Andre Tan's Surgery Notes (Ed 1)

8/21/2019 Andre Tan's Surgery Notes (Ed 1)

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Surgery Notes

For the M.B.B.S.

By Andre Tan

CONTENTS

Page

I TRAUMA (MULTI-SPECIALTY APPROACH) 2

II APPROACH TO ABDOMINAL PAIN 10

III A PPROACH TO ABDOMINAL MASSES 11

IV OESOPHAGEAL DISEASES 12

V UPPER BLEEDING GIT AND ITS CAUSES 21

VI COLORECTAL DISEASES 19

VII LIVER DISEASES 39

VIII PANCREA TIC DISEASES 45

IX BILIARY TRACT DISEASES 51

X BREAST DISEASES 59

XI HEAD AND NECK MASSES 69

XII SALIVARY GLAND SWELLINGS 74

XIII THYROID DISEASES 78

XIV PERIPHERAL ARTERIAL DISEASE 85

XV ABDOMINAL AORTIC ANEURYSM 93

XVI PERIPHERAL VENOUS DISEASE 95

XVII UROLOGICAL DISEASES 99

XVIII SURGICAL INSTRUMENTS 110

XIX IMPORTANT LUMPS & BUMPS AND OTHERS 119


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TRAUMA (MULTI-SPECIALTY APPROACH)

ADVANCED TRAUMA LIFE SUPPORT ALGORITHM

MAIN PRINCIPLES:

- Treat greatest threat to life first- Definitive diagnosis is less important- Time is important – the ―golden hour‖ after trauma is when 30% of trauma deaths

occur, and are preventable by ATLS

APPROACH

1. Primary survey and Resuscitation with adjuncts2. Re-evaluation of the patient3. Secondary survey with adjuncts4. Post-resuscitation monitoring and re-evaluation5. Optimise for transfer and definitive care

PRIMARY SURVEY – ABCDE

1. AIRWAY

Assessment of ai rway patency- Is patient alert, can patient speak?- Gurgling, stridor- Maxillofacial injuries- Laryngeal injuries- Caution: C-spine injury

Establ ish ing patent ai rway

- Chin-lift or modified jaw thrust (protect C-spine)- Remove any foreign objects in the mouth where possible- Oro/nasopharyngeal airway- Definitive airway – endotracheal tube, cricothyroidotomy, tracheostomy

2. BREATHING

Assessment of breath ing

- Look, listen, feel: chest rise, breath sounds – rhythm and equality bilaterally- Rate of respiration- Effort of respiration- Colour of patient- Percuss chest- Look for chest deformities e.g. flail chest

Management o f breath ing

- Supplemental oxygen- Ventilate as required if patient requires assistance with breathing- Needle thoracotomy for tension pneumothorax, followed by chest tube- Occlusive dressing for open pneumothorax

3. CIRCULATION

Assessment of organ perfusion

- Level of consciousness- Skin colour and temperature, capillary refill- Pulse rate and character – all major pulses- Blood pressure

Classes of haemorrhagic shock

I II III IVBld loss

Amt (ml)Percentage

40

Ht rate 100 >120 >140BP Normal Normal Decreased DecreasedCap refill Normal Prolonged Prolonged ProlongedResp rate 14-20 20-30 30-40 >35Ur output (ml/h) >30 20-30 5-15 Oliguric-anuricMental state Sl anxious Mild anxiety Anxious-

confusedConfused-lethargic

Fluidreplacement

Crystalloid Crystalloid Crystalloid +blood

Blood

Management

- Sources of bleeding apply direct pressure or pressure on proximal pressure point

- Be suspicious about occult bleeding e.g. intraperitoneal, retroperitoneal (pelvicfracture), soft tissue (long bone fracture)

- Venous access – large bore, proximal veins- Restore circulatory volume with rapid crystalloid infusion – Ringer‘s lactate - Blood transfusion if not responsive to fluids or response is transient- Reassess frequently


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4. DISABILITY

- Glasgow coma scale

Eye Verbal Motor

Spontaneous openingOpens to voiceOpens to painNo response

4321

Oriented speechConfusedInappropriateIncomprehensibleNo verbal response

54321

ObeysPurposefulWithdrawsFlexion responseExtension responseNo response

654321

GCS: 14-15 (minor); 8-13 (moderate); 3-7 (severe)

- AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive- Pupillary reactivity

- Call for neurosurgical consult as indicated

5. EXPOSURE

- Remove all clothes- Check everywhere for injuries (log-roll to look at the back)- Prevent hypothermia

6. ADJUNCTS TO PRIMARY SURVEY

Moni tor ing

- Vital signs – BP, pulse rate, saturation (pulse oximeter)- ECG monitoring- Arterial blood gas

Diagnost ic tools

- Screening X-ray films (trauma series): CXR, AP pelvis, lateral C-spine- Focused abdominal sonography in trauma (FAST)- Diagnostic peritoneal lavage

Urinary catheter

- Functions: decompress bladder, measurement of urinary output- Caution in urethral injury: blood at urethral meatus, perineal

ecchymosis/haematoma, high-riding prostate

Gastr ic catheter (orogastr ic or nasogastr ic) - Function: decompress stomach, look at aspirate (bloody? bilious?)- Caution in base of skull fracture: CSF otorrhoea/rhinorrhoea, periorbital

ecchymosis, mid-face instability (grab the incisors and rock), haemotympanum insert orogastric tube instead of nasogastric

SECONDARY SURVEY

When to do secondary survey

- Primary survey and resuscitation completed- ABCDEs reassessed- Vital functions returning to normal i.e. no need for active resuscitation at the moment

1. AMPLE HI STORY

- Allergy

- Medications- Past history- Last meal- Events leading to injury, Environment in which trauma occurred

2. C OMPLETE HEAD - TO - TOE EXAMINATION

Head

- Complete neurological examination- GCS or AVPU assessment- Comprehensive examination of eyes and ears for base of skull fractures- Caution: unconscious patient; periorbital oedema; occluded auditory canal

Maxil lofacial- Bony crepitus/deformity- Palpable deformity- Comprehensive oral/dental examination- Caution: potential airway obstruction in maxillofacial injury; cribriform plate

fracture with CSF rhinorrhoea do not insert nasogastric tube

Cervical spine

- Palpate for tenderness, any step deformity- Complete neurological examination- C-spine imaging- Caution: Injury above clavicles; altered consciousness (cannot assess

accurately); other severe, painful injury (distracts from cervical spine pain)

Neck (soft t issues)

- Blunt versus penetrating injuries- Airway obstruction, hoarseness- Crepitus (subcutaneous emphysema), haematoma, stridor, bruit- Caution: delayed symptoms and signs of airway obstruction that progressively

develop; occult injuries


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Chest

- Inspect, palpate, percuss, auscultate- Re-evaluate frequently- Look at CXR- Caution: missed injury; increase in chest tube drainage

Abdomen

- Inspect, palpate, percuss, auscultate- Abrasions and ecchymosis – ―seat- belt sign‖

- Lower rib fractures liver and spleen injury- Re-evaluate frequently- Special studies: FAST, DPL, CT scan- Caution: hollow viscus and retroperitoneal injuries; excessive pelvic

manipulation

Perineum

- Contusions, haematomas, lacerations- Urethral blood- DRE: Sphincter tone, high-riding prostate, pelvic fracture (may feel fragments of

bone); rectal wall integrity; blood

- Vaginal examination: blood, lacerations

Musculoskeleta l – extremi t ies- Contusion, deformity- Pain- Perfusion- Peripheral neurovascular status- X-rays as appropriate- Caution: potential blood loss is high in certain injuries (e.g. pelvic fracture,

femoral shaft fracture); missed fractures; soft-tissue or ligamentous injuries;examine patient‘s back

3. ADJUNCTS AND SPECIAL DI AGNOSTIC TESTS

- As required according to suspicion, but should not delay transfer

4. F REQUENT RE - EVALUATION

- Have a high index of suspicion for injuries to avoid missing them- Frequent re-evaluation and continuous monitoring rapidly recognise when

patient is deteriorating

5. P AIN M ANAGEMENT

- Intravenous analgesia as appropriate

ABDOMINAL TRAUMA

TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA

- Solid organ injury: spleen, liver – bleeding (may be quite massive)- Hollow viscus injury with rupture- Vascular injury with bleeding

INDICATIONS FOR IMMEDIATE LAPAROTOMY

- Evisceration, stab wounds with implement in-situ, gunshot wounds traversingabdominal cavity

- Any penetrating injury to the abdomen with haemodynamic instability or peritonealirritation

- Obvious or strongly suspected intra-abdominal injury with shock or difficulty instabilising haemodynamics

- Obvious signs of peritoneal irritation- Rectal exam reveals fresh blood- Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries

excluded as source of bleeding)

- X-ray evidence of pneumoperitoneum or diaphragmatic rupture

INVESTIGATIONS- If patient is stable: FAST and/or CT scan- If patient is unstable: FAST and/or DPL

FOCUSED ABDOMINAL SONOGRAPHY IN TRAUMA (FAST)

- Ultrasonographic evaluation of four windows: Pericardial, right upper quadrant, leftupper quadrant, pelvis

- Advantages Portable Can be done quickly in


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CT SCAN

- Only suitable for stable patient as quite long time involved in imaging with only patient in the room can collapse

- Advantages Able to precisely locate intra-abdominal lesions preoperatively Able to evaluate retroperitoneum Able to identify injuries that can be managed non-operatively Not invasive

- Disadvantages Expensive Time required to transport patient Use of contrast

DIAGNOSTIC PERITONEAL LAVAGE (DPL)

- Involves making a cut in the infraumbilical region and inserting a catheter into the peritoneal cavity, aspirate, then instillation of saline and re-aspiration

- Posi t ive DPL Frank blood (>5ml) or obvious bowel contents aspirated Lavage fluid seen to exit from chest drain or urinary catheter

RBC >100,000 per mm3, WBC >500, Gram stain positive for bacteria in effluent

- Ind icat ions: Any unstable patient with suspicion of abdominal trauma or where clinical exam

is difficult or equivocal Unexplained hypotension in multiple trauma Patient requiring immediate surgery for extra-abdominal injuries

- Contra indicat ions Absolute indication for laparotomy already exists Previous abdominal surgery or infections Gravid uterus Morbid obesity

Coagulopathy

- Advantages Can promptly reveal or exclude the presence of intraperitoneal haemorrhage Valuable in discovery of potentially lethal bowel perforation

- Disadvantages Morbidity involved – wound complications (haematoma, infection);

intraperitoneal injury False negative rate of 2% when there is failure to recover lavage fluid, early

hollow viscus injury, diaphragmatic injuries, injuries to retroperitoneal structures

CARDIOTHORACIC TRAUMA

There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving:

cardiac tamponade, airway obstruction, flail chest, haemothorax, and pneumothorax.

