Abdominal aortic aneurysm

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					Passing Surgery MB




                THE CHINESE UNIVERSITY OF HONG KONG

                             DEPARTMENT OF SURGERY

                             JUNIOR / SENIOR
                           SURGICAL CLERKSHIPS




              Passing Surgery MB
                                               Oct 2001




                                   Dr Paul Lai
                      Posted on Alumni Association Homepage




Page 1     Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB


Contents                                                                                          Page

1.       General Ideas                                                                              3
2.       Surgical Physical Examination                                                              6
3.       Preoperative Care and Evaluation                                                          14
4.       Postoperative Care                                                                        16
5.       Wound Management                                                                          19
6.       Abdominal aortic aneurysm                                                                 22
7.       Peripheral arterial disease                                                               23
8.       Vasculitis                                                                                26
9.       Evaluation of breast masses                                                               29
10.      Ca Breast                                                                                 31
11.      Abdominal pain                                                                            32
12.      Acute appendicitis                                                                        34
13.      Intestinal obstruction                                                                    35
14.      Renal failure                                                                             36
15.      Laparoscopy                                                                               39
16.      Gallbladder diseases                                                                      43
17.      Acute cholecystitis                                                                       45
18.      Disease of the Liver                                                                      46
19.      HCC                                                                                       52
20.      Recurrent pyogenic cholangitis                                                            57
21.      Primary liver cancer                                                                      59
22.      Pancreatic surgery                                                                        63
23.      CA Pancreas                                                                               66
24.      Acute pancreatitis                                                                        68
25.      CA Colon                                                                                  71
26.      CA Rectum                                                                                 73
27.      FAP                                                                                       75
28.      Anorectal disorders                                                                       76
29.      Hemorrhoids                                                                               79
30.      FIA                                                                                       80
31.      Rectal Prolapse                                                                           81
32.      Lower GIB                                                                                 82
33.      CRcancer                                                                                  86
34.      CA stomach                                                                                89
35.      Gastric outlet obstruction                                                                91
36.      Ca Thyriod                                                                                92
37.      Burn care                                                                                 94
38.      Brain abscess                                                                             97
39.      Neurosurgery Key Topics                                                                   104
40.      Commonly used suffixes in surgery                                                         107




Page 2       Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB


Chapter 1 General Ideas
Good preparation is the most useful way to reduce the stress of the final MB and to pass it.

Readings
read what you should read and what is ”bread and butter”
always ask yourself whether the ”investment” is worthwhile or not
value of group studying and discussion

Life style
avoid sleep deprivation
biological clock
don’t be late at exams

Long question / Essay
read all questions at the start carefully
logical thinking
essay plan
headings
write clearly if not beautifully
don’t rush
keep good timing
lots of practice before examination

Multiple choice questions
knowledge is required !
good thinking and guess work (i.e. good sleep)
MCQs are not negatively marked, do guess for all

Clinical examination
sleep well the night before
standard dress code for clinicals (shirt and tie / blouse and skirt of reasonable length + white coat)
? value of propanolol to clam your nerves
watch you finger nails
button up your white coat
keep cool and calm at all time
watch that can count seconds, stethoscope, tape, torch, ruler, pen
ask for help and don’t panic if you run into any trouble as there are a lot of helpful people around
in the viva, when you are asked, Are you sure?”, the examiner is probably giving you a chance to correct
yourself rather than trying to trick you.
the examiner will usually pick on something that you have said as the next question or subject for discussion,
therefore, try not to mention something you don’t really know.

Do you remember these ???

Features of pain
location
nature
time and mode of onset
severity
radiation
progression of pain
duration
exacerbating and relieving factors




Page 3         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Examination of an ulcer
position
colour
size
shape
edge
base
depth
discharge
temperature
tenderness
relationship to surrounding and underlying structures
regional lymph nodes
state of local tissues (vessels, nerves and soft tissues)

Types of ulcer edge
sloping (e.g. healing skin ulcer)
punch-out (e.g. DM, trophic or syphilitic ulcer)
undermined (e.g. TB ulcer)
rolled (e.g. basal cell carcinoma)
everted (e.g. squamous cell carcinoma)

Causes of ischaemic ulceration
large artery obliteration
         Atherosclerosis
         Embolism
small artery obliteration
         Raynaud's disease
         Scleroderma
         Buerger’s disease
         Embolism
         Diabetes
         Physical agents (pressure, radiation, trauma, electric burns)

Examination of a lump
position colour           size             shape
surface            temperature     tenderness         edge
composition (consistence / fluctuation / fluid thrill /translucency / resonance / compressiblity / pulsatility / bruit)
relationship to surrounding and underlying structures
regional lymph nodes
state of local tissues (vessels, nerves and soft tissues)




Page 4          Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Tumours

The simplest classification of tumours:
       1. benign
       2. malignant (further divided into primary and secondary)

For each particular tumour, the following headings are essential:
       1. incidence
       2. age distribution
       3. sex distribution
       4. geographic distribution
       5. predisposing factors
       6. macroscopic appearances
       7. microscopic appearances
       8. pathways of spread of tumour
       9. clinical features (history and examination)
       10. investigations and diagnosis
       11. treatment
       12. prognosis

You may laugh at the list and regard this as completely useless. However, it is surprising how many medical
students failed at their final examination as they just cannot recall one particular condition according to the
simple scheme above. Furthermore, you can also use the scheme to summarize and consolidate your
knowledge on other surgical conditions.

Long cases:
Malignant tumours are commonly selected as long cases at the final examination.

The simple scheme for history, physical examination and investigations can easily fit in as:
       1. effects of primary tumour itself
       2. effects of secondaries
       3. general effects of malignant disease

For treatment or management plan, the scheme can be:
        1. curative
        2. palliative

For curative and palliative treatment, the options are:
        1. surgery
        2. radiotherapy
        3. chemotherapy
        4. combination of the above




Page 5         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB


Chapter 2                 Surgical Physical Examination
Varicose Vein (Short Case)

[Greet patient, shade hand, introduce yourself, ask for permission to examine and any sore, etc.]

Situation: usually patient will be lying on the bed or sitting in a chair, should get him stand up

A. Inspection
        1. any obvious difference in limb size
        2. any dilated veins, (over what aspect of leg?)
        3. any surgical scars
        4. any ulcers (remember posterior aspect and groin)
                 (if present, at this moment describe fully on: -site, size, shape, base, edge, surround)
                 ( + ask the patient if it is painful or not)
        5. any skin color difference, pigmentation, scaling of skin, etc.
        6. rapid comment on nail bed & toe pulp (don’t forget the heel), any hair loss
        7. ask the patient if the limb is painful

B. Feel
          1. difference in skin temp
          2. ulcer surround & induration, lipodermatosclerosis
          3. quick check for perforators (above ankle x3 , one hand breath below knee, mid thigh)
          4. must look at the groin and feel the saphenous vein (perform tapping sign)

C. Get the patient to lie down
        1. quick feel the dorsalis pulse (if suspicious, proceed to proximal pulses as a vascular case)
        2. elevate the affected lower limb, empty the veins
                 * if veins can’t be empty when patient lies supine, look for A-V fistula (thrill on palpation &
                 bruit on auscultation)
        3. upper thigh tourniquet tests
                 (note: SF junction is 2cm below and 2 cm lateral to pubic tubercle)
                 Ask the patient to stand up:
                 1. see if veins dilated again (by Tourniquet control)
                 2. release the tourniquet, thus to see further dilation of vein.
                 * may have both above & below knee incompetence

** Tell your examiners that for completion, you would perform abdominal & PR examination
** Check both lower limb sensation as well if ulcer present
** You might be asked on Perthe’s test which is a test for deep vein patency




Page 6          Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Examine the neck (Short case)

1. General examination:
      nervousness, irritated patient?
      Hand for sweaty palm, radial pulse (? AF, tachycardia, etc.)
      Hand tremor
      Eye signs:       1.      exophthalmos (check from top)
                       2.      lid lag: (fix the head)
                    3. opthalmoplegia (fix the head, over upper & outer aspect for diplopia)

         *watch out for hypothyroid patient

2. Neck examination:
      * expose to upper chest (at least exposing both supraclavicular fossa)
      A. observe:          1. any obvious mass, describe
                           2. scar
                           3. dilated veins
                           4. supraclavicular fossa asymmetry
                           5. any respiratory distress
      B. give patient a cup of water & swallow
                * pharyngeal pouch would now appear if big mass move: swallowing?
                           (fixation to pre tracheal fascia)
                            feel from in front: (ask the patient if lump is painful)
      C. for possible thyroglossal cyst, fix the mass with fingers:
                - first, ask patient to open the mouth
                - then stick out the tongue
                            for thyroglossal tract to hyoid bone if it moves
      D. fell the mass for consistency, fluctulance, borders, measure the size, etc
      E. feel for tracheal deviation
      F. feel from the back: palpate both thyroid
                (normal thyroid shouldn’t be palpable!)
                - move any lump from side to side from fixation
                - pick up overlying skin to rule out skin fixation
                - systematically palpable LN groups:
                           from top: submental, submandibular, supperficial middle, lower cervical chains,
                           supraclavicular (ask the patient to raise his shoulder), back of the neck, occipital LN,
                           back of head, preauricular & parotid region
                           for any LN felt: site, size, consistency, number, matter, fixation, tenderness
      G. for mass of anterior triangle, one must test for
                           ? reducible
                           ? ???? with gurgles
                           ? pulsatile, expansile
      H. auscultate the thyroid mass and both carotid for bruit
      I. ask the patient to cough to test for recurrent laryngeal nerve palsy
      J. check oral cavity if LN origin suspicious or parotid mass, submandibular mass
      K. check facial nerve - to shut both eyes and show the teeth (paritcularly if parotid mass is felt)




Page 7         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Abdomen Examination (Short case)
Exposure: nipple to knee
1. observe: closely for obscure scar ( be aware in skin 1.crease 2.flank 3.groin 4.around umbilicus)
                then at end of table, ask the patient to take a deep breath
                      * any distension or obvious mass
                      * visible peristalsis - asymmetry
                      * caput medusae - dilated veins
                quick look over the genitalia
                      (told the examiner that you would leave the formal exam of genitalia till the end)
2. ask the patient to cough
                inspect the hernial orifices and then feel, tell the examiner whether they are clear or not
                      if hernia present, told the examiner you would stand the patient out at the end of the
                      examination to have a proper examination of the hernia
                feel the abdominal incision sites for any incisional hernia
3. test for direction of flow if there are dilated veins slow
                * veins inferior to level of umbilicus
4. tell patient you are going to palpate (knell down)
           (”if any pain or if you feel cold, just tell me, where is the sore?”)
5. superficial palpation (from non-tender quadrant)
6. deep palpation
7. liver - from level below umbilicus up to subcostal region
           percuss the upper border (normal 5 ICS at MCL)
8. palpate the spleen from right iliac fossa + hook the spleen (turn patient towards you )
9. palpate the left kidney (keep Rt hand - the watching hand still when patient inspire deeply)  then
            test for ballotability
10. palpate Rt kindey
11. percuss along gardner’s line
12. fluid thrill tests + shifting dullness (always repeat if not certain!)
13. auscultate x                1. Liver mass (bruit & rub)
                                2. Four quadrant B.S.
                                3. aorta + bifurcation (at umbilicus level)
14. lift the head of patient up to test for suspicious abdominal wall mass
15. told the examiner you want to check for (at last!) if you does not start with general examination
                      1. LN in supraclavicular fossa
                      2. PR examination
                      3. genitalia & scrotum (testicular mass, atrophy)
                      4. femoral pulses
                      5. formal hernia examination
                      6. other chronic liver disease stigmata
16. for A.A.A being found: check radial
                                         carotid
           (or told examiner                     femoral
           you want to examine) apex beat, H.S. as well
                                         (complete cardiovascular examination)




Page 8        Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Examine this patient’s groin:
1. get the patient down (stand up!)
2. observe & describe: groin mass
                            mass down to scrotum
                            ? both sides
                            ? scars
                            watch out for undescended testis
3. ask the patient to cough  see the cough impulse (without touching the patient)
          (tell the examiner that cough impulse is present or not)
   ask him to cough again  now feel both sides
                             ask if the mass is painful or not
4. for small hernia, define the neck at this juncture
5. for large hernia, get the patient back to bed
   * check the relation of the neck of the sac to the pubic tubercle
          (you can feel this landmark from above downward)
          * may need to reduce the whole mass to see the relationship of the neck to the tubercle if the hernial
          sac is large)
6. ask the patient to reduce it for you (if the patient is young and smart or you have to reduce it)
          *don’t hurt patient when reducing the hernia
          (tell examiner whether it is fully reducible)
7. stand over to right side of patient for right-sided hernia and vice versa
          right side - press with right hand finger tips over the deep ring
          (define ASIS & pubic tubercle)
8. support the back of the patient with the other hand
9. get the patient stand up (keep the compression)
10. ask patient to cough
           A. controlled  indirect inguinal hernia
          then release the hand
           if hernia comes out  indirect inguinal hernia OK!

           B. not controlled: probably direct inguinal hernia
          then release the hand
           B. if mass exaggerated
                    possible Pantaloon’s hernia
                   (direct + indirect inguinal hernia)
11. tell examiner that you would like to complete the examination by:
                   1. abdominal examination for ascites, mass, etc.
                   2. chest - COAD
                   3. PR examination

Noted: for suspect groin LN / femoral hernia
        * always say femoral hernia can’t be rule out completely (even if cough impulse is absent)
        * always check abdomen in cases of femoral hernia for any mass
        * check the lower limb in cases of groin LN for ulcers, melanoma, etc.

DDx for inguinal hernias include femoral hernia, vaginal hydrocele, hydrocele of cord / canal of Nuck,
undescended testis, lipoma of cord.

You need to know very well the anatomy of the inguinal canal and the femoral canal




Page 9         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Leg Ulcers:
Inspection: site, (pressure points?, toes? )
              size: in cm
              shape: oval, irregular?
1. ask patient if the ulcer is painful?
2. told examiner whether it is a shallow /deep ulcer
3. base - necrotic, dry, infected, covered & discharge, etc.
   edge - sloping /everted, rolled, etc.
   surrounding tissue: pigmentation, induration, cellulitis
   (tell the examiner you will check the groin LN at the end)
4. both legs: size
               scars
               dilated veins
               trophic skin changes, nail bed,
               flattened pulps of toes
5. feel for the temperature over both legs
6. capillary filling time
7. peripheral pulses
8. test for loss of sensation L1-S1
9. test proprioceptive if necessary / jerks / ask for a tuning fork for DM ulcers
10. do Buerger’s test (elevation blanching and dependent rubor)
11. tests for varicose vein (stand up) for any dilated veins, Perthe’s test for deep vein patency

Differential diagnosis:                                      base
4 common:                                                    depth
- Venous - USG dopper, ctc                                   discharge
- arterial - ankle, brachial index                           temperature
- DM neuropathy - check urine sugar                          tenderness
- neoplastic - BCC, SCC, melanoma                            relationship to surrounding and underlying
4 not uncommon                                               structures
- infective - TB syphilus, AIDS                              state of local tissues (vessels, nerves and soft
- trauma - self inflicted, work related                      tissues)
- insect bite, chemical contact, radiation                   regional lymph nodes
- topical /dressing allergy
3 unusual                                                    *Types of ulcer edge
- R.A.  vasculitis                                          sloping (e.g. healing skin ulcer)
- SLE, PAN, CREST                                            punch-out (e.g. DM, trophic or syphilitic ulcer)
- blood dyscrasis (sickle cell, leukaemia)                   undermined (e.g. TB ulcer)
                                                             rolled (e.g. basal cell carcinoma)
*Causes of ischaemic ulceration                              everted (e.g. squamous cell carcinoma)
large artery obliteration
         Atherosclerosis
         Embolism
small artery obliteration
         Raynaud’s disease
         Scleroderma
         Buerger’s disease
         Embolism
         Diabetes
         Physical agents (pressure, radiation,
trauma, electric burns)


Check list for examination of an ulcer
position
colour
size
shape
edge


Page 10         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Breast Examination:
1. ask for exposure of neck, chest and both shoulders
2. check the bra for discharge, blood clot, etc (if there is one!)
3. observe: at the end of bed        1 breast size difference
                                     2 nipple level
                                              retraction, ulceration, discharge, erythema
                                              (you may ask patient if it has been like that all along)
                                     3 skin over the breast for Peau d侊range
                                     4 dilated chest veins
                                     5. arm swelling (may well be a case of axillary vein thrombosis or post-RT
                                     lymphoedema)
4. ask the patient to raise both arms
          - look for skin tethering
          - exaggeration of above signs
5 ask the patient whether the breast is painful or not
          if painful, ask the patient to point to the mass
6. start palpate the normal side first
          don’t forget the nipple
7. palpate the abnormal side
9 fix the mass  define the mass
                            position
                            size (measure in cm)
                            temperature
                            shape, surface
                            pick the overlying skin x skin fixation
                            check if mass fix to chest wall
10. check the patient to push her hands on her waist
          check for mobility against pectoralis major in 2 planes
11. examine axilla (both side)
 * warm her it is going to be slightly uncomfortable and ask her to relax
          right axilla - support the elbow of patient with right hand and feel the axilla with the left hand
          Axilla LN grouping: apex, medial, lateral, anterior, posterior, interpectoral
12 go behind the patient: examine the LN in supraclavicular fossa
          percuss the thoracic spine x ? bone pain due to 2°
13. percuss lung bases x effusion if huge CA
14. lie patient flat for abdominal exam (liver edge & spleen)
15. if the lump is tender, may ask menstrual cycle

Arterial diseases (Short Case)
Exposure from groin to heel
1. look: leg size, color
          muscle wasting, joint swelling
          scars (*be ware of groin & popliteal fossa)
          trophic skin change, nail dystrophy (scaling ), hair loss
          flattened toe pulps
          (mention all small corns, callosity , psoriasis, eczema, etc. seen)
2. feel: temperature, capillary refill time
3. palpate the arteries: dorsalis pedis
                           posterior tibial
                           popliteal
                           femoral
          (kneel down on the side of bed, rest your elbow on bed)
          *palpate along the line of artery as below
4. Buerger’s test: elevate both legs x 30 sec. wait for blanching (stand at the end of the bed)
          release the both feet to one side of the bed for: 1. dependent rubor
                                                               2. slow refill of guttered vein
5. auscultate the femoral pulses all the way down the Hunter’s canal if there is a diminished
          femoral pulse on one side
6. ask for abdominal exam for ? AAA               ? aorto-iliac bruit (umbilical level)


Page 11         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

7. check carotid both sides + auscultate for carotid bruit (also heart sounds & murmur)
8. check the B.P (told the examiner that you want it be measured)
*? doppler x ankle / brachial index (usually not available)
        (normal > 1.1, abnormal < 0.9, worry < 0.6, critical limb / rest pain < 0.3)
Jaundice Patient:
History Taking
[shake hand with patient first. Introduce yourself: I am medical student of CUHK. May I have a word with you
about your problem recently?]

Age:              how old are you?
                  what kind of job / work are you now doing?

Jaundice:         1) onset - when do you start to have the yellow skin & duration
                  2) is persistent / comes & goes?
                  3) progression: is it getting worse /better?
                  4) what is the color of your water? (urine)
                  5) how is the bowel motion?
                           Is it pale, floats on water
                           very smelly? Blood, mucus, diarrhoea etc.
                  6) itchiness of skin?

Pain: do you have abdominal pain? (does the tummy sore?)
        characteristic site: where is it? how would you describe it?
                  (dull, sharp, colicky, cramps)
        radiation: does it goes to the back / shoulder?
        relief: can any thing like food or medicine that makes it better?
        aggravation: is the pain worsen by hunger?
                  does it wake you up at night?
                  does it occur after a full meal?
                  would squatting / bending the knee again the chest relief the pain?
                  (pancreatic nature?)

Fever: have you experience any temperature?
       have you measure it?
       how often do you experience it?
       do you got chills? Rigors?

GIT:      nausea / vomiting, malaise
          (how is your energy recently?)
          do you easily get tired?
          diarrhoea? loss of appetite?

Wt:     are you losing weight?
        losing how many pounds?
        over what period of time?
* do you have to take medicine regularly? For what reasons?
* do you have liver problem or hepatitis in the past? When?
        were you told that you are a carrier for the hepatitis?
* how you got other thing to tell me other than that I have been asking about you?

Social: smoker, drinker (details needed)

Past health: how is your previous health?
            any heart attack? H.T.?
            stroke? diabetes? how do you check for it?
            do you test your water? how many cross do you usually got in the urine test?




Page 12          Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB

Intermittent Claudication (Long Case)
History taking
1. Age, occupation, marital state, smoker, drinker

2. Onset of claudication
       Pain on walking (relief on rest, any paraesthesia or numbness,
                          any L.B.P / sciatica, any nocturnal pain)
       Since when do you start to have the leg pain
       Where is the pain?
       Is it most painful over (say the toes? the foot? calf? thigh?)
       Claudication distance (How far can you walk? How many feet
                                before you got the pain?)
       Progression of claudication (changes over a period of time)
       Pain severity (hang out of bed, rest pain, gangrene, analgesic requirement)

3. Risk factors
         Hypertension (for how long? what drugs? control?)
         Smoking (for how long? how many?
         DM (what kind? what drugs used? control?. Any systemic involvement? i.e. renal, ophthamological,
         cardiac problems)

4. Any impotence (How is your sexual life? Can you remain stiff? Any buttock pain?)

5. Any TIA, stroke (extend of recovery?), heart attack, chest pain, abdomen pain?

6. Operation, when, for what? Any relation to the vascular status?

7. Daily activities, social problems
         Housing area, shopping ?
         Need wheel chair?
         Do you still walk?
         Are you the sole bread winner?
         Anyone care for you now?
         How do you live with?




Page 13         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB


   Chapter 3 Preoperative Care and Evaluation
                                                                                               (last revised April 1998)

I. ADMIT ORDERS
A. Admit to the ward--primary physician

B. Diagnosis and planned procedure

C. Condition

D. Vital signs: for elective procedure, routine. For emergency procedure, increased frequency if unstable or if
attempting to adjust fluids before surgery

E. Allergies: medications and iodine

F. Activity: bed rest if unstable vital signs or other indication; otherwise encourage activity to avoid deep
venous thrombosis (DVT), muscle atrophy, pneumonia

G. Nursing: monitoring neurologic checks, monitoring lines (central venous pressure [CVP], Swan-Ganz
catheter), preoperative teaching, patient-controlled analgesia (PCA) pump, pulmonary toilet, etc.

H. Diet: determined by the rest of the medical history and the preparation required for surgery. The period of
nothing by mouth (NPO) before surgery depends on the age of the patient (infants may have clear liquids up
to 4 hours before surgery, adults should be NPO at least 6 to 8 hours)

I. Intakes and outputs (I&Os): fluids for rehydration (normal saline [NS] or lactated Ringer's [LR] solution),
maintenance and correction of electrolyte imbalance. Blood products if needed. Monitoring of fluids and fluid
status (CVP/Swan-Ganz, Foley)

J. Special tests. Chest x-ray: current to within 1 month unless likelihood of acute changes. Also depends on
emergency surgery, age, chronic illness. Electrocardiography (ECG): if older than 40 years, baseline ECG, or
if risk factors for coronary artery disease (CAD) or history of arrhythmias. Tests for specific surgery that might
help avoid problems during surgery (e.g., intravenous pyelography [IVP] to localize ureters for pelvic surgery)
or to identify concurrent problems (cholelithiasis and peptic ulcer disease [PUD], upper gastrointestinal [UGI]
and lower gastrointestinal [LGI] bleeding sources)

K. Special medications
        1. Patient's routine medications, change medications to intramuscular (IM) or intravenous (IV) as
        needed
        2. Increased steroids preoperatively if steroid dependent
        3. Pain medications as needed
        4. Antibiotics as indicated for infection/sepsis or prophylaxis of endocarditis, indwelling hardwear, or
        graft placement
        5. Preparation for surgery: bowel preparation, DVT prophylaxis with subcutaneous heparin, antiseptic
        shower and shave if indicated
        6. Premedication per anaesthesia to lower anxiety, lower secretions, and interact with narcotics for
        sedation

L. Laboratory tests
        1. Minimal: complete blood count (CBC) with platelets, urinalysis (UA)
        2. With any acute illness, medications affecting fluid/electrolyte balance, major surgery: electrolytes,
        urea & creatinine, glucose
        3. Consider calcium, total protein and albumin, prothrombin time (PT), partial thromboplastin time
        (APTT), liver enzymes, amylase, drug levels, marker levels before surgery (e.g. carcinoembryonic
        antigen [CEA])
        4. Pulmonary history: arterial blood gases (ABGs) and spirometry
        5. Type and crossmatch as indicated for the procedure



Page 14         Sing praises to God, sing praises: sing praises unto our King, sing praises. (Psalm 47:6)
Passing Surgery MB


II. MEDICAL HISTORY OF MAJOR IMPORTANCE

A. Neurologic
       Seizures: some anticonvulsants are oral only. May need to change medications if the patient will be
       NPO for a long period of time

B. Haematologic disorders
       1. Clotting disorders: may need evaluation, treatment
       2. Anaemia: ideally a haematocrit greater than 30%, with hemoglobin greater than 10 g/dL by the
       time of surgery

C. Integument disorders
        1. Active infections or open wounds in the area may delay elective surgeries because of
        postoperative infection risk
        2. Chronic skin disorders should be optimally controlled for postoperative healing
        3. Keloid formers: may need to consider different closure techniques

D. Nutritional status
         1. For elective or semielective surgery consider optimizing the nutritional status if the patient has
         chronic disease
         2. Obesity: weight loss to improve cardiopulmonary status and decrease problems with healing

E. Cardiac
        1. Congenital disease, rheumatic fever, unevaluated murmurs, coronary artery bypass grafting
        (CABG) within 6 months, post-n-valve replacement status: consider the need for prophylactic
        antibiotics. Aortic stenosis at high risk if there is a markedly decreased valve area
        2. Hypertension: diastolic blood pressure should be less than 110 and optimally in the normal range
        3. Atherosclerotic disease
                 a. Angina: mild, stable; eligible for minor elective surgery. More than this needs further
                 evaluation. For urgent procedures, may want to have an intraaortic balloon pump available
                 b. A history of myocardial ischemia (MI) less than 3 weeks has a 25% mortality rate; urgent
                 procedure only. At 3 months, a 10% mortality rate; semiurgent procedures. At 6 months, a
                 5% mortality rate; elective. At 1 year, the same risk as for an asymptomatic patient
                 c. Increased risk of MI within the first 48 hours; patients should have increased monitoring
                 postoperatively
        4. Arrhythmias
                 a. Increased risks with greater than five premature ventricular contractions (PVCs) per
                 minute, coupled PVCs, ventricular tachycardia, a history of cardiac arrest, second-or third-
                 degree heart block, bradyarrhythmias
                 b. Consider whether a preoperative pacemaker or postoperative cardiac monitoring is
                 appropriate
        5. Congestive heart failure: optimize control and fluid balance. Consider a preoperative Swan-Ganz
        catheter and evaluation of cardiac output with different pulmonary capillary wedge pressures
        (PCWPs) to find the optimal balance for postoperative control

F. Pulmonary
       1. Chronic obstructive airway disease (COAD): optimize the pulmonary toilet. Check for any change
       in sputum production or color indicating active infection; delay elective or semiurgent procedures
       2. Baseline spirometry and ABGs may help with postoperative management




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Chapter 4 Postoperative Care                                                      (last revised April 1998)


I. TYPICAL OPERATIVE NOTES
A. Preoperative diagnosis
B. Postoperative diagnosis
C. Procedure or operation performed
D. Surgeon, assistants
E. Anesthesia: general endotracheal, general mask, spinal, epidural, regional block, local, etc.; include the
specific agent used
F. Findings
G. Specimen: frozen section if obtained, pathology, microscopy, etc.
H. Estimated blood loss
I. Intraoperative fluids and blood products administered
J. Drains and tubes placed
K. Complications
L. Patient's condition and disposition


II. ORDERS
A. Admit to the ward, intensive care unit (ICU), or recovery room

B. Diagnosis, operation

C. Vital signs: every 30-60 minutes the first few hours, then reduce as stable

D. Allergies

E. Activity: bed rest until fully awake; up walking that night or the next morning depending on the surgery

F. Diet: NPO until nausea resolves or resumption of bowel activity as determined by bowel sounds, passing
gas, or having a bowel movement. Start with clear liquids and advance as tolerated

