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‫ كتابة و مراجعة الشيت‬، ‫الشكر لكل من ساهم في تفريغ‬

‫مع تمنياتنا بالتوفيق للجميع‬

"‫ "أواصف‬90 ‫ الدفعة‬-‫االمانة األكاديمية‬

❖ NOTE;
Some topics in this sheet are collected from different resources (Mr.
Mojahid records, bailey and love, kar-Alaini)

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Fluids and Electrolytes 4
Preoperative Preparations 7
Trauma 11
Thyroid 21
The Breast 41
Hernia 67
Diseases of The Esophagus 75
Stomach 81
Small and Large Bowel 89
Intestinal Obstruction 100
Acute Appendicitis 106
Hemorrhoids 110
Gallbladder 113
Obstructive Jaundice 116
Pancreas 119
Pediatric Surgery 128
Skin 136
Urology 146
Vascular Diseases 1643
Fluids and electrolytes

Fluids control depends on normal renal function.

❖ Urine :

Specific gravity ≥1.016

PH ≤5.8 ( Plasma pH 7.34 - 7.43)
Urine output per hour in adult: 30 – 50 cc/hr

❖ Serum electrolytes: (mmol/l)

*Na 135-145
Hypernatremia -> c/f ( seizure ( due to increase ICP)
Rx: diuretics / Restrict Na / in fasting pt give low conc. Of NS (1/5 saline)
Hyponatremia ->
Rx : normal or hypertonic saline .
Amount of Na in each one liter of NaCl = 77 ml/mol

*K 3.5-4.5
Hyperkalemia -> c/f ( arrhythmia = cardiac arrest = ECG change )
Rx: Ca gluconate / NaHCO3 / Salbutamol / insulin + glucose / Dialysis .
Hypokalemia -> c/f ( muscle weakness / paralytic ileus / arrhythmia)
Rx: K correction .

*Cl 85-115

*Ca 2.2-2.6 (9-11mg)

Hypercalcemia ->
Rx: bisphosphonate ( Ca chelating agent ) / diuretics
Hypocalcemia ->
Rx: Ca gluconate ( Ca correction )
*Hco 22-28

*Mg 1.5-2.5
Hypermagnesemia ->
Rx : Ca gluconate / insulin + glucose /Dialysis
Hypomagnesaemia ->
Rx : Magnesium sulphate ( Mg correction )

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 ❖ Diagnosis of fluid loss:
• Clinically:

Dehydrated and ill, collapsed veins , lethargic

Loss of skin turgor / dry mouth & mucous membrane / sunken eyes
Tachycardia (early) / Low volume pulse
Hypotension (late)
Reduced urine output oliguria
Normal urine output =0.5-1ml/kg /hour
=30-50ml/kg/hour
• Lab:

Increase Na, increased PCV, increased urea and creatinine

Total body water =42L
Daily water requirement 2-3L/day -> 1L(2 drip) every 8hrs -> ( total 6 drips )
=> Dextrose 5% (D5%)
Daily Na requirement 2mmol/kg/day=135- 150 mmol/day -> Normal saline (2d
rips, one drip contains 77 mmol of Na)
Daily K requirement 1mmol/kg/day=60-80mmol/day -> give 60 mmol to avoid
over correction -›3 ampules of K ( 1 ampule =20 mmol)
Formula = (2 D5% + 1 ampule K ) + (2 NS + 1 ampule K ) + ( 2D5% + 1 amp
ule K) + Replacement of loss ( RL )
In normal patient -> if have loss replace it (e.g. 1L give extra drip)

Note : Role of 4 in K replacement :

-Drip rate : 4 hrs
-UOP : 40 ml/hr
-serum level not exceed 4mmol
-Max ampules in a drip 40mmol ( 2 ampule)
Crystallized
-D5% contain -> water + glucose 200 kcal/drip ( distribute equally in all compa
rtment )
-NS 0.9% contain -> Na ( 77mmol/drip ) + water
-RL contain -> Na ( 135mmol) / K (5mmol) / Cl (120 mmol) / Water / HCO 3 (2
8 mmol) ( help in metabolic acidosis)
Close to blood / use as a replacement therapy & emergency fluid (except gastric
outlet obstruction, it is contraindicated due to metabolic alkalosis, inztead give
NS with ampulla of K) common exam Q
RL and NS distribute btw plasma (1/3) and ISF (2/3) .
Water distributes equally btw compartment.

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 ❖ Indications of IV therapy:

1. Fluid loss: shock, burn, bleeding, diarrhoea.

2. Pre and postoperative preparations.
3. Acute abdomen (intestinal obstruction, acute appendicitis).

❖ Sizes of intravenous cannulae:

Color Gauge Flow rate

Orange 14 240
Gray 16 180
Green 18 90
Pink 20 60
Blue 22 36
Yellow 24 20
Violet (purple, for neona 26 13
te)

Postoperative fluids:
1st day: 3L Dextrose (or D5%+1/5 saline)
2nd day: 2L Dextrose +1 L saline
(3 Ampoules)

Colloids : contain protein, use as plasma expanders ..) because they maintain th
e oncotic pressure and saved as the intravascular fluid -> so it use in the emerg
ency before blood
-albumin ( HAS = human albumin solution)
-hemigel
-dextran,hetastarch
-gelfusine

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 Preoperative preparations

1. Full History and examination :

Comorbidities / warfarin / bleeding tendency .
2. lab investigations: depend on the age and type of operation.
CBC / Hb ( minimum for surgery is 10 g )
BP / RFT / ECG (elderly) / CXR (>40)
Echo (>60) / Urine analysis / RBG / pulmonary Profile
3. Correct abnormalities / blood preparation ( depends on the type of surgery, p
t condition and emergency situation) )
4. mark site of the operation: ask the patient, see the image then see the mark.
5. Shaving on table (because decrease the risk of infection)
6. fasting 4-6 hours ( to empty the stomach so prevent the aspiration and mendil
son syndrome) or NG tube suction =intestinal obstruction plus prokinetics ( met
clopromide ) ->to increase the gastric empty rate
7. list the operation (start with pt having latix allergy -> DM -> cardiac proble
m -> end withbpts having infected wound or surgery )
8. consent ( competent elderly / Family )
9. patient transfer

❖ Specific preparations:

1. Obstructive jaundice:
-vit k 10mg
-antibiotics: to prevent ascending cholangitis.
-rehydration: to avoid hepatorenal syndrome.
-abd: lactulose (to prevent hepatic encephalopath), antipeptic ulcer, iv dextrose
and K correction)

2. Thyroid surgery:
-TFT ( euitis)
-Thoracic inlet xray & lateral cervical X-ray
-Indirect laryngoscopy: to visualize vocal cords.
-serum Ca ( baseline)
-tracheostomy tube (if expect tracheomalacia)
-Toxic=Beta Blocker + carbimazole 30mg for 6weeks