CARDIAC TAMPONADE

- High index of suspicion required

- Clinical features

Chest trauma and hypotension Beck‘s triad (hypotension, muffled heart sounds, distended neck veins) – only

seen in 50% of cases as hypovolaemia may prevent neck vein distension; muffled

heart sounds are least reliable Pulseless electrical activity Kussmaul‘s signs (increased neck distension during inspiration, pulsus paradoxus)

- Diagnost ic clues Enlarged cardiac shadow in CXR (globular heart – very rarely seen) Small ECG voltages, electrical alternans (uncommon) Pericardial fluid demonstrated on FAST or 2D-echo - definitive

- Management

Aggressive fluid resuscitation – helps maintain cardiac output and buys time Pericardiocentesis: ECG lead-guided or 2D-echo guided

AIRWAY OBSTRUCTION

- Chin lift or jaw thrust- Remove any foreign body manually, suction blood/secretions- Definitive airway – ETT, cricothyroidotomy, tracheostomy

FLAIL CHEST

- When 2 or more ribs are fractured at 2 points forming a flail segment that moves paradoxically with breathing

- Results in hypoxaemia mainly due to underlying pulmonary contusion, contributed to by pain with restricted chest wall movement

- Management: ensure adequate oxygenation and ventilation; judicious fluid therapy(avoid fluid overload); adequate intravenous analgesia

- Consider mechanical ventilation in high risk patients: shock, severe head injury, previous pulmonary disease, fracture of >8 ribs, age > 65, >3 associated injuries


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HAEMOTHORAX

- Chest tube insertion in the triangle of safety (bound by the lateral border of the pectoralis major medially, a line just anterior to the mid-axillary line laterally, and the

upper border of the fifth rib inferiorly)

- Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot- If blood >1500mls massive haemothorax, call urgent cardiothoracic consult

PNEUMOTHORAX (OPEN/TENSION)

- Tension pneumothorax is a clinical diagnosis (CXR will only delay treatment, andmay cause death) – signs of pneumothorax, hypotension, neck vein distension, severerespiratory distress

- Immediate needle thoracotomy in second intercostal space in mid-clavicular line- Followed by chest tube insertion

- Open pneumothorax occurs in a large chest wall defect with equilibration betweenintrathoracic and atmospheric pressure, producing a ―sucking chest wound‖

- Cover defect with a sterile dressing, taping it down on 3 sides to produce a flutter-valve effect, letting air out of the pleural cavity but not back in

- Insert chest tube (not through the wound)

NEUROSURGICAL TRAUMA

AIM in management of head injuries is the prevention of secondary brain injury (fromhypotension, hypoxaemia, increased ICP etc) since neuronal death is irreversible.

PATHOLOGIES:

1. Concussion

- Physiological dysfunction without anatomical or radiological abnormality- (Physiological dysfunction is the first step towards cell death, but is reversible if

no further insult occurs)

- Usually recovers in 2-3 hours

2. Contusion

- Small haematoma


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2. Fixed dilated pupil

- Constrictor fibres to the pupil run in the oculomotor nerve, which exits the brainstem at the upper midbrain – nerve fibres lie just under the tentorium

- Uncus of the temporal lobe sits on the tentorium- In raised ICP, the uncus herniates over the edge of the tentorium,

compressing the fibres of the oculomotor nerve just below

- Thus a fixed dilated pupil occurs on the side of the compression due tounoppressed sympathetic supply (dilates the pupil)

3. Cushing’s reflex - A triad of:

(a) Raised ICP(b) Hypertension(c) Bradycardia

- From Monroe-Kellie doctrine, an increase in mean arterial pressure helps tomaintain cerebral perfusion pressure when ICP is raised

- Increase in mean arterial pressure achieved by sympathetic overdrive:(a) Increased heart rate(b) Increased contractility(c) Increased vasoconstriction – increased total peripheral resistance(a) and (b) increase cardiac output increased BP; (c) increases BP

- Baroreceptors detect abnormally raised blood pressure and try to decrease it heart rate falls

MANAGEMENT

1. Assessment

- 3 important parameters: ABCs, GCS, pupil size- Glasgow coma scale (see above) – Minor head injury: 14-15; moderate injury: 8-

13; severe injury: 3-7

2. Minor head in jury

- Most common- Indications for admission: Persistent headache and/or vomiting CSF leak Neurological deficit Skull fracture History of loss of consciousness Amnesia

- In ward: NBM, IV drip (no dextrose saline!), no sedation, monitor GCS

- If patient deteriorates CT scan, exclude metabolic causes (e.g. hypoglyc), doseptic workup (exclude sepsis)

3. Moderate head injury

- All will be CT-scanned at ED NES will operate if any indication to do so- In ward: as per mild head injury

4. Severe head injury

- Must scan to look for reversible causes of raised ICP but stabilise patient first

- Medical methods to lower ICP(a) Intubate and hyperventilate(b) IV mannitol (must catheterise patient also; do not give if patient is unstable)

- Screen for other life-threatening injuries (likely to be multi-trauma patient)

- Achieve haemodynamic stability(a) Check for long bone fractures(b) FAST for bleeding into abdominal cavity(c) ABG to detect acidosis(d) Keep monitoring patient and re-investigate where appropriate

- Operate if reversible cause found(a) Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced

after blood evacuated) [Burrhole usually not big enough to drain an acute bleed]

(b) Evacuate clot(c) Insert endoventricular drain (EVD) if there is hydrocephalus

- Total sedation after operation, ward in ICU Prevents patient from struggling which will raise ICP

5. Depressed skull fractur e

- Can leave alone unless depression is greater than the thickness of the skull bone

6. Compound depressed fracture

- There is through-and-through skin laceration over the fracture- Always explore to ensure underlying dura is intact, and repair if dura is torn

(since meningitis can occur with a torn dura)


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MUSCULOSKELETAL TRAUMA

GENERAL POINTS

- Extremity trauma tends not to be life-threatening- But occult blood loss can occur in large volumes especially in certain types of

injuries – pelvic fracture (up to 3L), femoral shaft fracture (up to 2L)- Need to have high level of suspicion and treat with urgency- Look out for any tachycardia, early signs of shock- Prepare to resuscitate patient

ASSESSMENT OF THE EXTREMITY

- Perfusion: colour, pulses, skin temperature, capillary refill- Deformity- Wounds – open or closed injury; abrasion over a fracture is considered open fracture- Soft tissue assessment- Abnormal joint mobility – ligamentous injury around the joint; if in the knee, highly

likely that the popliteal artery is injured as well

- Neurological assessment- Viability of the limb

THE PULSELESS EXTREMITYThings to consider

- Is pulselessness due to shock?- Arterial or venous compromise?- Is there compartment syndrome (pulselessness is a very late sign)- Any pre-existing vascular disease?

Physical examinat ion

- Any limb deformity (can result in kinking of vessels)?- Any joint instability (dislocation of a joint can result in intimal tear in the major

vessel running across it, with thrombosis and occlusion)?

- Skin colour/temperature- Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent

angiogram!

