stool test
- Leucocyte (indicates inflammtory)
- Na & K concentration (if secretory, then very high)
- Fat content (malabsorptive or maldigestion)
- alpha-1 antitrypsin concentration (high = excessive GI protein loss)
- pH (if - Culture and stain (bacteria)
- ova and parasites (O&P) test
- C diffcile toxin (pseudomembraneous colitis)

3) Imaging
- AXR (esp calcification in chronic pancreatitis)
- Barium follow through, barium enema (IBD, mass)
- CT abdomen
- Labeled human serum scan (to localise source of protein losing enteropathy)

4) Endoscopy
Take biopsy too
- EGD, push enteroscopy
- Sigmoidoscopy
- Colonoscopy
- Capsule enteroscopy
- DB or SB enteroscopy
- etc


Name some Protein losing enteropathy 

- IBD (CD, UC)

- allergic gastroenteropathy 

- Whipple’s disease 

- intestinal lymphangiectasia (which is rarely secondary to chronic constrictive pericarditis)

- congenital hypogammaglobulinemia 


Diagnosing Protein losing enteropathy

1) Labeled human serum scan 
- Isotope-labelled albumin to look for the site of leakage

2) Faecal őĪ-1 antitrypsin concentration
- high

3) Blood őĪ-1 antitrypsin clearance
- high 


Irritable Bowel syndrome clinical features

- Psychiatric symptoms (e.g. depression, anxiety, somatisation) may precede GI symptoms; GI symptoms might worsen with stress and irritants

- Recurrent abdominal pain/discomfort ‚Č•3 days per month in the last 3 months

- Pain/discomfort improves with defaecation

- Onset associated with change in frequency of stool (diarrhoea or constipation)

- Onset associated with change in form of stool


Diagnosis of IBS

Diagnosis by exclusion, clinical diagnosis based on Rome III criteria:

Recurrent abdominal pain/discomfort ‚Č•3 days per month in the last 3 months, with¬†‚Č•2 of the following:

a) Pain/discomfort improves with defaecation

b) Onset associated with change in frequency of stool

c) Onset associated with change in form of stool


IBS Subtypes 

1) IBS with diarrhea [IBS-D]:
-¬†loose or watery stool ‚Č•25%
- hard stool

2) IBS with constipation [IBS-C]:
-¬†hard stool ‚Č•25%
-  loose or watery stool

3) Mixed IBS [IBS-M]:
-¬†hard stool ‚Č•25%
-¬†loose or watery stool ‚Č•25% of bowel movements

4) Unsubtyped IBS:
- insufficient abnormality of stool consistency to meet criteria for IBS-C, D or M. 


Pathophysiology behind IBS

‚ÄĘ Anomaly in¬†Brain Gut axis

‚ÄĘ Disregulation of Autonomic nervous system

‚ÄĘ Altered bowel motility [motor]

‚ÄĘ Visceral hypersensitivity [sensory]

‚ÄĘ Psychosocial factors (e.g. stress)

‚ÄĘ Neurotransmitter imbalance (serotonin)¬†


Features Against Irritable Bowel Syndrome 

- Weight loss
- Rectal bleeding
- Onset in older patients
- Family history of CA colon or IBD

- Positive FOBT
- Anemia, leucocytosis
- raised ESR
- Abnormal biochemistry 


Management of IBS

I. Education

II. Reassurance

III. Dietary modifications
1) FODMAP diet

IV. Psychological treatments
1) Talk therapy
2) Tricyclics, SSRI

V. Pharmacotherapy for Symptomatic Relief
1) Abdominal pain

- Antispasmodics: hyoscamine, dicyclomine
- Antibiotics: rifaximin
- Probiotics: bifidobacterium infantis
- Tricyclics: amitriptyline, nortriptyline
- SSRI: fluoxetine, citalopram, escitalopram

2) Diarrhoea
- antidiarrheals: loperamide, diphenoxylate
- Antibiotics: rifaximin
- Tricyclics: amitriptyline, nortriptyline
- SSRI: fluoxetine, citalopram, escitalopram

