Andre Tan's Surgery Notes (Ed 1)

Surgery Notes

For the M.B.B.S.

By Andre Tan

Page

I TRAUMA (MULTI-SPECIALTY APPROACH) 2

II APPROACH TO ABDOMINAL PAIN 10

III APPROACH 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 PANCREATIC 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

TRAUMA (MULTI-SPECIALTY APPROACH)

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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 adjuncts 2. Re-evaluation of the patient

3. Secondary survey with adjuncts

4. Post-resuscitation monitoring and re-evaluation 5. Optimise for transfer and definitive care

PRIMARY SURVEY – ABCDE

1. AIRWAY

Assessment of airway patency - Is patient alert, can patient speak? - Gurgling, stridor

- Maxillofacial injuries - Laryngeal injuries - Caution: C-spine injury Establishing patent airway

- 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 breathing

- 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 of breathing - 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 IV Bld loss Amt (ml) Percentage <750 <15 750-1500 15-30 1500-2000 30-40 >2000 >40 Ht rate <100 >100 >120 >140 BP Normal Normal Decreased Decreased Cap refill Normal Prolonged Prolonged Prolonged

Resp rate 14-20 20-30 30-40 >35

Ur output (ml/h) >30 20-30 5-15 Oliguric-anuric Mental state Sl anxious Mild anxiety

Anxious-confused

Confused-lethargic Fluid

replacement

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 (pelvic fracture), 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

4. DISABILITY

- Glasgow coma scale

Eye Verbal Motor

Spontaneous opening Opens to voice Opens to pain No response 4 3 2 1 Oriented speech Confused Inappropriate Incomprehensible No verbal response 5 4 3 2 1 Obeys Purposeful Withdraws Flexion response Extension response No response 6 5 4 3 2 1

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.ADJUNCTSTOPRIMARYSURVEY Monitoring

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

- Arterial blood gas Diagnostic 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

Gastric catheter (orogastric or nasogastric)

- 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 HISTORY - Allergy - Medications - Past history - Last meal

- Events leading to injury, Environment in which trauma occurred

2. COMPLETE 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 Maxillofacial

- 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 tissues)

- 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

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 Musculoskeletal – extremities

- 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 DIAGNOSTIC TESTS

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

4. FREQUENT 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. PAIN MANAGEMENT

- Intravenous analgesia as appropriate

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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 traversing abdominal cavity

- Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation

- Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising 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, left upper quadrant, pelvis

- Advantages  Portable

 Can be done quickly in <5min  Can be used for serial examination

 Does not require contrast, no radiation risk - Disadvantages

 Does not image solid parenchymal damage, retroperitoneum, diaphragmatic defects or bowel injury

 Compromised in uncooperative, agitated patient, obesity, substantial bowel gas, subcutaneous air

 Less sensitive, more operator-dependent than DPL and cannot distinguish blood from ascites

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

- Positive 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 - Indications:

 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 - Contraindications

 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

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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) - Diagnostic 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

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, and may cause death) – signs of pneumothorax, hypotension, neck vein distension, severe respiratory 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 between intrathoracic 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)

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AIM in management of head injuries is the prevention of secondary brain injury (from

hypotension, 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 <1cm 3. Intracranial haemorrhage

(a) Extradural haemorrhage

 Lens-shaped haematoma outside the dura (between skull and dura)  Pathology: expanding space-occupying lesion

 20% of patients with EDH are alert and well; underlying brain is minimally damaged, thus drainage gives good results

(b) Subdural haemorrhage

 Crescent shaped haematoma under the dura (between the dura and the arachnoid)

 More severe than EDH (usually due to nature of injury that causes SDH to occur – associated with higher impact, thus brain has other injuries)

 Pathology: underlying brain damage in addition to expanding SOL

 Removal of blood does not solve underlying brain damage  poorer results (c) Traumatic subarachnoid haemorrhage

 Usually only small amount of blood  conservative treatment sufficient (d) Intraparenchymal haemorrhage

 Any shape, size, location

 If large haematoma, will require evacuation 4. Diffuse axonal injury

- Global injury of axons

- Arises from injury that causes rotational and shearing forces (high impact injury) – rapid acceleration and deceleration of brain in the intracranial cavity against relatively fixed points of attachment at the falx and tentorium

- Maximal effects at corpus callosum and brainstem

- If severe, will see punctate haemorrhages at the grey-white border 5. Cerebral oedema (2 types)

(a) Hypoxic (cellular)

 Decreased blood supply (oxygenation)  loss of function of Na-K pump as ATP decreases  increased intracellular sodium  cellular swelling