SOFT TISSUE INJURIES

Types

- Open: laceration, abrasion- Crushing- Degloving: open or closed- Closed

Wound care

- Swabs of the wounds for culture and sensitivity- IV antibiotic prophylaxis- Tetanus toxoid cover- Photograph wound (to prevent re-opening of wound by every doctor that comes to

see patient)

- Betadine dressing- In OT: generous debridement, irrigation (within 4-8 hours, especially in open

fractures), fracture stabilisation (internal or external fixation depending on Gustilo

classification)- Leave wound OPEN

MANAGEMENT OF FRACTURES

- Recognise fracture and/or dislocation- Complete neurovascular examination of the limb involved before reduction- Appropriate X-rays (at least 2 planes)- Analgesia- Correction of deformity- Temporary immobilisation – backslab, malleable splint- Neurovascular examination; examine for compartment syndrome- Circulation chart

OPEN FRACTURES

Definition: there is communication between the fracture or fracture haematoma and theexternal environment

Gusti lo-Andersen classi f ication

Type I 1cm AND no extensive soft tissue damage, avulsions or flaps

Type II IA Extensive soft tissue damage, avulsions or flaps but adequate softtissue coverage of bone OR

High-energy trauma cause irregardless of size of woundType II IB Extensive soft tissue loss with periosteal stripping and exposure of

bone. Massive contamination common

Type II IC Arterial injury requiring repair


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- Grade I Low velocity injury, prognosis similar to closed fracture Treat with ORIF within 6 hours

- Grade II Moderate velocity, more trauma

- Grade IIIA Skin graft usually possible

- Grade IIIB

Skin graft alone often not adequate Local and free flaps will be necessary Secondary bone procedures

- Grade IIIC Neurovascular injuries present in addition to musculoskeletal injuries

Management of open fractures

- Recognise an open fracture- Stabilise patient first

- Pain relief and analgesia- Cover the wound with moist gauze- Temporary immobilisation and splinting- IV broad spectrum antibiotics- Appropriate X-rays- Nil by mouth- Pre-op investigations: FBC, U/E/Cr, PT/PTT, GXM, ECG, CXR- Arrange for emergency operation- Angiogram if needed

Surgery involves:

(a) Generous debridement of the wound with irrigation to decrease bacterial load

(b) Treat any soft-tissue injuries(c) Stabilise fracture – usually using external fixator


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ABDOMINAL PAIN

RHC Epigastr ic LHC

Thoracic

Pneumonia Pleural effusion

Biliary

Cholangitis Cholecystitis

Gallstone disease

Hepatic

Hepatitis (viral, autoimm etc) Hepatomegaly Abscess

Others

Subphrenic abscess

Pancreatitis PUD Appendicitis

Thoracic

MI Pericarditis Aortic aneurysm

Gastrointestinal

Oesophagitis

GERD PUD Gastric outlet obstructn CA stomach

Others

Pancreatitis Thoracic

Pneumonia Pleural effusion MI

Gastrointestinal

PUD

Diverticulitis Mesenteric ischaemia

Others

Subphrenic abscess Splenomegaly Pancreatitis

Rt Loin Per iumbi l ical Lt Loin

Biliary (see RUQ)

Urological

Infection

Pyelonephritis Abscess

Others

PKD

Renal cyst Angiomyolipoma Infarction

Obstruction

Hydronephrosis Nephrolithiasis Ureteral obstruction

CA

RCC TCC renal pelvis Bladder ca (ureteral obstructn)

Others

Appendicitis

Gastrointestinal

Appendicitis (early) I/O Mesenteric ischaemia Colitis IBD

Others

Aortic Aneurysm Pancreatitis

Spleni c disease

Urological (see Rt Loin)

RIF Hypog astric LIF

Gastrointestinal

Appendicitis Terminal ileitis Meckel‘s diverticulitis Mesenteric ischaemia Mesenteric adenitis IBD Colitis Colorectal CA

Hernia

O&G

Ovarian cyst Ovarian torsion Ectopic pregnancy PID

Orthopaedics (See LIF)

Gastrointestinal

Colorectal CA

Urological

ARU Bladder calculi Cystitis / UTI

O&G

Ectopic pregnancy Abortion PID Uterine rupture Fibroid complications Adenomyosis Endometriosis

Orthopaedics

Infection Septic hip arthritis TB hip

Degeneration

OA hip

Inflammation

RA hip Ankylosing spondylitis Reiter‘s syndrome

Inflitration

1o bone tumour (hip) Metastasis to hip

Destruction

# - NOF, pubic rami

Radiation

Back pathologies (referred pain)

Paediatric ortho condition s

Transient synovitis Perthes‘ dz SCFE

Gastrointestinal

Diverticulitis IBD

Colitis Colorectal CA Hernia

O&G (see RLQ)


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ABDOMINAL MASS

RHC Epigastr ium LHC

LiverMassive

Cancer: HCCMetastases

Myeloprolftve dz

Alcoholic liver dz Rt ht failure/tricuspid regurg

Moderate Above causes Lymphoprolftve dz Haemochromatosis Amyloidosis

Mild

Above causes Infxns: Viral – Hep, IMS

Bacterial – abscessParasitic – hydatidcyst, amoebic abscss

Biliary obstruction Cirrhosis

Gallbladder

Pancreatic/periampullary ca Acute cholecystitis Hydrops Empyema Mirizzi syndrome

Ascendin g colon

Cancer Diverticular mass/abscess Faeces

Right adrenal gland

Right k idney(see Rt lumbar )

Li ver (see RHC)

Pancreas

Pseudocyst Tumour

Transverse colon


Stomach

Cancer Distension (GOO)

Aorta

Aortic aneurysm

Retroperitoneal lNpathy

Lymphoma Teratoma Other malignancies

SpleenMassive

Infxns CML Myelofibrosis

Moderate

Above causes

Portal hypt Lymphoprolftve dz

(lymphoma, CLL)

H‘lytic anaemia (thal, HS) Storage dz (Gaucher‘s)

Mild

Above causes Infxns: Viral hep, IMS

Endocarditis

Autoimm – SLE, RA, PAN Myeloprolftve dz – PRV,

essential thrombocytopaenia

Infiltratn – sarcoid, amyloid

Stomach

Descending colon


Left k idney(see Rt lumbar)

Left adrenal gland

Right Lumbar Umbi l ica l Left Lumbar

Right Kidney

Hydro/pyonephrosis Cancer – RCC Polycystic dz Single cyst Amyloidosis Tuberous sclerosis, VHL

Right adrenal gland

Li ver (see RHC)

Ascending colon mass


Li ver (see RHC)

Stomach(see Epigastrium)

Small in testine

Obstruction

Mesenteri c cyst

Pancreas (see Epi gastri um)

Aorta

Aortic Aneurysm

Retroperitoneal lNpathy

Lymphoma Teratoma Other malignancies

Spleen (see LH C)

Left ki dney (see ri ght lumbar )

Descending colon


RIF Hypogastr ium LIF

Gastrointestinal

Appendiceal mass/abscess TB gut Ca caecum Distended caecum (due to

distal obstruction)

Crohn‘s dz (terminal ileitis)

Orthopaedics Chondroma/sarcoma of ilium Bony metastasis

O&G

Ovarian cyst/tumour Fibroids Urogenital:

Transplanted kidney Bladder diverticulum Ectopic or undesc testisVascular: Iliac artery aneurysm Iliac lymphadenitisSkin & Msk:

Psoas abscess

Bladder

Acute retention of urine Chronic retention of urine

Anal /rectal mass

Cancer

Uterus

Gravid uterus Fibroids Tumour

Ovary

Cyst Tumour

Gastrointestinal

Diverticular mass/abscess Ca colon/sigmoid Crohn‘s dz (terminal ileitis) Faeces

Similar causes as RI F mass


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OESOPHAGEAL DISEASES

ANATOMY

- Oesophagus is a muscular tube that is 25cm (10 inches) long

- Starts at the cricoid cartilage (C6 vertebra) from the oropharynx and continues intothe stomach at the level of T10

- Upper oesophageal sphincter is formed by cricopharyngeus muscle

- Lower sphincter is not an anatomical sphincter, but physiological:

(i) Increased tone of the muscularis propria at the lower oesophageal sphincter(ii) Fibres of the right diaphragmatic crus loop around the cardio-oesophageal

junction and ontract during coughing, sneezing etc when intra-abdominal pressure increases, thus preventing reflux

(iii) Angle of His where the oesophagus joins the stomach – acts as a valve

(iv) Intra-abdominal pressure being higher than intra-thoracic pressure

- 3 narrow points along the course of the oesophagus

(i) Cricopharyngeus muscle (15cm from incisor teeth)

(ii) Carina where the left bronchus crosses the oesophagus (27cm from incisors)

(iii) Where the oesophagus passes through the diaphragm (40cm from incisors)

- Structure: mucosa, submucosa, muscularis propria, adventitia (no peritoneal liningexcept for a short segment of intra-abdominal oesophagus)

Muscularis propria is composed of striated muscle in the upper one-third, striated andsmooth muscle in the middle third, and smooth muscle in the lower third

- Blood supply (roughly divided into thirds): Inferior thyroid artery to upper third,oesophageal branches of the aorta to the middle third, oesophageal branches of left

gastric artery to lower third

- Venous return also divided into thirds: Brachiocephalic veins (upper), azygos veins (middle), left gastric vein (lower) --- a portosystemic anastomosis exists at the lower

oesophagus thus leading to formation of varices in portal hypertension

PHYSIOLOGY OF SWALLOWING- Process of mastication forms a food bolus on the dorsum of the tongue

- The tongue then contracts upwards and backwards pushing the food bolus against thehard palate

- Soft palate elevates (contraction of palatoglossus) to close off nasopharynx

- Further elevation of tongue pushes food bolus into oropharynx

- As the base of the tongue is elevated posterior, the epiglottis falls back; at the sametime, the pharyngeal muscles contract to bring the posterior surface of the larynx

upwards to make the laryngeal inlet smaller closed off by the epiglottis

- Pharyngeal muscles contract to propel food bolus past the relaxed cricopharyngeusinto the oesophagus

- Once in the oesophagus, involuntary contractions of the muscularis propria form peristaltic waves to propel food bolus into stomach

APPROACH TO DYSPHAGIA

CAUSES OF DYSPHAGIA

- Dysphagia can be divided into oropharyngeal and oesophageal dysphagia- In each anatomic region the dysphagia can be caused by neuromuscular dysfunction

(impaired physiology of swallowing) or mechanical obstruction to the lumen

Oropharyngeal Oesophageal

Neuromuscular diseases Neuromuscular diseasesStroke

Parkinson’s disease

Brain stem tumours

Degenerative conditions e.g. ALS, MSPeripheral neuropathy

Myasthaenia gravisMyopathies e.g. myotonic dystrophy

Achalasia

Spastic motor disordersDiffuse oesophageal spasm

Hypertensive lower oesophageal sphincter

Nutcracker oesophagusScleroderma

Obstructive lesions Obstructive lesionsTumoursInflammatory masses e.g. abscess

Oesophageal webs

Pharyngeal pouch (Zenker‘s divert) Anterior mediastinal mass

Intrinsic structural lesionsTumoursStrictures: Peptic (reflux oesophagitis)