3) Constipation
- Bulking agents: methylcellulose, psyllium
- Osmotic laxatives: lactulose, polyethylene glycol
- Stimulant laxatives: senna, bisacodyl
- Emollient laxatives: docusates, mineral oils
- Chloride channel activator: lubiprostone


Compare the different inflammatory bowel diseases

Ulcerative Colitis vs Crohn's Disease:

1) Depth: UC is confined to mucosa and submucosa (this shallow ulcers), while CD extends from mucosa to serosa (i.e. transmural; deep ulcers)

2) Site: UC is confined to colon & rectum (rectosigmiod lesion always present!), while CD extends along the entire GI tract (commonly terminal ileum; only 50% involves rectosigmoid)

3) Lesion: UC is continuous while CD are skipped lesions

4) Clinical features:
- UC more likely to present with hematochezia and bloody diarrhoea, while CD usually non bloody diarrhoea
- Some different extraintestinal manifestationd

5) UC usually does not cause strictures fistula; while they are common in CD, as the lesion is transmural

6) Granuloma is rare in UC but common in CD

7) In histology, Goblet cell depletion in UC but present in CD 



Some risk factors for IBD

1) Genetics (Family History)
- Family aggregation of both UC and CD, suggesting genetic basis in both diseases and partially sharing the genetic basis 
- MHC gene, NOD2 gene

2) Environmental factors (postulated)
- smoking
- appendicectomy
- diet

3) Immunological


Clinical features of IBD in general

1) diarrhoea (more likely with blood in UC, but not CD)

2) Hematochezia (more common in UC)

3) abdominal pain, nausea, vomiting

4) Anorexia, malabsorption, weight loss

5) fever

6) anaemia

7) extraintestinal manifestations
- look at next


Extraintestinal manifestation of IBD

1) Eye lesion
- Episcleritis
- Anterior Uveitis

2) Mucocutaneous
- Pyoderma gangrenosum (especially UC)
- Erythema nodosum (especially CD)
- Oral aphthous ulcers

3) Arthropathy
- UC patients have greater incidence of ankylosing spondylitis
- Enteropathic arthropathy (migratory oligoarthropathy mainly affecting joints of lower limbs)
- Sacroilitis, dactylitis, heel ethesitis

4) Bone
- Osteoporosis

5) Biliary tract
- Primary sclerosing cholangitis in UC
- Gallstones in CD

6) Renal
- Renal stones

7) Hematological
- Hypercoagulable state (precipitates DVT, PE, stroke etc)
- Idiopathic thrombocytopenic purpura


Distribution of Ulcerative Colitis

Rectum is always involved, while colon is involved partially or completely:

1) Proctitis (10%)
- only rectum

2) Left sided Colitis (40%)
- rectum plus descending colon

3) Extensive colitis, pancolitis

4) Rarely, the distal ileum might be involved, aka "Backwash ileitis"


A image thumb

Classifications of Crohn's Disease

Based on the Vienna and Montreal classification for CD:

L1 = ileal
L2 = colonic
L3 = ileocolonic
L4 = isolated upper disease

B1 = non-stricturing, non-penetrating
B2 = stricturing
B3 = penetrating

p = perianal disease modifier


Complications of IBD

Ulcerative Colitis
1) GI haemorrhage with iron deficiency anemia

2) Toxic Megacolon (leading cause of death)

3) Electrolyte disturbances, dehydration, hypotension secondary to diarrhoea

4) Colorectal cancer & cholangiocarcinoma

5) Primary sclerosing cholangitis

6) Growth retardation

Crohn's Disease
1) Fistula
- enteroenteral
- enterovescial
- enterovaginal
- enterocutaneous

2) Abscess

3) Stricture, SBO
- oedema and spasm of bowel causes transient obstruction
- scarring and thickening of bowel wall cause chronic obstruction

4) Malnutrition and Malabsorption
- protein losing enteropathy
- lack of calorie, protein, Vitamin B12 and bile acid

5) Perianal disease
- perianal fistula
- anal fissures
- perianal abscess

6) Toxic megacolon (less common than UC)

7) Gallstone and renal stone

8) Growth retardation


Toxic megacolon (etiology, clinical features, Ix, Management)