G. I&Os
          1. Record I&Os every shift or more frequently if the patient's condition is unstable
          2. IV fluids: with surgeries involving third spacing replace with isotonic solutions or colloid for the first
          24 hours. Nasogastric (NG) losses should be replaced with 0.45 NS, and if there is an exceptionally
          large amount, then replace losses cubic centimeter for cubic centimeter. Maintenance fluids should
          generally be a mixture of sodium cholide and dextrose (e.g. alternating NS and D5 solution, half-half
          solution, etc.). Potassium is normally included in replacement solutions but is excluded from
          maintenance solutions until normal renal function is established (i.e., on first postoperative day). If
          hypotension and oliguria are both present, the cause is most likely volume depletion, and a bolus of
          500 or 1000 cc NS or LR may be tried. Urine output should be 0.5 to 1 ml/kg/hr at a minimum
          3. Instructions for care of all tubes and drains including a Foley catheter and nasogastric tube. The
          NG tube should be connected to low intermittent suction and irrigated frequently to ensure patency




H. Nursing
        1. Encourage turning, coughing, deep breathing, and incentive spirometry
        2. Dressing changes
        3. Parameters to notify the doctor such as urine output (1/2 cc/kg/hr), fever, hypertension or
        hypotension, tachycardia or bradycardia, inability to void within 8 hours of beginning surgery, or
        unusual drainage on dressings
        4. Specify neurologic or vascular checks




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I. Medications
        1. Pain medications: oral, IV (via PCA or injection), IM. Adequate doses improve mobility. High doses
        lead to hypoventilation and atelectasis
        2. Antiemetics: first consider whether medications may be causing nausea, whether tubes are
        plugged, or whether this is postanaesthetic nausea
        3. Antibiotics: for infection or for prophylaxis
        4. Routine medications that need to be renewed
        5. As-needed medications such as laxatives, sleeping medications, antacids, etc

J. Special tests such as follow-up chest x-rays or serial ECGs. Serial ECGs should be performed for high-risk
cardiac patients because the first 3 days have the highest risk of postoperative MI

K. Laboratory: follow-up CBC for the possibility of hemorrhage or for a large amount of blood loss. If the
patient continues on IV fluid, check electrolytes daily

III. POSTOPERATIVE FEVERS
A. Respiratory
        1. Initially may be secondary to aspiration
        2. Twenty-four to 48 hours postoperatively, most commonly due to atelectasis
        3. After 48 hours, most likely pneumonia developing

B. Wound infections
       1. First 24 hours, suggests Clostridium
       2. Forty-eight to 72 hours, most commonly due to Streptococcus species
       3. At 4 days, consider enteric aerobes and anaerobes and Staphylococcus

C. Thrombophlebitis: occurs intraoperatively and fever usually begins after 24 hours

D. Urinary tract infections: usually related to instrumentation or an indwelling Foley catheter and occurs after
24 hours

E. Less common causes of perioperative fever
        1. Transfusion reaction: immediate
        2. Malignant hyperthermia: starts intraoperatively
        3. Drug reaction
        4. Endocrine, such as thyroid storm
        5. Thrombophlebitis from the IV site

** There is a nice chapter in the Lecture Notes on General Surgery (by Ellis & Calne) on post-operative
complication, especially the table classifying the complications according to the time

IV. POSTOPERATIVE OLIGURIA
A. Oliguria is defined as urine output less than 30 cc/hr or 1 cc/kg/hr in infants. Postoperative oliguria can be
divided into
         1. Prerenal azotemia: caused by a decreased glomerular filtration rate secondary to hypovolemia or
         hypotension. This can occur with hemorrhage, GI loss, excessive renal loss, and sequestered loss
         (i.e., third-spacing)
         2. Acute tubular necrosis (renal failure): postoperatively it often develops when one or more
         conditions occur, including preexisting renal disease, long periods of hypotension, use of nephrotoxic
         agents, septicemia, or hemolysis (see Chapter 11 for a detailed discussion of diagnosis and
         management)
         3. Other causes
                    a. Reflex spasm of the voluntary sphincter because of pain or anxiety
                    b. Medications such as anticholinergics and narcotics
                    c. Detrusor atony as result of surgery and manipulation (especially after retroperitoneal or
                    pelvic surgery)
                    d. Preexisting partial bladder outlet obstruction such as an enlarged prostate
                    e. Mechanical obstruction such as an expanding haematoma or fluid collection or an
                    occluded Foley catheter


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B. Diagnosis: look for signs of hypovolemia such as decreased skin turgor or dry mucous membranes. If the
patient cannot or has no desire to urinate after several hours postoperatively, consider oliguria secondary to
hypotension. A palpable bladder is a sign of urinary retention

C. Treatment: relieve local pain. If the condition permits, perhaps standing or sitting may facilitate voiding.
Treat hypovolemia if present. Diuresis will worsen prerenal azotemia. If mechanical obstruction, e.g., an
enlarged prostate, is present, consider intermittent catheterization. If the patient already has a Foley catheter,
irrigate it to assess for obstruction




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Chapter 5 Wound Management                                                     (last revised April 1998)


I. GENERAL PRINCIPLES
The goal of wound management is primarily restoration of function, which requires minimizing the risk of
infection and repair of injured tissue with minimum cosmetic deformity.

II. SIGNIFICANT HISTORY

A. Mechanism of injury
       1. Blunt trauma: split or crush-type injuries will swell more and tend to have more devitalized tissue
       and higher risk of infection.
       2. Sharp trauma: clean edges, low cellular injury and risk of infection.
       3. Bite injury: high chance of infection, both superficial and deep.
       4. Examine the wound to rule out an underlying fracture or retained foreign body, which increases the
       risk of infection. X-ray suspicious injuries.

B. Contaminants: wound contact with feces, rust, dirt, etc., will increase the risk of infection. Wounds
sustained in barnyards or stables are considered contaminated. Clostridium tetani is indigenous in manure.

C. Time of injury: after 3 hours, the bacterial count in a wound increases dramatically. Wounds may be
closed primarily up to 18 hours out; clean well and use clinical judgment when choosing which wounds to
close. Wounds up to 24 hours old on the face may be closed after good cleaning. The blood supply in this
area is much better and the risk of infection therefore much less. All wounds should be rechecked for
infection between 24 and 48 hours. The risk of infection may be reduced in wounds by using tape closures.

D. Tetanus status: start full immunisation programme (immunoglobulin & tetanus toxoid) for patients not
previously immunized or if they were immunized more than 10 years ago. Booster dose of toxoid should be
given if the patient was immunized within the last 10 years.

E. Allergy history: check specifically for iodine, tape, lidocaine, and antibiotics.

F. Other medical illnesses
        1. Diabetes: small-vessel disease and immune suppression both increase the risk of infection.
        Antibiotics should be used for lower-extremity injuries with frequent rechecks.
        2. Chemotherapy or steroid dependence: immune suppressed. Need to use antibiotics orally for
        prophylaxis for any contaminated wound. Slowed healing may require sutures to remain in for 14 to
        21 days. After suture removal, reinforce the wound with wound tapes to avoid dehiscence.
        3. Peripheral vascular disease: increased risk of infection and delayed healing; watch the wound
        carefully.
        4. Malnutrition and other specific deficiencies: lack of protein, ascorbic acid, vitamin A, and other
        substances may inhibit or prolong healing. General nutritional support should be encouraged.

III. PHYSICAL EXAMINATION
A. Vascular injury: direct pressure is the first choice for controlling bleeding. If a fracture is involved,
immobilization will help control bleeding. Do not clamp vascular structures until it can be determined whether
this is a significant vessel needing repair. If the anatomy is suggestive of injury to major vascular structures,
obtain an angiogram. Capillary refill should be checked distally and be less than 2 seconds. Bleeding on the
scalp is best controlled by suturing the wound. For extremities, inflating a blood pressure cuff above systolic
pressure assists in wound inspection and repair.

B. Neurologic: check distal muscle strength and sensation. For hand and finger lacerations, check two-point
discrimination, which should be less than 1 cm at the fingertips. A crush injury may also decrease two-point
discrimination, and may take several months for recovery. A lacerated nerve may be repaired immediately or
delayed. Always check sensation before administering anesthesia. Numbness may also be the first sign of a
developing compartment syndrome.

C. Tendons can be evaluated by inspection, but individual muscles must also be tested for full range of
motion and full strength.


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D. Bones: check for open fracture or associated fractures. X-ray if there is any question. An open fracture is
an indication for surgical debridement and repair except in the case of a distal phalanx fracture, where
copious irrigation and oral antibiotics are acceptable treatment if the injury can be watched carefully for
infection. Even an obvious fracture should be radiographed in case comparison is needed in the future for
fracture healing or the development of osteomyelitis.

E. Foreign bodies: inspect and x-ray the area. Remember that wood or low lead glass may not show on
radiographs. Wound markers can be used during radiography, and views obtained in two planes can help
localize the object for recovery. During exploration spread the tissue; do not cut tissue and risk neurovascular
injury. Glass may penetrate at an angle and be buried deeper than it appears to be. Ultrasound is very
sensitive at picking up foreign bodies if x-ray findings are questionable.

IV. REPAIR
A. Wound healing
       1. Collagen formation peaks at day 7. The wound has 15% to 20% of its full strength at 3 weeks and
       60% of its full strength at 4 months. Epithelialization occurs in 48 hours under optimal conditions. The
       wound is then completely sealed.
       2. Scar formation: requires 6 to 12 months for a mature scar. Scars should not be revised until 12
       months have past. A wider scar or inadequate wound closure with dehiscence may occur with
       increased skin tension or if the wound is in an area of excessive motion. Contractures can develop
       when a scar intersects perpendicular to a joint crease. A Z-plasty or W-plasty may need to be revised
       in the future. Close approximation of portions of wounds gives the most pleasing scar, and frequently
       debriding jagged edges widens a scar or makes edges uneven and difficult to close.

B. Anaesthesia
       1. Local: over the edges of the wound. A small-gauge needle (27 or 30 gauge), slower infiltration, and
       deeper infiltration decrease the pain of infiltration. Subdermal injection may require 5 to 6 minutes for
       anesthesia to pinprick. Simple, effective, and quick.
       2. Regional: especially good for fingers, hands, feet, toes, mouth, and face.
       3. Anesthetics: true allergies to local anesthetics are rare and generally seen only with esters. Most
       "allergic'' reactions are actually vasovagal or other adverse response
                 a. Lidocaine is most frequently used and has an onset in 2 to 5 minutes and a duration of 60
                 minutes. Can use 3 to 5 mg/kg with not more than 300 mg total. Can repeat the dose after 30
                 minutes. Avoid the addition of epinephrine near end organs such as the fingers or toes
                 because it is a potent vasoconstrictor and may decrease blood flow and induce ischaemia.
                 b. Bupivacaine (Marcaine) has onset of 5 to 10 minutes and a duration of 90 to 120 minutes.

C. Wound preparation
      1. Debridement: with aseptic technique, devitalized tissue should be removed. Heavily contaminated
      tissue in sites free of critical tissue should be removed. High-pressure irrigation using a 35-cc syringe
      with a 19-gauge needle and normal saline is one of the most effective means of cleansing a wound.
      Scrubbing does not cleanse the wound as well, and using any disinfectant in the wound damages
      healthy cells needed for healing and resisting infection.
      2. Skin disinfection can be performed with povidone-iodine or chlorhexidine. Shaving the area may
      increase the risk of infection. However, hair can be clipped in the area if necessary. Never shave
      eyebrows because they are needed for alignment of the wound and may not grow back.

D. Wound closure
      1. Avoid primary closure of infected and inflamed wounds, dirty wounds, human and animal bites,
      and neglected and severe crush wounds. Stellate and missile wounds also fit this category.
      2. Tape closure: carries a lower risk of infection than suturing and may be a consideration for higher
      risk wounds. This may also be considered for small children to avoid a frightening surgical procedure.
      3. Open wound care: saline wet to dry dressings with gauze or antibiotic ointment dressings will keep
      the tissue moist. Gentle washing of the wound two to three times per day will remove bacterially
      contaminated secretions. Gauze dressing (especially larger pore size) will help gently debride dead
      and infected tissue. Avoid iodine dressings because this damages healthy tissue and will slow
      granulation. When clean tissue is apparent, closure with wound tapes can then be attempted.



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          4. Suturing: sutures are of two types--absorbable and nonabsorbable. Precision-point cutting needles
          and small-sized suture (5-0 or 6-0) should be chosen for skin when cosmetic closure is important. A
          conventional cutting needle is used for routine skin or dermal skin closure. A noncutting needle
          should be used for subcutaneous tissue. Extensor tendons are slow healing and should have a
          permanent suture of small size chosen. Muscle fascia layers may require nonabsorbable suture if
          under high tension. The majority of subcutaneous or dermal suturing may be performed with an
          intermediate duration absorbable suture. Skin suture should be chosen by the smallest size adequate
          for skin tension. Nonabsorbable monofilament suture gives the lowest risk of infection and lowest
          suture reactivity, thus minimizing scars.
          5. Dressings: consider antibiotic ointment to decrease infection until the skin surface closes (many
          surgeons do not believe in antibiotic ointment !). Immobilize if motion of a joint is going to increase
          skin tension and delay healing. Keep the wound dry for 24 hours; after this time most wounds do not
          require a dressing.

V. BITE WOUNDS
Good irrigation is mandatory for puncture wounds. All these wounds are much more prone to infection.

A. Human bites: multiple organisms are involved, including anaerobes. Osteomyelitis, septic arthritis, and
tenosynovitis are common complications. Any wound involving a joint should be irrigated in the operating
room and intravenous antibiotics used. Facial wounds are the only wounds that should be considered for
closure and must have antibiotics used in conjunction. Amoxicillin/clavulanate is the first choice followed by a
cephalosporin.

B. Cat bites: higher risk of infection than dog bites, particularly with Pasturella multocida as the major
pathogen present. Antibiotics should be used on all bites. Amoxicillin/clavulanate is recommended.
Doxycycline or tetracyclines in penicillin -allergic patients.

C. Dog bites: less prone to infection and may be treated without antibiotics if irrigated well, seen soon after
injury, and not complicated by devitalized tissue. If antibiotics are advisable, use ampicillin or penicillin VK.
Doxycycline or tetracycline in the penicillin allergic.

D. Rabies treatment
        1. Domestic dog or cat, in healthy condition and available for 10 days' observation: no treatment
        2. Domestic dog or cat, in rabid condition or suspected: human immune globulin and human diploid
        cell vaccine
        3. Domestic dog or cat condition unknown: consult public health in the area
        4. Wild animal: skunk, bat, fox, coyote, raccoon, carnivores--regard as rabid unless negative by
        laboratory tests
        5. Livestock, rodents, rabbits, hares: consult public health in the area

VI. FOLLOW-UP CARE
A. Risk of infection is highest in 24 to 48 hours, so if a high-risk wound is present, recheck during this period.
Consider antibiotic use for
        1. Patients prone to endocarditis
        2. Patients with hip prostheses
        3. Lymphedema
        4. Contaminated foot wound in diabetics or others with peripheral vascular disease
        5. Contaminated wounds that are primarily closed
        6. Human bites, which should always have antibiotic treatment
B. Suture removal; general guidelines
        1. Face: 3 to 5 days with tape reinforcement after suture removal
        2. Scalp: 7 to 10 days
        3. Trunk: 7 to 10 days
        4. Arms: 7 to 10 days
        5. Legs: 10 to 14 days
        6. Joints, dorsal surface: 14 days
        7. Increase the length for diabetics or steroid-dependent patients, who may require several weeks to
        heal



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Chapter 6 Abdominal aortic aneurysm
Introduction
    th
13 leading cause of death in USA
first successful resection and replacement in 1951
mortality of elective aneurysm repair ~2%
mortality of ruptured AAA >70-80%
the most important positive predictor of overall survival is early diagnosis as patients whose AAA are
discovered early and treated promptly have a mean 5-year survival rate only slightly lower than that of age-
matched controls

Definitions
irreversible, localized dilatation of an artery (alternatively, an aneurysm can be defined as an arterial segment
with a diameter at lease 50% greater than normal as a lesser dilatation is referred to as ctasia’)
normal external diameter of infra-renal aorta: about 2 to 2.5 cm

Risk factors
old age
males
racial difference (more in whites)
hypertension
smoking

Pathogenesis
atherosclerosis
genetically predisposed difference in the arteries
         Lapace Law (which states that the tension [lateral pressure] in the wall of a hollow viscus varies
         directly with its radius)
inherited connective tissue diseases (Ehlers-Danlos syndrome; Marfan syndrome)
inflammatory diseases (Takayasu arteritis; Kawasaki disease)
infective processess (mycotic anuerysms)




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Chapter 7 Peripheral arterial disease                                                          (last revised April 1998)


Peripheral arterial disease is characterized by intermittent claudication, consisting of exercise-induced lower
extremity pain that is relieved by rest. Claudication occurs when the blood supply is inadequate to meet the
demand of lower limb muscles as a result of atherosclerotic arterial stenosis.

I. Pathophysiology

A. The incidence of claudication rises sharply between ages 50 and 75 years, particularly in persons with
coronary artery disease.

B. This condition affects at least 10% of persons over 70 years of age and 2% of those 37-69 years of age.

C. Risk factors
        1.Cigarette smoking is the most important risk factor for PAD. 70-90% of patients with arterial
        insufficiency are smokers. Risk remains increased for up to 5 years after smoking cessation.
        2.Other risk factors include hyperlipidaemia, diabetes mellitus, and hypertension, and family history.

D. After five-years, 4% of patients with claudication lose a limb and 16% have worsening claudication or limb-
threatening ischaemia.

E. The five-year mortality rate for patients with claudication is 29%; 60% of deaths result from coronary artery
disease, 15% from cerebrovascular disease, and the remainder result from nonatherosclerotic causes.


II. Clinical Evaluation of Claudication

A. Evaluation consists of determining the location, extent, and severity of disease and the degree of
functional impairment.

B. Claudication
        1.The key clinical features of claudication are reproducibility of muscular pain in the thigh or calf after
        a given level of activity, and cessation of pain after a period of rest.
        2.Patients should be asked about the intensity of claudication, its location, and the distance they have
        to walk before it begins.
        3.Aortoiliac disease is manifest by discomfort in buttock and/or thigh and may result in impotence
        and reduced femoral pulses. Leriche's syndrome occurs when impotence is associated with bilateral
        hip or thigh claudication.
        4.Iliofemoral occlusive disease is characterized by thigh and calf claudication. Pulses are diminished
        from the groin to the foot.
        5.Femoropopliteal disease usually causes calf pain. Patients have normal groin pulses but
        diminished pulses distally.
        6.Tibial vessel occlusive disease may lead to foot claudication, rest pain, non-healing wounds, and
        gangrene.
                   a. Rest pain consists of severe pain in the distal portion of foot due to ischaemic neuritis.
                   b. The pain is deep and unremitting, and it is exacerbated by elevation and relieved by
                   dangling the affected foot over the side of the bed.




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III. Physical Examination

A. Evaluation of the Peripheral Pulses should include the femoral, popliteal, posterior tibial, and dorsalis pedis
arteries. The quality of the pulse and any pulse asymmetries between the limbs should be noted.

B. Other signs of chronic arterial insufficiency include brittle nails, scaling skin, hair loss on the foot and lower
leg, cold feet, cyanosis, and muscle atrophy. Careful inspection of the foot for skin breakdown or ulceration is
important. Buerger’s test is useful.

C. Bruits may be auscultated distal to the arterial obstruction.

D. Abdominal examination for a "pulsatile mass" is performed because of the strong association between
abdominal aortic aneurysm and peripheral arterial disease.


IV. Differential Diagnosis

A. Neurogenic Claudication (spinal stenosis)
       1.Neurogenic claudication is the clinical syndrome most difficult to distinguish from claudication.
       Neurogenic claudication is caused by osteophytic narrowing of the neural canal around the spinal
       nerves.
       2.This syndrome causes radicular leg pain that begins with a change of posture and is relieved by
       assuming the recumbent position. The leg pain is often accompanied by burning, tingling, and
       numbness.
       3.The pain of neurogenic claudication persists even after the patient has stopped walking or occurs
       with mere standing or after prolonged sitting. With neurogenic claudication, the distance walked until
       the onset of pain varies.

B. Nocturnal muscle cramps occur in older persons, but the cramps are not related to exercise.

C. Chronic compartment syndrome may occur in young athletes characterized by tightness and pain in the
calf after vigorous exercise. The pain does not quickly subside with rest.

D. Osteoarthritis of the hip may mimic thigh and buttock claudication. However, osteoarthritic pain occurs with
variable amounts of exercise,, and the pain changes in severity from day to day.


V. Laboratory Testing of Arterial Disease

A. Ankle-brachial Index (ABI)
        1.The ankle-brachial index (ABI) is the ratio of ankle systolic blood pressure to arm systolic blood
        pressure. It is highly sensitive and specific for peripheral arterial disease in nondiabetic patients.
                a.0.75 is considered normal
                b.0.40-0.75 suggests arterial obstruction with claudication
                c.<0.40 suggests significant arterial obstruction with critical ischaemia (i.e., non-healing
                wounds or rest pain).
        2.Patients occasionally have normal ABIs at rest, but their symptoms strongly suggest claudication.
        In these patients, ABIs should be obtained before and after exercise. Exercise may unmask
        obstruction.
        3.ABI and segmental blood pressure measurements are not accurate in patients with calcified
        vessels (especially diabetics) because ankle blood pressure readings tend to be falsely elevated.

B. Color Doppler imaging is a good diagnostic alternative for patients at high risk for calcification of vessels.

C. Arteriography is indicated following evaluation of ABIs if a patient with claudication is to undergo surgical or
endovascular treatment.

D. Magnetic resonance angiography has superior sensitivity over conventional angiography in detecting
disease in distal runoff vessels.


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VI. Management of Peripheral Arterial Disease

A. Risk Factor Modification
        1.Cigarette smoking is the most important modifiable risk factor. Claudication patients who abstain
        from tobacco usually do not progress to limb loss, whereas 11.3% of the patients who continue
        smoking require amputation.
        2.Meticulous care of skin of the lower limbs helps avoid ulcer formation and skin infection.
        3.Obese patients should be advised to lose weight through exercise and diet.
        4.Hypertension should be vigorously treated. Beta-blockers do not usually worsen claudication.
        5.Hyperlipidemia. Regression of femoral atherosclerosis is possible with lipid-lowering therapy. The
        goal should be to lower the low-density lipoprotein cholesterol level to below 100 mg/dL.
        6.Diabetes should be aggressively controlled in order to prevent further complications of
        microvascular disease.

B. Coronary and carotid artery disease assessment is essential because coronary disease accounts for 60%
of deaths.

C. Hormone replacement therapy after menopause may slow the progression of atherosclerosis.

D. Progressive Exercise Training
        1.Patients who have intermittent claudication but no rest pain or ischaemic ulceration should begin a
        walking program. They can usually increase their walking distance several times above baseline and
        can usually reduce the pain of claudication.
        2.Patients should walk to or through the onset of claudication, rest until the pain resolves, and then
        resume exercise; 30 minutes every day.

E. Pharmacological Management
       1.Pentoxifylline (Trental)
                a. The effect of pentoxifylline is only modest. Patients who take it may have a 20% increase
                in walking distance; however, exercise alone may increase walking distance up to 25%. This
                drug is useful only in patients who cannot benefit from exercise.
                b. Pentoxifylline is given in a dose of 400 mg tid. Gastrointestinal side effects may occur.
       2.Aspirin has no effect on claudication, but because of the high incidence of cerebrovascular and
       cardiovascular disease, aspirin, 160-325 mg per day, should be given.

F. Operative and Endovascular Procedures
       1.Most patients with claudication respond to conservative therapy. Surgery is reserved for patients
       with rest pain or tissue loss. Patients who have intermittent calf claudication alone are not surgical
       candidates unless the claudication severely limits their lifestyle or occupational functioning.
       2.Patients with rest pain, tissue loss as a result of gangrene, or non-healing ulcers, with an ABI in the
       range of 0.3, are surgical candidates.
       3.Percutaneous transluminal angioplasty has a greater than 90%success rate in the treatment of
       short-segment aortoiliac occlusive disease, and these results may be improved with the placement of
       an intra-arterial stent. However, five-year patency rates are only 40-60%.
       4.Surgical bypass therapy is an effective treatment for claudication; however, it is associated with 5-
       10% morbidity and mortality rates. Aortobifemoral grafting has a 90% 5-year patency rate. Aortoiliac,
       femoral-femoral crossover, and reversed and in-situ saphenous vein bypass grafting from the
       common femoral to the popliteal artery have 60-70% 5-year patency rates. A synthetic
       polytetrafluoroethylene graft (PTFE) is indicated for above knee femoral-popliteal bypass, and it has
       a 50% 5-year patency rate.

G. Axillofemoral Bypass. This procedure is useful for high risk, elderly patients who are unable to tolerate an
aortic procedure.




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Chapter 8 Vasculitis                                 Tam Tak Yau

Introduction
   Vasculitis is inflammation of blood vessel walls and, as such, may be associated with many types of
pathology, including infective foci and malignancy. On the whole, most authorities agree that it is the result of
immune complex deposition within or around blood vessels leading to overt clinical diseases.

Classification
   Recently, an international workshop agreed names and definitions for all major syndromes. The
classification is generally based on the size of vessels affected. This is adopted by the Consensus
Conference on the Nomenclature of Systemic Vasculitis as follows:

Large vessel vasculitis :-
          Giant cell ( temporal ) arteritis
          Takayasu’s arteritis

Medium vessel vasculitis :-
          Polyarteritis nodosa ( classic PAN )
          Kawasaki disease

Small vessel vasculitis :-
          Wegener’s granulomatosis
          Churg - Strauss Syndrome
          Microscopic polyangiitis
          Henoch - Scholein purpura
          Essential cryoglobulinaemic vasculitis
          Cutaneous leukocytolastic vasculitis

Note: Large artery refers to aorta and largest branches directed towards major body regions
      Medium-sized artery refers to main visceral arteries
      Small artery refers to distal arterial radicals that connect with arterioles.

   It can also occur as a secondary complication in a variety of systemic diseases such as collagen vascular
disease, malignancies, infection, radiation, hypertension and induced by drug.

   Discussion on all the above listed syndromes is beyond the scope of this presentation. Thereby
concentration on pathophysiology, signs and symptoms, diagnosis and current treatment on mainly large
vessel vasculitis is all that my concern in this paper.


TEMPORAL ARTERITIS
   Temporal arteritis, also referred to as cranial or giant cell arteritis, is characteristically involves one or
more branches of carotid artery, particularly the temporal artery. However, it is a systemic disease and can
involve arteries in multiple locations. It is a disease of the elderly, occurring almost exclusively in individuals
older then 50 years. It is more common in women than in men and is rare in blacks.

Pathophysiology
    Although the temporal artery is most frequently involved in this disease, patients often have a systemic
vasculitis of multiple medium- and large- sized arteries which may go undetected. Histopathologically, the
disease is a panarteritis with inflammatory mononuclear cell infiltrates within the vessel wall with frequent
giant cell formation. There is proliferation of the intima and fragmentation of the internal elastic lamina.
Pathophysiologic findings in organs result from the ischemia related to the involved vessels.
Immunopathogenic mechanisms, particularly cell-mediated immunity, are felt to be involved in this disease,
although the etiology is entirely unknown.




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Clinical Features
    The disease is characterized clinically by the classic complex of fever, anemia, and headaches in an
elderly patient. Other manifestations include malaise, fatigue, anorexia, weight loss, sweats, and arthralgias.
Temporal arteritis is closely associated with the polymyalgia rheumatica syndrome, which is characterized by
stiffness, aching, and pain in the muscles of the neck, shoulders, lower back, hips and thighs.

   In patients with involvement of the temporal artery, headache is the predominant symptom and may be
associated with a tender, thickened, or nodular artery which may pulsated early in the disease but may
become occluded later. Scalp pain and claudication of the jaw and tongue may occur. A well-recognized and
dreaded complication of temporal arteritis, particularly in untreated patients, is ocular involvement due
primarily to ischemic optic neuritis, which may lead to serious visual symptoms, even sudden blindness in
some patents. However, most patients have complaints relating to the head or eyes for months before
objective eye involvement.