Radiation

Chemical (caustic ingestion)

Medication Lower oesophageal rings (Schatzki‘s ring) Oesophageal webs (Plummer-Vinson)

Foreign bodies

Extrinsic structural lesionsVascular compression (enlarged aorta or

left atrium)Mediastinal masses – retrosternal thyroid,

lymphadenopathy

OthersOesophagitis: Reflux

Infectious (candida, herpes)

Radiation-induced

Medication-induced

Chemical-induced (alcohol)


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HISTORY:

1. Is there odynophagia (pain associated wi th di f f icu l ty swallowing)?

- Signifies some form of oesophagitis : infectious (candida, herpes), post-radiation,chemical-induced (usually alcohol), reflux oesophagitis

- Oesophageal spasm- Scleroderma- Pain occurs late in achalasia and oesophageal cancer (not painful from the start)

2. Di f ferent ia t ing oropharyngeal from oesophageal dypshagia

(i) Oropharyngeal- Presenting complaint is usually of difficulty in initiating swallowing - May be associated with choking, coughing, nasal regurgitation- Voice may sound nasal (bulbar palsy)- Cause of oropharyngeal dysphagia is usually neuromuscular rather than

mechanical; stroke is the most common cause

(ii) Oesophageal- Presenting complaint is that of food “getting stuck” in the throat or chest - Patient‘s localisation of the symptom often does not correspond to actual site

of pathology

- Can be due to either neuromuscular dysfunction or mechanical obstruction

3. Di f ferent ia t ing mechanical obstruct ion from neuromu scular dysfunct ion

(i) Mechanical- Patient complains of more difficulty swallowing solids than fluids- May have regurgitation of undigested food- Recent onset dysphagia that is progressively worsening, with loss of weight high suspicion of oesophageal cancer

- Intermittent symptoms are suggestive of webs, rings

(ii) Neuromuscular- Patient complains of more trouble swallowing fluids than solids- Dysphagia more long-standing, slowly progressive- Intermittent symptoms suggestive of diffuse oesophageal spasm, nutcracker

oesophagus- May have history of stroke, neuromuscular disease

4. History of predisposing condi t ions - Reflux symptoms e.g. retrosternal burning pain (heartburn), sour fluid reflux into

mouth (acid brash), excessive salivation (water brash), postural aggravation on

lying down

- Caustic chemical ingestion in the past- Smoking, chronic alcohol intake- Radiation to the chest

- Medication history- Symptoms of systemic disease e.g. stroke (focal neurological deficits),

scleroderma (telangiectasia, sclerodactyly, calcinosis, Raynaud‘s), Parkinson‘s

5. Systemic review - Loss of weight occurs in cancer and achalasia, but of much later onset in

achalasia compared to cancer

- Symptoms of anaemia (bleeding from tumour, or as part of Plummer-Vinsonsyndrome)

- Symptoms of aspiration pneumonia – fever, cough, shortness of breath

6. Tumour spread - Hoarseness (recurrent laryngeal nerve)- Fever, cough and haemoptysis (tracheo-oesophageal fistula)- Haematemesis (invasion into aorta)- Neck lump (lymph node)

PHYSICAL EXAMINATION

1. General condi t ion - Vitals: the patient may be hypovolaemic from vomiting/decreased intake- Nutrition: presence of cachexia

- Conjunctival pallor : bleeding from tumour, oesophagitis ulcerations, orassociated with P-V syndrome

- Scleral icterus: metastases to liver- Dehydration (mucous membranes, skin turgor, etc)

2. Disease

- Presence of cervical lymph nodes (esp Virchow‘s node) - Scars/marks over the chest and abdomen suggesting previous surgery, radiation- Palpable mass in abdomen (not likely)- Hepatomegaly- Ascites- PR examination for malaena

3. Compl icat ions of disease - Signs of pneumonia: patient febrile, may be toxic, lung crepitations, decreased

air entry usually over right lower lobe

4. Treatment - Tube feeding through NG tube, gastrostomy/jejunostomy – if aspirates seen,

what is the colour?- Total parenteral nutrition


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MANAGEMENT

1. Stabil ise patient - Resuscitate if patient is haemodynamically unstable- IV fluids (correct fluid deficits and also any electrolyte derangements)- Consider feeding with fluids if patient can tolerate it (only having problems with

solid food) otherwise consider tube feeding or TPN need to correct patient‘snutritionally debilitated state

- Keep NBM if patient cannot tolerate even fluids- Treat any aspiration pneumonia – NBM, IV antibiotics

2. Investigate for underlying cause and treat it

INVESTIGATIONS

Diagnost ic

1. Barium swallow

- Advantage of barium swallow is that it is less invasive than OGD, especiallywhen suspecting webs, diverticula in the oesophagus where OGD may cause

perforation; however if patient is at high risk of aspiration, barium swallow is

dangerous.

- Visualisation of obstructive lesions:o

Shouldering of a stricture (benign strictures form a smoother contour

whereas malignant strictures form a more right-angled contour)

o Bird‟s beak sign of achalasia

Achalasia Benign stricture Carcinoma

- Visualisation of pharyngeal pouch or oesophageal diverticulum- Diffuse oesophageal spasm gives a corkscrew appearance

2. Oesophagogastroduodenoscopy (OGD)

- Advantage is direct visualisation of the lesion and ability to take tissue biopsy (especially useful in malignancy), may also be therapeutic (stopping bleedingfrom a tumour, stenting the lumen, etc)

3. Manometry

- Gold standard for diagnosing achalasia:(i) Absence of peristalsis(ii) Very high pressures at the lower oesophageal sphincter(iii) Absence of relaxation at the LES on swallowing food

4. Videofluroscopic examination of swallowing (VFES) or flexible-endoscopicexamination of swallowing (FEES)

- Used to assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various consistencies of food during swallowing

Support ive

1. Blood investigations:

- Full blood count – Low Hb (anaemia from chronic blood loss)High TW (aspiration pneumonia)

- Urea, electrolytes, creatinine – electrolyte disturbances from vomiting, poorintake; raised creat and urea in dehydration (creat will be raised more than urea if

patient has prerenal failure from dehydration)

- Liver function tests – low albumin with nutritional deprivation

2. CXR- Consolidation (aspiration pneumonia)

3. 24-hour pH probe monitoring

- If patient complains of reflux symptoms and no signs are seen on OGD (see latersection on Gastro-oesophageal reflux disease)


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CANCER OF THE OESOPHAGUS

EPIDEMIOLOGY- Third most common gastrointestinal tract cancer in Singapore- Male predominance- Increasing incidence with age

RISK FACTORS

- Smoking (100x increased risk for SCC, 10x for adenocarcinoma)

- Alcohol (2x increased risk)

- Obesity (related to reflux, increases adenocarcinoma incidence)

- Diet: Hot beverages, preserved foods (nitrosamines), betel nuts; vitamin and mineraldeficiencies (selenium, vitamin E, beta-carotene)

- Tylosis (autosomal dominant disorder with keratosis of palms and soles

- Barrett‘s oesophagus (intestinal metaplasia of oesophageal mucosa due to reflux;increased risk of cancer due to metaplasia-dysplasia-carcinoma sequence; risk is 30-40x higher than in individual without Barrett‘s, and is about 1% per year)

- Achalasia (2-8% incidence of SCC)

- Caustic injury (ca occurs at site of scar/stricture, mostly middle third of oesophagus)

- Plummer-Vinson (or Paterson-Brown-Kelly) syndrome – Post-cricoid oesophagealweb and iron deficiency anaemia. (10% develop cancer in upper third of oesophagus)

PATHOLOGY

- 70% squamous cell carcinoma, 30% adenocarcinoma

- SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lowerthird and gastro-oesophageal junction (related to reflux and Barrett‘s oesophagus)

- Overall: 10% of cancers occur in the upper third, 60% in the middle third, 30% in thelower third

- Three growth patterns: Fungating (60%)

Ulcerative (25%) Infiltrative (15%)

- Tumour spread: direct extension into surrounding structures, vascular invasion,lymphatic spread

- Common sites of metastases: liver, lung, bone

STAGING

T Tis

T1a

T1b

T2

T3

T4

High-grade dysplasia/carcinoma in-situ

Tumour invading lamina propria or

muscularis mucosaTumour invading submucosa but does

not breach submucosaTumour invades the muscularis propria

Tumour invades adventitia

Invasion of surrounding structures

N N1 Regional node involvement (1-3 nodesinvolved =1a; 4-7=1b; >7=1c)

M M1a M1b

Nonregional lymph node involvementOther distant metastases

PRESENTATION

Usually of insidious onset, with earliest symptoms being non-specific e.g. retrosternal

discomfort, ―indigestion‖, and most patients already have advanced disease when theyare diagnosed – 75% have lymph node involvement at time of diagnosis.