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3. Bowel surgery:
( mechanical- enema- & chemical-laxative + antibiotics + PPI- bowel prepara
tion )
-Laxatives: eg.polyethelene glycol ,phosphate enema , Na picosulphate
-rectal washout
-antibiotics
-NG suction
-DVT prophylaxis

4. Steroid patient: stop the tabs and give high dose injectable steroid
3 doses of steroids (stress dose to overcome the situation of surgery)
1st dose = before surgery
2nd dose = at anesthesia
3rd dose =every 8hours
Complications of steroids :
-mask symptoms ( eg: peritonitis)
-decrease healing ( delayed)
-increase risk of infection (decrease immunity)

5. Anticonvulsants:
stop sodium valporate or phenytoin tabs in epileptic patients Terng for surgery ,
start iv drugs. :phentoin (complications: purple glove syndrome) or phenobarbit
one

6. Anticoagulants -> patient with metallic valve

Warfarin stop warfarin 3-5 days before operation and give sc heparin and contin
ue till 12 hours before surgery and return to heparin 12 hours postoperatively an
d return to warfarin when INR 2-3 then discharge.
If pt took aspirin stop before 2 weeks
Heparin antidote=protamin sulphate
Warfarin antidote= vitamin k and FFP
LMW heparin is preferable because it has less SE of unfractionated such as oste
oprosis and heparin induced thrombocytopenia HIT.
APTT for monitering of unfractionated heparin.

7. Antibiotics and infection control: (not mandatory in all operation)

Bowel= cephtriaxone + metro ( G +ve/ -be/ anaerobes)
Head and neck = vancomcin /fluxacillin (G+ve )
Bone = ampicillin
Single dose at anesthesia ( on table) +another one after 4 hours

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 ❖ Types of wound: The NICE classification:

1.Clean (<2% infection risk): varicose vein ( varicocele) , hernia (except mesh r
epair), thyroid. Exceptions of clean surgery: bone surgery, hernial repair with m
esh and heart or vascular surgery.
2-Contaminated (up to 20% ) : bowel surgery / appendicitis not perforated.
3- Clean contaminated ( infection risk 2-10%):give prophylactic dose after surge
ry Cholecystectomy / urinary tract surgery .
4. Dirty (20-25%): abscess, perforated appendix (peritonitis)
Give antibiotics during and after surgery

Sterilization Disinfection
Uses -To kill the bacteria/ org -To decrease the bacteri
anism a/ organisms
-For human body
-For instrument
Methods -heat ( autoclave is the b -iodine
est) -alcohol
- Radiation - chlorihexidine

❖ Postoperative complications:

1. Bleeding: -primary hemorrhage ( intraoperative)

-secondary hemorrhage (first 24 hr postoperative) e.g. Thyroid hematom
a
-reactionary hemorrhage (due to any maneuver by the pt)
2. Wound infection ->pain and pus on area of operation
Open the primary suturing -> dressing -> after 7days do secondary suturing
3. Wound dehiscence ( burst abdomen ( emergency ) / incisional hernia )
Causes:
wound -> infection/healing
Patient -> IMC / malnourished/ obese
Surgery->style of suturing ( primary / secondary /delayed primary )
4. Post operative fever:
Fever in day one = Atelectasis or lung collapse and this is because breathing con
trol the tempertur, occur after thorathic/upper Abdo in surgery. Anaesthetics dru
gs can cause 1st day fever also.
Ttt : physiotherapy
Fever in 2nd to the 7th day: due to wound infection, UTI.
Fever after 7th day: due to DVT or PE.
6. Stress peptic ulcer
8. Diabetic patient:

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Stop oral hypoglycemic agents (for 48 hr) start insulin short acting infusion(actr
apid regular) +dextrose +K and RBG monitoring and omit morning dose to pre
vent hypoglycemia intraoperative (sliding scale) and do FBG before surgery
9. DVT prophylaxis
Stop oral contraceptives, stop HRT 4 weeks before surgery
Low risk: young, minor surgery( like hernia) , no disease =Early mobilization
Moderate risk: elderly, DM, obesity, major surgery( e.g. Cholecystectomy) =ear
ly mobilization +TED stocking
High risk: elderly, Obese, abdominopelvic or orthopedic surgery ( hip and knee
surgery) = Early mobilization +TED
Stalking +Sc LMWt heparin ( stop12 hrs before surgery)
Revise well's criteria for DVT risk

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Trauma
Commonest cause of death from 1-40 years

• Mechanism of trauma:

1-blunt

2-pentrating (either low velocity (ex. stap wound) or high velocity (ex.gun
shot, here you expect more injuries and damage to the tissue )

✓ Trauma can be fetal in:

• Seconds: brain, heart, aortic rupture
• Minutes: ATOM FC

- airway obstruction

- tension pneumothorax

- open chest

- massive haemothorax

- flail chest

- cardiac tamponade

• Days: sepsis
✓ Triad of death in trauma:

Decrease temperature – acidosis – coagulopathy

❖ Advanced trauma life support ATLS:

1-Preparation: team of 4 or more

2-triage: black = dead

Red = need attention

Green = stable

3-primary survey: ABCDE

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 ✓ Airway:

1-check patency

- Remove any foreign body(blood, secretions, teeth,.....)

- modified jaw thrust or head tilt

- oropharyngeal airway (Guedel airway)

- tracheostomy

- intubation

2-maintence of cervical spine

- manually or Philadelphia collar

3-check the pupil

- if dilated this may indicate hematoma

✓ Breathing:

- respiratory examination

- Is Percussion dull or hyper resonance?

✓ Circulation:

- 2 wide bore cannula , take blood sample

- Start IV fluids

- Measure HR, BP (shock status)

- Cover wounds

- If there is signs of shock and no visible bleeding think of internal bleeding

(internal bleeding signs are similar to those of peritonitis; pain, tenderness,
rigidity) . Look for abdomen, pelvis, lower limbs

- Do FAST (focus abdominal Sonography of trauma)

- Primary survey end when the patient is stable

✓ adjuvants to primary survey:

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- 3 X-rays of trauma (lateral cervical, CXR, pelvic)

✓ Secondary survey

- Head to toe examination

✓ adjuvants to secondary survey

❖Head injury:

✓ Causes:

1-RTA 2-fall from height 3-voilence assault

Normal ICP 5-15 mmHg

Brain injury: either

1-primary: immediate like concussion, contusion

2-secondary: after 1-2 days (ex. Hypoxia)

✓ Glasgow coma scale:

Eyes: open spontaneous (4), open to command (3), open to pain (2), no
response (1)

Verbal: oriented (5), confused (4), inappropriate (3), incomprehensive sounds

(2), nothing (1)

Motor: respond to command (6), localize pain (5), withdrawal from pain (4),
flexed (3), extended (2), no response (1)

❖ Coma <9 GCS

✓ Important Points from history

- Mechanism of trauma

- If there is loss of consciousness even if for a while.