Diagnosis
   Characteristic laboratory findings of temporal arteritis is much elevated ESR. In addition, a normochromic
or slightly hypochromic anemia can be found. The diagnosis is confirmed by biopsy of the temporal artery.

Treatment
   Temporal arteritis and its associated symptoms are exquisitely sensitive to glucocorticoid therapy.
Treatment should begin with prednisolone, 40 to 60 mg per day followed by a gradual tapering to a
maintenance dose of 7.5 to 10 mg per day. When ocular signs and symptoms occur, it is important that
therapy be initiated or adjusted to control them. Because of the possibility of relapse, therapy should be
continued for at least 1 to 2 years. The prognosis is generally good, and most patients achieve complete
remission that is often maintained after withdrawal of therapy.




TAKAYASU㷧 ARTERITIS
   Takayasu’s arteritis is an inflammatory and stenotic disease of medium- and large-sized arteries
characterized by a strong predilection for the aortic arch and its branches. For this reason, it if often referred
to as the aortic arch syndrome. Takayasu’s arteritis is most prevalent in adolescent girls and young women
and more common in the Orient.

Pathophysiology
   The most common affected arteries seen by angiography are the subclavians, followed by the aortic arch,
ascending aorta, carotids, and femorals. The involvement of the major branches of the aorta is much more
marked at their origin than distally. Partial renal artery occlusion with resulting hypertension is common. The
disease is panarteritis with inflammatory mononuclear cell infiltrates and occasionally giant cells. There is
marked intimal proliferation and fibrosis, scarring and vascularization of the media, and disruption and
degeneration of the elastic lamina. Narrowing of the lumen occurs with or without thrombosis. The vasa
vasorum are frequently involved. Pathologic changes in various organs reflect the compromise of blood flow
through the involved vessels.       Immunopathogenic mechanisms, the precise nature of which is uncertain,
are suspected in this disease.

Clinical Features
   Takayasu’s arteritis is a systemic disease with generalized as well as local symptoms. The generalized
symptoms include malaise, fever, night sweats, arthralgias, anorexia and weight loss which may occur
months before vessel involvement is apparent. These symptoms may merge into those related to pain over
the involved vessels followed by symptoms of ischemia in organs supplied by the compromised vessels.
Pulses are commonly absent in the involved vessels, particularly the subclavian artery. The clinical course
may be fulminant, may progress gradually, or may stabilize. Complications are related to the distribution of
the involved vessels. Death usually occurs from congestive heart failure or cerebrovascular accidents.

  Characteristic laboratory findings include an elevated ESR, mild anemia, leukocytosis, and elevated
immunoglobulin levels.


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Diagnosis
     The diagnostic criteria have been summarized by Ishikawa:-

Obligatory criterion:      Age less than 40 years
Major criteria:            Left mid subclavian lesion
                           Right mid subclavian lesion
Minor criteria:            High ESR
                           Carotid artery tenderness
                           Hypertension
                           Pulmonary artery lesion
                           Left mid common carotid artery lesion
                           Distal brachiocephalic trunk lesion
                           Descending thoracic aorta lesion
                           Abdominal aorta lesion

   In addition to the obligatory criterion, the presence of 2 major criteria, 1 major criterion and 2 or more
minor criteria, or 4 or more minor criteria suggests a high probability of Takayasu’s artreitis.

Treatment
   The course of the disease is variable, and spontaneous remissions may occur. Although glucocorticoid
therapy in doses of 40 to 60 mg prednisolone per day alleviates symptoms, there are no convincing studies
which indicate that they alone increase survival. However, recent studies suggest that glucocorticoid therapy
can induce remissions in high percentage of individuals. In addition surgery and or angioplasty may
remarkable improve survival by decreasing the risk of stroke and correcting hypertension due to renal artery
stenosis. A few patients who were refractory to glucocorticoid therapy responded favorably to
cyclohposphamide, 2mg/kg per day.


REFERENCES
1.   Systemic vasculitis, Andrew Churg & Jacob Churg
2.   Medicine International. 1994 the medicine group (Journals) ltd
3.   Vasculitis, rheumatic disease & the nervous system. P. Berlit, PM Moore (eds), Springr-Verlag
4.   Am J Kidney (US) Mar, 1995.25 (3) p 380-9
5.   Z Rheumatol (Germany) Jan-Feb p 1995-54 (l) p26-38
6.   Harrison’s Principles of Internal Medicine, 12th edition
7.   Taylor. Treatment of vasculitis. Br. J. clin. Pharmac (1993) 35 p93-104.
8.   Joseph L. Jorizzo. Classification of Vasculitis. The J. of Investigative Dermat. 1993 vol 100 (1) p106s-
     110s




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Chapter 9 Evaluation of breast masses
I. HISTORY

A. General medical history
       1. Age, menstrual status, parity, history of breast-feeding, drug usage, any prior history of breast
       cancer
       2. Family history: a history of breast cancer in a first-degree relative increases the patient's risk of
       breast cancer twofold to fourfold
       3. The risk of breast cancer increases with age. Early menarche and/or late menopause also
       increases the risk. Risk is increased slightly in nulliparous women. If the patient has a prior history of
       breast cancer, her risk is increased fivefold for cancer developing in the contralateral breast

B. Mass
          1. How long has the mass been present
          2. Is the mass tender or painful
          3. Has the size been increasing, does the size of the mass vary with menstrual cycles
          4. History of nipple discharge


II. EXAMINATION
A. Look for asymmetry, fixation to underlying structures, skin retraction, elevation, change in color
B. Nipple: inversion, discharge, erythema, skin changes, eczematous changes. An inverted nipple can usually
be everted to normal position. Eczematoid changes of the areola or nipple can be indicative of Paget's
disease


III. COMMON BENIGN CONDITIONS
A. Fibroadenomas: peak incidence at age 20 to 25 years. May be multiple in 10% to 15% of patients. Usually
the nodule is smooth, firm, freely movable, and well circumscribed. Excisional biopsy is usually
recommended

B. Intraductal papilloma: often characterized by nipple discharge, which can be serosanguineous,
spontaneous, recurrent, or persistent. Must be excised to rule out intraductal papillary cancer

C. Fibrocystic breast disease: actually more a normal variant, not a "disease'' state. Can be characterized by
aching pain, nodularity, a premenstrual "lumpy'' feeling, with bilateral, diffuse, tender, easily movable ill-
defined masses. Usually most pronounced in the upper outer quadrants. Common recommendations include
wearing a support brassiere at all times and avoidance of caffeine; however, these measures have not been
shown to be definitely helpful. Danazol, a weak androgenic steroid, is sometimes prescribed for 4 to 6 months
if symptoms are severe


IV. SCREENING FOR BREAST CANCER

A. Breast self-examination is recommended, beginning at ages 20 to 25, to be done at least once per month,
early to midcycle when fibrocystic changes are likely to be less prominent

B. Physical examination by a physician: recommended annually for most patients. Patients at particularly high
risk, for example, patients with a previous history of breast cancer, may be recommended to have more
frequent examinations

C. Screening mammography: recommended beginning at age 40 for patients at average risk. To be done
every 1 to 2 years from ages 40 to 49, then annually from age 50 on




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V. MAMMOGRAPHIC SIGNS OF MALIGNANCY
A. Direct indications: appearance of a mass, clustered microcalcifications

B. Indirect signs: asymmetry, architectural distortion, focal duct dilatation, new density on sequential
screening

C. Masses
       1. Benign masses usually have sharply circumscribed margins
       2. Ultrasound may be helpful in differentiating solid from cystic masses
       3. Masses that have spiculated, irregular, or indefinite margins are suggestive of cancer and need to
       be biopsied

D. Calcifications
        1. Calcifications associated with malignancy are usually clustered, with pleomorphic sizes and
        shapes
        2. Calcifications associated with benign conditions are often scattered evenly throughout the breast


VI. EVALUATION OF A PALPABLE MASS

A. Fine-needle aspiration
        1. Usually done as an outpatient without general anesthesia
        2. Efficacious, cost-effective, and reliable when the cytologic preparation and sampling are done
        properly
        3. The false positive rate is very low (0% to 0.4%), so a positive result is often adequate to plan
        definitive therapy without an open biopsy
        4. False negative results happen quite frequently, (0.7% to 22%). If the result is unequivocally benign,
        then the lesion can be followed by examination and mammography, as appropriate to the individual
        case. However, if the lesion begins to increase in size, then excisional or incisional biopsy is indicated
        5. If the result is equivocal, then must proceed to open biopsy with frozen and/or permanent sections
        6. If the lesion appears benign cytologically, but mammographically was suggestive of malignancy,
        then proceed to biopsy

B. Young women
       1. Women less than 30 years of age have compact, fibroglandular breast tissue, which limits the
       accuracy of mammography
       2. Ultrasound can be quite helpful in this setting to differentiate cystic from solid masses
       3. Fine-needle aspiration may also be helpful if the lesion is palpable

C. Normal mammogram, palpable lesion
       1. Mammography has about a 10% to 15% false negative rate
       2. An abnormal mammogram may help confirm the diagnosis, but a normal mammogram does not
       exclude cancer, particularly in the presence of a palpable mass

D. Nonpalpable lesion detected by mammography
       1. If the lesion is possibly cystic, confirm with ultrasound. If the lesion is definitely cystic on
       ultrasound, it usually can be followed with serial examinations
       2. If the mass has a solid component on ultrasound, biopsy with a mammographically guided needle
       localization technique may be required (if the mass is nonpalpable)
       3. Specimen radiography is used to be sure that the suspicious area is included in the biopsy
       specimen




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Chapter 10                        Carcinoma of Breast
The carcinoma of the breast can be classified into which arised from mammary ducts(>90%)and that from
lobules. Then they can be further divided into non-infiltrating and infiltrating carcinoma.

For the carcinoma arising from ducts, the non-infiltrating cancer included intraductal carcinoma or
comedocarcinoma and intraductal papillary carcinoma. For the infiltrating cancer (70%) included Simple
type:scirrhous which is the commonest(70%) and special types, medullary, colloid, adenoid cystic, apocrine,
infillrating comedocarcinoma, infiltrating papillary, tubular and paget’s disease.

For the carcinoma arising from lobules, the non-infiltrating one is in-situ lobular carcinoma. The infiltrating one
(30%) is lobular carcinoma which tend to be multifocal and bilateral.

The CA breast mainly affects females, there is 100 times less common in males. the affected age usually
between 40-60 which increased incidence in the younger age. The risk groups included who have a family
history of CA breast, nulliparous, late age at first pregnancy, previous history of benign breast disease and
previous cancer in the opposite breast.

The clinical features of the carcinoma of the breast usually present as a lump at the upper lateral quadrant
which counts for 45%, next common site is around alveola which counts for 25% of incidence. other
presentations included nipple bleeding, abnormal distortion or retraction of nipple. In the advance cases,
ulceration, peau d侊range, or cancer en cuirasse can be presented. Some may present with metastatic
sympoms e.g. bone pain, ascites or hepatomegaly.

Investigations of the breast lump included physical examination, mammography, ultrasonography, and biopsy
included fine needle aspiration, trucut biopsy and excisional or incisional biopsy. preoperative assessment
include blood tests for complete blood picture, renal function test, liver function test and serum calcium for
screening hepatic metastasis. Chest X ray abdominal ultrasound and Bone scan for 2nd metastasis.

The cancer cells can spread locally, by lymphatic, and by haematologic systems. The TNM classification
which stands for the staging by the tumour, lymph node involvement and present of distant metastasis. The
other grouping system is divided the stage into stage 0 which means carcinoma in situ; stage I means tumour
is 2 cm; stage II is tumour sized less than 2 cm or 2-5 cm with cancer metastasis to ipsilateral axillary lymph
nodes; stage III means tumor sizec less than 2 cm, 2-5 cm or more than 5cm with metastasis to ipsilateral
axillary nodes fixed to one another or other structures; stage IV is presence of distant metastasis.

The treatment is depend on the staging of the breast cancer, age of the patients, and receptor status of the
cancer. For the stage I and II, the aims are control local cancer and decrease growth potential of
micrometasis. Total mastectomy + LN sampling and breast reconstruction are done if there is palpable LN or
LN clearance or lumpectomy + post op localized radiotherapy. If the LN is negative, observe and follow up the
patient is needed. Adjunvant therapy is only indicated if LN is positive. For the premenopausal patients, 6
cycles of chemotherapy are given included 5-fluorouracil, cyclophosphamide and methotrexate or ovarian
ablation is given. For the post-menopausal patient, if the cancer is estrogen receptor positive, hormonal
therapy is beneficial. Tamoxifen 20 mg/d for 2-5 years.

For the stage III, the treatment included surgery, chemotherapy, radiotherapy.

For stage IV, the aims for treatment are relieving symptoms and increase quality of life.

The prognosis depends on involvement of axillary LN, Histopathology, recepor status, and cell proliferative
index. The 10 years survial rate of stage I si 50%. and 25% for stage II and 5% for stage III.

The follow up of the post-operative patients included mammogram every 6 month for 2 years then annually,
and clinical breast examination every 3 months.




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Chapter 11                        Abdominal Pain                                               (last   revised   May
1998)

I. HISTORY
A. The area of the pain, including its origin and pattern of radiation, time of onset, nature, and associated
symptoms, will frequently make the diagnosis. A menstrual history should be obtained

B. Associated symptoms
       1. Weight loss: may be due to malignancy or decreased caloric intake secondary to pain. This can
       help identify significant intraabdominal disease with vague pains
       2. Vomiting of fecal material will indicate intestinal obstruction
       3. Diarrhea and constipation are mostly related to the small intestine and colon. Either can occur with
       near obstruction
       4. Blood per rectum, melena, hematemesis; always double-check with a Hemoccult test. Question
       foods or medicines taken that might confuse the observation
       5. Jaundice: biliary tract, pancreas. Remember that painless jaundice is the hallmark of pancreatic
       cancer. An episode of hemolysis such as with sickle cell disease or massive GI bleeding may cause
       abdominal pain and jaundice
       6. Reflux: characteristic of esophageal or gastric problems
       7. Dysuria, frequency, urgency, hematuria: renal problems are often manifested by a complaint of
       abdominal pain
       8. Sexual activity, last period, birth control, history of venereal disease, vaginal discharge, spotting or
       bleeding. Patients often neglect these associated symptoms; most often related to suprapubic/lower
       abdominal pain

C. Past medical history
        1. Other major illnesses
        2. Prior surgeries
        3. Prior studies performed for evaluation of abdominal problems
        4. Family history of any similar complaints
        5. Medications: especially digoxin, theophylline, steroids (causes ulcers), analgesics, antipyretics,
        antiemetics, barbiturates, diuretics


II. PHYSICAL EXAMINATION
A. General appearance: position in bed, whether restless or still

B. Vital signs: observe for signs of shock, elevated temperature

C. Signs of dehydration noted with mucous membranes and skin turgor

D. Abdominal examination
       1. Inspection: scaphoid/distended, movement, point of most severe pain, fullness of hernia sites,
       scars
       2. Auscultation: high-pitched bowel sounds suggest an obstructive process. Absent bowel sounds
       suggest an ileus
       3. Palpation/percussion: muscular rigidity (voluntary/involuntary), localized tenderness, masses,
       pulsation, hernias, peritoneal irritation (rebound, involuntary guarding, obturator or psoas sign,
       hyperesthesia, Murphy's sign), liver dimension/spleen dimension
       4. Costovertebral angle (CVA) tenderness
       5. Pelvic: mass, discharge, cervical excitation
       6. Rectal: localized tenderness, fluctuance, induration, masses, shelf, blood




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III. LABORATORY STUDIES
A. CBC with white blood cell (WBC) count and differential, platelet count, and urinalysis routinely done on
most cases of abdominal pain

B. Electrolytes with vomiting or diarrhea

C. Liver function tests and liver enzymes, amylase and lipase for upper abdominal pain

D. Other studies as indicated: chest x-ray (upright) for pneumonia or free air. Abdominal flat plate and upright
views for bowel obstruction, ileus, free air, abnormal calcification. Ultrasound to look for peritoneal fluid. ECG
for acute MI, ischemia, or arrhythmias. Paracentesis: may be important with fluid in the abdomen or in
evaluation of abdominal trauma.

E. Pregnancy test on all females except the very young and postmenopausal. This also needs to be done if
any radiographic studies are being considered


IV. INITIAL TREATMENT
A. Decide whether to
         1. Admit and observe
         2. Operate
B. Keep NPO until the diagnosis is clear
C. IV fluids: decide on expected fluid losses and current level of hydration
D. NG tube for vomiting, bleeding, or obstruction
E. Foley catheter to monitor fluids
F. Serial examinations for unclear diagnoses
G. Pain medications will often help clarify the diagnosis
H. Serial laboratory tests may be helpful, especially CBC, electrolytes, cardiac enzymes


V. DIAGNOSTIC STUDIES
A. Ultrasound
         1. Upper abdominal for gallstones, common duct obstruction, pancreatitis, pancreatic psuedocyst
         2. Kidney: may reveal obstruction, perinephric abscess
         3. Pelvic: appendicitis, diverticulitis, mass, ovarian cyst, ectopic pregnancy, PID with abscess

B. UGI: can use for questionable perforation if water-soluble contrast used. Small-bowel follow-through may
be useful for questionable obstruction

C. Lower GI for question of distal obstruction. Do not perform if acute diverticulitis is suspected or there is any
risk of perforation

D. IVP: masses, obstruction

E. Computed tomography (CT): especially for abscesses, pancreatic mass or pseudocyst, dissecting
aneurysm, ruptured liver or spleen




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Chapter 12 Acute appendicitis                                                  (last revised April 1998)


   most common cause of acute abdomen in Hong Kong.
   uncommon in people <age 2 as lumen is wide and short or > age 60 as lumen is most likely obliterated.

Pathophysiology
 accumulation of secretion in the obstructed appendix leads to distension, necrosis of the mucosa,
    invasion of the wall by gut bacteria.
 may resolves spontaneously, but usually progresses to gangrene and perforation.
 once perforated, if it can be contained, appendix abscess result. If not, generalize peritonitis ensues.

Clinical Features
Symptoms
 Pain:          typical periumbilical colic for several hours, then shifts to right iliac fossa, exacerbated by
    moving or coughing. in 1/3 cases, pain commence in right iliac fossa. site of pain also influenced by
    position of appendix (retrocaecal, retroileal, pelvic, etc.)
 G I upset with anorexia and nausea. Diarrhoea when rectum is irritated.
 (Ask for urinary and O&G symptoms).
Signs
 Tenderness, guarding, maximal over McBurney’s point. Associated with rebound tenderness.
 Rovsing’s sign pressure on the LIF producing pain in the RIF.
 Posas sign: pain during passive extension of right hip
 PR exam: tenderness in 1/3 patients
 In retrocecal appendicitis, tenderness is maximal on right flank or loin
 with perforation:  temp,  heart rate, T +, G +, R +, +/- appendix mass, & general peritonitis

Diagnosis
essential clinically

DDx
  Abdomen:               PPU, acute cholecystitis, acute I.O., Meckel’s diverticulitis, caecal diverticulitis
  Urinary:               UTI
  Chest:                 basal pneumonia, pleurisy
  Gynaecological:        acute salpingitis, ectopic pregnancy, rupture corpus luteal cysts.

Investigations
Urinalysis, MSU for C/ST & pregnancy test, CBP, RFT, AXR, CXR, USG to detect free fluid and other
gynaecological pathologies

Treatment
   NPO, IVF, monitor vital signs, analgesics
   Aims to remove appendix before gangrene and perforation occurs.
   Appendicetomy. but: *patient’s moribound with peritonitis  resuscitate first
                            *attack has already resolved  elective surgery
                *appendiceal mass has formed with no clinical sign of peritonitis and toxicaemia
   Prophylactic antibiotics (in PWH, combination of second generation cephalosporin and metronidazole is
    usually used) should be given to prevent wound infection for appendicetomy




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Chapter 13                        Intestinal Obstruction                                       (last revised April 1998)


I. CLASSIFICATION
A. Mechanical obstruction: complete or partial physical blockage of the intestinal lumen
B. Simple obstruction implies one obstruction point
C. Closed-loop obstruction: blockage at two or more points (e.g. carcinoma of ascending colon with
competent ileo-caecal valve, volvulus, afferent loop obstruction after Polya gastrectomy)
D. Paralytic ileus: impairment of muscle function (e.g. after abdominal surgery, trauma, peritonitis, electrolyte
imbalance, spinal injury)
E. Strangulating obstruction: when the obstructing mechanism occludes the mesenteric blood supply on the
wall of the lumen. Necrosis occurs in 3 to 4 hours. Difficult to diagnose preoperatively

II. SMALL-BOWEL OBSTRUCTION
A. Clinical manifestations
         1. Cramping abdominal pain--crescendo-decrescendo pattern. Continuous pain suggests
         strangulation
         2. Vomiting--earlier in high obstruction
         3. Faeculent vomiting--as a result of bacterial overgrowth, especially with distal obstruction
         4. Distension--more in lower obstruction
         5. Obstipation
         6. High-pitched bowel sounds
         7. Electrolyte abnormalities

B. Workup
       1. CBC with differential, electrolytes
       2. Supine and upright abdominal x-ray films with a stepladder pattern of air-fluid levels and no colonic
       gas suggest obstruction
       3. water soluble contrast meal

C. Treatment
        1. Fluid and electrolyte resuscitation and supportive care
        2. If partial obstruction with the patient passing gas, may treat with an NG tube. This will relieve
        vomiting and decompress distension
        3. Surgical intervention is indicated if the obstruction does not resolve with conservative treatment,
        development of peritoneal signs, or intestinal obstruction associated with an irreducible / strangulated
        hernia

III. LARGE-BOWEL OBSTRUCTION
A. Clinical manifestations
         1. Cramping pain
         2. Little vomiting (less with a competent ileocecal valve; vomitus is rarely fecal)
         3. Constipation and obstipation
         4. Distension (severe)
         5. Loud borborygmi
         6. Little loss of electrolytes


B. Workup
        1. Electrolytes
        2. Colonoscopy or flexible sigmoidoscopy may reveal an obstructive lesion
        3. Radiography will reveal a gas-filled colon with absence of gas beyond the obstruction
        4. Water soluble contrast enema
C. Treatment
        1. Nasogastric tube
        2. IV fluids, monitoring, with or without antibiotics
        3. Sigmoidoscopy may reduce a sigmoid volvulus
        4. Surgical intervention if the above measures are not successful in relieving the obstruction



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Chapter 14                       Renal Failure
I. ACUTE RENAL FAILURE
A. Sudden loss of renal function as evidenced by oliguria/anuria, increase in BUN and/or serum Cr levels

B. Etiology
         1. Renal: glomerular (rapidly progressive glomerulonephritis), vascular (renal artery or vein
         thrombosis, vasculitis), and tubulointerstitial (acute tubular necrosis [ATN] most common, see below)
         2. Prerenal: diminished renal perfusion resulting from volume depletion, inadequate cardiac output,
         volume redistribution ("third spacing'' from cirrhosis, burns, nephrotic syndrome, etc.)
         3. Postrenal: obstruction of the urinary tract from prostate disease, retroperitoneal disease

C. Diagnosis: may have urine output less than 400 mL/24 hr, elevated BUN and creatinine levels, decreased
Cr clearance. A progressive daily increase in the serum Cr level is diagnostic of acute renal failure

1. Estimated creatinine clearance =
[140 - age (yr)] [body weight (kg)]/(72) [serum Cr (mg/dL)]

          a) For women, multiply this figure by 0.85
          b) May not reflect early renal damage because of compensatory hypertrophy of the remaining
          glomeruli
          c) Normal for a healthy adult is 94 to 140 mL/min for men and 72 to 110 mL/min for women
          d) The Cr clearance normally lessens with age

D. To differentiate the causes of renal failure
        1. Prerenal azotemia: urine osmolality/plasma osmolality (U/P), more than 1.5; urine Na, less than
        20; fractional excretion of sodium [FeNa = (U/P Na)/(U/P Cr)], less than 0.01; [RFI urine Na
        (mmol/L)/(U/P Cr)], less than 1 (90% of cases)
        2. Postrenal azotemia (obstructive uropathy): U/P osmolality, 1 to 1.5; urine Na, more than 40; FeNa,
        more than 0.04; RFI, more than 2
        3. Renal (ATN): U/P, 1 to 1.5; urine Na, more than 40, FeNa, more than 0.02; RFI, more than 2
        (more than 90% of cases)
        4. Glomerulonephritis: U/P, 1 to 1.5; urine Na, less than 30; FeNa, less than 0.01; RFI, less than 1


II. ACUTE TUBULAR NECROSIS
A. Acute renal failure resulting from renal ischemia or renal damage from toxic insults. Renal function
generally returns to an adequate level if the patient survives the acute phase, which usually lasts 1 to 2
weeks. Sepsis is a major cause of death in renal failure

B. May progress from oliguric renal failure (urine output, less than 400 mL/day) lasting 1 day to 6 weeks
(average, 10 to 14 days) to nonoliguric renal failure, which may be manifested by massive urine output. There
is no prognostic difference. However, nonoliguric renal failure is easier to manage because of less need for
stringent fluid restriction

C. Laboratory findings: progressive hyponatremia, hyperkalemia, azotemia, and acidosis

D. Causes of ATN
       1. Ischemic: shock, sepsis, hypoxia, hypotension
       2. Toxic: radiologic contrast media, heavy metals, aminoglycosides, myoglobinuria from burns,
       trauma, polymyositis, etc.