1. Dysphagia- Present in 80% of patients – most common presentation- Pain develops late and is usually due to extra-oesophageal involvement

2. Weight loss

3. Regurgitation

4. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult)5. Vocal cord paralysis (left more than right)

6. Aspiration pneumonia

7. Tracheo-oesophageal or broncho-oesophageal fistula

INVESTIGATIONS

Diagnosis

1. Barium swallow- 92% accuracy in showing mucosal irregularity and annular constrictions but not

able to diagnose malignancy with confidence

2. Oesophagogastroduodenoscopy- Allows biopsy of the lesion confirmatory histological diagnosis

Staging

1. Endoscopic ultrasound- If endoscope can pass around the lesion, the EUS is good for T staging, and also

to identify enlarged regional lymph nodes

Stage T N M

0 is 0 0

I 1 0 0

IIA 2 / 3 0 0

IIB 1 / 2 1 0

III 3

4

1

any

0

0

IVA any any 1a

IVB any any 1b


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2. Chest X-ray- Presence of any lung metastases- Aspiration pneumonia- Pleural and/or pericardial effusion- Tracheal deviation or extrinsic compression of tracheobronchial system- Widened superior mediastinum in an upper oesophagus tumour- Raised hemidiaphragm with phrenic nerve involvement

3. CT scan or MRI of the thorax with extension to include liver and adrenals- Can be used for T, N, and M staging

4. Bronchoscopy- Exclude bronchial involvement especially in tumours involving upper two-thirds

of oesophagus

5. Bone scan for bony metastases

6. Laryngoscope to assess for vocal cord paralysis

Support ive

1. Full blood count – Low Hb (anaemia from chronic blood loss)High TW (aspiration pneumonia)

2. Urea, electrolytes, creatinine – electrolyte disturbances from vomiting, poor intake;raised creat and urea in dehydration (creat will be raised more than urea if patient

has prerenal failure from dehydration)

3. Liver function tests – low albumin with nutritional deprivation

TREATMENT

Princip les

- Three modalities available – surgery, chemotherapy, radiotherapy – used singly or incombination

- Aims of treatment: Curative or palliative (50% of patients have unresectable canceron presentation)

- Surgical treatment is usually performed with curative intention, but can also achievegood long-term palliation of symptoms

- Choice of treatment depends on several patient factors: age, co-morbidities,nutritional state, life expectancy, and prognosis of cancer

Surgery

- Curative in early lesions (in-situ, T1a) and part of multimodal therapy in moreadvanced stages

- Resection should not be done in patients with distant metastases or contraindicationsto surgery

- Endoluminal surgery – for early lesions; no attempt to remove any LNs (usually noLN involvement)

- Oesophagectomy

(i) Ivor-LewisTwo-stage procedure involving gastric mobilisation (first stage, done through

upper midline abdominal incision), oesophagectomy and gastro-oesophagealanastomosis in the chest (second stage, through right thoracotomy incision)

(ii) Trans-hiatal

Done via two incisions – one in the abdomen and one in the neckBlunt oesophagectomy, gastric mobilisation, and gastro-oesophageal

anastomosis in the neck

Less morbidity than Ivor-Lewis as the chest is not opened, but controversial

(iii) Tri-incisionalThree incisions – abdominal, chest, and also left neck incision for gastro-

oesophageal anastomosis in the neck

Performed with two-field lymphadenectomy (upper abdominal and mediastinal)

No difference in survival between trans-hiatal and I-L modalities; the stage of thecancer when the operation is performed is a greater factor influencing survival

Radical en-bloc dissections not shown to improve survival

Oesophagectomies have high mortality (5%) and morbidity (25%) rates, thus patients have to be carefully selected in order to maximise survival benefit fromsurgery

Complications of surgery dependent on extent of surgery and incisions used- Intraoperatively, injury to lung, thoracic duct, RLN can occur

- Respiratory complications higher in thoracotomies – atelectasis, pneumonia- Anastomotic leak and resultant mediastinitis (for chest anastomosis) most feared

- Reflux can result in the long term due to loss of the LES

- Anastomotic stricturing can also occur

- Palliative debulking for obstructive symptoms

Radiotherapy- Usually given in combination with chemotherapy- Primary treatment for poor-risk patients; palliation for unresectable lesions with

obstructive symptoms, pain and bleeding- SCCs are radiosensitive- Modalities: External beam radiation or brachytherapy- Obstructive symptoms may worsen temporarily after radiotherapy due to oedema- Complications: tracheo-oesophageal fistula, stricture

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Chemotherapy - Current regimen: 5-Fluorouracil and cisplatin- Addition of chemotherapy to external beam radiation for unresectable cancers shown

to have improved survival compared to EBRT alone

- Chemotherapy given preoperatively and postoperatively improves survival

Overall curativ e treatment

Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection),

oesophagectomy, and postoperative adjuvant chemoradiotherapy for responsive

tumours

Pall iative treatment

- Surgical debulking- Bypass surgery rarely done nowadays- Endoscopic laser fulguration to relieve obstruction- Photodynamic therapy is a new treatment option- Stenting to maintain lumen patency

Feeding in oesophageal obstruct ion

- Feeding via oropharyngeal route is preferred unless the passage is obstructed or it isunsafe for the patient to feed via that route (i.e. risk of aspiration)

- If still able to pass NG tube around tumour feed via NG (but also consider

complications with long-term NG placement e.g. erosions around nasal area,sinusitis); consider PEG placement for long-term feeding if able to get scope aroundtumour

- If unable to pass tube or scope around tumour, consider open gastrostomy- Total parenteral nutrition is another option but has more complications, more costly- Relief of obstruction via various techniques as listed above help to enable oral

feeding, but most techniques are not long-lasting and dysphagia will return withtumour growth

PROGNOSIS- 80% mortality at 1 year, overall 5-year survival


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- Reflux can also lead to pulmonary symptoms: chronic cough, chest infections(aspiration)

- Other symptoms: globus (feeling of a lump at the throat), chest pain (can mimicanginal pain with radiation to neck, jaw, arm), nausea, water brash (hypersalivation in

response to reflux)

COMPLICATIONS1. Pain and spasm

2. Stricture

3. Haemorrhage (occult more common than frank)4. Shortening of oesophagus

5. Ulceration

6. Barrett‘s oesophagus (see below) 7. Dysmotility

8. Schatzki‘s ring (constrictive ring at the squamocolumnar junction composed ofmucosa and submucosa)

9. Malignancy (adenocarcinoma arising from Barrett‘s oesophagus)

DIAGNOSIS

1. History is important as most patients with reflux are seen in the primary setting

with no facilities for detailed investigation- Exclude cardiac cause of chest pain, and exclude malignant cause of dysphagia

2. Oesophagogastroduodenoscopy- Cannot actually diagnose reflux- Can visualise and grade oesophagitis if present, and take biopsy specimens for

confirmation (see below)- May see a hiatal hernia which is associated with reflux (though not all patients

with hiatus hernia will have reflux)

3. Oesophageal pH probe

- Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probeespecially if oesophagitis is not seen on OGD

- Antimony probe most commonly used; alternative is the Bravo capsule (awireless capsule that is temporarily attached to the oesophageal wall)

- The probe is placed 5cm above the manometrically-determined upper limit of theLES (for the wired probe), or 6cm above the endoscopically-determined

squamocolumnar junction (for the wireless capsule)

- Diagnosis based on the percentage of time in 24hrs the pH reading is below 4

4. Barium swallow and follow-through- Not of much value in diagnosing reflux

- Can detect motility disorders that cause reflux, and also pick up oesophagealulceration and stricturing resulting from reflux

- Can sometimes see reflux of barium contrast into oesophagus

5. Manometry- No value in reflux except for detecting motility disorder

GRADING OF OESOPHAGITIS

1. Savary-Mil ler classi f icat ion

Grade I: One or more supravestibular non-confluent reddish spots, with orwithout exudates

Grade II: Erosive and exudative lesions, may be confluent but not circumferentialGrade III: Circumferential erosions covered by haemorrhagic and

pseudomembranous exudate

Grade IV: Presence of chronic complications such as deep ulcers, stenosis, orscarring with Barrett‘s metaplasia

2. Los Ang eles classi f icat ion

Grade A: one or more mucosal breaks, each 5cm long, but not between the tops of

adjacent mucosal folds

Grade C: at least one mucosal break that is continuous between the tops of adjacentmucosal folds, but which is not circumferential

Grade D: mucosal break that involves at least three-quarters of the luminalcircumference

- Relevance of classification schemes: subjective and dependent on assessment by theendoscopist; also, due to the multitude of classification schemes available, just

mentioning a grade may not have any meaning if the actual abnormalities are notdescribed

TREATMENT

Li festy le

1. Diet and eating habits

Avoid coffee, chocolate, fatty foods, or anything that worsens symptoms Do not eat 2 hours prior to sleeping Walk after eating Avoid excessive eating; eat small meals

2. Avoid drugs that relax LES e.g. anticholinergics, muscle relaxants, etc.

3. Weight reduction if obese

4. Elevate head of bed

5. Smoking and alcohol intake cessation

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Medicat ion

1. Acid suppression therapy: proton pump inhibitors or H2-receptor antagonists

2. Prokinetics to increase LES pressure e.g. domperidone, metoclopramide

Surgica l

- Indications: Failure of medical therapy (or incomplete resolution of symptoms) Oesophagitis with frank ulceration or stricture Complications of reflux oesophagitis – respiratory complications, Barrett‘s

oesophagus Severe symptoms or progressive disease Compliance problems - patient does not want to be on medication for life

(despite good results)

- Goal of surgery: Increase pressure at the gastro-oesophageal junction but not so much that it

prevents food from entering the stomach (too tight dysphagia)

- Surgery versus conservative treatment Surgery has higher rates of cure and better long-term results No need to adhere to strict lifestyle and diet change as well as long-term

medication

Disadvantage of surgery is the associated morbidity and mortality

- Fundoplication is the mainstay of surgical therapy

Can be done via open surgery or laparoscopic surgery (most laparoscopic now)

Nissen fundoplication is the most commonly done – a 360 degree (total) wrap ofthe fundus around the gastro-oesophageal junction

Partial fundoplications can also be done in patients where oesophageal motilityis poor or the oesophagus is foreshortened; anterior 90 degrees, anterior 180 deg,and posterior 270 deg fundoplications are various options available