- Amnesia and type (global, retrograde, anterograde)

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 - Symptoms of increased ICP (blurred vision, projectile vomiting, headache)

- Convulsions, seizures

- Drug history (anticoagulants)

• When to admit:

1-coma patients

2-signs of fracture base of the skull

(Anterior cranial fossa: CSF rhinorrhea, Raccoon eye, panda sign

Middle cranial fossa: CSF otorrhoea

Posterior cranial fossa: Battle’s sign)

3-alchoholic

4-epileptic patients

5-headache, confusion *

✓ Management:

We aim to reduce ICP

1- patient head in 45 degree

2- give O2

3- IV mannitol

4- Craniectomy

Steroids are not given*

❖ Extradural hematoma:
✓ History:

young patient, RTA, trauma to the side of the head and injury of middle cerebral
artery, patient have lucid interval (patient lose consciousness and become well
then deteriorate again)
✓ Signs: dilated pupils, contralateral hemiplegia
✓ Investigations:

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Brain CT: biconvex hematoma (hyper dense), sift of midline, collapsed
ventricles)

✓ Management:

Brain hole 2 cm in front of the ear and 3 cm above. Dramatic response once
evacuated

❖ Subdural hematoma:

Damage to the cerebral vein

✓ Acute < 10 days: white on CT

✓ Sub-acute 10 – 14 days: shifted midline, collapsed ventricle, gray on CT
(you can do CT with contrast or MRI for better visualization)
✓ Chronic > 14 days: black on CT, brain atrophy, patient may experience
hallucinations, amnesia

Subdural hematoma is Crescent shape on CT

✓ Complications:

- Abscess

After treatment and Mx pt may have

1. Psychosis

2. Depression

3. Parkinsonism

4. Miningitis

❖Chest trauma

• Airway obstruction:
✓ Causes:

1-forign body 2-blood

3-tongue 4-denture (teeth)

✓ Management:

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- Suction

- Oropharyngeal airway

- Cricothyrodotomy

• Tension pneumothorax:

Rupture of the lung and air accumulate resulting in lung collapse and trachea
and mediastinum shifted to the other side

✓ Clinical features:

- SOB

- Stabbing pain on the side of the lesion

- Hyper-resonance on percussion

- Dilated neck veins

- Decrease air entry

✓ Management:

- Emergency: wide bore cannula at the 2nd intercostal space mid clavicular
line

- Definitive: chest tube at the 5th intercostal space mid axillary line with
underwater sell

• Open chest wound:

It is also called sucking chest wound.

Wound > 3cm lead to new air path into the chest and pneumothorax develop.

Flatter valve mechanism

• Massive haemothorax:

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Bleeding from internal thoracic artery or intercostal artery

✓ Clinical features:

- SOB

- Trachea pushed to the other side

- Stabbing pain

- Dullness on percussion

✓ Management:

Chest tube

- If the chest tube drain >1.5 L of blood. Do lateral thoracotomy

- If the chest tube drain 200 cc/hour for 4-5 hours. Do thoracotomy

• Flail chest:

Two fractures or more in more than one rib

✓ Clinical features:

- Paradoxical movement

- Respiratory failure

✓ Management:

- ICU admission

- Mechanical ventilation

- Stabilization of fracture by k wire

• Cardiac tamponade:

Blood in the pericardium as result of stab wound

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Has the same findings of pericardial effusion on examination

✓ Clinical features:

- beck’s triad (muffled heart sounds, distented neck veins , hypotension

with a narrowed pulse pressure or weak*)

- pleuritic chest pain

- Dilated neck veins, raised JVP, increased HR and hypotension.

✓ Management:

- pericardiocentesis ( performed from xiphoid process 45° toward the left

shoulder, done under ECG monitoring)

- pericardiotomy

Other than ATOM FC

• Fracture rib :

Only one rib is fractured, not like flial chest

It just causes pain, may causes heamothorax, pneumothorax, injure the

underlying organs like spleen and liver

It isn't that dangerous, treated by analgesia and physiotherapy

❖Abdominal trauma

✓ Investigations:

- CT is the best for abdominal trauma

- Diagnostic peritoneal lavage DPL used to detect internal bleeding, bladder

injury, bowel injury. DPL is contraindicated in abdominal distension

- Laparotomy: indications for immediate laparotomy:

1-gun shot 2-peritonitis

3-prgoressive BP drop 4-presence of air under the diaphragm

• Stomach:

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Penetrating injury

Blood from N.G. Tube, air under diaphragm

Do laparotomy

• Duodenal:

Penetrating injury

Do laparotomy

• Pancreas:

Blunt trauma

Investigations: elevated serum amylase, CT

It is solid organ so first option of treatment is to treat conservatively

• Liver:

Commonly injured in blunt trauma because of its large size

Conservative treatment

• Spleen:

Injured by blunt trauma

Most common internal organ to cause internal bleeding

✓ Findings:

- Left hypochondrial pain

- Bruises

- Dull on percussion

- Fracture of lower ribs

- Sharp pain in left shoulder (Kher’s sign)

Do CT ( to assess the pt if he needs conservative treatment or laparotomy),

laparotomy

• Bowel:

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 ✓ Any bowel injury is for surgery, laparotomy
✓ and colostomy if large bowel is injured
✓ Grades of injury :

Any organ has a hilum that contains its own blood supply.

Grade 1: subcapsular hematoma, but the organ is intact

Grade 2: minor lacerations

Grade 3: major lacerations but does not reach the hilum

Grade 4: major lacerations till the hilum

Grade 5: avulsion of the organ, i.e total rupture of the hilum (this grade has
massive amounts of bleeding).

● Grades 1,2 and 3 are for conservative Mx. give blood, fluid, analgesia and
monitoring for vital signs…

● Grades 4 and 5 are for surgery…

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Thyroid

EMBRYOLOGY:
• Appears as an epithelial proliferation in the floor of the developing
pharynx (at a point later indicated by the foramen cecum) by the end of
the 3rd week.
• As the thyroid primordium descends to its final destination it remains
attached to the tongue by the thyroglossal duct which will later
disappear.
• Also as it descends it unites with the ultimobranchial body which arises
from the 4th pharyngeal pouch.
• Parafollicular cells that secret calcitonin are derived from neural crest
cells and reach the thyroid gland via the ultimobranchial body.
• The thyroid reaches its final position in the 7th week.
• It begins to function at the end of the 3rd month.

Developmental anomalies:
 Thyroglossal cyst:
▪ It’s a cystic remnant of the thyroglossal duct.
▪ May lie at any point along the migratory pathway of the
thyroid gland but is always near or in the midline of the
neck, usually just below the body of the hyoid bone.
▪ Clinically: presents most commonly during childhood.
Painless and moves up and down with swallowing and on
protrusion of the tongue. May present with infection
because it’s rich in lymphatics
▪ Treatment: Sistrunk’s operation; excision of the cyst with
and its associated tract entailing removal of the middle third
of the hyoid bone.
 Thyroglossal fistula:
▪ May result due to:
1. Infection of thyroglossal cyst leading to rupture
2. Incomplete removal of thyroglossal cyst.