E. Evaluation: diagnosis often apparent from the clinical history. Rule out an obstructive process (ultrasound
of kidneys, ureters helpful)
        1. Urinalysis may reveal renal epithelial cells, cellular casts
        2. See Section IC for differentiation from other causes




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III. PRERENAL AZOTEMIA
A. Commonly caused by dehydration (often due to excessive diuretic therapy). Indicated by signs of
decreased renal function with BUN elevated out of proportion to serum creatinine, often greater than 15 to
20:1

B. Treatment
        1. Adequate intravascular volume will prevent progression to oliguric/anuric failure
        2. Treatment is as below if renal failure results


IV. POSTRENAL AZOTEMIA
Usually caused in males by bladder outlet obstruction and is rapidly treatable with a Foley catheter. Other
causes include pelvic tumors


V. GLOMERULONEPHRITIS
A. Note the sudden onset of renal failure, hematuria, proteinuria, azotemia, and edema

B. Causes are legion, including poststreptococcal, hemolytic- uremic syndrome, Henoch-Schonlein purpura,
collagen vascular diseases, and others

C. Diagnosis is by renal biopsy. A nephrology consultation should be obtained


VI. TREATMENT OF ACUTE RENAL FAILURE
A. Careful monitoring of fluid and electrolyte status. Fluids should be restricted to replacement of losses
(urine output+ other losses [GI]+ approximately 500 cc/day for insensible loss). Dietary intake of K+ and
phosphates should be severely restricted. Hyperphosphatemia may be prevented by using oral aluminum
hydroxide antacids to absorb dietary phosphates and maintain PO4 less than 5.5. Calcium levels should be
monitored; they will tend to fall if phosphorus levels rise. Hyperkalemia should be treated as noted in Chapter
5. Fluid overload may require dialysis or diuretics, for example, furosemide, 20 mg IV or more

B. Monitor acidosis. Mild to moderate metabolic acidosis should be anticipated and may be well tolerated.
Severe acidosis may require oral bicarbonate solutions. These contain significant quantities of Na+

C. Monitor carefully for signs of infection (a common cause of mortality during acute renal failure)

D. Dialysis is indicated for symptomatic pericarditis, severe hyperkalemia or hyperkalemia that does not
respond to sodium polystyrene sulfonate (Kayexalate), severe acidosis, significant fluid overload, uremic
symptoms (especially neurologic)


VII. CHRONIC RENAL FAILURE (CRF)
A. Clinical syndrome of chronic compromise of renal function that can be categorized into three major groups:
         1. Inadequate renal reserve, characterized by the inability to compensate for extreme water/solute
         loading or deprivation
         2. Renal insufficiency, characterized by elevated BUN levels and a markedly diminished capacity for
         dealing with water/solute fluctuations, but otherwise can maintain homeostasis
         3. Renal failure, characterized by a progressive increase in BUN concentration to the point of causing
         uremia and fluid and electrolyte imbalance (glomerular filtration rate [GFR], less than 6 mg/min/m 2 )

B. Etiology: common causes include diabetes, hypertension, glomerulonephritis, polycystic kidney disease,
obstructive uropathy. Many other causes exist

C. Clinical manifestation: early symptoms may include only nocturia resulting from an inability to concentrate
urine. Fatigue, altered mental status, peripheral neuropathy, anorexia, nausea/vomiting, and pruritus indicate
uremia. Hypertension is common. Fluid and electrolyte imbalances result in varying signs and symptoms.
Loss of erythropoietin and vitamin D function results in anemia and osteodystrophy



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D. Laboratory findings: generally elevated BUN and Cr levels. Acidosis is usually present, as is a
normochromic normocytic anemia. Hyperkalemia and hyponatremia are often present

E. Treatment
        1. Dietary restrictions are required to maintain appropriate fluid and electrolyte balance. Protein
        restriction can reduce acidosis and symptoms from elevated BUN levels. Protein restriction may slow
        disease progression. Dietary K+ intake will generally require restriction only late in the course.
        Phosphate intake should be limited. Supplements of calcium and vitamin D will eventually be needed.
        Treatment with angiotensin-converting enzyme (ACE) inhibitors will slow progression of renal failure
        due to diabetes
        2. Fluid and sodium should be restricted only as indicated (generally required late in the course)
        3. Acidosis with plasma CO2 values less than 15 can be treated with oral bicarbonate. This may
        improve anorexia and lassitude
        4. Hyperphosphatemia should be treated with phosphate binders such as oral calcium acetate or
        calcium carbonate
        5. Dialysis: hemodialysis and chronic ambulatory peritoneal dialysis. Absolutely indicated for uremic
        pericarditis, progressive motor impairment, fluid overload not responsive to other interventions or
        producing congestive heart failure (CHF), severe acidosis, and hyperkalemia
        6. Transplant: an alternative to dialysis. The decision to proceed with dialysis and/or kidney
        transplantation requires the assistance of a nephrologist




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Chapter 15                      Laparoscopy
Background

Mark changes have occurred in the utilization of laparoscopy in the last decade.
In the 80’s CT & US/S had replaced Dx Laparoscopy in the Ix of liver disease.
         But problems with Imaging:
          lack histology
          limitation by its resolution ( 1cm, instrument & operator dependant)
          poor accuracy in determine peritoneal metastasis
             e.g. Warshaw et al, 35% (14/40) CA pancreas case, metastasis only seen by laparoscopy
             Kriplani et al, 40% (16/40) CA stomach case, metastasis reveal by laparoscopy
Late 80’s laparoscopy regain its attention
Both diagnostic and therapeutic
Low fatal complication 0.014 - 0.076%
Major complication                 0.095%
         Usually related to
          coagulation disorder
          portal hypertension, variceal umbilical / paraumbilical vein
All complications are related to
          operator experience
          equipment
          type of procedure
          anaesthesia
          anatomy & variation
          pre-existing condition
          patient cooperation
          poor general condition only relative risk

Complication of Anaesthesia

Rare with conscious sedation
Commonly due to synergism between sedation, analgesic & nacrotic
Increase intra-abdominal pressure
cf. Pre-existing cardio-pulmonary disorder
Problem
 cardiac arrhythmia
 hypercarbia & acidosis esp. CO2 is used
 vaso-vagal phenomenan - can cause mark bradycardia & hypotension
 aspiration pneumonia

Treatment
Prevention with better patient selection
Careful cardiopulmonary function evaluation
Avoid patient with known cardiopulmonary diseases
Atropine premedication reduce vaso-vagal reaction
Closing monitoring       oximeter
        `                ECG
Sedation                 slow & judicious




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Complication of Pneumoperitoneum

Overall < 1%
1) Increase intra-abdominal pressure can increase CVP, heart rate, mean artery pressure and cardiac
    output. But if pressure > 25 cm water it will decrease venous return, decrease CVP & cardiac output
2) Elevated diaphragm cause basal ateletesis, right to left shunt, ventilation : perfusion mismatch
3) CO2 can decrease oxygen tension and saturation, it also decrease tidal volume and minute volume but
    increase respiratory rate increase pCO2, decrease pH
4) Gas embolism when direct vessel injection --- fatal complication
5) Penetrating injury              viscera (e.g. liver, gut, etc.)
                                  usually due to adhesion
                                   vessel
                                  especially portal hypertension
vascular adhesion
6) Gas insufflation into the omentum, usually without consequence.
    Subcutaneous emphysema occur if gas leak into subcutaneous plan.
    Rarely pneumomediastinum, pneumothorax, pneumopericardium.
7) Pre-peritoneal insufflation of gas can preclude a successful study, but can repeat later when gas
    absorbed.

Complication of Trocar

1) Bleeding
    overall 0.21%
    a) epigastric and other small vessels
    usually cause haematoma, stop on its own with pressure
    1 : 10,000 adrenaline
    b) teared dilated vessels (usually veins)
    especially with portal hypertension
because of :-               size of vessel
                       clotting defect
                       thrombocytopenia (cf. hypersplenism)
therefore bleeding tendency, unlikely to stop on its own
surgical intervention is needed
high mortality :             Henning & Look
              17 patient-series –                  5 case of bleeding
                            1 need surgery
                            3 died
    c) major vessels injury
    e.g. aorta, iliac vessels or caval injury
    usually acute presentation
    minimal free blood but hyge retroperitoneal clot
    alert if blood pressure drop suddenly
     close monitor of blood pressure & pulse

2) Visceral injury
     colon > small bowel
     usually due to adhesion or inadequate pneumoperitoneum
     injury of omentum usually without problem
     precaution 2 - 5 cm from surgical scar
                         avoid patient with history of peritonitis
                         (cf. Open laparotomy)
                         insert trocar under laparoscopic vision
     Treatment           converted to open surgery
                         non-surgical --       immediate surgical repair in case of                    bowel
injury

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Complication during Laparoscopy

pain – in LA case
vaso-vagal reaction          especially when organs being pulled
                             treated with atropine
gas embolism is theoretically possible in patient with peritoneal-venous shunt if it is not clamp off before gas
insufflation

Complication of Liver Biopsy

                                      incident                           mortality

1. Bile peritonitis                0.05%                0.013 - 0.02% (1954 - 81)
    Incident decrease nowadays because no longer performed in obstructive   jaundice patient

2. Bleeding                         0.02 - 0.2%
    common in cirrhotic, liver secondary & vascular tumour
    usually presented acutely, but delayed as long as 13 days reported

    Related to :
     technique of biopsy
     angulation of 30 degree less likely to hit vessel than perpendicular
     caliber of biopsy instrument

    Treatment
    compression until clotted
    coagulation with diathermy
    FNA / brush cytology instead of biopsy
     no pain doesn’t mean no bleeding because blood is not that irritating

3. Infection
    Bacteriemia occur in 2.9 - 13%
    sepsis rare, 3 cases reported so far
    1 young lady died of septic shock and DIC
    commonest organism           Klebsiella pneumonia
                                 beta haemolytic streptococci
                                 E. coli

4. Perforation of viscera
    stomach is reported in biopsy of left lobe of liver
    Gall bladder is also known
    Pneumothorax can be avoid if the needle is below the insertion of the             diaphgram

Post-laparoscopy Complication

Delayed bleeding from biopsy site
Metastasis at trocar site
Herniation through the ports           avoid if the fascia is repaired
                                       risk of strangulation always exist, therefore always repair
Infection                              commonest umbilical port
                                       usually treated locally & antibiotic
                                       drainage rarely need




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Complication specific to Laparoscopic Cholecystectomy

Retained stone           1 - 3 % in conventional
                         0.4 % if endoscopic procedure done before
                         Same as open surgery

Treatment
laparoscopic exploration of CBD
converted to open
post operative ERCP
observe – especially < 5 mm

Bile duct injury
higher than conventional
Prevention better than cure
Principle               careful dissection of Calot’s triangle
                        avoid blind clipping of duct
                        beware of aberrant anatomy
Treatment               Converted to open
                        If no tension & / tissue loss – repair over a T tube
                        Otherwise biliary - enteric anastomosis

Occasionally, injury pass unnoticed during surgery
Patient will present late with abdominal or shoulder pain, with or without fever

Bile Leakage
Slipped clip
Tissue necrosis following cautery or extensive dissection
unsuspected duct damage
aberrant or accessory bile duct

Bile Duct Stricture
Misplaced clip - too much tension on the cystic duct
extensive dissection with ischaemia
Electro-cautery injury
treatment usually by biliary enteric anastomosis in good risk patients
stent, will need changes every 4 - 6 months, only if surgery is not indicated




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Chapter 16                        Gallbladder Diseases
I. OVERVIEW
       Asymptomatic cholelithiasis, choledocholithiasis, biliary colic, and acute cholecystitis are very
       common. The incidence of cholelithiasis increases with age and is more common in women. Other
       predisposing factors include obesity, pregnancy, diabetes, chronic hemolytic states.

II. ASYMPTOMATIC CHOLELITHIASIS
        Eighty percent of gallstones are asymptomatic, with a small percentage becoming symptomatic each
        year. Stones are composed of bile salts, cholesterol, phospholipids, or unconjugated bilirubin.
        Calcification may occur and results in about 10-15% of the stones becoming radiopaque.

          Management
          A. Asymptomatic patients do not require surgery. However, the presence of pancreatitis, or
             cholangitis warrants considerations for surgery.
          B. Gallstone dissolution may be considered in asymptomatic patients with normal gallbladder
             function or if a patient refuses or is not a candidate for surgery. The recurrence rate is high if
             medication is not continued, the dissolution rate is slow, and side effects are common. However,
             as most of the gallstones in Chinese patients are mixed stones (unlike cholesterol stones which
             response to dissolution therapy quite well), dissolution therapy is not commonly given to our
             patients.
          C. Lithotripsy dissolution is an option for treatment if available.

          * Relative indication of surgery in asymptomatic gallbladder problems : salmonella carrier, diabetes,
          porcelain gallbladder, limy bile, GB polyp >1cm, suspected malignancy.

III. EVALUATION OF THE GALLBLADDER
        A. Laboratory tests may include liver function tests, amylase for evidence of pancreatic damage,
           and a WBC count if symptoms are acutely present. Alkaline phosphatase is possibly the most
           sensitive indicator of biliary disease.
        B. Plain x-ray films may help because about 10-15% of stones are radiopaque.
        C. Ultrasound is often the initial examination used to evaluate for cholelithiasis. Can visualize stones
           and evaluate biliary ducts and pancreas. Obesity and overlying abdominal gas decrease the
           quality of the examination.
        D. Oral cholecystography is performed by having the patient ingest 3 g of iopanoic acid about 12
           hours before the study. Failure of the gallbladder to opacify indicates gallbladder disease. It is
           now rarely used to diagnosis gallstone diseases.
        E. Radionuclide excretion scans (e.g. E-HIDA scan) can be used in the setting of moderately
           elevated bilirubin levels and acute cholecystitis. Failure of the gallbladder to be visualized with the
           presence of radioisotope in the common bile duct 4 hours postinjection indicates acute
           cholecystitis.

IV. BILIARY COLIC
         A. Caused by intermittent obstruction of the cystic duct by gallstones. The history will generally
            include episodes of epigastric and right upper quadrant (RUQ) pain that may radiate to the back.
            Pain is usually constant and abrupt in onset and subsides slowly. Nausea is commonly
            associated. Attacks may be precipitated by ingestion of fatty foods.
         B. Physical examination will reveal the absence of fever, possible RUQ or epigastric tenderness
            without rebound. The gallbladder may be palpable.
         C. Laboratory evaluation: a CBP with differential should be obtained. The WBC count should not be
            significantly elevated. Liver function test (LFT) findings are usually normal.
         D. Treatment: analgesics and antiemetics should be provided acutely. Morphine may increase
            biliary pressure and is contraindicated. Further evaluation may be obtained as convenient in the
            next few days with the patient instructed to avoid fatty foods. Cholecystectomy should be
            performed electively.




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V. ACUTE CHOLECYSTITIS
      A. Cholecystitis, often due to a bacterial infection of the gallbladder, will develop in a significant
          percentage of patients with biliary colic and gallstones.
      B. Symptoms are similar to biliary colic with the additional features of low-grade fever, leukocytosis,
          mild elevation of bilirubin, and elevated alkaline phosphatase levels. Murphy's sign may be
          present (sudden increase in pain and inspiratory arrest with palpation of the RUQ during deep
          inspiration).
      C. Treatment: consultation with a surgeon is required. Antibiotics are indicated for acute
          cholecystitis. A third-generation cephalosporin and metronidazole will cover the most common
          organisms. There are advantages and disadvantages to both early and delayed surgery,
          although early surgery appears to generally result in lower morbidity and shorter periods of
          hospitalization. The surgeon will ultimately need to base decisions on the particular features of
          the case.

VI. CHOLEDOCHOLITHIASIS
       A. Stones in the common bile duct can give rise to jaundice when the flow of bile into duodenum is
          blocked.
       B. Patient may also present with right upper quadrant pain, fever when the biliary tract is infected
          (acute cholangitis)
       C. Initial management includes intravenous fluid resuscitation and antibiotics. For severely sick
          patient, endoscopic retrograde choledocho-pancreatography (ERCP) percutaneous biliary
          stenting (PTBD) should be performed as emergency basis.
       D. If the patient has also got gallstones, cholecystectomy should be considered to prevent recurrent
          attack


TERMS AND THEIR MEANING
     Cholelithiasis              presence of stones in the gallbladder, does not imply disease
     Acute cholecystitis         acute inflammation of the gallbladder
     Choledocholithiasis         stones in the common bile duct
     Cholecystectomy             surgical removal of gallbladder




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    Chapter 17                       Acute cholecystitis
                                                                                               (last revised April 1998)
   commonly caused by obstruction of the cystic duct by a stone, with proximal distention, stasis and
    secondary infection.
   acalculous cholecystitis - no stone, similar clinical picture, non-specific inflammation of the gall bladder
    wall or cholestoses (chronic inflammatory change with hyperplasia of all element), common in patients
    recovering from major surgery, trauma and burns (? stasis due to fasting or splanchnic vasoconstriction)

Clinical features
1. People - commonly 30-60 yrs old , F>M
2. Symptoms -
    a) sudden onset RUQ or epigastric pain,             iliary colic’ - persistent colicky pain, usu > 12 hrs,
        precipitated by heavy meal or fatty and protein rich diet, radiate to right shoulder and/or angle of the
        right scapular, aggravated by respiration, relieved by analgesic only.
    b) fever (38-9 C), chills and rigor.
    c) nausea, vomiting and anorexia
3. Signs -
    a) Inspection
         general : distressed, shallow breath, tachycardia, pyrexia
         abdomen : movement of the abdomen with respiration is diminished, distention
    b) Palpation
         RUQ tenderness and guarding,
         Murphy’s sign : If the patient is asked to take a deep breath while you are palpating the tender
             area, the downward movement of the gall bladder striking the palpating hand may cause a sharp
             pain that prevents further inspiration
         Boa’s sign        : hyperaesthetic area at angle of the scapula when pain radiate to the back
    c) Rectal examination - normal

Investigations
1. Blood test : CBP - neutrophilia
                LFT - bilirubin may increase
                Blood and bile culture and sensitivity test (C/S)
2. Imaging : Ultrasonogram GB - detect any gallstone (underlying pathology), distended
                                     GB with oedematous wall, free fluid in RUQ, ultrasonic
                                      Murphy’s sign
                                EHIDA scan - absence of GB filling (non-functioning gallbladder)

Management
1. NPO, Ryle’s tube (if patient vomits), IV fluid, frequent monitoring of BP/P, Temp., I/O chart, repeated
   abdominal examination for generalized peritonitis.
2. Conservative treatment (Bed rest, broad spectrum antibiotics then change according to C/S, analgesic) is
   offered as the initial management.
3. Conservative treatment should not continued if diagnosis is uncertain e.g. PPU, high retrocaecal
   appendicitis need to be excluded by laparoscopy or laparotomy.
4. Condition contraindicated for conservative treatment if there is generalized abdominal pain + increased
   pulse rate --> laparotomy if the patient’s general condition is good / a percutaneous cholecystostomy
   under ultrasound guided should be performed if patient is unfit.

Early cholecystectomy (within 48 hrs) versus Delayed cholecystectomy (after 6-8 weeks): Studies have
shown early cholecystectomy has the same morbidity and mortality as in delayed cholecystectomy. However,
early surgery has the advantage of short duration of hospitalisation, no chance for failed conservative
treatment, swift resolution of symptoms after operation although it might be technically more demanding. This
applies to both open cholecystectomy and laparoscopic cholecystectomy.




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Chapter 18   Disease of the Liver, Biliary tract
and Pancreas
                                                   Liver 
   One of the largest organ in the body with a lot of function in metabolism
   dual blood supply   25% from the hepatic artery
                              75% from the portal vein
   Blood flow  1500 ml / min. i.e. ¼ of cardiac output


Hepatic Trauma

   Rare because the liver is well protected by the rib cage and the diaphragm
   Serious condition

Cause : Road traffic accident or industrial accident
                Civilian injury - usually stab

Treatment
 Resuscitation with intravenous fluid and / or blood
 laparotomy to repair the damage


Infections
Viral infection       - Hepatitis
commonest :           Hepatitis A
                       from faecal - oral route
                       contaminated food especially the shellfish
                       usually recover without consequence
                       few acute fulminating hepatitis - died
                       no chronic carrier state
                      Hepatitis B
                       from blood or body fluids e.g. transfusion
                       can recover with antibody rpoduction
                       chronic carrier state
                        10% Hong Kong population is carrier, chance increase with age
                       lead to cirrhosis
                       associated with Hepatocellular carcinoma
Pyogenic infection
uncommon
source of organism :          abnormal biliary tract
                              portal pyaemia
                              systemic septicemia
                              parasite infestation e.g. Amoebae

Treatment
Antibiotic according to sensitivity
Metronidazole for amoebae
Drainage of the pus         -       percutaneous under imaging guidance


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Cirrhosis
a disease with necrosis of liver parenchyma followed by fibrosis and regeneration of liver cell
common courses               :    Hepatitis B
                                  Alcoholism
                                  Others          chronic biliary obstruction
                                                  haemochromatosis
                                                  Chemical poisoning e.g. cholorform
                                                  Primary biliary cirrhosis
                                                  Parasite infestation
Morphologically :
 Micronodular Vs Macronodular
Pathology :
 parenchymal destruction with overgrowth of fibrous tissue
 portal and hepatic vein will be compressed by the fibrosis
                           Portal hypertension


Portal hypertension
5 portal-systemic circulation pathways where blood get back to systemic circulation

Esophageal varices
can extend into the stomach i.e. gastric varices
Problems :     bleeding - profusely
               first presentation of cirrhosis
               high mortality

Management
Resuscitation :      Blood and intravenous fluid
Diagnosis :          urgent upper endoscopy (OGD)
                     confirm bleeding from the varices
                     high chance of having gastric and duodenal ulcer

Treatment :          1)    Endoscopic injection sclerotherapy
                            usually STD, glue
                     2)    Sengstaken / Minnesota tube
                            simple and easy
                            tamponade effect
                            cannot use > 24 hours because of pressure necrosis of underlying tissue
                            aspiration possible
                            buy time to stabilize the patient
                            during emergency situation where endoscopy is not available
                     3)    Surgery - high mortality in emergency situation
                                      difficult, technically demanding
                                      Choices :
                                  a) Esophageal transection
                                       simpler
                                       good for controlling bleeding in emergency
                                  b) Shunt operations
                                       difficult
                                       higher mortality and complications
                                       definitive treatment for stable cases
                                       post-operative hepatic encephalopathy because bleed bypass the
                                           liver



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Neoplasm of the Liver

Benign - not very common

Haemangioma
 usually the carvenous type
 ultrasound examination is good enough to diagnose most of the cases
 if still in doubt - isotope scan +/- angiogram
 follow up imaging
 avoid needle biopsy because bleeding can be heavy at the biopsy site

Adenoma
 uncommon
 usually in the female sex
 history of taking contraceptive pills with high estrogen component
 safe to observe
 for surgery if enlarging

Malignant - very common

Primary hepatocellular carcinoma
  1000 death / year in Hong Kong
 Hepatitis B carrier  Hepatitis B cirrhosis  Hepatocellular carcinoma
 Median survival around 10 weeks from diagnosis

Treatment
 Surgical resection
 only  10% of case is suitable for surgery
 technically difficult
 usually associated with cirrhosis
 Operative Mortality 10 - 15%
 cause of post-operative death - bleeding
                                            liver failure
                                            infection
 Poor respond to systemic chemotherapy and irradiation
 better result with immuno-chemotherapy and selective irradiation - only for palliation in most of the cases.
    In rare situation, an inoperable tumour might become operable after shrinkage of tumour.

Secondary deposit from other malignant tumour
 very common
 usually signify terminal stage of disease
 occasional still amenable to treatment, e.g. solitary metastasis from colorectal secondary


                                  Biliary Tract Disease 

Gall stones
very common problem
 10% is radiopaque therefore can be seen in the plain X ray

3 types of stones:
                     Cholesterol stone
                    almost entirely composed of cholesterol
                    6% of all
                    solitary


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                       Mixed stone
                      90%
                      mixture of cholesterol, calcium salts (bilirubinate, phosphate, carbonate, palmite) and
                       proteins
                      multiple
                      faceted

                       Pigmented stone
                      common in the Far East
                      almost entirely calcium bilirubinate
                      small, black and multiple
                      can be as hard as coral or soft like mud

Effect and complications of Gall Stone
in gall bladder           Silent
                          Chronic cholecystitis
                          Acute cholecystitis         gangrenous
                                                       empyema
                                                       perforation
                          Mucocele
                          Carcinoma

in the bile duct          obstructive jaundice
                          cholangitis
                          pancreatitis

in the intestine          intestinal obstruction (gallstone ileus)


Treatment of gall bladder stone

Asymptomatic
Nothing                  patient may never develop any problem
                         risk for surgery is higher than waiting
Exception                diabetic patient
                               chance of having complications is higher than usual if
                       complication arise, more serious
                        limy bile
                               increase chance of carcinoma of gall bladder
                        typhoid carrier
                               bacteria hide inside the gall bladder
                               continue produce bacterial to infect other people
Symptomatic
always advice on surgery
Choices            Open cholecystectomy
                       traditional
                       easy
                   Laparoscopy cholecystectomy
                       new
                       technically more demanding
                       expensive in setting up the equipment and in running
                        5% of patient is impossible / unsafe and need to
                      convert to open surgery
                       less wound / pain


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                         quicker recovery, shorter hospital stay
Treatment of bile duct stone
Cholangitis         resuscitation
                    antibiotics
                    remove of sources
Stone removal       endoscopy  ERCP
                               (Endoscopic retrograde cholangio-pancreatogram)
                    open surgery e.g. Common bile duct exploration (ECBD)
                               less common


Malignancy of Bile Duct - Cholangiocarcinoma
uncommon
associated with              clonorchosis
                             choledochocyst
common adenocarcinoma
presented with obstructive jaundice and / or cholangitis
investigations reveal stricture in the bile duct

Treatment
Surgical excision        only way of cure

Surgical bypass              if tumor found to be irresectable at operation
                             better way of palliation than stent

Stenting                     can be done in very ill patient who cannot withstand surgery
                           done endoscopically or percutaneously
                           blockage is a common problem, need to be replace periodically
                           increased chance of infection

                                               Pancreas 

Pancreatitis

Causes :
Biliary                   common problem in Hong Kong
Alcoholic                 more common in the Western society, also seen in Hong Kong
Others                    Trauma
                          Metabolic e.g. Hyperlipidaemia
                          Infection e.g. mumps, Coxsackie B
                          Drugs e.g. steroid
                          Idiopathic – no cause found after thorough searching

Severity varies
Mild abdominal pain  Shock, Multi-organ failure

Diagnosis
Hyperamylasaemia – amylase > 6 times normal

Treatment
Supportive                   intravenous fluid
                           correction of electrolyte disturbances
                           correction of hypoxia

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                         removal of cause if possible
Malignancy of pancreas
more common in the West although not rare in Hong Kong
70% in the head
30% in the body and tail
Better prognosis in the head because causing symptoms earlier
Classically              Painless Progressive Jaundice
                         Others :     Weight loss
                                       Anorexia
                                       Pain

Investigations
Ultrasound
Computerized Axial Tomography (CT Scan)
ERCP         Diagnostic
             Therapeutic by putting biliary stent to relieve the obstructive jaundice
Treatment
Surgery            the only hope of cure
                    Pancreatic head lesion - Whipple’s Operation
                               major operation
                               high mortality
                    Body and Tail lesion - Total / distal pancreatectomy
                    Bypass surgery - palliation for obstructive jaundice and / or
                associated duodenal obstruction

Stenting            for palliation of jaundice only
                     also have problem of blockage of stent and infection

No response to systemic chemotherapy or irradiation




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Chapter 19                         Hepatocellular Carcinoma                                              July 1998


>90% patients present with symptomatic tumour

85-95% inoperable          all dead within 1 year, mostly within 6 months with a median survival
                           of 10 weeks

10-15% operable            operative mortality 10% (mainly due to infection & liver failure)
                           5 year survival rate 30%
                           operability depends on patient factor, LFT factor and tumour factor
LFT factor
when patient has normal non-cirrhotic liver
 can take away 3/4 of liver
 regeneration will be completed and recovered in 2 weeks (10days to 2 weeks time regenerate LFT)

          Definition of regeneration:
          - cell division
          - replacement of injured tissue by cells of the same type
          Non-cirrhotic (normal) liver:
          - good regenerative power
          Cirrhosis:
          - repeated cell destruction follow by regeneration and fibrosis
          - gradually regeneration becomes limited

Tumour factor
- extrahepatic dissemination, e.g. porta hepatis LN metastasis, lung secondaries
- tumour invades major vessels, e.g. main portal vein, IVC
- extensive bilobar involvement

          5 year survival after resection:
          Ca stomach                5-10%
          Ca oesophagus             10-15%
          Ca head of pancreas       10%
          Colorectal cancer         depends on Dukes’ staging

Try to detect tumour when the patient is asymptomatic
        · screening (aim detect 2 cm tumour)
         - detect smaller / earlier tumour
         - operation rate (80-90%)
         - lower operative (less trauma, less liver resection)
         - improves 5 year survival (70-80%)
primary screening - detect a disease which is totally asymptomatic
        sensitive
        specific (no need very specific)
        acceptable (non-invasive)
        cost effective
                 prevent disease in community
                 there is high risk group (more effective screening procedure)
                 relative cheap
        screening test follow by specific test
        screening: diagnosis  effective treatment
Screening tests in practice: Ca breast; G6PD deficiency; congenital hypothyroidism

10-15% HBV carrier (Red Cross reported 10% HBV carriers in blood donor)
HBV carrier  HCC (> 100x risk increase)




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Screening Tests
- screen AFP + USG
- AFP not a very sensitive test
 therefore patient. With SOL in liver on USG even no increase in AFP  refer to specialist
- USG : can detect SOL >2cm
- AFP: sometimes increase in HCC not detected in USG (<2cm)
 therefore, do both
-testicular tumour also increase AFP, because AFP in mail exam the testis.
- conditions of increase in AFP: pregnancy, chronic liver disease (because regeneration of liver, e.g. chronic
hepatitis)

Frequency of Screening
- biological behaviour of tumour: doubling time of tumour ~4 months (double size)
- therefore ideally once every 4 months, but compromised once ever 6 months

6 month screening programme
- HK population 6,000,000
- HK carrier 600,000
- 1.2 million/year USG  problem
- 1.2 million/year AFP  OK.
- therefore screening group:
         relatives of HCC patients
         HBV carrier  screening

Aetiological factors of HCC
- HBV
- HCV (1-% serological +ve)
- cirrhosis
- aflatoxin (aspergillus flavor)
- aerobic steroid

Route of transmission
- blood fluid transmission
         - vertical transmit from one generation to another
         - most important in H.K
         - transmission rate ~100%
         - mother is HbeAg carrier
         - baby’s early exposure to HBV
         - high % develop chronic hepatitis:
         - in family members
- Horizontal (relatively unimportant)
         - sexual
         - sharing needles (IVDA)