(b) Interstitial

 Breakdown of blood-brain barrier  proteins enter interstitial space  oedema

PATHOPHYSIOLOGY

1. Monroe-Kellie doctrine

- Intracranial cavity is of fixed volume and its contents (brain, CSF, blood) are relatively incompressible

- Thus increase in intracranial volume  raised ICP

Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure

- Compensatory mechanisms:

(a) Hyperventilation  vasoconstriction of cerebral vessels due to increased partial pressure of carbon dioxide  decrease in blood volume

(b) CSF pushed into spinal canal (but limited volume available)

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 to

unoppressed 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 to maintain 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 injury - 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), do septic 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 fracture

- 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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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 EXTREMITY

Things 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 examination

- 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 the external environment

Gustilo-Andersen classification Type I  <1cm AND clean

Type II  >1cm AND no extensive soft tissue damage, avulsions or flaps Type IIIA  Extensive soft tissue damage, avulsions or flaps but adequate soft

tissue coverage of bone OR

 High-energy trauma cause irregardless of size of wound

Type IIIB  Extensive soft tissue loss with periosteal stripping and exposure of

bone.

 Massive contamination common

- 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

ABDOMINAL PAIN RHC Epigastric 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 Periumbilical 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 Splenic disease Urological (see Rt Loin)

RIF Hypogastric 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 conditions

 Transient synovitis  Perthes‘ dz  SCFE Gastrointestinal  Diverticulitis  IBD  Colitis  Colorectal CA  Hernia O&G (see RLQ)

ABDOMINAL MASS RHC Epigastrium LHC Liver Massive  Cancer: HCC Metastases 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 – abscess Parasitic – hydatid cyst, amoebic abscss  Biliary obstruction  Cirrhosis Gallbladder  Pancreatic/periampullary ca  Acute cholecystitis  Hydrops  Empyema  Mirizzi syndrome Ascending colon  Cancer  Diverticular mass/abscess  Faeces

Right adrenal gland Right kidney(see Rt lumbar)

Liver (see RHC) Pancreas  Pseudocyst  Tumour Transverse colon  Cancer  Diverticular mass/abscess  Faeces Stomach  Cancer  Distension (GOO) Aorta  Aortic aneurysm Retroperitoneal lNpathy  Lymphoma  Teratoma  Other malignancies Spleen Massive  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

 Cancer

 Diverticular mass/abscess  Faeces

Left kidney(see Rt lumbar) Left adrenal gland

Right Lumbar Umbilical Left Lumbar

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

Right adrenal gland Liver (see RHC) Ascending colon mass

 Cancer  Diverticular mass/abscess  Faeces Liver (see RHC) Stomach(see Epigastrium) Small intestine  Obstruction Mesenteric cyst

Pancreas (see Epigastrium) Aorta  Aortic Aneurysm Retroperitoneal lNpathy  Lymphoma  Teratoma  Other malignancies Spleen (see LHC)

Left kidney (see right lumbar)

Descending colon

 Cancer

 Diverticular mass/abscess  Faeces

RIF Hypogastrium 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 testis Vascular:

 Iliac artery aneurysm  Iliac lymphadenitis Skin & 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

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 into the 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 lining

except for a short segment of intra-abdominal oesophagus)

Muscularis propria is composed of striated muscle in the upper one-third, striated and smooth 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 the hard 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 same time, 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 cricopharyngeus into the oesophagus

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

A

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 diseases

Stroke

Parkinson’s disease

Brain stem tumours

Degenerative conditions e.g. ALS, MS Peripheral neuropathy

Myasthaenia gravis

Myopathies e.g. myotonic dystrophy

Achalasia

Spastic motor disorders Diffuse oesophageal spasm

Hypertensive lower oesophageal sphincter Nutcracker oesophagus

Scleroderma

Obstructive lesions Obstructive lesions Tumours

Inflammatory masses e.g. abscess Oesophageal webs

Pharyngeal pouch (Zenker‘s divert) Anterior mediastinal mass

Intrinsic structural lesions

Tumours

Strictures: Peptic (reflux oesophagitis) Radiation

Chemical (caustic ingestion) Medication

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

Extrinsic structural lesions

Vascular compression (enlarged aorta or left atrium)

Mediastinal masses – retrosternal thyroid, lymphadenopathy

Others

Oesophagitis: Reflux

Infectious (candida, herpes) Radiation-induced

Medication-induced Chemical-induced (alcohol)

HISTORY:

1. Is there odynophagia (pain associated with difficulty 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. Differentiating 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. Differentiating mechanical obstruction from neuromusculardysfunction