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 ▪ Treatment: excision of the fistula along with the central part
of the hyoid bone.
 Intralingual thyroid:
▪ Due to failure of descent of the thyroid
▪ Patient presents with tongue swelling and obstruction
manifestations (dysphagia, dyspnea, difficult swallowing)
▪ Thyroid scans: absence of thyroid tissue in the normal site of
the neck.
▪ Treatment: thyroxine replacement + surgery or radioactive
iodine ablation.

ANATOMY:
• A brownish-red highly vascular endocrine gland consisting of 2 lobes
connected in the midline by an isthmus.
• Each lobe extends superiorly up to the oblique line of the thyroid
cartilage and inferiorly to the 4th or 5th tracheal rings.
• The isthmus overlies the 2nd and 3rd tracheal rings.
• The gland weighs around 20-25 gm.
• Main blood supply:
1. Superior thyroid artery, a branch of the external carotid artery
2. Inferior thyroid artery, a branch of the thyrocervical trunk of the
subclavian artery.

• Venous drainage:
1. Superior and middle thyroid veins drain into the internal jugular
vein.
2. Inferior thyroid vein drains into the left brachiocephailc vein (the
innominate vein)

• Lymphatic drainage:
There is an extensive lymphatic network within and around the gland:
▪ The subcapsular plexus drains principally to the central
compartment juxtathyroid – ‘Delphian’ and paratracheal nodes and
nodes on the superior and inferior thyroid veins (level VI), and
from there to the deep cervical (levels II, III, IV and V) and
mediastinal groups of nodes (level VII).

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 ▪ Some lymphatic channels pass directly to the deep cervical lymph
nodes.

PHYSIOLOGY:
• The functioning unit of the gland is the lobule, supplied by a single
arteriole and consisting of 20-40 follicles. The resting follicle contains
colloid in which thyroglobulin is stored.
• Synthesis and liberation of thyroid hormones are stimulated by thyroid
stimulating hormone (TSH) which is secreted from the anterior pituitary.
Circulating thyroid hormones have a –ve feed back effect on TSH while
Thyrotropine releasing hormone (TRH) secreted from the hypothalamus
increases its production.
TSH
• Thyroid hormones synthesis: 3HYPER +TOB+CSR
1) trapping of inorganic iodide from the blood;
2) oxidation of iodide to iodine; by perioxidase enzyme
3) binding of iodine with tyrosine to form iodotyrosine; called
organification
4) coupling of monoiodotyrosines and di-iodotyrosines to form tri-
iodotyrosine(T3) and L-thryoxine (T4)
5) Release of the hormones into the circulation when needed. When
released, the hormones are bound to serum proteins: albumin,
thyroxine-binding globulin(TBG) and thyroxine-binding prealbumin
(TBPA).
• The metabolic effects are due to the unbound free T3 & T4.
• T3 is the most important physiological hormone and is also produced in
the periphery by conversion from T4. T3 is quick acting (within a few
hours) whereas T4 acts more slowly (4-14 days).
• Calcitonin is secreted by parafollicular C cells. It’s a serum marker for
recurrence of medullary thyroid cancer.

INVESTIGATIONS:

1) Thyroid function test (TFT):

To measure serum T3, T4 & TSH
- Hyperthyroidism: ↓TSH and ↑T3 & T4
- Hypothyroidism: ↑TSH and ↓T3 & T4.
- Sub-clinical hyperthyroidism: normal T3 & T4 while ↓TSH
- Sub-clinical hypothyroidism: normal T3 & T4 while ↑TSH.

2) Thyroid auto-antibodies:
- Grave’s disease: long-acting thyroid stimulating antibodies (LATs)

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 - Hashimoto thyroiditis: anti-TPO antibodies.

3) Thyroid imaging:
❖ Chest and thoracic inlet X-rays: to confirm retrosternal goiter
and if there’s tracheal deviation and compression.

❖ Ultrasound (US):
1. Differentiates solid from cystic masses
2. Guides fine-needle aspiration
3. Differentiate between a solitary nodule and a dominant nodule
in multinodular goiter.
❖ Isotope scanning:
▪ Uptake of either radiolabelled iodine (123I) or technetium
(99mTc) will demonstrate the distribution of activity in the
whole gland.
▪ Warm nodule: active, the nodule takes up the isotope and
so does normal thyroid tissue around it.
▪ Hot nodule: when a nodule is hyperactive and takes up
isotope while the rest of the gland is inactive and does not
take up the isotope.
▪ Cold nodule: a non – functioning nodule that doesn’t
uptake iodine at all. In 15% it’s malignant.
▪ When to do isotope scanning? When a patient presents
with a solitary nodule with features of hyperthyroidism, to
localize the site of overactivity in the gland (whether the
nodule alone or the whole gland) which will govern the
choice of surgery:
➢ If the whole gland: do Total thyroidectomy
➢ If the nodule alone: do lobectomy

4) Fine-needle aspiration cytology (FNAC)

▪ It’s the investigation of choice in discrete (nodular) thyroid
swellings.
▪ To differentiate between malignant & benign nodules.
▪ Usually surgery decision is based on FNAC results, except
in case that FNAC shows follicular cells (it can’t
differentiate between follicular adenoma and follicular
carcinoma) so a true-cut biopsy here is needed (in biopsy
if there’s invasion of the basement membrane then it is
carcinoma, if there’s no invasion then it’s adenoma).

5) Biopsy: to differentiate between follicular adenoma and carcinoma, also

between lymphoma and anaplastic carcinoma.

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 Disorders of thyroid function
➢ Hypothyroidism (Myxoedema):
▪ Etiologies:
1) Autoimmune thyroiditis (chronic lymphocytic thyroiditis): non-
goitrous (primary myxoedema), goitrous (Hashimoto thyroiditis)
2) Iatrogenic: after thyroidectomy, after radioiodine therapy, or drug
induced (anti-thyroid drugs)
3) Dyshormonogenesis: the most common cause of congenital
hypothyroidism is Sudan. Genetic deficiencies of thyroid enzymes e.g
affecting TPO activity (Pendred syndrome) and thyroglobulin synthesis.
4) Goitrogens (e.g lithium, iodides in large amounts, carbimazole, para-
aminosalicyclic acid)
5) Thyroid agenesis
6) Endemic cretinism

▪ Symptoms:
• Tiredness
• Mental lethargy
• Cold intolerance
• Weight gain
• Constipation
• Menstural disturbance
• Carpal tunnel syndrome
• Alopecia
• Loss of lateral third of eyebrows.