- Complications of surgery

Perforation of the oesophagus – most feared complication, may result in

mediastinitis if not promptly detected and repaired intraoperatively Excessively tight wrap resulting in dysphagia

Excessively loose or short wrap – reflux recurs (failure of treatment)

―Slipped- Nissen‖ occurs when the wrap slides down, the GE junction retractsinto the chest, and the stomach is partitioned; usually due to a foreshortenedoesophagus unrecognised in the first operation

―Gas bloat syndrome‖ – patient experiences difficulty burping gas that isswallowed

- Outcome of surgery 80-90% Excellent to good (no symptoms, no medications and lifestyle changes

required) 10-15% Satisfactory (some residual symptoms)


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Management

1. Treatment of underlying reflux- Lifestyle changes, acid suppression, surgery etc- Not shown to decrease risk of cancer still requires surveillance

2. Endoscopic surveillance- Not certain regarding benefit for surveillance if patient has Barrett‘s but no

dysplasia if 2 scopes in a year reveal no dysplasia, repeat OGD once every 3years

- Main purpose of surveillance is to pick up dysplasia- If patient has high grade dysplasia, it should be treated (see below), otherwise toundergo intensive surveillance (q3mths for at least one year) to detect cancer

development

3. Treatment of high-grade dysplasia- Endoscopic therapies to ablate the dysplastic tissue e.g. photodynamic therapy,

laser therapy, argon plasma coagulation will not remove all dysplastic cells

thus potential for malignancy still remains- Oesophagectomy is the only definitive treatment to remove all dysplasia, but is

associated with high morbidity and mortality (worth it?)

- Possibility of endoscopic mucosal resection as a treatment modality (researchstill undergoing)

ACHALASIA

FEATURES

- Abnormal peristalsis secondary to absence or destruction of Auerbach‘s (myenteric) plexus and failure of the LES to relax; affects body and distal oesophagus

- Aetiology unknown

- Patients present with dysphagia, regurgitation, weight loss, retrosternal chest pain,and recurrent pulmonary infections

- Barium swallow demonstrates ―bird‘s beak‖ narrowing of distal oesophagus with proximal dilatation

- Manometric studies (required for diagnosis) show abnormally high pressures at theLES, with incomplete LES relaxation on swallowing, and lack of progressive

peristalsis (often aperistaltic)

- 1-10% of patients develop SCC after 15-25 years of disease

TREATMENT

- Mainly palliative in nature

- Non surgical treatment:

Injection of botulinum toxin (problem is that it is not long lasting and only usedin patients not fit for surgery)

Pneumatic balloon dilatation (about 65% of patients improve, 40% response rateat 5 years)

- Surgical treatment

Laparoscopic Heller cardiomyotomy (much like Ramstedt pyloromyotomy for pyloric stenosis) – good results with 85% symptom-free after 5 years; there is a3% chance of developing reflux addition of fundoplication helps prevent this

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UPPER BLEEDING GIT AND ITS CAUSES

APPROACH TO BLEEDING UPPER GIT

CAUSES

1. Peptic ulcer disease (bleeding peptic ulcer)2. Gastritis, gastric erosions, duodenitis

3. Gastric malignancy

4. Gastro-oesophageal varices

5. Mallory-Weiss tear6. Rare causes: AV malformation (Dieulafoy lesion), aortoenteric fistula7. Bleeding from other sources: Haemoptysis, nasopharyngeal bleeding

HISTORY (if patient is stable)

1. Nature of bleeding

Haematemesis

- Can be fresh red blood as in variceal bleeding, Mallory-Weiss tear, AVmalformation

- Coffee grounds vomitus is altered blood (due to gastric acid) and can come fromgastric ulcer, gastritis/erosions, or variceal blood that has entered the stomach

Malaena- Altered blood; malaena indicates bleeding from the upper GIT i.e. above the

ligament of Treitz

- Different types of malaena:

(a) Fresh malaena – jet black with sheen, tarry, non-particulate (almost liquidin consistency)

(b) Stale malaena – black-grey, dull, mixed with normal stool, occasionally particulate

(c) Iron stool – greenish hue on rubbing between gloved fingers, particulate.

- If gloved finger is stirred in a cup of water, malaena will ―dissolve‖ completelywith no sedimentation and turn the water black, but iron stool will sedimentate

and turn the water green

Frank PR bleeding

- Very brisk upper GI bleed can present as frank PR bleeding as blood passesdown so fast it doesn‘t get altered

2. Amoun t of blood

- If patient is having haematemesis, ask how much blood Cup? Bowl?

3. Aetiolog ical clues

Gastric ulcer/gastritis/erosions

- Any history of dyspepsia, gastric ulcer (any OGD done in the past showing these problems? On any ―gastric‖ medications?)

- Any drugs that may predispose – NSAIDs, antiplatelets, steroids, anticoagulants,TCM

Varices

- Any history of chronic liver disease

Mallory-Weiss tear- Binge-drinking with subsequent severe retching and vomiting leading tohaemetemesis

Malignancy

- Recent constitutional symptoms e.g. LOA, LOW, malaise- Early satiety- Dyspepsia

4. Compl icat ions

- Symptoms of anaemia: postural giddiness, shortness of breath, lethargy,decreased effort tolerance, palpitations, chest pain

- AMI esp. if it‘s an old patient with previous history of IHD

5. Comorbid i t ies

- Elderly patient (>60) high risk

- Other comorbidities: liver disease, renal disease, IHD high risk

PHYSICAL EXAMINATION

1. Vitals!

- Blood pressure, heart rate stable? Any postural hypotension? (Tachycardia is anearly sign of shock)

- Patient‘s conscious level – confused?- Compare current vitals with vitals in ambulance, ED – is there a worsening trend?

2. General inspec tion- Pallor- Cold clammy peripheries impending shock- Stigmata of chronic liver disease

3. Abdomen - Any tenderness (not very helpful)

4. Digital rectal examinatio n

- Malaena or frank blood


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IMMEDIATE MANAGEMENT

1. Resuscitation

- Protect airway, supplemental oxygen, 2 large-bore IV cannula in antecubitalfossa

- Take blood for investigations: FBC, U/E/Cr, PT/PTT, LFT, GXM 4 pints

- ECG to detect any acute myocardial ischaemia/infarction

- 1 pint N/S over half to one hour if patient is in shock, followed by more fluids ifnecessary (be wary in patients with renal failure, heart failure)

- Packed cells if Hb is less than 10, to keep Hb above 10g/dL

- May consider platelets if patient is on antiplatelet medication (qualitative defectin platelets)

- FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K)

2. Adjuncts

- NG tube if patient is having haematemesis – prevents aspiration, allows gastriclavage prior to OGD (DO NOT insert if suspecting varices)

- Catheterisation – monitor input/output balance especially in elderly patient orwhen large amount of fluid resuscitation required, or anticipating surgery

- IV omeprazole 80mg bolus (increases stomach pH and stabilises clot formation)

- If suspecting varices – IV somatostatin/octreotide, IV antibiotics, vitamin K

3. Close moni tor ing

- Monitor for: Increase in heart rate Decrease in BP Decrease in urine output Increasing confusion and lethargy

4. Emergency oesophagogastroduodenoscopy

- Indications: Shock (resuscitated) Ongoing BGIT Suspected variceal bleed

- Role of endoscopy Diagnostic: confirm UBGIT & identify source of bleeding, Therapeutic: injection of ulcer, ligation/sclerotherapy for varices

- Repeat OGD with greater detail if it is normal the 1st time.

Exclude haemoptysis & bleeding from nasopharynx Look for Mallory weiss tear and posterior wall duodenal bleeding ulcer

VARICEAL BLEEDING

PATHOPHYSIOLOGY

A result of portal hypertension (i.e. portal venous pressure >20 cmH2O or >12 mmHg – normal should be 7-14 cmH2O or 5-10 mmHg)

WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT

- Previous history of variceal bleed- Chronic alcohol intake

- Jaundice or stigmata of chronic liver disease

MANAGEMENT OF VARICES can be divided into three categories:1. Acute bleeding2. Prophylaxis3. Chronic management

I. ACUTE BLEEDING – MANAGEMENT

1. Resuscitate

- Airway, breathing, circulation- If patient appears well, look for early signs of shock – tachycardia, postural

hypotension- Look at hydration status

2. Ass ess mental state

- If patient has altered mental state (encephalopathy) need to protect airway(may require intubation)

3. Vascular access, f lu ids/b lood resusci tat ion, and blood invest igat ions

- 2 large-bore IV cannula in proximal veins (cubital, EJV, IJV)- Send bloods – GXM 4 pints, FBC, U/E/Cr, LFT, PT/PTT- Infuse fluids- Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9, as

enthusiastic transfusion can increase portal pressure and cause more bleeding

4. Management of severe bleeding

- If patient is hypotensive and bleeding is still continuing – may require use ofSengstaken-Blakemore tube for up to 48hr

- Protect airway before inserting tube.- Inflate gastric balloon and pull upwards against cardioesophageal junction

(balloon will press on perforator veins entering oesophagus from stomach, and

thus decrease oesophageal variceal bleeding); oesophageal balloon is not inflatednowadays

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5. IV som atostatin/oc treotide

- Not given in ulcer bleed; mode of action is as a splanchnic vasoconstrictor whichdecreases portal blood flow and hence portal pressures decreased variceal

bleeding

- Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow

6. Acid suppression

- Increasing intragastric pH increases clot stability, aids haemostasis- Agents available: omeprazole, esomeprazole, pantoprazole, etc.