(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 predisposingconditions

- 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. Systemicreview

- 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-Vinson syndrome)

- Symptoms of aspiration pneumonia – fever, cough, shortness of breath 6. Tumourspread

- Hoarseness (recurrent laryngeal nerve)

- Fever, cough and haemoptysis (tracheo-oesophageal fistula) - Haematemesis (invasion into aorta)

- Neck lump (lymph node)

PHYSICAL EXAMINATION

1. Generalcondition

- Vitals: the patient may be hypovolaemic from vomiting/decreased intake - Nutrition: presence of cachexia

- Conjunctival pallor: bleeding from tumour, oesophagitis ulcerations, or associated 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. Complicationsof 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?

MANAGEMENT

1. Stabilisepatient

- 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‘s nutritionally debilitated state

- Keep NBM if patient cannot tolerate even fluids - Treat any aspiration pneumonia – NBM, IV antibiotics 2. Investigate for underlying cause and treatit

INVESTIGATIONS

Diagnostic

1. Barium swallow

- Advantage of barium swallow is that it is less invasive than OGD, especially when 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 bleeding from 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-endoscopic examination of swallowing (FEES)

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

1. Blood investigations:

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

- 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)

- 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 later section on Gastro-oesophageal reflux disease)

C

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 mineral deficiencies (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 oesophageal

web 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 lower third 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 the

lower 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 mucosa

Tumour invading submucosa but does not breach submucosa

Tumour invades the muscularis propria Tumour invades adventitia

Invasion of surrounding structures N N1 Regional node involvement (1-3 nodes

involved =1a; 4-7=1b; >7=1c) M M1a

M1b

Nonregional lymph node involvement Other 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 they are 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

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 Supportive

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

Principles

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

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

- Surgical treatment is usually performed with curative intention, but can also achieve good 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 more advanced stages

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

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

- Oesophagectomy

(i) Ivor-Lewis

Two-stage procedure involving gastric mobilisation (first stage, done through upper midline abdominal incision), oesophagectomy and gastro-oesophageal anastomosis in the chest (second stage, through right thoracotomy incision)

(ii) Trans-hiatal

Done via two incisions – one in the abdomen and one in the neck

Blunt 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-incisional

Three 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 the

cancer 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 from surgery

 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

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 curative treatment

Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection), oesophagectomy, and postoperative adjuvant chemoradiotherapy for responsive tumours

Palliative 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 obstruction

- Feeding via oropharyngeal route is preferred unless the passage is obstructed or it is unsafe 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 around tumour

- 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 with tumour growth

PROGNOSIS

- 80% mortality at 1 year, overall 5-year survival <10%

G

-

(GORD)

EPIDEMIOLOGY

Incidence in Singapore not known

Increasing prevalence, more common in males than females

PATHOPHYSIOLOGY

- Lower oesophageal sphincter is a physiological sphincter with various mechanisms that help to prevent reflux (see above, Anatomy of the oesophagus)

- Some physiological reflux occurs that is rapidly cleared by peristaltic movements in the oesophagus

- GORD results from various pathophysiological factors (loss of the normal protective mechanisms, or the mechanisms are overwhelmed) singly or in combination:

 Loss of LES function – decreased tone, hiatal hernia, iatrogenic injury  Delayed gastric emptying

 Increased intra-abdominal pressure – obesity, tight garments, large meal  Motor failure of oesophagus with loss of peristalsis

- Acid incites inflammation in the lower oesophagus – extent of inflammation increases with increasing duration of contact with acid

- Chronic inflammation results in complications of GORD: oesophagitis, stricture, Barrett‘s oesophagus

CAUSES/RISK FACTORS

- Malfunction of LES

- Motility disorder of oesophagus e.g. scleroderma - Hiatal hernia (loss of normal LES mechanisms)

- Chronically increased intra-abdominal pressure – pregnancy, chronic cough, obesity, constipation, etc

- Drugs that cause smooth muscle relaxation e.g. calcium channel blockers, sedatives, beta agonists, anticholinergics, etc. Coffee and smoking also cause LES relaxation. - Eating habits – lying down after a heavy meal

- Any cause of decreased gastric emptying

PRESENTATION

- Heartburn: retrosternal pyrosis

- Acid brash: reflux of sour gastric juices into back of mouth i.e. regurgitation

- These symptoms occur usually after food, particularly a heavy meal, and are aggravated by lying flat (posturally related)

- Long-standing disease can lead to dysphagia due to stricture formation; dysphagia can also result from an underlying oesophageal motility disorder; odynophagia suggests oesophagitis with ulceration