Vaccinations
baby
-passive immunization + follow up active immunization

          Summary
          - HCC is a disease of bad prognosis, because of its late presentation
          - concept of screening
          - primary prevention of HCC




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Clinical features of HCC
1. asymptomatic
- incidental finding
- discovered by screening
2. local s/s
- RUQ mass /pain
-stigmata of chronic liver disease
-liver failure: encephalopathy
3. general s/s
- wt loss
- anorexia , nausea
4. metastasis
- blood spread
           -lung: sob
           -bone: pain
           -skin: mass
-intraperitoneal (most common)
           ascites
-lymphatic (only 10% by this spread)
5. Cx
i. rupture
           acute  hypovolaemic shock
                    acute abdomen
                    sign and symptom of peritonitis (haemoperitoneum)
           ddx: ectopic preg.
           Chronic  slow oozing of blood
                    progressive increase pain
                    pallor
                    abd distension with blood stained ascites
           Mx: resuscitation
                    find the cause: USG, diagnostic tapping or lavage
                    definitive Tx
                             -angiographic embolization of the bleeding vessels
                             -surgery: packing, suturing, injection of sclerosant (e.g. 100% alcohol)
ii. bleeding varices
           -HCC invade portal vein/ hepatic vein
           - much higher mortality
           -more difficult to control
iii. OJ
           -uncommon but treatable, may be operable
           -90% because parenchymal insufficiency and die within 1 months.
           -causes: intrahepatic: multiple tumour compression
                    extrahepatic:     tumour cast
                                      tumour fragment shed in CBD
                                      haemobilia
                                      LN at porta hepatis
6. Paraneoplastic symdrome.
i. insulin-like subs hypoglycaemia (no history of DM)
ii. PATIENTH like subs.  hypercalcaemia
iii. non-erythropoiteic polycythaemia




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P/E:
- stigmata of chronic liver disease
- signs of bleeding tendency
          decrease LFT, decrease clotting factor, decrease platelet
- portal HT
          caput medusae
          splenomegaly
          ascites
          varices
- hypersplenism
          splenomegaly
          pancytoopenia
          hypercellular/ normal BM
          recersible by splenectomy
- sign of liver failure
- s/s of liver failure
- s/s of 1°
- s/s of 2°

Ix: reasons to do Ix
i. Dx
         direct vs indirect
         histology- biopsy.            Incisional
                                       excisional
                                       needle
                                       trucut
                                       punch biopsy (using endoscope)
           guided by : endoscope, USG/CT, Laparoscopic
           blind Bx.
           Cytology (individual cells) Vs histology (architecture of tissue)
                    endoscope Vs radio (e.g. Barium meal)
                    1. diagnosis of lesion     missed of lesion
                       diagnosis early tumour
                    2. no irradiation hazard
                    3. take biopsy.
           Indirect: radiology
ii. Assess GC of patient.
           -assess the patient. Factor
iii. Extent of disease
           e.g. a malignant condition
                    -local extent (it may affect management)
                    - distant metastasis
iv. prognosis
           e.g. receptor status of CA breast  hormonal treatment
           e.g. HCC with AFP +ve  poor prognosis
v. facilitate FU
           e.g. colorectal CA
                    CEA before op
                    post op decrease CEA (success)
                    FU increase CEA recur
           e.g. HCC - AFP

Diagnosis of HCC
-direct -biopsy (reluctant to do)
- indirect -SOL, AFP




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What is the danger of biopsy?
1. bleeding. Esp. in cirrhotic patient. (because increase patient, decrease pit. Portal HT  severe bleed liver
subs is firm  not easy to contract)
          risk of major bleeding from biopsy ~1% (even with careful and good technique)
2. tumour dissemination
I/C of liver biopsy:
-liver biopsy would determine the treatment plan

Indirect diagnosis
1. SOL in liver
2. increase in AFP e.g. pregnancy, testicular tumour, regeneration of liver( chronic hepatitis, cirrhosis)
AFP > 500  investigate
therefore in patient. With SOL & AFP>500 R/O testicular tumour & pregnancy.  assume it is HCC  op

Hepatoma Clinic
- CXR
        -heart size
        -chronic chest
        -2°
-USG
-CBP platelet. (decrease in hypersplenism)
        increase in paraneoplastic syndrome
-LFT / PT/ APTT
        PT for Pugh’s Child grading
- HBV serology
- AFP
(HCV not routinely done, for research purpose, account for ~10% of HCC)

USG
-liver size ? shrunken
-small ant of ascites
-extent of tumour: size, solitary Vs multiple
-status of portal vein (even better than CT)
  st
*1 choice of treatment of HCC is surgery because make sure that the tumour is operable or not
If operable  further Ix
some/most centers  CT / detect small SOL (especially in lung base)
PWH              HAG (hepatic angiogram)

                                  HAG (2-D image)

in-operable                       ?                          Operable
(Ytrium90 TcMAA)                  Lipiodol
                                  -retain in tumour                  CT scan

CT scan                                    CT D10                    if still operable
radio isotope scan                (USG better show SOL)
                                  but regeneration                            OT
                                  nodule haemangioma
                                  also retain lipiodol

MRI
- still in research stage




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Chapter 20                        Recurrent                     pyogenic                  cholangitis
(RPC)                               (last revised April 1998)


  PC is a disease characterized by the formation of calcium bilirubinate stones in the intra-hepatic bile ducts
leading to biliary obstruction, strictures formation and repeated attacks of cholangitis.”

This is a surgical condition that a Hong Kong medical student must learn and know quite a bit. It is also called
oriental cholangitis. Furthermore, it comes up rather frequently in the clinical examination. It is a condition that
carries a lot of names: primary cholangitis, asiatic cholangitis, oriental cholangiohepatitis, hepatolithiasis, etc.

Incidence
the disease is endemic in East Asia
both sexes are affected equally
affects people of lower social class
number of new cases and admissions decreasing in the last 10 years
peak age of presentation: 30-40

Pathology
characterized by the presence of sludge and pigment stones, in a background of strictures and dilatation in
the intra-hepatic and extra-hepatic bile ducts due to inflammation and infection
left hepatic duct is more commonly affected (drainage of the left lobe is worse than the right)
extra-hepatic ducts are often grossly dilated and contain stones in 2/3 of cases
10-20% of cases has stones in gallbladder

Clinical features
RUQ pain, fever and jaundice (Charcot’s triad)
septicaemia (Reynold’s pentad)
abdominal signs over RUQ
gallbladder palpable in one third of patients, invalidating Courvoisier’s law

Laboratory and radiological investigations
blood: CBP, LFT, PT/APTT, amylase, blood culture
urine: bile and urobilinogen
CXR (erect): to detect free gas under diaphragm, basal pneumonia, etc
AXR: may detect pneumobilia
USG: dilated biliary tree, stones, any liver abscess
Cholangiogram: by ERCP or PTBD

Management
Patients with an acute attack of recurrent pyogenic cholangitis are managed conservatively except when
complication such as abscess or peritonitis occur which require emergency treatment. The patient is kept nil-
by-mouth and N/G tube is placed to rest the bowel. Intravenous fluid is given. Blood pressure, pulse,
temperature are monitored regularly. IV antibiotic therapy is given after blood culture taken. Analgesic is also
prescribed.

Majority (>80%) will resolve on conservative treatment. If the condition is deteriorated (septic shock) or not
response to conservative treatment after 2 to 3 days, biliary tree decompression is required.

Biliary tree decompression can be achieved by endoscopy, percutaneous approach or surgery. If the stone is
impacted at the lower end of CBD, ERCP with papillotomy and nasobiliary drainage is indicated. Stones can
then be extracted in later ERCP sessions when the acute cholangitis is under control after decompression.
Percutaneous transhepatic biliary drainage (PTBD) is indicated when there is intraheptic obstruction or the
CBD is not accessible (e.g. after gastrectomy). Laparotomy with CBD exploration and T-tube insertion is the
intervention employed in emergency situation when endoscopy and interventional radiology are not available
or failed.




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To prevent the recurrence of the disease, more definitive treatment is required. The principles are: (1).
eradication of stones in biliary system, (2). drain the obstructive segment, (3). resect non-functioning
segments of liver. The stones can be removed by surgery, endoscopic approach or percutaneous approach.

At open surgery, choledochotomy is performed and the stones are extracted by forceps or Forgarty balloon
catheter with the aid of flexible choledochoscope. Large stones can be fragmented mechanically by means of
wire basket or electrohydraulically or laser. If the stone is impacted at the lower end of CBD, transduodenal
sphincterotomy is performed to remove the stone and then the duct mucosa sutured to that of
duodenum(transduodenal sphincteroplasty). Then the choledochotomy is closed with fine absorbable sutures
around T-tube. The long limb of T-tube is brought through the abdominal wall via a stab wound. T-tube
serves to drain the bile if there is obstruction CBD after exploration. Postoperative cholangiography is carried
out 7-10 days to confirm the free flow of bile before the removal of T-tube. If there is residual stone, the T-
tube is left in-situ for 4-6 weeks allowing tract to form. Then the stones can be removed under direct vision by
choledochoscope after dilatation of the tract percutaneously.

      Besides surgery, stones can be removed following endoscopic papillotomy. Also stones can be
removed through choledochoscopy inserted through the dilated PTBD tract.

         Drainage procedures are indicated when the surgeon cannot clear all the stones or when there is
recurrent choledocholithiasis. The aim of biliary drainage is to allow newly formed stones to pass
spontaneously into the bowel. This can be achieved by choledocho-duodenostomy, hepato-jujenostomy,
sphincteroplasty. For those patients with recurrent attacks, hepatico-cutanous jejunostomy can be
constructed to allow access to bile duct without operation. Segmental liver resection is indicated only when
there is substantial liver parenchymal damaged.




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Chapter 21                       Primary liver cancer
(adopted from CancerNet from the National Cancer Institute, Information for Health Care Professionals)

Adult primary liver cancer

PROGNOSIS
Hepatocellular carcinoma is a tumor that is relatively uncommon in the United States; however, it is the most
common cancer in some other parts of the world. Hepatocellular carcinoma is rarely curable by surgical
resection, but surgery is the treatment of choice for the small fraction of patients with localized disease.
Prognosis depends on the degree of local tumor replacement and the extent of liver function impairment.
Therapy other than surgical resection is best administered as part of a clinical trial. Such trials evaluate the
efficacy of systemic or infusional chemotherapy, hepatic artery ligation or embolization, and radiolabeled
antibodies, often in conjunction with surgical resection and/or radiation therapy. In some studies of these
approaches, long remissions have been reported. Hepatocellular carcinoma should be distinguished from
bile duct cancer (cholangiocarcinoma) as well as from metastatic cancer that originates in another organ.

Hepatocellular carcinoma is associated with cirrhosis in 50%-80% of patients; 5% of cirrhotic patients
eventually develop hepatocellular cancer, which is often multifocal.

Hepatitis B infection and hepatitis C infection appear to be the most significant causes of hepatocellular
carcinoma worldwide, particularly in patients with continuing antigenemia and in those who have chronic
active hepatitis.

Aflatoxin has also been implicated as a factor in the etiology of primary liver cancer in parts of the world
where this mycotoxin occurs in high levels in ingested food. Workers who were exposed to vinyl chloride
before controls on vinyl chloride dust were instituted developed sarcomas in the liver, most commonly
angiosarcomas. Other sarcomas of smooth muscular and vascular origin are also found.

The primary symptoms of hepatocellular carcinoma are those of an hepatic mass. However, in patients with
underlying cirrhotic disease, a progressive increase in alpha-fetoprotein (AFP) and in alkaline phosphatase or
a rapid deterioration of hepatic function may be the only clue to the presence of the neoplasm. Infrequently,
patients with this disease have polycythemia, hypoglycemia, hypercalcemia, or dysfibrinogenemia.

The biologic marker AFP is useful for the diagnosis of this neoplasm. By a radioimmunoassay technique,
50%-70% of patients in the United States who have hepatocellular carcinoma have elevated levels of AFP.
However, patients with other malignancies (germ cell carcinoma and, rarely, pancreatic and gastric
carcinoma) also demonstrate elevated serum levels of this protein. AFP levels have been shown to be
prognostically important, with the median survival of AFP-negative patients significantly longer than that of
AFP-positive patients. Other prognostic variables include performance status and liver functions.

Patients scheduled for possible resection require preoperative assessment with angiography in conjunction
with computed tomographic (CT) scan, CT scan with arterial portography, or dynamic CT and magnetic
resonance imaging (MRI) scanning. Information on the arterial anatomy is helpful for the operating surgeon
and may eliminate some patients from consideration for resection. Selective angiography also helps
differentiate the tumor from lesions that may not require active therapy, such as hepatic hemangioma.
Dynamic CT and MRI scans can document the relationship of the tumor to the hepatic and portal veins (and,
on occasion, involvement of these structures), delineating tumors for which the chances for surgical cure are
remote.

CELLULAR CLASSIFICATION
Malignant tumors of the liver are primarily adenocarcinomas, with two major cell types: hepatocellular and
cholangiocellular.




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Histologic classification is as follows:
 hepatocellular carcinoma
  (liver cell carcinoma)
 hepatocellular carcinoma
  (fibrolamellar variant)
 cholangiocarcinoma
  (intrahepatic bile duct carcinoma)
 mixed hepatocellular cholangiocarcinoma
 undifferentiated

 Hepatoblastoma rarely occurs in adults.

 Note: The fibrolamellar variant is important because an increased proportion of these patients may be
cured if the tumor can be resected. It is more frequent in young women.

STAGING INFORMATION
For purposes of treatment, patients with liver cancer are grouped as localized resectable, localized
unresectable, or advanced disease. These groups are described with the following TNM correlations:

-- Localized resectable --
(T1, T2, T3, and selected T4; N0; M0)

This type of liver cancer is confined to an anatomically solitary mass in a portion of the liver that allows the
possibility of complete surgical removal of the tumor with a margin of normal liver. Liver function tests are
usually minimally abnormal, and there should be no evidence of cirrhosis or chronic hepatitis. Only a small
percentage of liver cancer patients will prove to have such localized resectable disease. Preoperative
assessment that includes computed tomography and angiography should be directed toward determining the
presence of extension across interlobar planes, involvement of the hepatic hilus, or encroachment on the
vena cava. A resected specimen should contain a 2-cm margin of normal liver. Patients with chronic
hepatitis and nutritional cirrhosis are at high risk when surgical resection is performed.

-- Localized unresectable --
(selected T2, T3, and T4; N0; M0)

This type of cancer appears to be confined to the liver, but surgical resection of the entire tumor is not
anatomically possible. Some cases may be inoperable despite a localized mass because of serious
anatomic or functional impairment of the noncancerous hepatic tissue. Patients with locally unresectable
fibrolamellar variant hepatomas may be considered for liver transplantation.

-- Advanced --
(any T, N1 or M1)

Advanced liver cancer is cancer that has spread through much of the liver or to distant metastatic sites.
Median survival is usually 2-4 months. The most common metastatic sites of hepatocellular cancer are the
lungs and bone. Multifocal disease in the liver is common, particularly when cirrhosis or chronic hepatitis is
present.

TREATMENT OPTION OVERVIEW
The designations in PDQ that treatments are "standard" or "under clinical evaluation" are not to be used as a
basis for reimbursement determinations.

LOCALIZED RESECTABLE ADULT PRIMARY LIVER CANCER
-- T1, T2, T3, and selected T4; N0; M0 --




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Treatment options:
Standard:
  Surgery: Resection of the localized liver cancer varies from segmental resection to trisegmental (80%)
resection. In series of carefully selected patients, partial hepatectomy has resulted in a 5-year survival of
10%-30%. Many of these patients present with the fibrolamellar variant. Hepatic carcinoma is frequently
multifocal and may involve multiple sites throughout the liver at the time of exploration, even when a dominant
mass is found on preoperative assessment. Preoperative assessment should also include a search for
extrahepatic metastases, since this condition will also preclude the planned hepatic resection. Resection that
involves more than a wedge of liver is poorly tolerated (high mortality rate) in patients with cirrhosis or chronic
active hepatitis. These are generally contraindications to major hepatic resection but may not contraindicate
hepatic transplantation.

Under clinical evaluation:
  Because of the high proportion of patients who experience relapse following surgery for localized hepatic
cancer, adjuvant approaches have been employed using regional arterial infusion of the liver or systemic
therapy with chemotherapeutic agents. Chronic intermittent infusion chemotherapy and new anticancer
agents have re-established interest in this area, but there are no data, thus far, that support improved survival
with adjuvant approaches.

LOCALIZED UNRESECTABLE ADULT PRIMARY LIVER CANCER
-- selected T2, T3, and T4; N0; M0 --

Clinical trials that use systemic chemotherapy, regional chemotherapy, external radiation and chemotherapy,
and/or labeled or radiolabeled antibodies have demonstrated remission of unresectable hepatoma. Other
approaches currently under evaluation include hepatic artery ligation and embolization of the hepatic artery.
These approaches often produce central tumor necrosis, reduction in tumor size, and relief of pain, but the
benefits are usually transient. Hepatic artery ligation may offer the same benefit. However, any interference
with arterial blood supply (including infusion chemotherapy) may be associated with significant morbidity and
is contraindicated in the presence of portal hypertension or clinical jaundice. Liver function should be
relatively unimpaired, and there should be no evidence of portal vein thrombosis in patients in whom these
approaches are undertaken. Recent trials include cryosurgical destruction or injection of alcohol into the
cancer in attempts to destroy the tumor.

Treatment options:
Standard:
 There is no standard therapy for unresectable disease. Such patients should be considered candidates for
clinical trials.

Under clinical evaluation:
1. For selected patients with localized unresectable hepatoma, particularly patients with fibrolamellar
hepatomas, liver transplantation may offer a potentially curative treatment option.

2. Chemotherapy (regional infusion of the liver): Chemotherapeutic agents may be infused with a
subcutaneous portal or implantable pump via a catheter placed in the hepatic artery. Older studies that use
standard agents have demonstrated responses in 15%-30% of such cases, but newer agents and techniques
(that is, biodegradable microspheres) have been evaluated in pilot trials, as has regional chemotherapy with
external-beam radiation therapy. Many patients are not candidates for these approaches, which often require
surgical intervention.

3. Systemic chemotherapy: Several centers are evaluating combination chemotherapy programs. Long
remissions have rarely been reported, and no significant survival benefits have been conclusively
demonstrated.

4. Surgery, chemotherapy, and radiation therapy: These modalities may be combined in clinical trials for
patients with a dominant hepatic mass and multifocal involvement with small amounts of tumor; surgical
resection of the mass may be followed by hepatic infusion of the remaining liver with chemotherapeutic
agents alone or in combination with hyperthermia, radiation, or radiation with radiosensitizers.




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5. Cryosurgical destruction of hepatomas and intratumor injections of alcohol are newer modalities,
particularly for patients with cirrhosis for whom resection is unsafe.

6. Other approaches include the use of radiosensitizers and external-beam radiation therapy without
chemotherapy. The relative radiosensitivity of normal liver tissue compared with tumor tissue must always be
considered when radiation therapy is contemplated.

ADVANCED ADULT PRIMARY LIVER CANCER
-- any T, N1 or M1 --

There is no standard therapy for advanced metastatic liver cancer. Such patients should be considered
candidates for clinical trials exploring the usefulness of new biologicals or antitumor drugs (phase I and II
studies) or combinations of existing drugs, radiosensitizers, and radiation therapy. Palliation may sometimes
be achieved in such studies.

External-beam radiotherapy and chemotherapy followed by radiolabeled polyclonal antiferritin antibody
produces objective response in up to 50% of patients, but it is a localized treatment and does not address the
question of systemic disease.

RECURRENT ADULT PRIMARY LIVER CANCER
The prognosis for any treated primary liver cancer patient with progressing, recurring, or relapsing disease is
poor. The question and selection of further treatment depends on many factors, including prior treatment,
site of recurrence, presence of cirrhosis, and hepatic function as well as individual patient considerations.
Resection may be possible. Clinical trials are appropriate and should be considered whenever possible.




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Chapter 22                        Pancreatic Surgery                                  (last revised April 1998)



ACUTE PANCREATITIS
Acute pancreatitis usually is a nonbacterial inflammation of the pancreas caused by activation, interstitial
liberation, and the digestion of the gland by its own enzymes. It is characterized clinically by acute abdominal
pain, elevated concentrations of pancreatic enzymes in blood, and an increase in the amount of pancreatic
enzyme in the urine. In Hong Kong, the most common cause of acute pancreatitis is cholelithiasis and
second is alcohol.

During a mild attack, the morphologic changes are characterized by pancreatic and peripancreatic edema
and fat necrosis, but pancreatic necrosis is absent. This often is referred to as edematous pancreatitis. This
mild form may become severe (or it may be severe from the onset); in its severe form, extensive pancreatic
and peripancreatic fat necrosis, pancreatic parenchymal necrosis, and hemorrhage into and around the
pancreas is evident. This form of disease is referred to as haemorrhagic or necrotizing pancreatitis. During an
episode of acute inflammation, both exocrine and endocrine functions of the gland are impaired for weeks or
months. If the cause (cholelithiasis) and any complications (pseudocyst) are eliminated, the pancreas usually
returns to normal. Acute pancreatitis, even multiple attacks of acute pancreatitis, rarely lead to chronic
pancreatitis.

Surgery
In acute pancreatitis a diverse spectrum of illness is seen, varying from a mild, short-lived, self-limited
disease to a severe toxic condition associated with shock, hypovolaemia, multiple medical derangements,
and ultimately death. The clinical presentation alone may be quite suggestive of the diagnosis. The
predominant clinical feature of acute pancreatitis is abdominal pain. The pain normally begins in the
epigastrium, achieving maximal intensity several hours into the illness. In most patients, the pain has a
penetrating quality, radiating to the back. In patients with alcohol-induced pancreatitis, the pain often
commences 12 to 48 hours after an episode of inebriation. In contrast, patients with gallstone pancreatitis
typically experience the pain after a large meal.

Typical findings on physical examination include tachycardia, fever, epigastric tenderness, and abdominal
distension. Abdominal distension may be the result of a paralytic ileus arising from the retroperitoneal
irritation or it may be secondary to a retroperitoneal phlegmon. Severe pancreatitis associated with
hemorrhage into the retroperitoneum may produce two distinctive physical signs: Turner’s sign (bluish
discoloration of the flank) or Cullen’s sign (bluish discoloration around the umbilicus). These signs are seen in
less than 3% of patients with pancreatitis and result from the tracking of blood-stained fluid through the tissue
planes of the abdominal wall to the flank or along the falciform ligament to the umbilical region.

The diagnosis is often suspected on the basis of clinical presentation and is supported by finding elevated
amylase level. Clinical and laboratory evidence of pancreatitis can be supported by radiographic procedures.
Currently, computed tomography (CT) is the most widely accepted and sensitive method used to confirm the
diagnosis of pancreatitis. The clinical course of up to 80 to 90% of patients with acute pancreatitis follows a
mild, self-limited course; in 10% to 20% of patients, however, a severe form of illness develops. It is possible
to predict the severity of an attack of pancreatitis and the overall prognosis using routine available clinical and
laboratory determinations. The most widely used predictive criteria involve 11 prognostic signs identified by
Ranson in 1974.

Ranson’s Early Prognostic Signs of Acute Pancreatitis
       At Admission                        During Initial 48 Hours
       Age > 55                            Hematocrit fall > 10%
                               3
       WBC > 16,000 cells/mm               BUN elevation > 5 mg/dL
                                                      2+
       Serum LDH > 350 IU/L                Serum Ca fall to < 8 mg/dL
       SGOT > 250 U/dL                     Pao2 < 60 mm Hg
       Blood glucose > 200 mg/dL           Base deficit > 4 mEq/L
                                           Estimated fluid sequestration > 6L




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          Number of Criteria                   Mortality
                0-2                                 Essentially no mortality
                3-4                                 15% (half require ICU admission)
                5-6                                 50% (almost all require ICU admission)
                >7                                  > 50%

Management of Acute Pancreatitis
The treatment of uncomplicated acute pancreatitis is medical and is directed primarily toward the restoration
of fluid and electrolyte balance and avoidance of secretory stimulation of the pancreas. Complications of
acute pancreatitis include adult respiratory distress syndrome (ARDS), pseudocyst formation, infected
pancreatic necrosis, and pancreatic or peripancreatic abscess. Surgical intervention in the management of
acute pancreatitis is reserved for patients who develop those complications previously noted.


CHRONIC PANCREATITIS
Chronic pancreatitis is characterized clinically by recurrent, acute episodes of abdominal pain
indistinguishable from those of acute pancreatitis. Diabetes and exocrine insufficiency occur as the disease
progresses. In Hong Kong, the most common cause of chronic pancreatitis is alcoholism. Morphologically,
chronic pancreatitis is characterized by a permanent and usually progressive destruction of pancreatic
parenchyma. The acinar cells are destroyed first, replaced by dense fibrosis. In chronic pancreatitis, unlike
acute pancreatitis, the morphologic changes are irreversible and progressive, even if the cause (e.g.
alcoholism) is removed. Management of acute exacerbation of chronic pancreatitis is similar to the
management of acute pancreatitis. Surgical intervention for relief of chronic pain is possible, but it is
impossible to state in precise terms.


PANCREATIC CYSTS
Three types of pacnreatic cysts occur: (1) congenital, (2) pseudocysts, and (3) neoplastic. Of these,
pseudocysts are the most common.
     Congenital cysts are of little clinical importance except when they are multiple and part of the systemic
     disease cystic fibrosis.
     Pseudocysts are localized collections of fluid with high concentrations of pancreatic enzymes; they
     usually occur as a complication of pancreatitis. They are located either within the parenchyma or in one
     of the potential spaces that separate the gland from the adjacent abdominal viscera. They usually are
     found in the lesser sac behind the stomach. If mature pseudocysts are less than 5cm in diameter, they
     may not require treatment but should be followed by serial ultrasound. Cysts requiring surgical
     intervention are usually drained internally, although external drainage and excision are other options. A
     portion of the wall should always be biopsied to exclude a diagnosis of cystadenocarcinoma of the
     pancreas.
     Neoplastic cysts are of clinical importance that it can be benign or malignant. Surgery is usually
     indicated if a diagnosis of malignant cyst is suspected.

PANCREATIC CARCINOMA
In the United States, cancer of the exocrine pancreas is the fourth leading cause of death in men and the fifth
in women. It is also quite common in Hong Kong. At the time of diagnosis, the tumor is confined to the
pancreas in fewer than 10% of patients, and in 75% of cases, pancreatic cancer occurs in the head of the
pancreas. Approximately 75% of patients with pancreatic head carcinoma present with obstructive jaundice,
weight loss (average of 20 pounds), and deep-seated abdominal pain.

A CT scan should be done after baseline laboratory studies confirm an elevated bilirubin. A dynamic CT scan
with fine cuts through the head of the pancreas often defines a mass in the head of the pancreas. Evidence
of metastatic spread or involvement of the superior mesenteric artery may be noted; these two features deem
the patient unresectable. Fine-needle aspiration (FNA) can be performed for accurate tissue diagnosis in
patients who are not candidates for surgery.




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Endoscopic retrograde cholangiopancreatography (ERCP) is indicated for the relief of biliary obstruction for
carcinomas that are not resectable, or if a definite mass is not seen on CT scan. In those patients determined
preoperatively to be resectable, pancreatoduodenectomy (Whipple resection) is the most commonly
performed surgery for carcinoma of the pancreatic head. Surgical palliation in patients with unresectable
pancreatic carcinoma is directed toward relief of obstructive jaundice, gastric outlet obstruction, and pain.

ISLET CELL NEOPLASMS
Insulinoma
These tumors arise from beta cells and are the most common islet cell neoplasms. The classic diagnostic
criteria (Whipple’s triad) are usually present: (1) hypoglycemic symptoms produced by fasting, (2) blood
glucose concentrations less than 50 mg/dL during symptomatic episodes, and (3) relief of symptoms during
intravenous administration of glucose. The most useful diagnostic test is the demonstration of fasting
hypoglycemia with inappropriately high serum levels of insulin. A ratio of plasma insulin to glucose of greater
than 0.3 is diagnostic. Treatment consists of removal of the adenoma. Surreptitious self-administration of
insulin may mimic this tumor. Circulating C-peptide levels are normal in these patients but are elevated in
patients with insulinoma.