- usually complication of Ulcerative Colitis, rarely Crohn's Disease

Clinical features:
- Diarrhoea
- Fever, anaemia, low albumin
- Dehydration, electrolyte imbalance, mental changes
- hypotension, tachycardia

- confirm by AXR (thumb signs)
- rule out pseudomembranous colitis, CMV infection

- Bowel rest by NPO and TPN
- fluid and electrolyte resuscitation
- corticosteroids
- urgent colectomy if no response to medical therapy (~50%)


Investigations in suspected IBD

Confirm the diagnosis by:
- Endoscopy with biopsy (no goblet cells, granuloma in UC, but present in CD)
- Barium follow through or enema
- AXR, CR and MRI
- p-ANCA in UC; ASCA in CD

*** Screen for TB (tuberculin & CXR) and HBV status, as we will consider biological agents that might cause relapse

Investigations to be done is same as chronic diarrhoea Ix:

1) Blood test
- CBC (anemia? leucocytosis? eosinophilia? neutrophilia for infection?)
- ESR, CRP (CRP higher in inflammatory diarrhoea)
- Serum electrolyte panel (Na, K, Ca, albumin)
- Thyroid function test (TSH) 
- RFT (baseline for contrast, sometimes ARF causes vomiting, also for electrolytes)
- ANF, p-ANCA, ASCA (for Crohn's disease, ulcerative colitis)

2) Stool test
- Leucocyte (indicates inflammtory)
- Na & K concentration (if secretory, then very high)
- Fat content (malabsorptive or maldigestion)
- alpha-1 antitrypsin concentration (high = excessive GI protein loss)
- pH (if - Culture and stain (bacteria)
- ova and parasites (O&P) test
- C diffcile toxin (pseudomembraneous colitis)

3) Imaging
- Barium follow through, barium enema (IBD)
- CT abdomen
- Labeled human serum scan (to localise source of protein losing enteropathy)

4) Endoscopy
Take biopsy too
- EGD, push enteroscopy
- Sigmoidoscopy
- Colonoscopy
- Capsule enteroscopy
- DB or SB enteroscopy
- etc


Management of IBD

"Traditional step-up pyramid approach"

Mild disease:
1) 5-aminosalicylic acid (5-ASA)
- Sulphasalazine (sylphapyridine + 5-ASA)
- 5ASA analogues e.g. Mesalazine, olsalazine

2) Budenoside, antibiotics for Crohn's Disease

3) Corticosteroids

4) Immunosuppressants
- Azathioprine (delay onset of action for 3 months, so not good for initiation of therapy)
- 6-Mercaptopurine 
- Methotrexate (for Crohn's disease)

5) Biological agents
basically anti-TNF agents:
- Etanercept 
- Infliximab (chimeric, more allergy)
- Adalimumab (human, better)
- Certolizumab 

6) Surgical therapy
Not curative, disease recurs close to the anastomosis.
- Stricturoplasty
- Colectomy
- Proctocolectomy 


Indications of different therapy in IBD

1) 5-ASA agents
- Mild to moderately severe CD & UC
- Maintenance of remission
- Local anti-inflammatory action

2) Steroids
- Frequently relapsing disease

3) Immunosuppressants
- Frequently relapsing disease
- Steroid sparing effects
- Fistulating CD 

4) Biological agents
- only drug that can induce mucosal healing whilst improving symptoms
- standard treatment not working
- extra-intestinal manifestations
- fistulising CD  

5) Surgery
- failed medical treatment
- severe bleed, perforation
- stricture, fistula, abscess
- High risk of cancer 


ADR of anti-TNF agents

1) Infection:
- reactivation of latent TB & latent viral e.g. HBV

2) Malignancy:
- Lymphoma

3) Autoimmunity:
- hemolytic anaemia
- lupus-like, anti-dsDNA, ANA


History of anorectal disease

- present illness (pain? bleeding?)