▪ Signs:
• Bradycardia
• Cold extremities
• Dry skin and hair
• Periorbital puffiness
• Hoarse voice
• Bradykinesis, slow movement
• Delayed relaxation phase of ankle jerks (the most useful clinical
sign in making the diagnosis)

▪ Treatment: Oral thyroxine (0.1 to 0.2 mg/day). The dose is lowered in

elderly patients or those with cardiac disease to 0.05 mg/day.

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▪ Complications:
• Myxoedema: signs and symptoms of hypothyroidism are
accentuated. Typical facial appearance and supraclavicular
puffiness with malar flush and yellow ting to the skin.
• Myxoedema coma characterized by altered mental state, severe
bradycardia (sometimes without a pulse), hypothermia and a
precipitating medical condition, e.g heart failure or infection. It
carries a high mortality rate. You might think he is dead!!
• Treatment: admit to ICU, warming if temp >30C, give IV
thyroxine and hydrocortisone ± ventilation.

➢ Hyperthyroidism (Thyrotoxicosis):
• Clinical types:
1) Diffuse toxic goiter (primary thyrotoxicosis, Grave’s disease):
autoimmune where long-acting thyroid stimulating Ab (LATs
Ab) binds to TSH receptor and stimulate it, the most common
form, more common in young females, abrupt onset, more
severe but no cardiac failure.
Exophthalmos + pretibial myxoedema + thyroid acropachy =
Grave’s disease.
2) Toxic multinodular goiter (secondary thyrotoxicosis,
Plummer’s disease): insidious onset and occurs on top of a
long-standing simple nodular goiter. May present with cardiac
failure or atrial fibrillation, affects middle aged & elderly
females, hyperthyroidism is not severe. Eye signs only lid lag
and lid spasm (other eye signs are rare).
3) Toxic nodule, a solitary overactive nodule (may be a true toxic
adenoma or part of a multinodular goiter)
4) Hyperthyroidism due to rarer causes:
 Thyrotoxicosis factitia: due to excess intake of thyroxine
 Jod – Basedow thyrotoxicosis: when large doses of iodide
are given to patient with a hyperplastic endemic goiter.
 De Quervain’s thyroiditis: hyperthyroidism occurs early in
subacute/acute forms of autoimmune thyroiditis due to
liberation of thyroid hormones from damaged tissues.
 Hashitoxicosis: about 5% of patients with Hashimoto’s
thyroiditis may have thyrotoxicosis in early stages.
 Secondary carcinoma: a large mass of functioning 2ndry
carcinoma secreting thyroid hormones.
 Neonatal thyrotoxicosis: in babies born to hyperthyroid
mothers or euthyroid mothers who have had thyrotoxicosis.

26
• Symptoms:
▪ Tiredness
▪ Emotional lability
▪ Heat intolerance
▪ Weight loss despite good appetite
▪ Palpitations

• Signs:
▪ Tachycardia
▪ Hot, moist palms
▪ Exophthalmos (a sign of grave’s disease), due to infiltration
of the retro-bulbar tissues with fluid and round cells.
▪ Eyelid lag/retraction
▪ Agitation
▪ Thyroid goiter and bruit
▪ Rapid pulse during sleep (more than 90bpm)

• Treatment:
❖ Grave’s disease:
▪ Medical Tx: Carbimazole 30mg/day for 18 months. You
start with 30mg/day till the patient becomes biochemically
euthyroid, then you shift the dose to 15mg/day. Another
method is maintaining a high dose (30-50mg/day) the whole
18 months (Block & replacement theray). Permanent cure
in 50% of patients. For Exophthalmos give prednisone
▪ Surgery: Total thyroidectomy + thyroxine replacement
(only after failure of medical Tx). Orbital decompression
for exophthalmos.
▪ Radioiodine, the Tx of choice in case of recurrent
thyrotoxicosis after surgery. Absolutely contraindicated in
pregnancy.

❖ Toxic multinodular goiter & toxic nodule:

▪ Toxic multinodular goiter: Total thyroidectomy +
thyroxine replacement for life
▪ Toxic adenoma: ipsilateral lobectomy (total lobectomy +
isthmusectomy)

• Preoperative preparations:
▪ Control toxicity; make the patient biochemically euthyroid:
✓ Carbimazole 30mg/day + propranolol for 8-12 weeks. Also
given for 1 week post-operatively.

27
 ✓ Lugole’s iodine can be given for 10 days before surgery; it
reduces vascularity of the gland and makes the patient
euthyroid. Can be used after failure of medical Tx along with
the above therapy to help make the patient euthyroid.
✓ Carbimazole is contraindicated in pregnancy, use
propythiouracil (PTU)

• Preoperative investigations:
▪ TFT and thyroid antibodies.
▪ Thoracic inlet CXR & lateral cervical X-ray: to detect if there’s
retro-sternal extension of the thyroid or tracheal deviation and
compression. Retro-sternal extension may mandate sternotomy. In
case of tracheal compression removing the thyroid may lead to
tracheomalcia so a tracheostomy tube might be needed.
▪ Serum Calcium estimation: because it might drop after the
surgery due to either accidental removal of the parathyroid gland or
injury to the blood supply of the parathyroid gland.
▪ Indirect laryngoscopy: to assess the movement of the vocal cords
(medico-legal importance)
▪ Isotope scan: is necessary in case of toxic nodular goiter if total
thyroidectomy is not planned.

• Complications of surgery:
1) Immediate complications:
a. Bleeding, usually from the superior thyroid artery
b. Injury to surrounding structures:
▪ Recurrent laryngeal nerve (RLN): hoarseness of voice
▪ External branch of the superior laryngeal nerve: weak
voice
▪ Trachea, esophagus, carotid sheath, … etc.
c. Thyrotoxic crisis (storm): severe hyperthyroidism;
agitation, tachycardia & palpitation, dehydration and
hyperthermia. It’s an emergency.
▪ Management:
✓ Admit to ICU
✓ IV Rehydration
✓ Rectal carbimazole
✓ IV propranolol
✓ Cooling
✓ Lugole’s iodine

2) Early complications:

28
 • Respiratory distress; patients presents with stridor 4-6 hours
post-operatively, DDx:
• Hematoma, open the wound
immediately (don’t wait to take the
patient to the theater) and evacuate the
hematoma
• Tracheomalacia, put a tracheostomy
tube
• Bilateral injury to recurrent
laryngeal nerves.
• Hypocalcemia; occurs 2-5 days (24-48h as Dr. Mojahid said)
postoperatively due to injury to the parathyroid.
• Patient presents with numbness and
paraesthesia around thigh and groin or
convulsions.
• Treat the convulsions, and then request
serum Ca2+ level to compare it with the
baseline Ca2+ level. If low means the
parathyroid gland is injured
• Give IV Ca gluconate
• Alfacalcidol may be required to maintain
normocalcemia.
• Less frequently, the hypocalcemia might be
due hungry bone syndrome. Grave’s
patient may develop osteoporosis so after the
gland is removed serum calcium shifts to
bone formation leading to hypocalcemia.
• Patient may have hypocalcemia without
overt symptoms, this is called
asymptomatic hypocalcemia. The
symptoms can be elicited via:
i. Chovestek sign: tapping the facial
nerve will elicit twitching of the face.
ii. Trousseau sign: you bring the
sphygmomanometer cuff and inflate it
around the arm above the systolic
blood pressure, this will induce
carpopedal spam

3) Late complications:
• Hypothyroidism; if patient didn’t stick to Tx

29
 • Recurrence; if the gland is not removed properly and as
in case of subtotal thyroidectomy.
• Hypertrophic or keloid scar; if incision overlies the
sternum and in dark-skinned people.