Gastrinoma (Zollinger-Ellison Syndrome)
The principal manifestation of Zollinger-Ellison syndrome (ZES) is due to gastric acid hypersecretion caused
by excessive gastrin production by tumor. Although the normal pancreas does not contain gastrin-producing
cells, most gastrinomas arise in the pancreas. Other gastrinomas are found chiefly in the duodenum. One-
fourth of gastrinomas are associated with multiple endocrine neoplasia type I (MEN-I) syndrome, in which the
tumors are usually multiple and benign; those without MEN-I (sporadic gastrinomas) are more often single
and malignant.

Symptoms of gastrinomas are those of gastric acid hypersecretion: severe refractory peptic ulcer disease
and diarrhea (resulting from fat malabsorption as massive quantities of acid destroy pancreatic lipase). The
diagnosis of gastrinoma requires the demonstration of fasting hypergastrinemia (greater than 200 pg/mL) in
the presence of gastric acid hypersecretion. A paradoxical increase in serum gastrin levels in response to
intravenously administered secretin (secretin stimulation test) confirms the diagnosis. The medical
management of gastrinomas is treatment with hydrogen potassium proton pump inhibitor. In patients with
MEN-I, the tumors are multiple and generally unresectable. All patients with sporadic gastrinoma should
undergo surgical exploration unless there is evidence of extensive metastatic disease.




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Chapter 23                         CA Pancreas                               (last revised April 1998)


Anatomical location
head 70 % -- head proper (47%), periampullary region (23%)
body 30%
average age of 60, slight male preponderance

Risk factors
high saturated fat diet, smoking

Pathology
Histological types : majority are ductal adenocarcinoma
(a) Periampullary Ca
duodenal papilla, ampulla of Vater, duodenal mucosa (earliest presentation)
(b) Ca head proper
usu. small at presentation because tumour obstruct CBD
(c) Ca body and tail
greater size with advance local disease and metastasises more often

Spread
(1) local -- occurs in (b) and (c)
-- to adj. structures: duodenum, pyloric antrum, transverse colon and mesocolon
(2) lymphatics -- head: nodes along hepatic artery
-- body and tail: gastric, coeliac, mesenteric, para-aortic
(3) blood-stream -- late, esp. to liver
(4) peritoneal implantation -- 10 %

Clinical Presentation
Symptoms:
(1) As painless progressive obstructive jaundice
pruritus -- coincides with onset of jaundice
jaundice -- steadily progressive
pain -- steady dull ache, in epigastrium, radiate to back, (can be colicky and simulate biliary colics)
anorexia
weight loss
(2) As intractable pain without jaundice -- due to ca tail
pain -- in back at L1-2, worsen when lies down, not related to food, persist for weeks
diarrhoea,anorexia,weight loss
(3) Other related conditions
thrombophlebitis migrans -- thrombophlebitis appear spontanously in almost any superficial vein ; resolve and
re-appear
DM -- suspected when adequate DM treatment with continue weight loss.
pancreatic calcinosis--almost an pre-carcinomatous condition
acute cholecystitis and /or acute pancreatitis -- occasionally the first indication of ca pancreas.

Signs:
(1) Palpable gallbladder (60 %, Courvoisier's law) with jaundice
(2) Palpable liver (60%)
(3) Palpable epigastric mass
(4) Ascitis




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Investigation
(1) Barium meal (rarely used)
'pad' sign
reverse '3' sign

(2)hypotonic Duodenography (rarely used)
--'rose-thorning' distortion (duodenal wall invasion)
N.B. chronic pancreatitismedial duodenal wall straighten
      ampullary CA filling defect

(3)Laboratory test
stercobilinogen <10mg/d (not routinely performed)
faecal occult blood esp. in periampullary CA.

(4)ERCP
confirm the presence or absence of a surgical cause of jaundice.
main pancreatic duct narrowed or completely obstructed
cytological exam of pancreatic juice can confirm radiological diagnosis
can performed endoscopic stenting at the same session
complications: cholangitis, acute pancreatitis

(5)U/S
jaundice is one of the major indication for U/S
best in thin object
CA head and body can be identified in most patient when present clinically
tumor<2cm usually not detected
The use of percutaneous imaging-guided biopsy or FNAC is controversial

(6)CT scan (most useful)
>2cm usually detected irrespective of the site
best with patient with well developed fat plane

Management
(1) operative treatment
(a) (Whipple’s operation / pylorus-preserving pancreatoduodenectomy)
fixity of the tumour, involvement of major vessels (e.g. SMA, SMV, portal vein), and presence of liver
secondaries rule out radical surgery
general mortality 5-10%
5 years survival rate for Ca head of pancreas is only 5% while Ca ampulla >30%
(b)palliative operations
for jaundice and gastric outlet obstruction when radical resection is not indicated
* choledochojejunostomy + gastroenterostomy ( ouble bypass” procedure)
         [some surgeon may prefer cholecystojejunostomy instead of choledochojejunostomy]
(c)treatment of intractable back pain
splanchnic or caelic plexus block as part of open procedure (can also be performed percutaneously through
the back)

(2) non-operative treatment for jaundice
(a) palliative endoscopic stenting
(b) percutaneous transhepatic biliary drainage (PTBD)




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Chapter 24                            Acute Pancreatitis
                                                                                                    (last revised April 1998)

Acute pancreatitis : an acute pancreatic inflammation usually resolve with no structural or functional damage
if the primary cause is removed.

EPIDEMIOLOGY : - male : female = 1 : 1                                        - peak at 40 -50’s

AETIOLOGY :
(1) biliary tract disease e.g. gallstone , RPC.
(2) idiopathic
(3) alcoholism
(4) traumatic
(5) post-operative e.g. ERCP
(6) rare causes :          infection - mumps, Coxackie virus, parasites (ascaris / clonorchis)
                           drugs - steroids, cytotoxic drugs, diuretics (thiazide / frusemide)
                           metabolic - hypercalcaemia, hyperlipidaemia
                           inflammatory - peptic ulcer
                           vascular - PAN, SLE
                           obstruction - Ca pancreas, calculi
                           congenital - familial hereditary pancreatitis
                           hypothermia

PATHOGENESIS:
- mainly due to autodigestion of the gland

                                                                  * cholelithiasis
        * virus
        * drugs                                                   * alcoholism
        * ischaemia
        * nutritional deficit
                                                                  ductal obstruction
        * trauma
                                                                  + biliary reflux
                                                                  + duodenal reflux

        acinar cell injury            * hypercalcaemia             interstitial leakage
                                      * hyperlipidaemia

        cell necrosis


                                      interstitial enzymes



          lecithin              phospholipase A              elastase                kallikrein
                                                                                     bradykinin


        lysolecithin              fat necrosis         vascular damage                 local
                                                                                      edema


                                      pancreatitis




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CLINICAL PRESENTATION

SYMPTOMS:
onset - any time, frequently follows ingestion of heavy meal/alcohol.
pain - severe constant epigastric, radiate to the back, crescendo over several hours,
       increase on lying flat and decrease on sitting up & bending forward
nausea, vomiting & retching frequent.
muscle twitching, cramps & spasms less common.

SIGNS:
          general:- shock
                  - faint jaundice
                  - fever occasionally
                  - rarely cyanosis
          local: - tenderness, sometimes rigidity & rebound tenderness
                  - Cullen’s sign and or Grey Turner’s sign
                  - ileus
                  - tender mass in epigastrium (pseudocyst/abscess formation)

RADIOLOGICAL FEATURES:
      (1) sentinel loop
      (2) colon cut off sign
      (3) air-fluid level in D-J junction plus expanded C-loop
      (4) left pleural effusion, elevation of left hemidiaphragm, basal atelectasis
      (5) gallstones
      (6) pancreatic calcification - if underlying chronic pancreatitis present

INVESTIGATION
      AXR, CXR
      U/S abdomen
      serum amylase
      RFT
      LFT, LDH, AST
      CBP (WCC)
      glucose
      Ca
      PT/APTT
      X-match
      ABG
      urinalysis

DIAGNOSIS
- Hx and P/E
- clinical picture (high index of suspicion)
- high serum amylase (>1000 I.U./l) highly suggestive
- serum calcium decreases
- exclude other DDx
To confirm diagnosis: U/S abdomen or CT scan abdomen

DIFFERENTIAL DIAGNOSIS:
(1) PPU
(2) Acute cholecystitis
(3) MI
(4) I.O.
(5) leaking aortic aneurysm
(6) mesenteric vascular occlusion




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MANAGEMENT:

conservative treatment: supportive            - resuscitation
                                              - rest pancreas and bowel (NPO +/- NG suction)
                                              - pain relief by opiates
                                              - respiratory support
                                              - treat infection
                                              - monitor renal output (Foley)
                           specific           - resist enzymatic activity by drugs e.g. octreotide

if        impacted stone at ampulla                   ERCP + NB drainage/

if:       uncertain diagnosis
          condition deteriorate
          fulminant acute pancreatitis
          complications occurs
          failure of conservative treatment
                   CONSIDER SURGERY                   peritoneal lavage/
                                                      pancreatic resection and drainage/
                                                      necrosectomy/
                                                      surgical management of complications

COMPLICATIONS:

EARLY:            CVS: shock, AMI
                  RESP: ARDS, pulmonary edema, hypoxaemia, AV shunting if sepsis
                  RENAL: renal failure
                  GI: superior mesenteric obstruction ---> thrombosis ----> segmental infarction
                      infective pancreatic necrosis, ileus
                  SEPTIC COMPLICATION: toxaemia, DIC
                  ELECTROLYTE DISTURBANCE
                  METABOLIC DISTURBANCE: hyperglycaemia, acidosis, hypocalcaemia

LATE:             Pseudocyst formation
                  Abscess formation
                  Acute relapsing pancreatitis
                  Chronic pancreatitis

PROGNOSIS:
Short term --- by Ranson’s criteria (>3 criteria - severe attack)
Long term --- depends on causes e.g. good for gallstone, bad for alcoholism
Death rate: 6 - 20%     Complete resolution: 20%             Relapse rate: 40%
Chronic pancreatitis: 10%




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Chapter 25                       Colorectal carcinoma
Epidemiology:
 common in the west, but our incidence is catching up
 recto-sigmoid colon and caecum are common sites
 M:F = 3:2
 usually over 50 years old

Pathology:
 columnar-celled carcinoma originating in epithelial lining or in crypts of Lieberkuhn.

Predisposing factors:
 familial adenomatous polyposis
 inflammatory bowel disease
 colorectal polyps
 high fat and low fibre diet
 positive family history

Spread of carcinoma:
 direct extension
 lymphatic permeation
 haematogenous dissemination
 transcoelomic spread

Clinical features:
1) left colon:
          25% present with increasing intestinal obstruction
          intestinal colic
          alteration of bowel habits
          palpable abdominal mass
          abdominal distension
2) sigmoid colon:
          bleeding
          colicky pain
          tenesmus
          bladder symptoms
3) rectum:
          bleeding
          sense of incomplete defaecation
          alteration of bowel habit
4) transverse colon:
          lassitude
          anemia
5) caecum and ascending colon:
          anaemia
          mass in right iliac fossa
          general malaise, weight loss and anaemia indicates advanced disease.

Physical examination:
 pallor
 groin or supraclavicular lymph nodes
 abdominal mass
 organomegaly
 mass or blood detected in digital rectal examination




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Investigation:
    1. Blood test            CBP,LFT,RFT,CEA
    2. Stool                 occult blood
    3. Imaging               CXR
                             double-contrast barium enema
                             ultrasound abdomen
                             CT scan for locally advanced tumour
   4.   Endoscopy            proctosigmoidoscopy
                             colonoscopy
                             biopsy during endoscopic examination

   Stages of progress:
      Dukes’ staging
          A:       growth is limited to muscularis mucosa
          B 1:     growth extended into but not through the muscularis propria
          B 2:     growth penetrates the entire thickness of the muscularis propria
          C 1:     secondary deposits in pericolic lymph nodes
          C 2:     secondary deposits in distant lymph nodes
          D:       wide spread metastasis

   Preoperative management:
    Mechanical :           4L of PEG as bowel preparation
                        whole bowel irrigation or enema to cleanse the bowel
               :    high-calorie and low-residue diet
    Chemical :             ampicillin(for Gram -positive bacteria)
                            cefuroxime(for Gram - negative bacteria)
                            metronidazole(for anaerobes)
   Treatment:
    caecum or ascending colon - right hemicolectomy
    hepatic flexure - extended right hemicolectomy
    transverse colon - excision of transverse colon and 2 flexures, transverse mesocolon and greater
       omentum (transverse colectomy)
    splenic flexure or descending colon - similar to that of transverse colon, and resection of descending
       colon (left hemicolectomy)
    sigmoid colon - sigmoid colectomy
    upper 2/3 rectum -anterior resection / low anterior resection
      lower 1/3 rectum - abdomino-perineal excision

   when irresectable
    palliative resection is the best treatment for overcoming obstruction
    others        :transverse colostomy for left upper colon carcinoma
                   :left iliac colostomy for pelvic colon carcinoma
                   :ileocolostomy for ascending colon carcinoma

   adjuvant therapy
    Chemotherapy: 5-fluorouracil and levimisole or folinic acid for staging B2 or above
    Radiotherapy: rectal tumour is sensitive

   Treatment of complication:
   1. obstruction - immediate resection (one stage or two stages)
   2. perforation - proximal end is exteriorized as a colostomy(or ileostomy)
                  - distal end is exteriorized or closed
                  - secondary anastomosis after inflammation subsided
   3. direct extension - resection en bloc with the colon

   Prognosis:
       5 year survival rates are :
           Dukes A - 90%             B - 60% C - 30%            D - 5%


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Chapter 26                       Carcinoma of Rectum                                           (last revised April 1998)


Epidemiology
Age 50-60
male > female

Risk factors
genetics, polpys, western diet (?high saturated fat & low fiber), inflammatory bowel disease (UC)

Origin
Adenoma-carcinoma sequence: most rectal carcinoma arise from an adenoma

Pathology
microscopic:
1. well differentiated adenocarcinoma
2. averagely differentiated adenocarcinoma
3. anaplastic, undifferentiated adenocarcinoma
 more malignant variety contain large number of mucin-producing cells
 prognosis after treatment is influenced by histological grading

macroscopic:
1. ulcer (commonest)
2. papilliferous
3. infiltrative

Spread
1) Local spread:
        circumferentially (18-24 months for complete encirclement) penetrating:
             anteriorly:         male: prostate, seminal vesicles, bladder
                         female: vagina, uterus
             posteriorly:        sacrum and sacral plexus
             laterally:          ureters
1) Lymphatic spread:
   usually upwards (for upper rectal tumour)
   lateral spread along middle rectal artery lymphatics for tumour 4-8cm from anus
2) Venous spread:
        usually late
        principal sites: liver (34%), lung (22%), adrenal (11%) other (33%)
4) Peritoneal spread:
        penetration of peritoneal coat by a high-lying rectal carcinoma

Duke’s Staging
A     growth is limited to rectal wall                                 15%      5 yr survival 90%
B     growth is extended to the extrarectal tissue, but no             35%      5 yr survival 60%
      metastasis to regional LN
C     secondary deposition on regional LN                              50%      5 yr survival 30%
D*    distant metastasis                                                        5 yr survival <5%
*not originally included




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Clinical features:
1. PR bleeding (+/- mucus)                2. Sense of incomplete emptying
3. Alternation in bowel habit             4. Pain
5. Weight loss, loss of appetite, anaemia
Physical examination
1. Abdominal: usually NAD, +/- hepatomegaly
2. Rectal: 90 percent of tumours can be felt digitally
3. Vaginal: anterior wall lesion
4. Protosigmoidoscopy: always positive if present, provided that rectum is emptied of faeces

Investigation:
Baseline blood tests and others bedside investigations (ECG, lung function test) for assessment of fitness for
general anaesthesia and major surgery

For diagnosis:
        1. Biopsy (through sigmoidoscopy / colonosocopy)
        2. Colonoscopy (useful to rule out synchronous tumour)
        3. Ba enema
        4. CEA (helpful)

For staging:
        1. CXR
        2. USG abdomen
        3. CT abdomen + pelvis (for locally advanced tumour)

Treatment
 Mainly surgical
      1) Anterior resection of rectum: sphincter-saving operation, for tumor in upper two-thirds
      2) Abdomino-perineal excision of rectum (APR): removal of rectum with a permanent colostomy, for
          tumor in lower one-third
      3) Abdominotransanal coloanal anastomosis (for very low rectal tumour)
      4) Pelvic exenteration
      5) Hartmann’s operation
      6) Palliative colostomy
      7) Local resection

   Principles:
        1) Radical excision of the rectum and mesorectum, together with associated lymph nodes should
             be the aim.
        2) The presence of solitary liver metastasis dose not necessarily rule out the feasibility of radical
             excision (Hepatectomy for liver secondaries can be performed later).
        3) When a tumour appear to be locally advanced, preoperative radiotherapy may reduce its size
             and make it more amenable to radical excision.
        4) When a rectal excision is possible, whenever feasible, the aim should be restore gastrointestinal
             continuity and continence by preserving the anal sphincter.

   Radiotherapy:
        1) Pre-operative: reduce tumor mass
        2) Post-operative adjuvant radiotherapy (for local control of recurrence)

   Post-operative adjuvant chemotherapy (for LN metastasis)




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Chapter 27                      Familial Adenomatous Polyposis
(FAP)                                             (last revised April 1998)


Aetiology
 an inheritable disease which is transmitted as autosomal dominant mode
 defect gene located on chromosome 5 in q21 region (5q21)
 about a third of the affected individuals are sporadic cases because of new mutation

Clinical features
asymptomatic patients
         * usually members of affected families attend for screening
symptomatic patients
         * colonic manifestation
                  1. loose stool
                  2. passage of blood and mucus
                  3. lower abdominal pain
                  4. weight loss
    * extracolonic manifestation
                  5. desmoid tumour
                  6. osteoma
                  7. epidermoid cyst
                  8. CHRPE (congenital hypertrophy of retinal pigment epithelium)
                          pigmented spots in retina - pathognomonic for the disease
                  9. brain tumour (Turcot syndrome)

Diagnosis
 by colonoscopy showing presence of more than 100 polyps and histological confirmation that these are
   adenoma

Course
 patients who inherits the gene for FPC is usually asymptomatic until after puberty, at which time polyps
   may begin to appear in some patients
 polyps almost always be visible by 30
 carcinoma of large bowel develop 10 to 15 years after onset of polyposis
 life-time risk of malignant change approaches 100%

Management
Aim   early diagnosis
      removal of vulnerable large bowel
      surveillance of any remaining large bowel

Screening is IMPORTANT because
carcinoma rate in FAP patients who present with symptoms is more than 50%, while the malignant rate for
affected individuals who are identified by screening of at-risk family members is below 5%

Screening can be done by CHRPE, DNA tests for FAP gene and colonoscopy
Surgery is the only reasonable management of FPC
        proctocolectomy and ileostomy
                adv.: most effective in eliminating risk of rectal carcinoma recurrence
                dis.:    unacceptable to some patients
        restorative proctocolectomy with ileo-anal anastomosis
                adv.: does not require permanent ileostomy yet they are continent
                dis.:    higher morbidity and results in longer hospitalization
        total colectomy and ileorectal anastomosis
                adv.: rectal preservation
                dis.:    risk of carcinoma formation in remaining rectum even with surveillance


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Chapter 28                        Anorectal disorders (last revised May 1998)
I. Haemorrhoids

A. Haemorrhoids are dilated veins located beneath the lining of the anal canal.

B. Internal haemorrhoids are located in the upper anal canal. External haemorrhoids are located in the lower
anal canal.


II. Internal Haemorrhoids

A. Internal haemorrhoids become symptomatic when constipation causes disruption of the supporting tissues
and resultant prolapse and excessive of the vascular anal cushions.

B. The most common symptom of internal haemorrhoids is painless rectal bleeding, which is usually bright
red and ranges from a few drops to a spattering stream at the end of defecation.

C. If internal haemorrhoids remain prolapsed, a dull aching may occur.

D. Blood and mucus stains may appear on underwear, and itching in the perianal region is common.

          ** Classification of Internal Haemorrhoids
          Grade 1         Non-prolapsing (Minimal bleeding)
          Grade 2         Prolapse with straining, reduce when spontaneously prolapsed
                          (Bleeding, discomfort, pruritus)
          Grade 3         Prolapse with straining, manual reduction require when prolapsed
                          (Bleeding, discomfort, pruritus)
          Grade 4         Cannot be reduced when prolapsed (Bleeding, discomfort, pruritus)

E. Management of Internal Haemorrhoids
       1. Grade 1 and uncomplicated grade 2 haemorrhoids are treated with avoidance of nonsteroidal anti-
       inflammatory drugs and dietary modification (increased fiber and fluids and avoidance of binding,
       spicy, and fatty foods).
       2. Symptomatic grade 2 and grade 3 haemorrhoids
               a. Treatment consists of hemorrhoid banding. An proctoscope is used to place a rubber band
               ligature above and around the haemorrhoid. The tissue sloughs in about a week, leaving an
               ulcer. Two or three bandings at separate visits are often required.
               b. Major complications are rare and consist of excessive pain, bleeding, and infection.
               Discomfort after banding is usually relieved by warm baths and oral analgesics.
       3. Grade 4 haemorrhoids require surgical haemorrhoidectomy.




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III. External Haemorrhoids

A. External haemorrhoids occur most often in young and middle-aged adults, becoming symptomatic only
when they become thrombosed.

B. External haemorrhoids are characterized by rapid onset of constant burning or throbbing pain
accompanying a new rectal lump. Bluish skin-covered lumps are visible at the anal verge.

C. Pain is maximal in the first 48 hours and decreases thereafter to minimal discomfort after the 4 days.

D. Management of External Haemorrhoids
       1. If patients are seen in the first 48 hours, the entire lesion can be excised in the office. Local
       anesthetic is infiltrated, and the thrombus and overlying skin are excised with scissors. The resulting
       wound heals by secondary intention.
       2. If thrombosis occurred more than 48 hours prior, spontaneous resolution should be permitted to
       occur; symptoms may be relieved by pain medication, sitz baths, and stool softeners. Thrombosed
       external haemorrhoids may erode through the skin, leading to hematochezia. The problem requires
       only direct pressure for haemostasis.


IV. Anal Fissures

A. Anal fissures are linear ulcers that extend from just below the dentate line to the anal verge, occurring
most often in young and middle-aged adults but can they affect all ages.

B. These lesions are most common in the posterior midline, but they may in the anterior midline in 10%.
Chronic lesions can cause a skin tag at the outermost edge (the sentinel pile).

C. Chronic fissures can undergo suppuration and extend into the surrounding tissues, causing a perianal
abscess.

D. Trauma to the anal canal during defecation is the cause of anal fissures.

E. Anal fissures cause a tearing anal pain during defecation and gnawing or throbbing discomfort after
defecation. Any bleeding is usually slight.

F. Anal fissures are confirmed by inspection of the anus.

G. Treatment of Anal Fissures
        1. Medical management:
                a. Bulking fiber supplements together with warm sitz baths and a high-fiber diet are the most
                effective treatment methods.
                b. Topical medication and suppositories are not effective when used alone but are not
                harmful.
        2. Lateral Partial Internal Sphincterotomy
                a. This procedure is indicated when medical therapy fails. It consists of surgical division of a
                portion of the internal sphincter, and it is highly effective in relieving pain.
                b. Adverse effects include temporary incontinence to flatus and liquid faeces.




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V. Perianal Abscess

A. The anal glands, located in the base of the anal crypts at the level of the dentate line, are the most
common source of perianal infection.

B. Acute infection presents as an abscess, and chronic infection results in a fistula. Infections start in the
intersphincteric plane and can extend upward, downward, and circumferentially around the anus.

C. The most common symptoms of perianal abscess are swelling and pain that is throbbing, continuous, and
progressive. Fevers and chills may occur. Perianal abscess is common in diabetic and immunosuppressed
patients, and there is often a history of chronic constipation or previous abscesses.

D. A tender mass with fluctuant characteristics or induration is apparent on rectal exam.

E. Management of Perianal Abscess
       1. A perianal abscess is treated with incision and drainage. Antibiotic therapy alone is not adequate. If
       the abscess is small, incision and drainage as an office procedure using a local anesthetic is usually
       possible. Large abscesses require regional or general anesthesia for adequate drainage.
       2. A cruciate incision is made close to the anal verge and the corners are excised to create an
       elliptical opening, which promotes drainage.

F. An anorectal abscess can progress readily to Fournier's gangrene (necrotizing fasciitis of the perineum
and abdominal wall), especially in diabetic or immunocompromised patients. This life-threatening condition
requires immediate, radical debridement.

G. About half of patients with anorectal abscesses will develop a fistula tract between the anal glands and the
perianal mucosa, known as a fistula-in-ano, which manifests as either incomplete healing of the drainage site
or recurrence. All patients with anorectal abscess should be reexamined 4 weeks after treatment to
determine if a fistula has formed. Permanent healing of a fistula-in-ano requires a surgical fistulotomy.


VI. Condylomata Acuminata

A. Condylomata acuminata, or genital warts, are a common venereal disease caused by the human
papillomavirus. They are spread by intimate contact, including autoinoculation, and have an incubation period
that ranges from weeks to months.

B. An estimated 1% of sexually active adults have visible lesions. Several subtypes of human
papillomaviruses are associated with malignancy.

C. Patients with small lesions usually have few symptoms. Bleeding, discharge, itching, and pain may occur.
Warts appear pink or white with a papilliform surface.

D. Treatment of Condylomata
        1.Topical caustic agents, such as podophyllum resin or trichloroaceticacid, work best on small
        lesions when applied repetitively.
        2.Lesions that are persistent despite topical treatment, extensive, or that extend into the anal canal
        are managed with surgical ablation.
        3.Recurrence is common.




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Chapter 29                      Haemorrhoids                                   (last revised April 1998)


   hypertrophy of vascular cushions due to stretching of the submucosal smooth muscle
   classically positions : 3, 7 and 11 o lock [terminal branches of superior rectal (haemorrhoidal) artery]
   associated with low dietary fiber intake, pregnancy, chronic constipation, laxative abuse, chronic
    diarrhoea of the inflammatory bowel disease and heredity.

Classification
 according to symptoms or appearance into three degrees :
   First degree         haemorrhoids within anal canal and detectable only on proctoscopy
   Second degree        haemorrhoids which prolapse on defecation but reduce
                        spontaneously or require manual replacement
   Third degree         permanently prolapsed haemorrhoids
 It can also be classified to four degrees (first degree the same as above, second degree as prolapsed
    haemorrhoids which reduce spontaneously, third degree as prolapsed haemorrhoids which require
    manual replacement, and fourth degree as permanently prolapsed haemorrhoids) , but clinically, second
    and third degree haemorrhoids are treated in the same way

Clinical Features
 rectal bleeding is the commonest presentation (intermittent small amount of fresh blood, stained tissue
    paper or drip from the anus into the toilet)
 other presentations include perianal irritation and discomfort due to soiling of the perianal skin,
    prolapse of the haemorrhoids, and severe pain due to prolapse and thrombosis which require
    emergency treatment

Diagnosis
 general physical examinations (especially the nutritional state, the presence of pallor, lymph nodes,
     abdominal masses and chronic chest problems)
 a complete anorectal examination is essential :
(1) Inspection : excoriation of perianal skin, fistula openings, ulcers, fissure and external haemorrhoids
(2) Ask the patient to strain down to see any prolapse of haemorrhoids
(3) Digital examination : masses such as polyps or tumors, and colour of the stool
(4) Proctoscopy and Sigmoidoscopy : bleeding points and masses e.g. haemorrhoids
 Colonoscopy or Barium enema should be indicated :
(1) patients over the age of 50 where the blood is not clearly coming from the anal canal (altered
blood, or blood mixed with stool)
(2) where there is a change in bowel habit and mucus in the stool
(3) altered blood or mucus is seen on sigmoidoscopy
 Other differential diagnosis should be considered: fissure-in-ano, perianal haematoma, perianal abscess,
     tumour of the anal canal, proctalgia fugax, etc.