- past health (medical disease, previous surgery)

- family history

- sexual history 


PE of anorectal disease

1) General examination

2) Abdominal examination

3) Perianal examination
- Patient in lithotomy position (left lateral) or prone jackknife position (better exposure)
- inspection for scars, fissure, stretch mark, haemorrhoid
- ask patient to bear down for prolapse

4) Digital rectal examination
- ask patient to bear down for anal tone
- feel for the four walls (Do not mistake cervix as mass in women)
- look at finger for stool, blood
- note internal haemorrhoids cannot be felt by PR

5) Proctoscopy
- visualise lesion
- assessment and confirmation


Investigations of anorectal disease

1) Endoscopy
- Rigid sigmoidoscopy 
- Flexible endoscopy
- to exclude proximal bowel lesion 

2) Transrectal ultrasound 
- Assesses the sphincter muscles in patients with faecal incontinence 
- Staging of rectal cancer 
- Assesses complex fistula 

3) Contrast study
- Barium enema
- Defaecography: in patient with constipation
- Fistulogram 

4) CT, MRI
- Very accurate, but usually unnecessary
- primary track of fistula and any extensions 

5) Anorectal manometry

6) Electromyogram

7) Pudendal nerve latency test 


What are haemorrhoids? What are their functions?

Cushions of vascular tissue (arterioles, venules, AV connections) at the anal canal, which can:

i) Aid in continence(act as a plug)
ii) Protect sphincters/anus from the trauma of defecation 


How to differentiate anal haemorrhoids from anal varices?

We can differentiate the two by the color of the blood:

Haemorrhoids: Fresh, bright red blood

Varices: Dark coloured blood


Compare internal and external haemorrhoids

External haemorrhoids
- Distal to the dentate line
- from ectoderm
- covered by squamous epithelium
- innervated by pudendal nerve & sacral plexus, thus causes pain
- drains by inferior rectal vein into IVC

Internal haemorrhoids
- Proximal to dentate line
- from endoderm
- covered by columnar epithelium of anal mucosa
- Not supplied by somatic sensory nerve, thus usually do not cause pain
- drains by superior rectal vein into portal system


How does internal haemorrhoids cause pain?

Internal haemorrhoids are not supplied by somatic sensory nerves, and therefore cannot cause pain per se.

However, prolapse of internal haemorrhoid will cause spasm of sphincter, thus causing perianal pain. Incarceration and strangulation of an internal haemorrhoid will cause pain too.


Etiology of haemorrhoids

‚ÄĘ Constipation

‚ÄĘ Straining

‚ÄĘ Pregnancy

‚ÄĘ Low fibre diet

‚ÄĘ Family history¬†


Symptoms of haemorrhoids

- Rectal Bleeding (bright red fresh blood, coated or dripping from faeces, but not mixed with stool)

- Prolapse

- Mucus discharge, thus pruritus

- Pain occurs only when complications are present (thrombosis, prolapse, incarceration, strangulation) 


Classifications of internal haemorrhoids

Goligher Classification:
For internal haemorrhoids only!!

1st degree:
- not prolapse out of anal canal

2nd degree:
- prolapse out of anal canal (usu during straining) and reduce spontaneously

3rd degree:
- requires manually reduction

4th degree:
- cannot be manually reduced & thus remain out of anal canal (due to considerable swelling preventing back flow of blood)
- result in thrombosis, prolpase, and ulcer


Treatment strategy for haemorrhoids

Depends on the classification:

1st degree
- Diet, banding, sclerotherapy, infrared coagulation

2nd degree
- Diet, banding, sclerotherapy, infrared coagulation

3rd degree
- Diet, banding, sclerotherapy, surgery

4th degree
- haemorrhoidectomy
1) Non-operative
- diet modification with high fibre diet
- sitz bath: for prolapsed haemorrhoids 

2) Office procedures
- banding (rubber band ligation)
- sclerotherapy
- Infrared coagulation

3) Surgical Hemorrhoidectomy 
- Excision (conventional haemorrhoidectomy)
- Stapled haemorrhoidectomy


Indications of haemorrhoidectomy

- 4th degree haemorrhoid (i.e. cannot be manually reduced)

- Mixed internal and external

- Failureof other treatment

- Patient preference

- In conjunction with another procedure 


Complications of haemorrhoidectomy

‚ÄĘ Bleeding
‚ÄĘ Pain
‚ÄĘ Infection

‚ÄĘ Incontinence¬†
‚ÄĘ Urine retention
‚ÄĘ Faecal impaction

‚ÄĘ Anal tags
‚ÄĘ Anal stenosis


Pros and cons of stapled haemorrhoidectomy

- less pain (less analgesics, quicker patient recovery)