7. Antib iot ics

- Not given in ulcer bleed- Studies have shown that cover with broad spectrum antibiotics (with Gram neg

cover) decreases infectious complications, possibly mortality, and also risk of

recurrent bleed

- Preferably started before endoscopy (procedures increase bacteraemia)

8. Endoscopy

- Purpose: confirm diagnosis and institute management- Needs to be done emergently (on that night of admission) as soon as patient is

stabilised since bleeding can be torrential and life-threatening

- Banding is the best modality for stopping oesophageal variceal bleeding(sclerotherapy is associated with higher morbidity e.g. mucosal ulceration)

- Gastric varices are usually too large to be banded, sclerotherapy used instead

9. Observation

- Continue antibiotics and omeprazole- Continue somatostatin up to the point where haemostasis is achieved or 5 days

(exact ideal duration not well studied)- Anticipate complications:

(a) encephalopathy – fleet and lactulose, treat hypokalaemia from vomiting(b) aspiration – protect airway; ?benefit of gastric decompression using NG tube(c) risks of procedure – OGD-related risks

10. Secondary prophylaxis- Best option is combination of band ligation and non-selective beta-blockers e.g. propranolol unless propranolol is contraindicated

11. Management of possib le precip i tants

- NSAIDs; Hepatic vein thrombosis

I f b leeding is no t remediable by endoscopic intervent ion:

- Insert Sengstaken-Blakemore tube (only temporary) and repeat endoscopy 10-12hours later

- Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt(TIPSS) if in good Child‘s score to avoid ppt. encephalopathy

- Shunt surgery Portocaval shunts (joining portal vein to IVC) – side-to-side, end-to-side Mesocaval shunts (joining superior mesenteric vein to IVC)

Proximal splenorenal shunt (splenectomy with end-to-side anastomosis of portalside of splenic vein to left renal vein)

Distal splenorenal shunt (Warren-Zeppa shunt – splenic vein divided and splenicside anastomosed end-to-side to left renal vein)

- Sugiura procedure (last resort): splenectomy, proximal gastric devascularisation,selective vagotomy, pyloroplasty, oesophageal devascularisation, oesophageal

transection

II. PRIMARY PROPHYLAXIS OF VARICEAL BLEEDING

Use of non-selective beta-blocker e.g. propranolol can be used to prevent developmentof varices in patients without varices, and can decrease the size of and prevent bleeding

from varices in patients who already have them. In patients with small varices with no

risk of bleeding, the use of propranolol is of questionable benefit – repeat OGD tomonitor varices.

Predictors of var iceal haemorrhage:

1 Site: varices at the gastro-oesophageal junction have the thinnest coat of supporting

tissue and are at highest risk of rupture and bleeding

2 Size: F1: Small straight varices

F2: Enlarged tortuous varices that occupy less than one-third of the lumenF3: Large coil-shaped varices that occupy more than one-third of the lumen

3 Child‘s score – patients with higher Child‘s score have higher risk

4 Red signs: Red wale marks (longitudinal red streaks)

(ESRH) Cherry red spots (flat discrete spots)Haematocystic spots (raised discrete spots – resemble ―blood blisters‖) Diffuse erythema

5 Previous variceal haemorrhage:

70% of patients will have further variceal bleeds after an index bleed

30% rebleed within 6 weeks (risk highest in first 48 hours after first bleed); 30%

rebleed after 6 weeks


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III. CHRONIC MANAGEMENT

- Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapyand subsequent endoscopic monitoring and repeated ligation/sclerotherapy asrequired to completely ablate varices)

- If patient bleeds again failed ablation consider surgery (as above – shunts, orSugiura)

PEPTIC ULCER DISEASE

EPIDEMIOLOGY- Incidence about 100 per 100,000 per year- 68% of patients are over 60 years of age- Overall mortality is 7-10%, unchanged for last 2 decades – mostly due to ulcer

bleeding especially in elderly with significant comorbidities

MAIN AETIOLOGICAL FACTORS

H. pylor i

- 60% of population are positive for H. pylori by age 21

- About 10-20% of infected patients develop an ulcer- Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers

NSAIDs

- Accounts for most of the rest of ulcer disease not caused by H. pylori- 30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a clinically

significant ulcer i.e. symptomatic, bleeding

Other factors

- Cigarette smoking- Alcohol- Steroids and anticoagulants do not increase the risk of ulcer formation, but increase

the risk of bleeding in an existent ulcer

PATHOGENESIS

- An imbalance between mucosal protective mechanisms against acid, and aggressiveforces that damage the gastric mucosa

- Aggressive forces: gastric activity and pepsin activity

- Protective mechanisms: mucus secretion, bicarbonate secretion into mucus, robustmucosal blood flow to remove protons, epithelial regenerative capacity,

prostaglandin secretion by mucosa to maintain blood flow

- H. pylori causes a local inflammatory reaction and secretes enzymes that break downthe gastric mucosal barrier, and also enhances gastric acid secretion and decreases bicarbonate production

- NSAIDs impair mucosal prostaglandin production (through non-selective COXinhibition) prostaglandins are important for mucosal bicarbonate and mucin

production and inhibiting gastric acid secretion, as well as maintaining mucosal blood

flow

PRESENTATION

1. Incidental ly detected on OGD

2. Symptoms of dyspepsia

(a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom(b) Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen,

associated with upper abdominal fullness, early satiety, bloating, belching,

nausea(c) Unspecified dyspepsia- Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a

duodenal ulcer

3. Bleed

- As above, presenting with haematemesis (coffee-grounds vomitus) or malaena

4. Perforation

- Patient presents with sudden generalised abdominal pain that is aggravated byeven the slightest movements

- Board-like rigidity, guarding will be present on examination (signs of peritonism)- Erect CXR will show air under diaphragm

ENDOSCOPY (OGD)

- The most important and valuable investigation

- Roles of endoscopy:

(a) Diagnosis

Confirmation of ulcer disease Location of ulcer Biopsy to rule out malignancy (usually 6 bites) Biopsy of antral tissue for CLO (Campylobacter-like organism) test for H.

pylori

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(b) Pro gnos tication of bleeding risk (in UBGIT)

Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH)

Forrest grade Bleeding risk

1a Spurting (arterial) 90%1b Non-spurting, ooze (venous) 20%

2a Non-bleeding ulcer with visible vessel 40%

2b Non-bleeding ulcer with adherent clot 20%2c Ulcer with haematin-covered base (flat spot) 10%

3 Ulcer with clean base 5%

(c) Endot herapy (in UBGIT)

Injection with adrenaline (1:10,000) or absolute alcohol Thermal coagulation (heater probe) Haemostatic clipping (endoclip) Argon plasma coagulation

CONSERVATIVE MANAGEMENT

1. Gastroprotect ion

(a) Standard dose proton pump inhibitor 20mg OM Promotes ulcer healing even with ongoing NSAID use

(b) Double dose famotidine 40mg BD Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs

are stopped; ulcers will not heal with ongoing NSAID therapy

2. H. pylori eradication

First line triple therapy: omeprazole 20mg BD, amoxicillin 1g BD,clarithromycin 500mg BD for 7 days

In penicillin-allergic patients, substitute amoxicillin with metronidazole 400mgBD

Document eradication by endoscopy with CLO test, urea breath test or stoolserology testing

Treatment failure occurs in up to 20% - treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS, tetracycline 500mg QDS, metronidazole 400mg

BD, omeprazole 20mg BD for 7 days

Re-scope in 6 weeks to docum ent ulcer heal ing

If ulcer still present, biopsy ulcer again (exclude malignancy for gastric ulcer) and also

do antral biopsy for CLO test (to confirm eradication of H. pylori)

SURGICAL MANAGEMENT

D UODENAL ULCER

Ind icat ions for surgery:

1. Persistent bleeding (e.g. erosion of a posterior duodenal ulcer into gastroduodenalartery)

2. Perforation

3. Gastric outlet obstruction (patient presents with vomiting of undigested food notlong after meal, succussion splash, air-fluid levels on AXR; characteristic

electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria)

4. Failure of medical management (ulcer does not heal)

Surgery:

1. Oversewing the bleeding vessel2. Vagotomy with gastric drainage procedures

- Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastricsecretion; parietal cells also become less responsive to histamine and gastrin, and

vagal stimulus for gastrin release is abolished- Vagotomy can be truncal, selective, or highly selective- Drainage procedures usually done with vagotomy as gastric emptying is

decreased with denervation gastrojejunostomy or pyloroplasty3. Antrectomy with truncal vagotomy

4. Gastrectomy

5. Omental patch repair is sufficient for small perforated ulcer

Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)

G ASTRIC ULCER

Ind icat ions for surgery

1. Failure to heal after 3 months of conservative therapy2. Dysplasia or carcinoma3. Recurrence4. Perforation, persistent bleeding

Surgery

1. Oversewing the bleeding vessel2. Gastrectomy3. If prepyloric ulcer, can treat similar to duodenal ulcer


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GASTRIC CARCINOMA

EPIDEMIOLOGY- Fourth most common cancer in males, sixth most common in females in Singapore- Female to male ratio 2:1- Incidence 10-18 per 100,000 per year- Incidence increases steeply after 50 years old

RISK FACTORS

1. Envi ronmenta l- Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons- Smoking- Alcohol- Occupational exposure: asbestos, heavy metals, rubber- Low socioeconomic status

2. Genetic

- Blood type A- HNPCC – Lynch syndrome II- P53 mutation- Germline mutation of e-cadherin- Family history of gastric cancer