4) Other complications:
• Wound infection
• Stitch granuloma, seen after the use of non-absorbable
suture material (particularly silk)

THYROID ENLARGEMENT
• Goiter: means generalized enlargement of the thyroid gland
• Solitary (isolated) swelling: a discrete swelling (nodule) in one lobe with no
palpable abnormality elsewhere.
• The swelling can be simple (without features of hyperthyroidism, nor
inflammation, nor neoplasm) or toxic (with features of hyperthyroidism)
• It can be nodular (with multiple nodules) or diffuse (the whole gland is
equally enlarged).
• So thyroid enlargement can present as:
1) Simple diffuse goiter (diffuse hyperplastic)
2) Simple multinodular goiter (the most common goiter)
3) Simple solitary nodule
4) Toxic diffuse goiter (Grave’s disease)
5) Toxic multinodular goiter (Plummer’s disease)
6) Toxic solitary nodule (toxic adenoma)

➢ Simple goiter – endemic or sporadic:

• Due stimulation of the thyroid gland by TSH, either due to:
1. Inappropriate secretion from a microadenoma in the anterior
pituitary (rare), or
2. In response to a chronically low level of circulating thyroid
hormones.

• Etiologies
1. Iodine deficiency, which is responsible for endemic cases in areas
with low iodide content in water and food like mountainous areas or
low-land areas (endemic goiter). Relative deficiency occurs in
females during puberty, pregnancy and lactation making them
susceptible to goiter.
2. Enzymatic deficiency (dyshormonogenesis), responsible for many
cases of sporadic goiter. Often being associated with a +ve family

30
 history reflecting an underlying genetic defect. Pendred’s syndrome
is due to deficiency of perioxidase enzyme. in this syndrome there’s
goiter, sensorineural deafness and mutism. Deficiency of
dehalogenase enzyme is also responsible for sporadic goiter
3. Goitrogens
4. Iodides in large amounts are goitrogenic.

• Stages in goiter formation:

1. Diffuse hyperplastic goiter: Persistent growth stimulation causes
diffuse hyperplasia; all lobules are composed of active follicles and
iodine uptake is uniform.
2. Later, as a result of fluctuating stimulation, a mixed pattern
develops with areas of active lobules and areas of inactive lobules.
3. Active lobules become more vascular and hyperplastic until
hemorrhage occurs, causing central necrosis and leaving only a
surrounding rind of active follicles.
4. Necrotic lobules coalesce to form nodules filled either with iodine-
free colloid or a mass of new but inactive follicles.
5. Continual repetition of this process results in a nodular goiter. Most
nodules are inactive, and active follicles are present only in the
internodular tissue.

• Types of simple goiter:

All types of simple goiter are more common in females due to the
presence of estrogen receptors in the thyroid gland.
A) Diffuse hyperplastic (simple physiological) goiter: appears in
childhood in endemic areas, but in sporadic cases it usually occurs with
puberty. Soft, diffuse and may become large enough to cause discomfort.
A colloid goiter is a late stage of diffuse hyperplasia when TSH
stimulation has fallen off and when many follicles are inactive and full of
colloid.
• Treatment: thyroxine 0.15-0.2 mg/day for few months.
• Prevention: usage of iodized table salt in endemic areas.

B) Simple multinodular goiter: usually multiple nodules are grossly

present. Occasionally, only one nodule is present and the rest of the
nodules are not palpable, here it’s called a dominant nodule.
• Clinical picture:
▪ Patient is euthyroid

31
 ▪ Nodules are palpable and visible, smooth, firm and not
hard.
▪ Goiter is painless and moves freely on swallowing.
▪ Hardness & irregularity, usually due to calcification,
may simulate carcinoma.
▪ A painful nodule, sudden appearance, or rapid
enlargement of a nodule maybe due to:
1. Hemorrhage into a simple nodule (more
common)
2. Follicular Carcinoma.
3. Thyroiditis
4. Development of toxicity (plummer syndrome)

• Investigations:
▪ TFT, to exclude mild hyperthyroidism
▪ Thyroid antibodies, to differentiate it from autoimmune
thyroiditis
▪ Thoracic inlet CXR
▪ FNAC, in case of dominant nodule.

• Complications:
1. Tracheal obstruction due to gross lateral displacement or compression
in compression by retrosternal extension of the goiter.
2. Secondary thyrotoxicosis, in up to 30% of patients.
3. Carcinoma (follicular carcinoma) the incidence is 3%.
4. Cyst formation
5. Hemorrhage into a nodule
6. Calcification may occur in long-standing cases

• Treatment:
▪ Preoperative investigations + Surgery, because
multinodular goiter is irreversible by medical Tx.
▪ Indications of surgery:
1) Compression symptoms; stridor, dyspnea, hoarseness
of voice, dysphagia (never mention dysphagia first)
2) Retrosternal extension

32
 3) Suspicion of cancer (hard, irregular, solid nodule,
lymph node, weight loss… etc)
4) Cosmetic.

▪ Options of surgery:
1. Total thyroidectomy + thyroxine replacement for life.
Do in case of carcinoma or toxicity signs.
2. Subtotal thyroidectomy (2 subtotal lobectomy +
isthmusectomy): is obsolete now due to the high
recurrence rate
3. Near – total thyroidectomy (Dunhill operation): the
best option (total lobectomy + isthmusectomy + subtotal
lobectomy). Do in case of pressure symptoms or
cosmetic.

➢ Solitary thyroid nodule:

• May be:
1. A dominant nodule in a multinodular goiter
2. Follicular adenoma (Toxic adenoma)
3. Carcinoma
4. Colloid nodule
5. Cyst (treated by aspiration)

• Features that raise suspicion of cancer in solitary nodule:

1. History of previous irradiation
2. Sex (thyroid cancer is more common in females) & age (young and
elderly patient)
3. Recent onset & rapid growth
4. Bloody aspirate
5. Rapid recurrence of fluid
6. Pain
7. If the nodule is hard, irregular with limited mobility
8. Presence of local invasion or lymphatic or blood borne metastasis.
- A thyroid nodule in a male is much more likely to be malignant than
in a female.