- Higher patient satisfaction, more aesthetically pleasing

- less post operative bleeding, wound complications

- More serious complications (e.g. rectal perforation, severe pelvic sepsis, rectovaginal fitula)

- more recurrence than conventional haemorrhoidectomy


Site of Fissure-in-ano 

- A split in the anoderm at the dentate line

- at posterior midline in 90%

- at anterior midline in 10% of women

- Think about secondary causes if at atypical sites


Chronic anal fissure features

Associated with:

1) sentinel pile

2) hypertrophic papilla

3) internal sphincter muscles visualisation at the base of the fissure 


Etiology of fissure-in-ano

If typical (i.e. posterior midline), then:

1) hard stool

2) tight internal anal sphincter

3) ischaemia of the overlying anoderm at the posterior midline (due to poor blood supply over the area)
if atypical position and multiple in number, then suspect:

- inflammatory bowel disease
- tuberculosis
- syphilis, HIV, CMV infection


Clinical features and investigations of anal fissure

Clinical feature:
- pain on defaecation
- fresh rectal bleeding

- diagnosis is by spreading the buttock to reveal the fissure

- PR examination and proctoscopy are painful and not indicated 


Fissure-in-ano management

Non-operative treatment
1) Manage contipation & hard stool
- bulk agents, stool softeners and topical anaesthetics

2) Reduce internal sphincter pressure 
- nitroglycerin ointment
- topical Ca channel blocker
- Botulinium toxin injection

Surgical treatment
1) lateral internal sphincterotomy (complication being minor incontinence, e.g. flatus incontinence)


Anorectal abscess clinical features

- Pain

- Swelling

- Drainage

- Constipation and urinary difficulties due to associated pain


Site of anorectal abscess

1) Ischiorectal 60%

2) Perianal 20%

3) Intersphincteric 18%

4) Supralevator 2% 

A image thumb

Anorectal abscess etiology

1) cryptoglandular infection

2) specific infections (esp when multiple abscesses)
‚ÄĘ inflammatory bowel disease
‚ÄĘ tuberculosis
‚ÄĘ actinomycosis
‚ÄĘ foreign body
‚ÄĘ surgery
‚ÄĘ malignancies¬†


Anorectal abscess management

- incision and drainage of abscess

- consider primary fistulotomy as high number of abscess will develop into a fistula

- little role for antibiotics except in patients with severe cellulitis, valvular heart disease, prosthetic heart valves and immunosuppression


Anal fistula definition and etiology

Abnormal tracts (usu lined with granulation tissue) communicating between the rectum/anal canal with perineal skin

Formed from anorectal abscesses, which can be due to:
1) cryptoglandular infection

2) specific infections (if multiple anal fistulas)
‚ÄĘ inflammatory bowel disease
‚ÄĘ tuberculosis
‚ÄĘ actinomycosis
‚ÄĘ foreign body
‚ÄĘ surgery
‚ÄĘ malignancies¬†


Classification of anal fistula

i.e. the Parks Classification

1) intersphincteric

2) transphincteric

3) suprasphincteric 

4) extrasphincteric

A image thumb

Clinical features of anal fistula

- Pain

- Swelling

- Drainage

- Constipation and urinary difficulties due to associated pain

- Bleeding

- external opening over skin

- PR will feel induration with cord like structure 


Management of anal fistula (and complications)

Depends on types (Parks classification)

1) Intersphincteric
- Fistulotomy (lower risk of incontinence)
- Fistulectomy
- Ligation of intersphincteric fistula tract (LIFT)

2) Transsphincteric
if low:
- Fistulotomy (for those with good pre-op anal sphincter function)
- Fistulectomy

if high/anterior fistula
- Cutting Seton
- Partial fistulectomy & endoanal flap
- Injection of fibrin glue

3) Suprasphincteric
- Cutting seton
- Endorectal advancement flap
- Sphincter reconstruction

4) Extrasphincteric
- Endorectal advancement flap
- Laparatomy & resection & fistula curettage
- incontinence
- recurrence 