Treatment
 a high dietary fiber (fruits, cereals and vegetables) intake and regular bowel habit are advised
 conservative management includes the use of creams, ointments, and a bulk laxative
 first degree haemorrhoids : injection sclerotherapy (5% solution of phenol in almond oil, phenol as
   antiseptic and almond oil as sclerosant in Gabriel syringe)
 second degree haemorrhoids : injection sclerotherapy and / or rubber band ligation The
   complications of banding include haemorrhage when the band separates, sepsis and pain (usually hours
   later and last for a few days)
 third degree haemorrhoids : haemorrhoidectomy ( ligation excision haemorrhoidectomy, submucosal
   haemorrhoidectomy or closed haemorrhoidectomy ). The complications of haemorrhoidectomy include
   pain, and acute retention of urine, secondary haemorrhage and later anal stenosis if too much skin has
   been removed (anal stenosis usually responds to an anal dilator used regularly for 2 months)
 strangulated or thrombosed haemorrhoids : conservative or operative treatment. Operations include
   manual dilatation of the anus and various forms of emergency haemorrhoidectomy



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Chapter 30                       Fistula-in-Ano (FIA)                            (last revised April 1998)


* A fistula is an abnormal communication between two epithelial surface

Aetiology
 not exactly known
 infection commences in an anal gland
 intersphincteric abscess
 tract into the perianal or ischiorectal region
 Surgical discharge complete the fistula
 keep open by continuing infection from the anal lumen.
 Association:
         1. Crohn’s disease
         2. Ulcerative colitis
         3. Tuberculosis
         4. Colloid carcinoma of the rectum / Ca anal canal
         5. lymphogranuloma venereum
         6. HIV infection

Classification (*always recall the diagram of anal canal)
1. Low level
         the internal orifices open into anal canal below the anorectal ring
         including subcutaneous, submucous and low anal in the standard classification
2. High level
         the internal orifices open into anal canal at or above the anorectal ring fistula
         including high anal and pelvirectal in the standard classification

Goodsall’s Rule
 Fistula with the external opening in relation to the anterior half of anus tends to be of the direct type.
 Those with the external opening in the posterior half usually open internally on posterior midline, and may
   extend behind the anal canal on both sides, forming a horseshoe fistula.

Clinical Features
Presentation
 As an abscess, surgical incision of which complete the fistula
 As a small discharging sinus with excoriation and pruritus.
 Painless unless blockage of fistula leads to abscess formation

Physical examination
 Inspection: external opening or openings
 PR exam: induration along the fistula track,
               pressure on the induration part may express pus from the external opening.
 EUA:         use a malleable probe to define the course

Treatment
Course of the fistula must be define before embarking in a surgery and anorectal ring must be preserved.
1. Low level fistula
        laid open along the entire length and allowed to heal by granulation and epithelialization
            (fistulotomy / fistulectomy)
2. High level fistula
        staged procedure: passing a suture (seton) along the track and out through the anal canal, the
            suture is then tied at anal verge (with or without tension, also known as cutting and non-cutting
            seton insertion) and allow fibrosis to occur before the seton divide the sphincter muscles.




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Chapter 31                        Rectal Prolapse                             (last revised April 1998)



Partial prolapse
        The mucosa and submucosa of the rectum protrude outside the anus
                usually find in infants and children
                associate with haemorrhoid in adult

Complete prolapse (procidentia)
      Protrusion of all layers of the rectal wall outside the anus
              usually find in old woman F : M = 6 : 1
              associated with prolapse of uterus, past history of gynaecological operation
Mechanism
      Weakness of the structure of the pelvic floor e.g. levator ani muscle + straining

History
          lump appears in anus after defecation or spontaneously when standing, walking or coughing
          uncomfortable, anal pruritis, not painful unless ulcerated
          bleeding, mucus secreting
          persistent desire to defecate, fecal incontinence or double incontinence
          reduced spontaneously or manually, or not reducible
          urinary symptoms

Past History
       chronic cough or constipation or urinary obstruction (for old man)
        prolonged and difficult labor, multipara, gynecological operation (for old woman)
        occupation like manual worker

Physical Examination
       pink color tubular mass protruding through anus
       mucosa thrown into circumferential concentric folds around a central pit
               (sometimes have to ask the patient to strain down to produce the prolapse)
       non-tender, differentiate partial from complete prolapse by the wall thickness
       mucosa of the mass is continuous to the anal skin ---> rectal prolapse
               (if there is a gap between mucosa of the mass and skin of anal skin, think of intussusception
               protruding from anus)
       associated uterine prolapse

Treatment
      Partial prolapse
      ~ in children
               1. conservative --- digital reposition
                        gently replace the protrusion after each defecation, place gauze pad against anus
                        and tape buttocks together until next defecation
               2. sclerotherapy --- if conservative treatment failed
                        submucosal injection of phenol in almond oil

          ~ in adult
                  1. try sclerotherapy
                  2. excision of the prolapsed mucosa +/- haemorrhoidectomy




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   Chapter 32 Lower Gastrointestinal Bleeding
                                                                                               (last revised April 1998)

The spontaneous remission rate for lower gastrointestinal bleeding, even with massive bleeding, is 80% (the
same as for upper gastrointestinal bleeding). No source of bleeding can be identified in 12%, and bleeding is
recurrent in 25%.

Bleeding has usually ceased by the time the patient presents to the emergency room, although copious
amounts of blood and clots may continue to be passed from the rectum.

I. Initial Clinical Evaluation
A. The severity of blood loss and hemodynamic status should be assessed immediately. Initial management
consists of resuscitation with colloidal solutions (haemacel) or crystalloid solutions (NS / lactated Ringers
solution) and with blood products if necessary.

B. An initial diagnostic evaluation, to determine the source of bleeding, is performed while the patient is being
resuscitated.

C. The duration and quantity of bleeding are assessed; however, the duration of bleeding is often
underestimated and the quantity is often overestimated.

D. Risk factors that may have contributed to the bleeding should be assessed, such as the use of
nonsteroidal anti-inflammatory drugs, anticoagulants, history of colonic diverticulosis, renal failure,
coagulopathy, colonic polyps, hemorrhoids, chemotherapy or radiotherapy.

E. Hematochezia. Bright red or maroon blood per rectum suggests a lower GI source; however, 11-20% of
patients with an upper GI bleed will have hematochezia as a result of rapid blood loss (these patients are
usually in shock).

F. Melena. Sticky, black, foul-smelling stools suggest a source proximal to the ligament of Treitz, but can
result from bleeding in the small intestine or proximal colon. Iron and bismuth can turn stools black but not
melanotic (shiny and tarry).

G. Malignancy may be indicated by a change in bowel habit or stool caliber, tenesmus, anorexia, weight loss
and malaise.

H. Patients may have a history of hemorrhoids, diverticulosis, inflammatory bowel disease, peptic ulcer,
gastritis, cirrhosis or esophageal varices.

I. Associated Findings
        1. Abdominal pain may result from ischaemic bowel, inflammatory bowel disease, or a ruptured aortic
        aneurysm.
        2. Painless, massive bleeding often indicates vascular bleeding from diverticula, angiodysplasia or
        hemorrhoids.
        3. Bloody diarrhea suggests inflammatory bowel disease or an infectious origin.
        4. Bleeding with rectal pain is seen with anal fissures, hemorrhoids, and rectal ulcers.
        5. Chronic constipation suggests hemorrhoidal bleeding; new onset constipation or thin stools
        suggests a left-sided colonic malignancy.
        6. Blood on the toilet paper or dripping into the toilet water after a bowel movement suggests a
        perianal source.
        7. Blood coating the outside of stool suggests a lesion in the anal canal.
        8. Blood streaking or mixed in with the stool may result from a polyp or malignancy in the descending
        colon.
        9. Maroon colored stools often indicate small bowel and proximal colon bleeding.




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II. Physical Examination
A. Postural hypotension suggests a 20% blood volume loss; whereas, overt signs of shock (pallor,
hypotension, and tachycardia) indicate a 30-40% blood loss.

B. The skin may be cool and pale with delayed capillary refill if bleeding has been significant.

C. Stigmata of chronic liver disease including jaundice, caput medusae, gynecomastia, and palmar erythema
should be sought since these patients frequently have GI bleeding.


III. Approach to the Diagnosis of Lower Gastrointestinal Bleeding
A. Rapid clinical evaluation and resuscitation should precede diagnostic or therapeutic studies. Intravenous
fluids (1-2 liters) should be infused over 10-20 minutes to restore intravascular volume, and blood is
transfused if there is rapid ongoing blood loss or if hypotension or tachycardia is present. Coagulopathy is
corrected with fresh frozen plasma or platelets.

B. When small amounts of bright red blood are passed per rectum, the lower gastrointestinal tract can be
assumed to be the source.

C. In patients with large-volume maroon stools, nasogastric tube aspiration can be performed to exclude
massive upper gastrointestinal hemorrhage. Upper GI endoscopy (OGD) is performed to exclude bleeding
source from oesophagus down to duodenum. Occult blood testing of lavage fluid is useless because mild
trauma from tube placement may cause a false positive result.

D. If upper GI source of bleeding is excluded, proctoscopy and sigmoidoscopy should be performed to
determine whether a colonic mucosal abnormality (ischaemic or infectious colitis) or haemorrhoids might be
the cause of bleeding.

E. Emergency diagnostic colonoscopy without bowel preparation should be considered to locate the possible
bleeding source. Bowel preparation is recommended if the colonoscopy is to be done in an elective setting.

F. In cases where persistent bleeding is evident, visceral angiography should be performed to located the
possible bleeding source.


IV. Causes of Lower Gastrointestinal Bleeding
A. Angiodysplasia and diverticular disease of the right colon account for the vast majority of episodes of acute
lower gastrointestinal (LGI) bleeding.

B. Most acute LGI bleeding originates from the colon; however, 15-20% of episodes arise from the small
intestine and the upper gastrointestinal tract.

C. Elderly patients. Diverticulosis and angiodysplasia are the most common causes of lower GI bleeding.

D. Younger patients. Haemorrhoids, anal fissures, and inflammatory bowel disease (IBD) are more common
causes.

E. Angiodysplasia
        1. Angiodysplastic lesions are small vascular tufts that are formed by capillaries, veins, and venules.
        2. Angiodysplastic lesions are commonly noted during colonoscopy, appearing as red dots or spider-
        like lesions 2 to 10 mm in diameter.
        3. Angiodysplastic lesions develop secondary, to chronic colonic distention, which leads to
        obstruction of venules.
        4. Angiodysplastic lesions are associated with advanced age, and they have a prevalence rate of
        25% in elderly patients These lesions have also been associated with chronic renal failure, CREST
        syndrome, Rendu-Osler-Weber syndrome, and cirrhosis.
        5. Even though angiodysplasia may be present throughout the entire colon, the most common site of
        bleeding remains the right colon. Most patients with angiodysplasia have recurrent minor bleeding;
        however, massive bleeding is not uncommon.


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F. Diverticular Disease
        1. Diverticular disease is the most common cause of acute lower gastrointestinal bleeding.
        2. 60% to 80% of bleeding diverticula are located in the right colon.
        3. 90% of all diverticula are found in the left colon.
        4. Diverticular bleeding tends to be massive, but it stops spontaneously in 80% of patients with only
        supportive care, and the rate of rebleeding is only 25%.


V. Definitive Management of Lower GI Bleeding
A. Colonoscopy
1. Colonoscopy is the procedure of choice for diagnosing colonic causes of gastrointestinal bleeding. It
should be performed after adequate preparation of the bowel, which permits identification of 80% of all
causative colonic lesions. If the bowel cannot be adequately prepared because of persistent, acute bleeding,
a red cell scan or angiography is sometimes more preferable.
2. Endoscopy may be therapeutic for angiodysplastic lesions, polyps, and tumors, which can be effectively
coagulated.
3. If colonoscopy fails to reveal a source for the bleeding, the patient should be observed, since in about 80%
of cases, bleeding ceases spontaneously.

B. Red cell scan
        1. The technetium-labeled ("tagged") red blood cell bleeding scan can detect bleeding sites when
        bleeding is intermittent.
        2. If the result is positive, the next step is colonoscopy or angiography.

C. Angiography
        1. Selective mesenteric angiography detects arterial bleeding that occurs at a rate of 0.5 mL/min or
        faster.
        2. Diverticular bleeding classically causes pooling of contrast medium within a specific diverticulum
        (extravasation).
        3. Bleeding angiodysplastic lesions demonstrate abnormal vasculature.
        4. Bleeding from angiodysplastic lesions usually is slow and rarely necessitates therapeutic
        intervention. However, when active bleeding is seen with diverticular disease or angiodysplasia,
        surgery should be considered. In patient where surgery is too risky or if patient is unfit, selective
        arterial infusion of vasopressin is effective in arresting hemorrhage in many cases.

D. Evaluation of the Small Bowel
        1. If bleeding persists but no source is noted, the small bowel must be considered as a possible
        source.
        2. The preferred technique for evaluating the small bowel is push enteroscopy (with an overtube) in
        combination with small bowel enema (barium) study.
        3. Meckel's diverticulum, which usually presents in younger patients, is a common site of bleeding in
        the small intestine. The diagnosis can be confirmed by radionuclide Meckel's scanning, which
        identifies the ectopic gastric mucosa.

E. Surgery
        1. If bleeding continues and no source has been found, surgical intervention is warranted.
        2. Surgical resection may be indicated for patients with recurrent diverticular bleeding, or for patients
        who have had persistent bleeding from colonic angiodysplasia and have required blood transfusions.
        3. Treatment of lower gastrointestinal bleeding involves resection of the involved segment--for
        example, a right hemicolectomy or sigmoid resection. Patients with a diffuse process, such as
        ulcerative colitis, require a total proctocolectomy with ileostomy.
        4. When laparotomy fails to identify a definitive source of bleeding, intraoperative endoscopy may be
        a useful adjunct.




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VI. Colon Polyps and Colon Cancers
A. These rarely cause significant acute LGI hemorrhage.

B. Left-sided and rectal neoplasms are more likely to cause gross bleeding than right sided lesions. Right
sided lesions are more likely to cause anemia and occult bleeding.

C. Diagnosis. Colonoscopy.

D. Treatment. Colonoscopic excision or surgical resection.


VII. Inflammatory Bowel Disease
A. Ulcerative colitis can occasionally cause severe GI bleeding associated with abdominal pain and diarrhea.
B. Diagnosis. Colonoscopy and biopsy.
C. Treatment. Medical treatment of the underlying disease; operation is required on rare occasions.


VIII. Ischemic Colitis
A. This disorder is seen in elderly patients with known vascular disease; abdominal pain may be postprandial,
and is associated with bloody diarrhea or rectal bleeding. Severe blood loss is unusual but can occur.

B. Diagnosis. Abdominal films may reveal "thumbprinting", caused by submucosal edema. Colonoscopy
reveals a well-demarcated area of hyperemia, edema, and mucosal ulcerations. The splenic flexure and
descending colon are the most common sites.

C. Treatment: Most episodes resolve spontaneously; however, vascular bypass or resection may be required.


IX. Hemorrhoids
A. Hemorrhoids rarely cause massive acute blood loss. In patients with portal hypertension, rectal varices
must be sought.

B. Diagnosis. Proctoscopy and sigmoidoscopy.

C. Treatment. High fiber diet, stool softeners, or haemorrhoidectomy.

Complete prolapse
      ~ perineal approach
          advantage: can be applied in very and frail patients, or patients with spinal cord injury
          disadvantage: higher recurrent rate
      e.g. Delorme’s operation
              the rectal mucosa is removed circumferentially from the prolapsed rectum, the underlying
              muscle is then imbricated with a series of sutures such that when these are tied, a ring of
              muscle within anal canal which narrows the orifice is created

          ~ abdominal approach
             advantage: less recurrent rate
             disadvantage: can only be applied in relatively fit patients, increased anaesthetic risk,
             complications of abdominal surgery
                 e.g. Well’s operation
                 rectum is fixed firmly to the sacrum by inserting a sheet of polyvinyl alcohol sponge between
                 them, the sponge is fixed by a series of sutures to the periosteum over the midline of the
                 sacrum and is then wrapped loosely about the rectum covering all except the anterior wall




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Chapter 33                     Colorectal carcinoma
Epidemiology
     Next common to Ca lung in male and breast in female, second commonest cause of death from
       malignancy
     Ca colon is more frequent in female; Ca rectum is equal in both sexes
     Age : peak at 60-70
     Common in Westernized society
Etiology
     Genetic predisposition
           o Family history
           o Familial adenomatous polyposis : ~1% of colorectal cancer
           o Hereditary non-polyposis colorectal cancer : ~5%
     Diet
           o Low fibre
           o Animal fat
     Pre-existing colonic disease : adenoma, ulcerative colitis
Pathology
     Distribution
           o Most common at rectosigmoid region : 40%
           o Caecum
           o Other area less common
     Macroscopic
           o Polypoid
           o Ulcerative
           o Stenotic
           o Colloid
     Microscopic
           o Adenocarcinoma 90%
           o Colloid 9%
           o Anaplastic : rare
           o Squamous cell carcinoma : 10% of lower rectal cancer
     Spread
           o Local
           o Lymphatic
           o Blood
           o Trans-coelomic
     Staging
           o The tumour is confined to bowel wall
           o The tumour extends beyond the bowel wall
           o Lymph node involved
           o Distant metastasis
    .  Pathogenesis
           o Adenoma carcinoma sequence, double hit theory.




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Clinical features
     Local symptoms
            o Distal tumour (recto-sigmoid region)
                     Rectal bleeding
                     Altered bowel habit : constipation, diarrhea
                     Mucus
                     Tenesmus
            o Proximal tumour
                     May be silent at early stage
                     Rectal bleeding / melaena,
                     Anaemia
                     Abdominal mass
     Metastasis
     Complications
            o Obstruction
            o Perforation
            o Severe bleeding : rare
     Systemic symptom : weight loss, loss of appetite
Investigations
     Sigmoidoscopy
     Complete blood picture & other base line biochemical tests
     Carcino-embryonic antigen (CEA) : non-specific for diagnosis but useful for monitoring
     Barium enema and/or colonoscopy
     Biopsy
     USG abdomen
     CT scan if tumour is bulky or local invasion suspected
     Chest X ray
Treatment
     Curative resection in patients with reasonable general condition, no metastasis
            o Principles : an adequate margin & lymphatic clearance.
            o Mucosal margin : 5cm for poor, 3cm for moderate and 2cm for well differentiated tumour.
                Some surgeons accept 2cm irrespective of the differentiation.
            o Lymphatic clearance : lymphatic run along mesenteric vessels, colorectal resection falls into
                a few patterns according to the specific mesenteric vessel sacrified
                     Tumour at caecum and ascending colon : Right hemicolectomy (ileocolic and right
                        colic vessels)
                     Hepatic flexure : Extended right hemicolectomy (ileocolic, right colic and middle colic
                        vessels))
                     Transverse colon - two options : Extended right hemicolectomy or Transverse
                        colectomy (only the middle colic vessel)
                     Splenic flexure : Extended left hemicolectomy (middle colic vessel and inferior
                        mesenteric vessel close to aorta)
                     Descending colon : Left hemicolectomy (inferior mesenteric vessel close to aorta)
                     Sigmoid colon - two options : Left hemicolectomy or Sigmoidectomy (inferior
                        mesenteric vessel distal to take off of left colic vessel)
                     Rectosigmoid junction and upper rectum : Anterior resection (similar to
                        sigmoidectomy)
                     Lower rectum : Low anterior resection or Abdomino-perineal resection

         Adjuvent therapy after curative resection
              o Indicated for Dukes' C disease. Effectiveness in Dukes' B disease controversial. Not
                 necessary in Dukes' A.
              o Radiotherapy for Ca rectum (not for colon) : to reduce local recurrence.
              o Chemotherapy for both Ca colon and rectum : 5 fluorouracil based, may improve survival.




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         Palliative excision
               o Shall be considered for the following groups of patients
                        Symptomatic (e.g. troublesome bowel symptom, anaemic) but reasonable general
                            condition.
                        With potentially resectable metastasis (e.g. metastasis confined to one side of the
                            liver)
                        With metastasis that may be benefited from chemotherapy
               o The procedures are similar to those of curative resection

Specific complications of surgery
     Massive bleeding, from presacral venous plexus
     Damage to neighboured organ, e.g. ureter, bladder, duodenum
     Anastomotic leakage
     Urinary / Sexual dysfunction
     Colostomy problems : erosion, stenosis, prolapse, herniation
     Perineal wound infection / dehescience (after AP resection)
Prognosis
After curative resection, the 5 years survival is ~90% for Dukes' A, 60% for Dukes' B and 30% for Dukes' C
disease

Supplementary information
    Total mesorectal excision (TME)
    Pre-operative radiotherapy for rectal cancer
    Solitary metastasis
    Salvage chemotherapy




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Chapter 34                         Carcinoma of stomach                                                   (last revised
April 1998)

EPIDEMIOLOGY
      - the second commonest cause of death from G.I. malignancy
      - 10 % of all cancer deaths
      - most common in Japan
      - male : female is 2 :1
      - peak age : 40 - 60

AETIOLOGY
      - 3 -4 times more common in patients with pernicious anaemia
      - predisposing factors : - atrophic gastritis
                               - achlorhydria, hypochlorhydria
                               - adenomatous polyps
                               - previous partial gastrectomy
                               - H. Pylori infection
                               - blood group A
                               - genetic
      - occupational factors : - mining, rubber, asbestoes
      - dietary factors :      - smoked foods ( 3,4- benzpyrene )
                               - low intake of fresh fruit and vegetables
                               - formation of carcinogenic nitrosamines (from nitrates)

PATHOLOGY
        - almost all (95%) adenocarcinoma derived from the mucus-secreting epithelial cells              - other 5%
consists of lymphoma, leiomyosarcoma, etc.
         most common in antrum

MACROSCOPIC CLASSIFICATION
     1. cauliflower-like growth with sharply defined edges
     2. ulcerative with irregular indurated edges
     3. colloid (infiltration of all layers by kind of aerolar tissue, interspaces of which contain transparent
     gelatinous substance)
     4. linitis plastica
     5. carcinoma secondary to chronic GU

MODES OF SPREAD
     1. direct extension : pancreas, transverse colon, mesocolon, oesophagus or liver
     2. lymphatic spread : by emboli & permeation
        * regional nodes follow the course of arterial supply
        * left supraclavcicular node ( Troisier’ s sign)
     3. transcoelomic spread : peritoneal and omental seedlings, ovary (Krukenberg’s
                                  tumour)
     4. blood-borne spread : to liver, lung, bone, etc.

CLINICAL FEATURES
       * early disease : no symptoms or vague dyspepsia only (difficult to diagnose)
       * classical symptoms : anorexia, vomiting, anaemia, weight loss

          1. local symptoms : epigastric pain, vomiting, dysphagia, GIB, perforation (rare)
          2. general symptoms : weight loss, anorexia, anaemia
          3. metastasis : ascites, lymph node enlargement, jaundice, bone pain
          4. paraneoplastic : acanthrosis nigricans, migrating thrombophlebitis




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DIAGNOSIS
      -P/E:                weight loss, +/- epigastric mass +/- ascites +/- hepatology +/-
                   supraclavicular nodes +/- PR bleeding
          - Investigation: 1. occult blood ,full blood count , LFT
                            2. endoscopy + biopsy
                            3.double contrast barium studies
                           * irregular ulcer base, interruption and rigidity of mucosal folds, ulcer
                              with raised margins and raised base, unusual site (e.g. greater
                              curve) ----> suggesting malignancy
                                     * differential diagnosis: - benign gastric ulcer
                                                               - lymphoma
                                                               - giant mucosal hypertrophy

TREATMENT
      - the only treatment that has any success is surgical removal of the lesion
      - Curative resection ( i.e. excision of tumour + local LN)
               a). CA involving distal stomach :
                        subtotal gastrectomy + regional LN
               b). CA involving upper 2/3 stomach :
                        total gastrectomy + regional LN + distal 2-3 cm of oesohagus
                        + Roux en Y reconstruction
               c). CA involving lower oesophagus or cardia :
                        trans-abdominal or thoraco-abdominal gastrectomy
      - Palliative operation ( i.e. to reduce symptoms of bleeding, pain or obstruction)
               a). symptoms due to blood loss :
                        resection of involved part of stomach
               b). symptoms due to obstruction of distal stomach :
                        gastrojejunostomy, gastroduodenostomy
               c). proximal tumors causing dysphagia :
                        endoscopic stenting procedure
      - Radiotherapy : no use !
      - Combination chemotherapy : as adjuvant treatment at the time of surgery

PROGNOSIS
     - LN involvement is a major determinant of survival in patient undergoing gastric                   resection.
     - 5 year survival rate in patient with uninvolved nodes is 50 % , whereas with
        involved nodes only 10 %        .
     - the overall outlook is gloomy : < 15 % of patient surviving for 5 year survival




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Chapter 35                       Gastric outlet obstruction
                                                                     (last revised April 1998)


When the gastric outlet is obstructed, the site of obstruction can be inside the lumen, in the wall and outside
the wall.

Causes
 Peptic ulcer disease
 Tumours e.g. gastric carcinoma, lymphoma, pancreatic carcinoma.
 Duodenal web
 Annular pancreas
 Adult hypertrophic pyloric stenosis
 Crohn’s disease
 Cholecystitis
 Pancreatitis
 Superior mesenteric artery syndrome (although it is not strictly gastric outlet)

Pathophysiology
 excessive vomiting of hydrochloric acid leads to dehydration and hypochloremic, hypokalemic metabolic
                                             +     +                                   +
   alkalosis, further aggravated by loss of K and H from the kidney, in exchange for Na to conserve water.

Presentation
History
 Vomiting of stale food (ingested over 4 hours previously)
 Repetitive vomiting often projectile or nocturnal
 Epigastric pain or fullness, nausea and vomiting, anorexia, fatigue, weight loss
Physical Examination
 Visible gastric peritalsis
 Sucussion splash more than 4 hour after eating
Gastric aspirate
 Gastric residue >300ml 4 hour after eating
 Overnight fasting gastric residue
Radiology
 Retention of barium 50 percent at 4 hour.
 large atonic stomach
Special studies
 Oesophageal-gastroendoscopy: to detect any ulcer.
 Saline load: to find out the severity of gastric fluid retention. (700ml of NS at room temperature infused
    over 3-5 minutes via the NG-tube which is then clamped. Aspirate 30 minutes later and see if the aspirate
    is more than 350ml)
 External scanning technique: e.g. USG, CT to localize source of external compression.

Management in general
Medical
 Correction of volume and electrolyte disturbance by adding solution of NaCl and KCl.
 NG suction with H2-blockers, iv hyperalimentation.

Surgical
 Vagotomy and antrectomy, with gastroduodenal anatomosis
 Truncal vagotomy with drainage
 Gastrojejunostomy in severe scarring
 Partial gastrectomy with pyloroduodenal dilatation
 Dilatation endoscopically placed balloon catheter
 Feeding jejunostomy in anticipation of slow return of gastric emptying.
 Surgical resection of any compressing tumour.