- 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 mimic anginal pain with radiation to neck, jaw, arm), nausea, water brash (hypersalivation in response to reflux)

COMPLICATIONS

1. 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 of mucosa 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 probe especially if oesophagitis is not seen on OGD

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

- The probe is placed 5cm above the manometrically-determined upper limit of the LES (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 oesophageal ulceration 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-Millerclassification

Grade I: One or more supravestibular non-confluent reddish spots, with or without exudates

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

pseudomembranous exudate

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

2. Los Angelesclassification

Grade A: one or more mucosal breaks, each <5cm in length

Grade B: at least one mucosal break >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 adjacent mucosal folds, but which is not circumferential

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

- Relevance of classification schemes: subjective and dependent on assessment by the endoscopist; also, due to the multitude of classification schemes available, just mentioning a grade may not have any meaning if the actual abnormalities are not described

TREATMENT

Lifestyle

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

Medication

1. Acid suppression therapy: proton pump inhibitors or H2-receptor antagonists 2. Prokinetics to increase LES pressure e.g. domperidone, metoclopramide Surgical

- 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 of

the fundus around the gastro-oesophageal junction

 Partial fundoplications can also be done in patients where oesophageal motility is 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 retracts into the chest, and the stomach is partitioned; usually due to a foreshortened oesophagus unrecognised in the first operation

 ―Gas bloat syndrome‖ – patient experiences difficulty burping gas that is swallowed

- Outcome of surgery

 80-90% Excellent to good (no symptoms, no medications and lifestyle changes required)

 10-15% Satisfactory (some residual symptoms)  <5% Unsatisfactory

 <1% Mortality

 5-40% need for acid suppression therapy at 5 years due to symptoms - Management of stricture

 Rule out malignant cause of stricture by taking biopsy  Dilatation (variety of means available – balloon, dilators, etc)  Treatment of underlying reflux

 If resistant to dilatation  resection and reconstruction

BARRETT’S OESOPHAGUS

Features

- Intestinal metaplasia of the oesophageal epithelial lining (stratified squamous epithelium converted to mucus-secreting columnar epithelium with goblet cells) - Associated with long-term reflux – an adaptation mechanism where intestinal

epithelium withstands exposure to acidic reflux better than oesophageal epithelium - Diagnosed on endoscopy and histology:

 The squamocolumnar junction (or Z line) is visible on endoscopy as gastric and intestinal type epithelium is pink and granular in appearance, but stratified squamous epithelium is smooth and pale

 The gastro-oesophageal junction is defined as the point where the gastric folds begin

 If the squamocolumnar junction is above the gastro-oesophageal junction (i.e. they do not align) and biopsy of the junction shows intestinal metaplasia, the patient is diagnosed to have Barrett‘s oesophagus

- Short segment Barrett‘s is defined as the squamocolumnar junction being <3cm above the gastro-oesophageal junction, while in long segment Barrett‘s the distance between the two junctions is >3cm.

- Long segment Barrett‘s is associated with more severe reflux, as well as higher risk of dysplasia and subsequent adenocarcinoma development than short segment Barrett‘s

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 3 years

- Main purpose of surveillance is to pick up dysplasia

- If patient has high grade dysplasia, it should be treated (see below), otherwise to undergo 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 (research still undergoing)

A

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 the LES, 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 used in patients not fit for surgery)

 Pneumatic balloon dilatation (about 65% of patients improve, 40% response rate at 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 a 3% chance of developing reflux  addition of fundoplication helps prevent this

UPPER BLEEDING GIT AND ITS CAUSES

A

GIT

CAUSES

1. Peptic ulcer disease (bleeding peptic ulcer) 2. Gastritis, gastric erosions, duodenitis 3. Gastric malignancy

4. Gastro-oesophageal varices 5. Mallory-Weiss tear

6. Rare causes: AV malformation (Dieulafoy lesion), aortoenteric fistula 7. 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, AV malformation

- Coffee grounds vomitus is altered blood (due to gastric acid) and can come from gastric 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 liquid in 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‖ completely

with 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 passes down so fast it doesn‘t get altered

2. Amount of blood

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

3. Aetiological 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 to haemetemesis

Malignancy

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

- Dyspepsia 4. Complications

- 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. Comorbidities

- 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 an early sign of shock)

- Patient‘s conscious level – confused?

- Compare current vitals with vitals in ambulance, ED – is there a worsening trend? 2. General inspection

- Pallor

- Cold clammy peripheries  impending shock - Stigmata of chronic liver disease

3. Abdomen

- Any tenderness (not very helpful) 4. Digital rectal examination