Pruritus ani (epidemiology, etiology, management)

Pruritus of perianal area, scratching leads to excoriation and secondary infection

- men to female ratio: 4:1
- common in 5th and 6th decades 

- personal hygiene
- diet
- systemic diseases
- dermatogical conditions
- neoplasm 
- infection
- psychogenic
- drugs
- diarrhoea
- idiopathic 

‚Äč‚Äď Identify etiology and treat appropriately¬†
‚Äď reassurance
‚Äď keep perianal skin dry
‚Äď avoid soap and local applications
‚Äď avoid prolonged topical steroids
‚Äď dietary change¬†


Rectal prolapse etiology

Neurological disorders (e.g. pudendal neuropathy)



If childhood, consider: cystic fibrosis, whooping cough, developmental abnormalities and malnutrition 

Anatomical anomalies, e.g.:
‚Äď Rectal intussusception
‚Äď Deep cul de sac
‚Äď Loss of rectal fixation
‚Äď Redundant sigmoid
‚Äď Levator ani diastasis
‚Äď Patulous anal sphincter¬†


Treatment of rectal prolapse

Abdominal repair 
- Rectal fixation (e.g. Laparascopic ventral mesh rectopexy - never insert dorsally due to potential nerve damage)

- Sigmoidectomy

- Proctectomy

- Combination of rectal fixation and sigmoid resection 

Perineal repair
- Full thickness resection

- Mucosal resection with muscular reefing

- Anal encirclement

- Concomitant sphincter repair and/or levator reinforcement. 


Name some Anal neoplasms 

1) Epidermoid carcinoma of anal canal 
- Risk factors: anal sex, STD, HPV
- Treatment: Chemoirradiation

2) Malignant Melanoma 

Tumours at anal margins:
3) Squamous cell carcinoma 

4) Basal cell carcinoma

5) Kaposi's Sarcoma
- HHV 8 infection in HIV patients


Faecal incontinence etiology

‚Äď perineal soiling (pseudoincontinence)

‚Äď overflow incontinence

‚Äď diarrhoea states

‚Äď sphincter injury (obstetric, surgical and traumatic)

‚Ästcongenital abnormality

‚Äď pelvic floor denervation¬†


Treatment of fecal incontinence

Medical management
‚Äď diet and medication to change stool consistency¬†and transition time

‚Äď colonic irrigation

‚Äď biofeedback¬†

‚Ästanorectal muscle repair: overlapping¬†sphincteroplasty, post anal repair

‚Äď neosphincter procedure: dynamic graciloplasty, artificial sphincter

‚Ästsacral nerve stimulation


‚Ästothers:¬†continent colonic conduit¬†


What are Pilonidal cysts? (epidmiology, symptoms)

A cyst or abscess near or on the natal cleft of the buttocks that often contains hair and skin debris

- more common in male
- puberty to 40yo

- Pain/discomfort or swelling above the anus
- purulent/bloody discharge from the tailbone area
- Unexpected moisture in the tailbone region


Treatment of Pilonidal sinus

‚Ästincision and drainage of abscess

‚Ästwide excision of sinus to fascia

‚ÄstZ-plasty, myocutaneous flap for complex and recurrent disease

‚Äď meticulous hair control¬†


RLQ Pain DDx

* = both sides

1) Acute appendicitis 
2) Caecal diverticulitis
3) Mesenteric Adenitis
4) Ileitis 
5) Meckel’s diverticulitis 
6) Caecal ischaemia 
7) Cancer of caecum 
8*) Ureteric colic 
9*) Ruptured ectopic pregnancy
10*) Torsion of ovarian cyst 
less likely
11*) Inguinal/femoral hernia 
12*) Testicular pathology
13) Perforated peptic ulcer 
14) Acute cholecystitis


LLQ Pain DDx

1) Sigmoid diverticulitis
2) Cancer of the sigmoid colon 
3*) Ureteric colic
4*) Ruptured ectopic pregnancy 
5*) Torsion of ovarian cyst 

Less likely
6*) Inguinal/femoral hernia 
7*) Testicular pathology


Central abdominal pain DDx

Either periumbilical or hypogastrium pain:

1) SBO
2) Gastroenteritis 
3) Early acute appendicitis 
4) Bowel ischaemia (mesenteric ischemia)
5) IBS
6) Ruptured AAA
7) Acute pancreatitis

Suprapubic or Hypogastrium
1) Cystitis
2) Pelvic inflammatory disease 
3) Large bowel obstruction 
4) Acute retension of urine


Diffuse abdominal pain DDx

1) Peritonitis

2) Gastroenteritis

3) bowel obstruction 

4) Poor description from Hx


Visceral pain and its location

Result of stretching of hollow or solid organ, dull and vaguely localized - Via slow C fibers in sympathetic nerves: 

1) Epigastrium Visceral Pain
- Foregut (i.e. stomach, biliary tree, D1, D2)

2) Umbilical visceral pain
- Midgut (i.e. D2 to proximal 2/3 of transverse colon)

3) Suprapubic visceral pain
- Hindgut (i.e. distal 1/3 of transverse colon to rectum)


Parietal pain explained

Sharp pain caused by irritation of pain fibers of the parietal peritoneum, localized to the dermatone at the site of the stimulus (via A-őī fibers of somatic nerves):

1) Referred Pain
- R diaphragm irritation at right shoulder tip
- Gallbladder irritation at right scapula tip

2) Radiation of pain
- Pancreatitis, AAA rupture radiates to back
- Ureteric colic radiates to ipsilateral testicle
- Testicular pain radiates to ipsilateral flank

3) Shifting pain
- Acute appendictitis pain might shift from periumbilical (even LLQ) to RLQ


Colicky pain explained

On-and-off pain and spasm resulting from contraction of a hollow organ against an obstruction:

- Ureteric colic
- Biliary colic
- Small or Large Bowel obstruction


Acute appendictitis presentation

Commonly presented in young people; Gradual onset of:

1) Abdominal pain 
- Classically present with periumbilical pain (visceral pain) which later shifted to RLQ (somatic pain)
- Rovsing's sign, obturator sign, psoas sign

2) Peritonism
- Localized tenderness and guarding at the McBurney’s point 

3) Anorexia
- appendictitis unlikely if patient is hungry

4) Nausea, vomiting, diarrhoea, dysuria and fever 


Where is the McBurney's Point?

2/3 of the distance from umbilicus to right ASIS


Diagnosis and Ix in appendicitis

1) Mostly a Clinical diagnosis

Supportive Ix:
2) CBC shows leucocytosis

3) US & CT scan may be helpful if uncertain about the diagnosis


Treatment of acute appendicitis

1) Anticbiotics

2) Appendectomy (laparascopic or open)


Mesenteric adenitis presentation

Usually presented in children:

1) Recent sore throat & high fever

2) RLQ pain

3) Not much peritoneal sign 

4) Presence of enlarged lymph nodes found during operation 


Mesenteric adenitis causative agents

- ő≤-hemolytic strep,¬†Strep viridans
- E coli
- Yersinia

- Coxsackievirus
- Rubeola virus
- Adenovirus 


Ileitis etiology

1) Crohn’s disease (or rarely backwash ileitis in UC)

2) TB

3) Radiation enteritis

4) Bacterial infection e.g.
- Campylobacter
- Yersinia
- Salmonella 


Ectopic pregnancy overview

Most common site at the Fallopian tube 

Higher risk in previous PID, ectopic pregnancy 

Causes rupture at 6 weeks 


Ruptured ectopic pregnancy management

- Large bore IV cannula and resuscitation

- Urgent laparoscopy and salpingotomy / salpingectomy 


PID pathogens

- Chlamydia trachomatis

- Neisseria gonorrhoeae 


Management of PID

1) Antibiotic

2) Drainage of tubo-ovarian abscess (image guided/ laparoscopic) 


Painful testes DDx

1) Testicular torsion (usually younger age)

2) Epididymo-orchitis 

3) testicular tumour 


Peritoneal spaces

- Right & left subphrenic spaces

- Hepatorenal recess (Morrison's pouch)