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Chapter 36                       Thyroid Cancer                                                (last revised April 1998)


   incidence increases with age
   female to male ratio is about 3 to 2

Etiology
   previous radiation exposure especially at the neck region
   hereditary factors such as the evidence of MEN II syndrome
   prolong stimulation of elevated TSH
   Hashimoto thyroiditis predisposing to malignant lymphoma

Clinical features
   most commonly enlarging mass in the neck, either present as thyroid lump or lymph nodes

Pathology
A) Papillary CA 60%
   wide age range but usually younger than the other CA thyroid
   lymph node spread very common
   diagnosis depends on cytological feature (psammonma bodies)
   size influence prognosis ( <1.5 cm, best prognosis , usually survive more than 10 years )

B) Follicular CA 20 %
   diagnosis depends on capsular and vascular invasion, not on cytological appearance
   haematological spread occurs early
   size has no influence on prognosis

C) Medullary CA 5%
   primary malignant tumor arising from the parafollicular 鏠-cells” within the thyroid
   capable of secreting calcitonin (used as a tumour marker), ACTH and histamines
   metastasis often occur in neck and mediastinal LN, distant metastasis occur late
   size is not important on prognosis
   may occur in combination with adrenal phaeochromocytoma and hyperparathyroidism (due to parathyriod
    hyperplasia) in MEN type IIa
   when the familial form is associated with prominent mucosal neuromas involving the lips, tongue, and
    inner aspect of the eyelids, with the occasionally a Marfanoid habitus, the syndrome is known as MEN
    type IIb

D) Anaplastic CA 10%
   occur in old people with rapid growth of hard neck mass
   highly aggressive and usually inoperable, median survival 4 months
   year survival rate is only 3.6%

E) Malignant lymphoma
   occur in old age
   may arise de novo or secondary to Hashimoto’s thyroiditis
   may have synchronous or metachronous involvement of gastrointestinal tract

Investigations of thyroid cancer
   baseline tests
   iodine isotopes uptake
   ultrasonography
   serum calcitonin assay
   fine needle aspiration biopsy
   open biopsy and frozen section




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Management of thyroid cancer
A) Surgery
totoal or near total thyroidectomy (except minimally invasive follicular CA & lymphoma)
clinically involved neck lymph nodes should be removed by neck dissection

B) Thyroxine suppression
suppressive dose of thyroxine (0.25 to 0.3 mg daily) should be given to suppress TSH

C) Radioactive iodine

D) External beam radiotherapy

E) Chemotherapy




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Chapter 37                         Burn Injury                                 (last revised April 1998)


I. INITIAL ASSESSMENT

A. Assess airway, breathing, and circulation (ABCs). Check for singed nares, cough, wheezes, hoarseness,
facial burns, charred lips, carbonaceous secretions, or a history of an enclosed-space fire. May need to
intubate early because maximal edema occurs at 12 hours. Baseline ABGs and carbon monoxide level.
Chest x-ray; may not show changes for 24 to 72 hours

B. Check the fire history for chemicals that might have been inhaled and lead to pulmonary toxicity

C. Check for other injuries. ECG for electrical injuries

D. Fluid resuscitation for burns over 15% to 20% of body surface area (BSA) in adults and less than 10%
BSA in small children. Estimate with the Parkland formula: TBSA burn (%) x weight (kg) x 4 cc/24 hours (half
in the first 8 hours, other half in the next 16 hours). Do not use colloid in the first 24 hours; use lactated
Ringer's solution

E. NG tube for ileus if the burn is greater than 25% of BSA

F. Foley catheter for fluid monitoring if burns are significant

G. Pain medications

H. Cardiac monitoring for severe burns


II. ASSESSMENT OF BURNS

A. Surface area (Rule of nines)

B. Depth
        1. Superficial (first degree): epidermis only, painful and erythematous
        2. Superficial partial thickness: epidermis and the outer half of the dermis with sparing of hairs
        3. Deep partial thickness: epidermis and destruction of reticular dermis. Can easily convert to full
        thickness with secondary infection, mechanical trauma, or progressive thrombosis (partial-thickness
        burns previously classified as second-degree burns)
        4. Full thickness: dry, pearly white, charred, leathery. Heals by epithelial migration from the periphery
        and by contracture. May involve adipose, fascia, muscle, or bone (full-thickness burns previously
        classified as third degree burns)

C. Severity
       1. Minor: first-degree and partial-thickness burns less than 15% BSA in adults and less than 10%
       BSA in children younger than 6 years old; full thickness burns less than 2% BSA in adults
       2. Moderate: partial-thickness burns 15% to 25% BSA in adults and 10% to 20% in children; full
       thickness burns less than 10% BSA
       3. Major (requires burn unit or burn center care): partial-thickness burns over 20% to 25% BSA in
       adults and over 20% in children; full-thickness burns over 10% BSA; burns of hands, face, eyes,
       ears, feet, perineum; inhalation burns, electrical burns, burns complicated by fracture or major
       trauma, all burns in infants or elderly, patients at poor risk secondary to prior medical conditions




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D. Cause of burn
       1. Thermal
                a. Flame, especially with clothing, tends to cause full-thickness burns
                b. Molten metal, tars, or melted synthetics lead to prolonged skin contact, should be cooled
                as rapidly as possible, and should not be removed immediately after injury because this
                causes increased depth of injury. Tar may be softened with antibiotic ointments or cream
                c. Liquid burns should be cooled rapidly and any clothing in contact with the area rapidly
                removed to decrease the contact time
       2. Electrical burns may have extensive underlying tissue necrosis. Consider admission for cardiac
       monitoring. Observe for compartment syndrome, myoglobinuria
       3. Chemical agents
                a. Strong acids are quickly neutralized or quickly absorbed. Rinse off skin and call the poison
                control center for specific instructions
                b. Alkalis cause liquefaction necrosis and can penetrate deeply and lead to progressive
                necrosis up to several hours post-contact
       4. Radiation burns initially appear hyperemic and may later resemble third-degree burns. Changes
       can extend deeply into the tissue. Sunburns are of this type and involve moderate superficial pain


III. TREATMENT OF BURNS

A. Emergency room: cover wounds with cool, normal saline-soaked gauze for pain control until suitability for
narcotics can be determined. Intravenous narcotics can help for initial wound care. Tetanus immunization
status should be checked and the patient treated accordingly
        1. Clean with bland soap and water
        2. Debride loose and foreign material. May leave blisters intact if relatively small and the patient is
        reliable
        3. Rinse well with normal saline
        4. Wound dressing choices
                 a. Nonadherent inner layer of water-soluble porous material followed by soft bulky absorbant
                 gauze and covered with a semielastic outer layer
                 b. Topical antibacterial agents such as 1% silver sulfadiazene, mafenide (Sulfamylon), or
                 silver nitrate are applied and then covered with gauze pads. Dressings should be done once
                 to twice daily with washing to remove the old cream. Absolute contraindications to silver
                 sulfadiazene are term pregnancy, premature infants or infants less than 1 month old,
                 hypersensitivity, glucose-6-phosphate dehydrogenase (G6PD) deficiency. Relative
                 contraindications are possible cross-sensitivity to other sulfonamides, pregnancy
                 c. Heterograft, allograft, or xerograft dressings can be used on an inpatient basis for partial-
                 thickness wounds. These should be examined daily and debrided as needed or removed if
                 signs of infection develop
        5. Chemical burns should be washed with tap water at least 15 and preferably 30 minutes in duration;
        this should be started at the scene if possible. Alkali burns should be irrigated for 1 to 2 hours
        postinjury. Chemical binding may be required for certain burns
        6. Tar burns need cooling, gentle cleaning, and application of a petrolatum-based antibacterial
        ointment for 24 hours to help dissolve tar. After 24 hours the tar can be washed away and the injury
        treated as a thermal burn
        7. Electrical burns should be cleaned as for thermal burns and a topical antibacterial agent applied




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B. Follow-up care
        1. Daily to twice-daily dressing changes should be performed. Mild soap such as dish soaps can be
        used for cleaning. Necrotic debris and eschar may require debridement as healing occurs. Tub soaks
        can help loosen coagulum and speed separation of necrotic debris. Absolute sterility is not
        mandatory for dressing changes; however, cleanliness and thorough cleaning of hands, sinks, tubs,
        and any instruments used must be emphasized
        2. Contractures may not be apparent for weeks to months, therefore, range-of-motion exercises
        should be started during the early healing period. Any person with burns across joints should practice
        range-of-motion exercises frequently. If the hands are involved extensively, early excision and
        autografting may decrease the scarring of deep partial-thickness and full-thickness burns. Splinting
        and prolonged physical therapy may be required for rehabilitation. If the patient is prone to keloids,
        special garments may be used to reduce this scarring
        3. Pain medications may be necessary for sleep at night or for dressing changes. Codeine or
        hydrocodone is normally adequate after the initial emergency department visit. If the dose is taken a
        half hour before the dressing change, it will facilitate cleaning and debridement
        4. All burns should be seen within 24 hours of initial treatment, and if any signs of infection develop,
        cultures should be performed and hospitalization considered
        5. Prophylactic antibiotics should rarely be required but may be considered for immune-compromised
        hosts, patients at high risk of endocarditis, or patients with artificial joints. Broad-spectrum coverage
        with a first-generation cephalosporin or with a penicillinase-resistant penicillin plus an aminoglycoside
        may be used if necessary
        6. In circumferential burns, extensive extremity burns, or electrical burns, watch for vascular or
        neurologic compromise indicating a compartment syndrome developing. Immediate escharotomy is
        then required. Extremities should be elevated to minimize swelling
        7. In extensive burns, nutritional support is extremely important. The metabolic rate may be increased
        100% to 200% above normal. Electrolytes must be frequently checked to replace maintenance
        needs, loss through the burn wound, and loss secondary to elevated body temperature. Intravenous
        hyperalimentation may be required until the gastrointestinal tract is functioning.




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 Chapter 38                         Brain Abscess
 Clinical manifestation
       classical triad
               fever, headache, and focal neurologic signs-occurs
                       only a minority of patients
               presents as a rapidly or subacutely developing space-occupying lesion
               fever or other signs of active infection are often absent
               75% present with symptoms of less than 2 weeks' duration
       Clinical signs
               may develop so rapidly as to suggest cerebral infarction or acute meningitis
               may evolve over weeks or even months
               Headache 75%
               nausea and vomiting 50%
               Fever < 50%
                       may be attributed to coexisting sinusitis, otitis, or systemic infection
               Focal neurologic signs < 50%
                       may be extremely subtle (Wispelwey et al 1997)
               ~ 1/3 present with seizures
                       most frequently generalized
                       most closely associated with frontal lobe abscesses
               Nuchal rigidity 25%
               Papilledema < 25%
                       frequently absent in rapidly developing abscesses

 Etiology

          causative agents of brain abscess
                 vary according to the age and immunological status
                 Wispelwey et al 1997

          adults
                   aerobic, microaerophilic, and anaerobic streptococci
                   Streptococcus milleri group
                   (Streptococcus anginosus and Streptococcus intermedius)
                          60% to 70%
                          common in abscesses arising from sinusitis or dental infections
                   Bacteroides species
                          and enteric bacteria
                          Escherichia coli, Proteus species, and Pseudomonas species
                          20% to 40% of cases
                   Staphylococcus aureus
                          10% to 15%
                          associated with penetrating trauma or neurosurgical procedures

                   Multiple organisms
                           may be present
                           particularlly associated with sinusitis or otitis




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                 Staphylococcus aureus
                        may be present as a single organism
                        associated with trauma or endocarditis

                 less frequently isolated organisms
                         Listeria monocytogenes
                         Clostridium, Fusobacterium, and Actinomyces species

          neonates
                frequently a complication of meningitis
                gram-negative organisms are thus the most frequent isolates
                       Proteus mirabilis
                       Escherichia coli
                       Serratia marcescens
                       Citrobacter species
                               especially Citrobacter diversus

          immunocompromised
               Enterobacteriaceae and Pseudomonas aeruginosa
                      immunosuppressed children and adults (Brook 1995)
               Fungi
                      Cryptococcus neoformans, Candida, Mucor, and Aspergillus species
               Nocardia asteroides
                      can occur in immunocompetence subject
               AIDS
                      Toxoplasma gondii
                      Cryptococcus neoformans
                      Mycobacterium tuberculosis


 Biological basis

 Source
 hematogenous dissemination of organisms
      from distant sites of infection
              cyanotic congenital heart disease with right-to-left shunt
             hereditary hemorrhagic telangiectasia
             acute infective endocarditis
             IV drug abuse
             chronic, pyogenic lung abscess
             AIDS and other conditions of impaired host immune response
      from spread of organisms through emissary veins
             during sinusitis, otitis, or mastoiditis
                      historically --> otitis
                      at present --> frontal, ethmoidal, and sphenoidal sinusitis

 Less frequent causes
       penetrating trauma
       neurosurgical procedures
       facial infections
       dental sepsis



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 Location of Abscess

 hematogenous origin
       most common in the distribution of the middle cerebral artery
       then ACA --> PCA
 frontal and ethmoidal sinusitis
       within the frontal lobe
 Sphenoid sinusitis
       frontal or temporal lobe abscesses
 middle ear or mastoid infection
       spread through emissary veins
       into the middle fossa
               temporal lobe abscesses
       into the posterior fossa
               cerebellar abscess

 Development of Abscess
 begin as a microscopic focus of septic
        microvascular injury
        usually within white matter or at the gray-white junction
 localized encephalitis or "cerebritis,"
        undergoes liquefaction
 inflammatory response
        lymphocytes and polymorphonuclear leukocytes
        intense cerebral edema
 abscess capsule
        both fibrotic and gliotic elements
        thickest on its cortical surface
        thinnest medially
        causing the abscess to expand toward and rupture into the ventricular system

 Death in brain abscess
      tonsillar herniation
              from mass effect of the abscess and its surrounding cerebral edema
              from rupture of the abscess into the ventricular system

 Epidemiology

 occurs worldwide
 incidence of approximately 4 per million population
 ~1 in 10,000 hospitalizations
 males > females

 most common in third decade
      may occur at any age
      paranasal infections
              ages of 10 and 30
      Otogenic abscesses
              childhood and after age 40
      children
              a peak incidence between 4 and 7 years
              25% cyanotic congenital heart disease


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 Differential Diagnosis
       Rapidly developing brain abscess
              bacterial or aseptic meningitis
              epidural abscess
              subdural empyema

         temporal lobe abscesses
               herpes simplex virus encephalitis

         Slowly developing abscesses
                primary or metastatic tumors

         abrupt change
                evolving cerebral or brainstem infarction
                brain hemorrhage
                subarachnoid hemorrhage

 Diagnostic Workup
      recent onset of severe headache
              with symptoms or signs of a rapidly developing intracranial SOL
      new onset of focal or generalized seizures
      history
              systemic infection, sinusitis, otitis, carious teeth, drug abuse
      risk factors for AIDS

 Fever                 50%
                       may be 38oC or less
 WCC                   normal in 40%
                       elevated above 20,000 cells/mm³ < 10%
 ESR            minimally elevated but
                       may be normal
 CRP            frequently elevated
                       do not correlate with ESR
 MRI
       gadolinium enhancement
       diagnostic procedure of choice
 Diffusion-weighted MRI
       differentiation between brain abscess and tumor with central necrosis
 Contrast-enhanced CT
       may fail to detect lesions easily discernible on MRI
       should be used if MRI is not available
       sensitivity increase if scan is repeated 30 to 60 minutes after contrast infusion
 Lumbar puncture
       contraindicated
       CSF abnormalities are usually nonspecific
       10% to 18% risk of brain herniation and death




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 Prognosis and Complications

 Survival
       depense on condition at presentation
       fully alert                               100%
       stuporous but not comatose >90%
       responsive only to pain              41%
        without pain response              18% (82% mortality)

 Adverse prognostic factors
      delay in diagnosis
      choice of inappropriate antibiotics
      inadequate aspiration or drainage
      multiple, large, deep, or multiloculated abscesses
      posterior fossa abscesses
      intraventricular rupture

 Severity of residual neurologic defects
      secondary to the abscess itself or to complications of surgical intervention
      influenced by neurologic status at the time of admission
      may also be better in cases successfully treated with
               antibiotics alone or with antibiotics plus aspiration
      30% to 55%
      incapacitating in 17%
               Seizures                35%
                       occur up to 12 months after surgery
                       ? may be reduced by early therapy with anticonvulsant medication

 Management
 appropriate antibiotics
 surgical drainage or removal
 control of cerebral edema

                  Table 1. Antibiotics for Empiric Therapy of Brain Abscess

Suspected Organism                                                Recommended Antibiotic
Streptococci and other Gram-positive organisms                    Penicillin, ceftriaxone, or cefotaxime
       excluding S. aureus
Staphylococcus aureus                                             Vancomycin;
                                                                  If nafcillin resistance is suspected,
                                                                  neurosurgical procedures or head
                                                                 trauma; If patient is allergic to penicillin,
                                                                 Oxacillin or Nafcillin
Gram-negative organisms                                           Ceftriaxone or cefotaxime
       excluding Pseudomonas aeruginosa
Pseudomonas aeruginosa                                            Ceftazidime
Bacteroides species                                               Metronidazole or chloramphenicol




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 Initial therapy
                worry of mixed culture of organisms
                combined use of oxacillin + ceftriaxone + metronidazole / chloramphenicol
                         for at least 8 weeks if surgery is not undertaken
                        or at least 4 weeks if the abscess is drained
 ceftriaxone and metronidazole
                has been reported following surgical drainage
                ? efficacy of this regimen
 Pseudomonas aeruginosa
                strongly suspected
                ceftazidime should be used in place of ceftriaxone
 AIDS
                treated initially as being due to Toxoplasma gondii
                 with sulfadiazine and pyrimethamine

 Surgical therapy
       aspiration or excision

       Aspiration
               particularly under stereotactic CT guidance
               less traumatic to the CNS
               removes the purulent center
               more amenable to antibiotic therapy
               effectively reduces intracranial pressure
               may require repeat aspiration

       Excision
              large or multiloculated abscesses
              abscesses located in the posterior fossa or brainstem
              abscesses that do not respond to aspiration
              cases in which ventricular rupture is considered imminent

       Cerebellar abscesses
             may require aggressive CSF diversion
             to avoid further increase in ICP

       brain abscess with intraventricular rupture
              80% fatality rate
              open craniotomy with debridement of abscess cavity and ventricular lavage
              + 6 weeks of intravenous antibiotics
              + intraventricular gentamicin twice daily for 6 weeks
              + intraventricular drainage for 6 weeks

 Abscesses treated with antibiotics alone
      Abscesses at the stage of cerebritis
             do not contain material that can be drained
      Surgery may be deferred
             if the abscess is less than 3 cm in diameter
             the patient is neurologically stable

       followed with great care, by MRI or CT within 24 to 48 hours after initiation of therapy
              then every 3 to 5 days in the first 2 weeks
              abscesses may enlarge despite antibiotic therapy

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Cerebral edema
      emergent treatment
             hyperventilation
                    short-term to a pCO2 of < 28 torr
             mannitol
                    20% solution
                    initial dose of 0.5 to 1.0 g/kg over 10 minutes
                    followed by 0.25 to 0.5 g/kg every 3 to 5 hours
                    monitor IO, electrolyte, osmolarity
             dexamethasone
                    effective in reducing vasogenic edema
                    short course of 10 mg intravenously initially
                    followed by 4 mg intravenously every 4 to 6 hours
             transcranial or intraventricular pressure monitor

 Inappropriate secretion of antidiuretic hormone
 diabetes insipidus
 Prevention of DVT
 Seizure
       phenytoin in normal saline at a rate no faster than 50 mg/min (1 mg/kg per minute in
 neonates)

 Anesthesia
 significantly elevated intracranial pressure
        caution with halothane, methoxyflurane, or ketamine
                cause intracranial vasodilatation
                may further increase ICP




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Chapter 39                         Neurosurgery Key Topics
                                                                                      Mr R. Boet     (1999)

1. Neurological examination :
Refer to a standard textbook on clinical neurological examination.

2. Special investigations :
Plain X-ray : skull, C-spine, thoraco-lumbar spine
Myelogram : indications, contra-indications
CT Scan principles : iso-, hypo- and hyperdense lesions, contrast enhancement, good for bone and trauma,
poor for posterior fossa and intramedullary spinal cord lesions, CT angiography
MRI principles : iso-, hypo- and hyperintense lesions, flow void, T1, T2, contrast enhancement, poor for bone
and trauma but good for all soft tissue pathology.     MR angiography.

3. General care :
Fluid and electrolyte disturbances ie. hyponatraemia , SIADHS and              diabetes insipidus, diagnosis and
management
Anticonvulsants and treatment of status epilepticus.
Steroid use, indications and complications

Raised intracranial pressure :
Concept of the pressure/volume curve, cerebral perfusion pressure, methods of measuring ICP, hyperemia
vs edema , herniation syndromes, RICP treatment, general principles eg patient position, control of pain,
empty bladder, no restriction of chest movement; specific treatment eg removal of mass lesions, steroids for
edema , mannitol, hyperventilation, drugs eg barbiturates.

4. Head injury :
General : coma, Glasgow Coma Score, approach to a comatose patient ie ABC, blood investigations esp.
glucose !, look for lateralising signs then consider CT scan, teat seizures, consider medical causes eg,
metabolic coma, diabetes, drug overdose , C2H5OH, infections, organ failure, hypertensive encephalopathy.
Always remember the collateral history. Brain death : criteria and consideration for organ donation.

Blunt head injury vs penetrating head injury ( stab and gunshot )

Diffuse head injury vs focal injury.

Skull fractures : Open vs closed, linear #, depressed #, base of skull #, growing skull #

Haematomas ; Traumatic SAH, extradural, subdural (acute vs chronic), intracerebral and intraventricular
haemorrhage.

Diffuse head injury : concussion, diffuse axonal injury

Subdural hygroma
Child abuse




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5. Cerebrovascular disease :
SAH and aneurysms, arteriovenous malformations, spontaneous intracerebral haemorrhage and stroke.

Aneurysmal SAH : clinical features, grading SAH, investigations (ie. CT scan, CSF, MRA, CTA, DSA),
general management ie. bed rest, analgesia, neuro-observations, BP control, electrolyte management,
calcium channel blocks, stool softeners. specific problems : rebleeding, hydrocephalus and vasospasm. :
diagnosis and management. aneurysm management : conservative vs clipping vs coiling.

Arteriovenous malformations : presentation : haemorrhage (ICH, SAH), seizures, mass effect, ischemia,
headache, bruit (eg dural avm), increased ICP (eg hydrocephalus in pediatric malformations). Treatment
options : observation vs surgery vs radiosurgery. carotid-cavernous fistula : clinical features, diagnosis
and treatment.

Spontaneous ICH : primary (hypertensive) vs secondary, position of haemorrhage ( ie lobar / putamen /
thalamic / brainstem / cerebellar ) management of hypertensive ICH, medical vs surgical. Investigation of
secondary (non-hypertensive haemorrhage)

Ischemic stroke : embolic vs thrombotic. Regarding embolic stroke, role of carotid stenosis, diagnosis and
medical vs surgical treatment thereof.

6. Brain tumour :
General principles : presentation ie raised intracranial pressure, seizures progressive neurological deficit,
changes in mental state, endocrine disturbances (pituitary pathology)

Classification ; Primary vs secondary

Secondary tumours : metastases are the most common brain tumour. etastatic” work up to look for primary
disease, management : medical, steroids, anticonvulsants.
radiotherapy, surgery ( indications, diagnosis unknown, symptomatic or life threatening, primary disease
controlled or life expectancy reasonable, solitary lesion).

Primary tumours :
Gliomas : most common primary tumour. types : astrocytoma, oligodendroglioma, ependymoma. Grading of
astrocytomas, broad principles of treatment ie medical, surgery, radiotherapy, chemotherapy,
Meningiomas : usually benign and slow growing, common, treatment : observation, surgery plus or minus
radiotherapy.
Vestibular schwannoma (acoustic neuroma) : symptoms and signs, investigations, treatment, conservative vs
surgery (radiosurgery), link this tumour up with the disease neurofibromatosis
Pituitary tumours : NB appreciate the anatomy and physiology of the hypothalamic- pituitary axis !! Secretory
vs non-secretory tumours. general clinical symptoms and signs, specific syndromes ie acromegali, Cushing’s
disease, prolactinoma. Medical and surgical treatment of pituitary disease (general principles)

Posterior fossa tumours in children :
Four common types 1. Medulloblastoma 2. Ependymoma 3. Cerebellar pilocytic astrocytoma 4. Brainstem
glioma. General principles of clinical presentation and treatment. Hydrocephalus, surgery, radiotherapy,
craniospinal metastatic disease.

Spinal tumours :
Clinical features, radiological investigations, treatment : surgery/radiotherapy.
Pathology : 1. Extradural disease : metastases
              2. Intradural disease : Extramedullary - meningioma , neurofibroma
                   Intramedullary - astrocytoma, ependymoma




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7. Infections :
Brain abscess, subdural and extradural empyema, parasitic infections, tuberculosis. AIDS.

Abscess, SDE, EDE :
Etiology: ENT infections ie sinusitis and mastoiditis, hematogenous spread ie congenital heart disease,
endocarditis, lung infections, penetrating trauma, post surgical infection.
Principles in treatment: drainage of the abscess, treatment of the primary disease and prolonged antibiotic
therapy.

Neurocysticercosis : infection by the larval stage of Taenia Solium. Multiple lesions, may be calcified or cystic.
often ring enhancing, may cause hydrocephalus. Treatment: Medical : Praziquantel or Albendazole
            Surgical : Hydrocephalus, mass lesions, diagnosis unsure.

Tuberculosis : neurosurgical involvement is mainly to confirm the diagnosis or treat hydrocephalus

AIDS : Aids is a disease that will come more on the forefront in the future. Neurosurgical involvement is
common. Mass lesions found : toxoplasmosis, cryptococcus, fungi, tuberculosis, other lymphoma, PML
(progressive multifocal leukoencephalopathy)

8. Spinal disease :
Degenerative spinal disease, spinal trauma, spinal infections :

Degenerative spinal disease : most common sites are cervical and lumbar.
Cervical disease: Clinical features : myelopathy vs radiculopathy, special investigations: plain X-rays and
MRI, treatment : indications are pain not responsive to consvervative management and neurological deficit
especially if progressive. Surgery involves either an anterior or posterior surgical procedure depending on
the pathology and involved anatomical level/levels.
Lumbar disease:
Lumbar spinal stenosis. Clinical features ie neurogenic claudication. Treatment ie decompression most
commonly a laminectomy
Lumbar disc prolaps : Radiculopathy, clinical features treatment ie conservative eg bed rest, analgesia,
physiotherapy, surgery ie discectomy.
Cauda equina syndrome is a neurosurgical emergency. Clinical features (pain, paraparesis/plegia, bladder
and/or fecal incontinence) Requires urgent neurosurgical referral.

Spinal trauma :
Principles of the management of a spinal injury ie. ABC, immobilization, maintain BP, maintain oxygenation,
methylprednisolone, clinical examination, radiological identification of pathology (X-ray C-spine C1/T1 , open
mouth view, thoracic and lumbar AP and lateral views if fracture suspected ) Urgent MRI required if :
incomplete lesion, neurological deterioration noted, no bony pathology noted in presence of neurological
deficit ( ? disc prolaps or epidural haematoma) . Surgical treatment is specialized and taken care of by the
orthopedic/neurosurgical specialities.

Spinal infection :
Spinal epidural abscess is a neurosurgical emergency. Clinical features : Back pain, fever, spinal
tenderness, neurological deficit. Risk factors : DM, IV drug abuse, immunocompromised state. Treatment :
urgent drainage.




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9. Congenital abnormalities :
Common abnormalities include arachnoid cysts, craniofacial abnormalities eg synostosis, encephalocele,
Chiari malformations, Dandy-Walker malformation, aquaduct stenosis, spina bifida (dysraphism), tethered
cord syndrome.

Hydrocephalus : communicating vs non-communicating. Clinical features in children vs adults. Treatment
options : conservative vs surgical, shunt/ ventriculostomy.

Spina bifida : spina bifida occulta vs aperta(open). Tethered cord syndrome, clinical features, radiological
investigations and treatment. Myelomeningocele, clinical features , treatment and comprehension of the long
term multidisciplinary involvement in the care of these patients ( neurosurgery, urology, orthopedics, pediatric
surgery, physiotherapy and occupational therapy, psychological support)

10. Functional neurosurgery :
Neurosurgery also involves the treatment of pain (eg trigeminal neuralgia and other chronic pain syndromes),
movement disorders (eg parkinsonism), the surgical treatment of epilepsy , the treatment of spasticity etc.
Understand the concept of       unctional neurosurgery” and appreciate some of the common conditions ie
trigeminal neuralgia, parkinsonism, temporal lobe epilepsy.



Chapter 40:
Commonly used suffixes in surgery
Suffix                   Use

-ectomy                  removal of a segment or all of an organ e.g. appendicectomy

-otomy                   1. surgical incision into an organ or cavity, e.g. laparotomy,
                         enterotomy
                         2. cutting of a structure, e.g. vagotomy

-ostomy                  1. surgical created connection between 2 organs,                                    e.g.
                         gastroenterostomy
                         2. connection between an organ and the skin, e.g. colostomy

-oscopy                  visualization of the inside of a duct, cavity or organ by means of an
                         endioscope, e.g. colonoscopy

-orrhaphy                a repair operation, e.g. herniorrhaphy

-pexy                    an operation to secure an organ or structure, e.g. rectopexy

-desis                   an operation to fuse 2 structures together, e.g. arthrodesis

-plasty                  an operation to alter structure or function, e.g. arthroplasty,
                         rhinoplasty




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