33
 - Evidence of RLN paralysis, suggested by hoarseness and a non-
occlusive cough and confirmed by laryngoscopy, is almost
pathognomonic.
- Deep cervical lymphadenopathy along the internal jugular vein in
association with a clinically suspicious swelling is almost diagnostic
of papillary carcinoma.

• Investigations:
 TFT, if hyperthyroid associated with a solitary nodule it’s either a
toxic adenoma or a dominant nodule in a multinodular goiter
 Isotope scanning, the mainstay of investigation of nodular thyroid
swelling to determine the functional activity relative to the
surrounding thyroid tissue. Can be either hot (overactive), warm
(active) or cold (underactive). About 80% of solitary nodules are cold,
but only 15% are malignant.
 FNAC, the investigation of choice in solitary thyroid nodule. FNAC
can not differentiate between follicular carcinoma and follicular
adenoma.
 Tru-cut biopsy
 US
 Radiology
 Laryngoscopy

• Treatment:
▪ The main indication of surgery is risk of neoplasm, which
includes follicular adenoma as well as malignant swellings. Other
indications are the same as for simple multinodular goiter surgery
(compression symptoms, retrosternal extension, cosmetic)
▪ Toxic adenoma: excise the adenoma or do ipsilateral lobectomy.
Radioiodine ablation is also an option

34
 The indications for operation in solitary or dominant thyroid
nodule

➢ Retrosternal goiter:
- Usually arise in a normally placed thyroid from ectopic thyroid tissue;
most arise from the lower pole of a nodular goiter.
- The goiter might be malignant or toxic
Clinical features:
It’s often symptomless and discovered on a routine chest radiograph.
However there may be severe symptoms:
▪ Trachea compression leading to dyspnea, particularly at night,
cough and stridor
▪ Sometimes dysphagia may be present.
▪ Engorgement of facial, neck and superficial chest wall veins; in
severe cases there may be obstruction of the superior vena cava.
▪ RLN paralysis is rare

Signs:
▪ Inspection: dilated superficial veins of the upper part of the chest.
There may be cyanosis and edema of the face.
▪ Palpation of the neck may reveal an enlarged thyroid gland
▪ Percussion of the sternum may reveal retrosternal dullness.

35
 Treatment:
Surgery is the only treatment.

Thyroiditis
 Hashimoto’s thyroiditis:
o Chronic lymphocytic (autoimmune) thyroiditis
o Starts with mild hyperthyroidism then progresses to
hypothyroidism.
o Most common in females at the menopause, but may occur at any
age. Usually there’s a +ve family history (presentation: female
with family history presenting with hypothyroidism)
o Commonly presents as goiter (diffuse or nodular) a characteristic
“bosselated” feel or with established or subclinical thyroid failure.
o The autoantibodies are Anti-TPO.
o There’s risk of developing lymphoma
o Investigations:
▪ Biochemical test: are of diagnostic value only if
hypothyroidism is present.
▪ FNAC is the most appropriate investigation
▪ Biopsy: when there’s doubt about neoplasm.

o Treatment: thyroxine 0.1 – 0.2 mg/day ± surgery

 Granulomatous thyroiditis (Subacute thyroiditis, De Quervain’s

thyroiditis):
▪ May follow a viral infection
▪ Presents pain in the neck, fever, malaise and a firm, irregular
enlargement of one or both thyroid lobes.
▪ In 10%, the onset is acute, goiter is very painful and
hyperthyroidism maybe present.
▪ There’s raised inflammatory markers, absent thyroid antibodies.
▪ Serum T4 is slightly elevated, with low uptake of iodine by the
gland.
▪ Diagnosis is confirmed by FNAC, radioactive iodine uptake and
rapid symptomatic response to prednisone.

36
 ▪ Treatment: Prednisone 10 – 20 mg/day for 7 days for the acute
case.
▪ Give thyroxine if there’s prominent thyroid failure.

 Riedel’s thyroiditis:
▪ Very rare (0.5% of goiters)
▪ Thyroid tissue is replaced by cellular fibrous tissue which
infiltrates into muscles and adjacent structures.
▪ It may occur in association with retroperitoneal and mediastinal
fibrosis.
▪ It’s probably a collagen disease
▪ It presents as woody hard fixed goiter (DDx: anaplastic carcinoma)
▪ Treatment: high – dose steroid + Tamoxifen + thyroxine
replacement.
▪ Surgery if pressure symptoms are present.

Neoplasms of the thyroid

• Benign: Follicular adenoma
• Malignant:
▪ Differentiated: papillary &follicular carcinomas
▪ Undifferentiated: anaplastic carcinoma
▪ Lymphoma
▪ Medullary carcinoma (from parafollicular cells)
▪ Secondary tumors: metastatic or local infiltration.

• Investigations: TFT, FNAC, Biopsy, staging

• Imaging: CXR, abdominal US, bone scan
❖ When a preoperative diagnosis is made, imaging with US of MRI
is required (to give an information about the extent of the primary
tumor and nodal involvement)
❖ CT, particularly with iodine-containing contrast media, should be
avoided. Iodine – containing contrast agents may interfere with
radioactive iodine uptake used for diagnostic scanning or therapy.

37
 Papillary carcinoma:
▪ The most common thyroid neoplasm (60%)
▪ Common in young females, lump in the neck or lymph node for
many years (slow growth)
▪ The most important risk factor is irradiation of the thyroid under 5
years of age.
▪ Occasionally associated with Hashimoto’s thyroiditis.
▪ Multiple foci may occur in the same lobe.
▪ Histopathology: papillary projections with Orphan Annie – eyed
nuclei and psammoma bodies (concentric calcifications)
▪ Spread is via lymph nodes
▪ The term extrathyroidal indicates that the primary tumor has
infiltrated through the capsule of the thyroid gland.
▪ O/E: hard solid & irregular. Enlarged cervical lymph nodes may be
the presentation.

 Follicular carcinoma:
▪ The 2nd most common (20% of cases)
▪ May arise on a background of endemic goiter
▪ Presents in middle-aged females (20 – 40 years)
▪ Metastasis is more via the blood, especially to the skull. (A
common OSCE picture, a female with neck swelling and skull
swelling -> follicular carcinoma of the thyroid)
▪ Hurthle cell tumors are a variant of follicular neoplasm where
oxyphil (Hurthle cell) cells predominate histologically.

 Surgical treatment of differentiated carcinoma (papillary &

follicular):
▪ In high-risk patients with nodal involvement and distant
metastasis: total thyroidectomy + radioactive iodine.
▪ In low-risk patient with a single focus of the disease limited to the
thyroid: thyroid lobectomy. This has the significant advantage of
protecting the contralateral RLN and parathyroid gland. This
approach is now considered appropriate unless there are high-risk
features of the disease. (Bailey & love 27th edition)

38
 ▪ Or, if the tumor is less than 1 cm you can do lobectomy, but if the
tumor is >1 cm then do total thyroidectomy in all cases la
lobectomy la 3’ero (Dr. Mojahid)
▪ After surgery you give thyroxine, to suppress endogenous TSH
production to prevent recurrence and as a replacement therapy.
▪ Summary: Surgery + Thyroxine. If there’s lymph node
involvement do lymphadenectomy.
▪ Thyroglobulin is used for follow-up to detect recurrence.