- Splenorenal recess

- Lesser sac 

- Left & right paracolic gutter

- Interloop space 

- Pelvis  


Peritoneal Response to Infection 

1) Rapid absorption of bacteria via diaphragmatic stomata and lymphatics

2) Opsonization and destruction of bacteria via the complement cascade

3) Localization of bacteria within fibrin to promote abscess formation 
Liver will filters portal circulation while spleen filters systemic circulation


Peritoneal cellular response to infection

4 types of cells:

1) Mast cell
- histamine
- vasodilation
- influx of fluid & complements & Ig

2) Macrophage
- cytokine production, phagocytosis 

3) PMN (neutrophils)
- phagocytosis 

4) Peritoneal mesothelial cells
- downregulate fibrinolysis in case of inflammation
-> facilitating entrapment and isolation of bacteria within the fibrin matrix 


Peritonitis classifications

1) Primary Bacterial Peritonitis
- SBP (in ascites in cirrhosis)
- TB peritonitis
- Peritonitis associated with chronic ambulatory peritoneal dialysis 

2) Secondary bacterial peritonitis
Infection arising as a result of intra-peritoneal processes:
- Perforated GI Tract (e.g. pancreatitis, appendicitis)
- unrecognized operative injuries or dehiscence of anastomoses 
- Bowel ischemia

3) Tertiary bacterial Peritonitis 
Opportunistic infection with normally non-pathogenic gut flora; associated with prolong use of antibiotics:
- Candida, Enterococcus, Staphylococcus 

4) Acute non-bacterial peritonitis


Acute Non-bacterial Peritonitis 

- Chemical irritation by gastric juice, bile, urine and blood

- May become infected within 6-12 hours 


Bacteriology of peritonitis

Primary peritonitis
Hematogenous origin of bacteria:
- Strep. pneumonie 
- Strep pyogenes
- Enteric organisms 
- Chronic: TB, Actinomycosis 

Secondary peritonitis
Usually mixed:
- Gram Negs e.g. E coli, Klebsiella, Proteus, Pseudomonas
- Gram Pos e.g. Enterococcus, Staphylococcus, Streptoccus , Clostridium


Risk factors of primary bacterial peritonitis

- intra-abdominal malignancy

- malnutrition, immunosuppression, splenectomy

- chronic liver & renal disease 


Pathophysiology in secondary bacterial peritonitis

1) Exudative inflammation
- large amount of protein rich ascitic fluid
- high PMN count

2) Peritoneum becomes edematous, hyperarmic, covered with fibrinous exudates

3) Paralytic ileus

4) Hypovolemia

5) septicaemia, endotoxaemia and shock 


Acute Secondary Bacterial Peritonitis Treatment 

1) Supportive
- IV fluid replacement, nasogactric tube suction 
- Urinary catheter 
- Oxygen
- Analgesics
- Close monitoring

2) Broad spectrum Antibiotics 

3) Drainge
- percutaneous drainage of abdominal abscess 
- ERCP for biliary drainage 

4) Surgical correction
- Laparoscipic surgery (e.g. ulcer repair, bowel resection)
- Laparotomy surgery 

5) Peritoneal toilet 
- Necrosectomy
- Abscess drainage

6) Planned Abdominal Re-exploration 
- Planned repeated laparotomy for peritoneal toilet 


Peritonitis in the Elderly 

1) Poor historian
- patient often confused or demented
- rely on family members & caretakers for history

2) Minimal peritoneal signs 

3) Suspect peritonitis if:
- abdominal pain
- abdominal distention
- sepsis


Peritonitis in the Tropics 

1) Typhoid fever
- enteritis, perforation 

2) Amoebiasis 
- colitis & perforation; liver abscess 

3) Ascariasis 
- intestinal obstruction in children
- biliary obstruction or pancreatitis 


Peritonitis in HIV Patients 

Related to immunocomprimised state:

1) TB peritonitis
- primary bacterial peritonitia

2) CMV colitis causing perforated bowels

3) CMV cholecystitis

4) Lymphoma causing Bowel obstruction or perforation 


Peritonitis in Pregnancy 

A natural reluctance to operate; usually atypical presentation due to:

1) Enlarged uterus alters the location of organs
- e.g. caecum and appendex is pushed to RUQ