PRECURSOR CONDITIONS

1. Part ial gastrectomy for benign disease wi th Bi l ro th II reconstruct ion

- Usually occurs >15 years after surgery- Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal

secretions at the anastomotic zone

2. Gastr ic polyps

- Highest risk in inflammatory polyps: 75-90%- 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those

with villous histology

- Also increased risk of adenocarcinoma elsewhere in the stomach

3. Chronic atrophic gastr i t is

- Hypertrophic gastritis (Menetrier‘s disease) – inflammatory disease of gastricepithelium, up to 10% risk of malignant change

- Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10%risk of gastric cancer

4. Peptic ulcer disease

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SPREAD

- Direct extension to neighbouring organs

- Lymphatic spread(a) Regional nodes(b) Supraclavicular nodes (Virchow‘s node) (c) Umbilical (Sister Joseph‘s node)

- Haematogenous spread – liver, lung, bone, brain

- Peritoneal seeding to omentum, parietal peritoneum, ovaries (Krukenberg‘s tumour),or cul-de-sac (Blumer‘s shelf)

PRESENTATION

Very non-specific symptoms and signs:- Abdominal pain 60%- Weight loss 50%- Nausea/vomiting 40%- Anaemia 40%- Palpable mass 30%- Haematemesis/malaena 25%- Early satiety 17%- Metastatic symptoms late (bony tenderness, neurological deficits, etc)

New onset dyspepsia at age>35 years old should cause concern

COMPLICATIONS

- Bleeding- Gastric outlet obstruction vomiting (dehydration, hypokalaemic metabolic

alkalosis, aspiration ± pneumonia)

- Perforation- Malnutrition

INVESTIGATIONS

Diagnosis

OGD – visualisation and biopsy (ulcer with heaped-up edges)

Staging invest igat ions

1. CXR/ CT thorax – lung mets2. Endoscopic ultrasound – gold standard for T staging and good for N staging3. CT abdo pelvis – good for T, N & M staging4. Staging laparoscopy prior to operation – picks up small peritoneal metastases that

are occult on CT scanning (up to 1/5 of patients) upstage of disease

Support ive invest igat ions

5. FBC – low Hb6. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis7. LFTs – albumin as a marker of nutritional status (alb15 regional LN involved

CURATIVE TREATMENT

S URGERY

Princip les of surgery:

- Wide resection of the tumour to negative margins (at least 6cm margins)- En-bloc excision of regional lymph nodes- Choice between total gastrectomy and subtotal gastrectomy Subtotal gastrectomy leaves a small portion of proximal stomach – easier to

anastomose to jejunum than oesophagus since oesophagus does not have serosa(higher risk of leak)

Subtotal gastrectomy is associated with less morbidity, better functional outcome(some residual reservoir function preserved)

Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia, body) as well as diffuse-type tumours and cardio-oesophageal junction tumours

- Reconstruction Bilroth I (end-to-end gastroduodenostomy) – rarely done as it is difficult to

mobilise duodenum up to anastomose with residual stomach

Bilroth II/Polya (gastrojejunostomy) – no protection against biliary reflux intostomach

Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higherchance of leak

Oesophagojejunostomy (after total gastrectomy)

Compl icat ions of gastrectomy:

Early1. Bleeding2. Infection3. Anastomotic leak

1. Asymptomatic: from histology ofulcer biopsy

2. symptomatic: non specificabdominal pain, early satiety, N/V,

LOW, LOA3. Complications: s/s of anaemia, s/s

of UBGIT, s/s of GOO, s/s of

metastasis, peritonism (perforation)

L t


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Late

Early satiety

Retained antrum syndrome- Not enough antrum removed leads to increased acidity in residual stomach, with

formation of marginal ulcers on the jejunal side of the anastomosis

Intestinal hurry- Inadequate reservoir function leads to poor digestion may have phytobezoar

formation

Dumping syndromes- Early dumping syndrome: due to increased osmotic load in bowel occurringhalf to one hour after meal, resulting in flushing, palpitations, dizziness, nausea;

treat by eating small frequent meals with low carbo and high protein/fat- Late dumping syndrome: reactive hyperinsulinaemia with hypoglycaemia; treat

by eating more carbohydrates

Biliary/intestinal reflux into stomach- Leads to symptoms of dyspepsia

Afferent limb syndrome- Occurs in Bilroth II/Polya reconstruction- Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic

narrowing, or adhesions postprandial epigastric pain with non-bilious

vomiting- Can be decreased by doing Roux-en-Y surgery (but may s till occur)

Nutritional deficiency- Iron deficiency – mixed picture

(a) Loss of intrinsic factor B12 deficiency(b) Decreased conversion of iron from Fe

3+ to Fe

2+ by gastric acid decreased

iron absorption in terminal ileum

- Need to supplement with B12 injections and iron supplements

C HEMOTHERAPY /R ADIOTHERAPY

Adjuvant therapy

5-fluorouracil with chemotherapy5-fluorouracil with epirubicin for advanced disease

Neoadjuvant therapy

- 5-FU and cisplatin can be used to downstage unresectable, locally advanced diseasewith a significant increase in resectability (61% 79%)

- For resectable disease: preoperative 5-FU, cisplatin, doxorubicin, methotrexate,followed by intraperitoneal 5-FU improved resection rates, response rates, median

survival

PALLIATIVE THERAPY- For palliation of symptoms such as pain, bleeding, obstruction- Endoscopic laser ablation for obstruction- Embolisation for bleeding- Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%),

gastrojejunostomy for obstruction

- External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy bleeding as it takes weeks to cause fibrosis)

PROGNOSIS

- Stage I 90% 5-year survival- Stage II 70%- Stage III 40%- Stage IV 0%

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COLORECTAL DISEASES 2 Defects in DNA mismatch repai r


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COLORECTAL DISEASES

COLORECTAL CARCINOMA

EPIDEMIOLOGYCommonest cancer in Singapore men, number 2 cancer in Singapore womenPeak incidence at 60-70 years of age

PATHOLOGY- Almost all tumours are adenocarcinomas- 90% of tumours are sporadic- 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and

1% in association with familial adenomatous polyposis (APC)

- 1% arise in association with long-standing ulcerative colitis (>10 years)

PATHOGENESIS

There are 2 pathways for cancer development in the colorectal mucosa:

1. APC pathw ay (adenoma-carcino ma sequenc e)

- Accounts for 80% of sporadic colorectal carcinomas

- Characterised by chromosomal instability - Stepwise accumulation of mutations in a series of oncogenes and tumour

suppressor genes:

Loss of the APC suppressor gene on 5q21 (congenitally absent in patientswith familial adenomatous polyposis – APC) is the earliest event in adenomaformation

APC is required to break down beta-catenin; with the loss of APC, beta-catenin accumulates and activates various genes in the nucleus (such as MYC

and cyclin D1) which promote cell proliferation

K-RAS (12p12) mutation follows the loss of APC – an activating mutationthat causes the RAS to keep delivering mitotic signals and prevent apoptosis

Loss of tumour suppressor gene at 18q21

Loss of p53 late in carcinogenesis

- The molecular evolution of colon cancer through this pathway occurs through aseries of morphologically identifiable stages: localised epithelial proliferation small adenoma large, more dysplastic adenoma carcinoma in-situ

invasive cancer

2. Defects in DNA mismatch repai r

- Involved in 10-15% of sporadic cases

- Like the APC pathway, there is accumulation of mutations, but due to a differentmechanism, and without clearly identifiable morphologic correlates i.e. no

adenomas

- Due to mutations in one of the five DNA repair genes (MSH2, MSH6, MLH1,PMS1, PMS2) of which MSH2 and MLH1 are the most commonly involved in

sporadic colorectal carcinomas

- Loss of DNA mismatch repair results in microsatellite instability which affects

coding or promoter regions of genes involved in cell growth such as the BAXgene and the type II TGF-β receptor

- Tumours that arise from this pathway have a better prognosis than tumours thatarise from the APC pathway

SITE:

- 25% in caecum and ascending colon,- 25% in transverse colon,- 25% in descending colon and proximal sigmoid,- 25% in distal sigmoid and rectum

- Most are left-sided though there is an increasing incidence of right-sided tumours

MORPHOLOGY

1. Polypoid – more common in the right colon as there is more space to grow

2. Scirrhous – annular ―apple-core‖ lesions, more common in the left colon 3. Ulcerated

4. Nodular

SPREAD

1. Intramural – along bowel wall or Intraluminal2. Direct extension into surrounding tissues e.g. small bowel, ovary

3. Lymphatic

4. Haematogenous – to liver, lungs5. Transcoelomic

RISK FACTORS HISTORY


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RISK FACTORS

1. Age >50 years

2. Envi ronmenta l factors

- Diet: high in red meat, preserved foods (nitrosamines), low in fibre, vitamins,minerals

- NSAIDs may be protective against CRC

3. Genetic predisposi t ion

(a) Personal history of CRCs Metachronous colorectal cancers occur at a rate of 3-5% in the first

five years after resection of a primary CRC, while metachronous

adenomas occur at a rate of 25-40%(b) Family history of CRCs

1 first-degree relative with CRC increases risk of CRC 1.7X, Risk is further increased if there are 2 1 st-degree relatives with CRC,

or if the relative had CRC


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Iron deficiency anaemia: fatigue, SOB, CP, decreased ET, palpitations, postural giddiness,

Intestinal obstruction: abdominal distension, abdominal colick pain,vomiting, absolute constipation

Symptoms of peritonism: perforation Symptoms of metastasis: bone pain/ #, SOB, LL weakness with loss

or bowel and urinary continence, RHC discomfort

B) Strong-r isk factors

Positive Family history- 1 or more 1st deg relative with CC at age 10 years

PHYSICAL EXAM

1. Abdominal mass

2. Mass on DRE: (rectal

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Andre Tan's Surgery Notes (Ed 1)