 Undifferentiated (anaplastic) carcinoma:

▪ Occurs mainly in elderly women (10%)
▪ Local infiltration is an early feature of these tumors
▪ Spread by lymphatics and by the bloodstream.
▪ Extremely lethal
▪ Most patients are inoperable when first seen.
▪ If there’s trachea compression do isthmusectomy.
▪ Managed by palliation. Rarely it is managed by surgery
▪ Radiotherapy should be given in all cases

 Medullary carcinoma:
▪ Arise from parafollicular (C cells) derived from the neural crest.
▪ High levels of calcitonin and carcinoembryonic antigen (CEA)
▪ Calcitonin can be used for monitoring and follow up.
▪ Diarrhea is a feature in 30% of cases, may be due to 5-
hydroxytryptamine or prostaglandins produced by the tumor cells
▪ 10-20% of cases are familial and part of MEN-2 (Multiple
endocrine neoplasia)
▪ Lymph nodes involvement occurs in 50-60% of cases.
▪ Blood borne metastasis is common.
▪ The tumor is not TSH dependent and does not uptake radioactive
iodine.
▪ Treatment:
• Total thyroidectomy & either prophylactic or therapeutic
resection of central and bilateral cervical lymph nodes.
• Genetic screening for the RET mutations and prophylactic
surgery for infants with the genetic trait.

39
 Malignant lymphoma:
▪ Most lymphomas arise on a background of Hashimoto’s thyroiditis.
▪ Treated by radiotherapy, no need for surgery.

40
The Breast
Surgical anatomy:
• Development: the breasts are modified sweat glands arising from 2
ectodermal thickening right & left (mammary ridges). These ridges
extend from the axillae to the groin.
• Position and extent:
▪ Between the skin and the pectoralis fascia.
▪ Overlies the area from the 2nd to the 6th ribs, from the lateral border
of the sternum to the anterior axillary line.
▪ The axillary tail (of Spence) is a prolongation of the parenchyma
which passes deeply through an opening in the deep fascia to blend
with the axillary fat.
▪ The breast actually extends:
 Upwards to the clavicle
 Downwards to below the costal margin
 Medially to the middle line
 Laterally to the posterior axillary line
• Breast components:
▪ Epithelial component: responsible for milk secretion and
transport. Each breast consists of 15 – 20 radially – arranged lobes,
each lobe is drained by a lactiferous duct. The ducts converge at
the nipple. A lobe is made up of 20 – 40 lobules, each of which
consists of 10 – 100 alveoli. The main ducts lie behind the areola,
while the lobules occupy the more peripheral part of the breast.
▪ The supporting tissue (stroma). Fibrous septae (Cooper’s
ligament) extends from the pectoral fascia to the skin, and are
responsible for division of the parenchyma into lobes.

Blood supply & lymphatic drainage:

• Arteries:
▪ Internal thoracic artery (internal mammary artery), through
branches that perforate the intercostal spaces and pectoralis major

41
 muscle. The internal thoracic artery is a branch of the subclavian
artery.
▪ lateral thoracic artery, a branch of the axillary
▪ The pectoral branch of the acromiothoracic artery
▪ The intercostal perforators.
• Veins:
▪ Primarily through the axillary and internal mammary veins.
▪ The intercostal veins are clinically important as they drain into the
azygos system and communicate with the valveless vertebral
venous plexus. This communication could explain the tendency of
breast cancer deposits to affect the axial skeleton.

• Lymphatics:
▪ Drains mainly to the axillary (receives about 75% of breast lymph)
and internal mammary lymph nodes.
▪ Axillary lymph nodes:
o Anterior (pectoral) group: at the lower border of pectoralis
minor muscle
o Posterior (subscapular) group: along the subscapular
vessels.
o Central group: embedded in the axillary fat behind
pectoralis minor
o Apical (subclavian) group: lying between the pectoralis
minor and the clavicle, and situated behind the clavipectoral
fascia. It receives lymph from all other groups, and is in
continuity with the lower posterior deep cervical nodes, that
ultimately drain into the subclavian lymph trunk.
Lymphatics from the upper lateral part of the breast may
drain directly into the apical group.
o Lateral (humeral) group: along the axillary tail
o Interpectoral (Rotter) group: a few lymph nodes lying
between the pectoralis major and minor muscles.

The sentinel node is defined as the first lymph node draining

the tumor – bearing area of the breast. Injection of methylene
blue 1% near the tumor will allow identification, excision and
immediate pathological examination of the sentinel lymph

42
 node. This is indicated in N0 patients (clinically &
radiologically negative axillary lymph nodes)

For the purpose of the operative technique of axillary dissection,

the axillary lymph nodes are divided by the pectoralis minor
muscle into three levels:
✓ Level I nodes, located low in the axilla below the muscle
✓ Level II nodes, located behind the pectoralis muscle
✓ Level III nodes, located medial to the muscle at the apex
of the axilla.

▪ Internal mammary nodes:

o There are 3 or 4 internal mammary nodes on each side,
lying along the internal mammary vessels in the 1st three
intercostal spaces.
o They receive part of the lymph from the medial half of the
breast.
o They also drain the posterior third of the breast, and are not
routinely dissected.

▪ Further lymphatic spread:

o Lymph channels from the breast do not cross the midline,
but they do cross the diaphragm, where they communicate
with liver lymphatics.
o Lymphatics from the lower inner quadrant may pierce the
recuts sheath to reach the peritoneal lymphatic plexus.

Investigations of the breast symptoms:

❖ Mammography:
▪ Sensitivity increases with age as the breast becomes less dense
▪ For women > 35 years
▪ A normal mammogram does not exclude carcinoma (5% of breast
cancer are missed the population-based mammographic screening
programs)
▪ Types: 1) Craniocaudal 2) Oblique
▪ Uses:
✓ Screening, screening age is 50-70 years every 3 years

43
 ✓ Management, Triple assessment (see below)

▪ Cancer features on mammography:

1. A dense opacity
2. Clustered micro-calcifications (a feature of DCIS, whereas
macro-calcification is called coarse calcification and is benign)

❖ Ultrasonography (US)
▪ Used in young females (<35 years)
▪ A speculated hypo-echoic mass more deep than wide suggests a
malignant lesion.
▪ The addition of color duplex US identifies the vascularity of the
lesion. Malignant lesions receive blood flow from all around with
turbulent speed, whereas benign lesions receive blood flow from
one side at a low speed.
▪ US Uses:
1. Differentiate cystic from solid masses
2. Guide biopsy
3. Management of the axilla (to check if there's lymph node
enlargement.)
4. To localize impalpable areas of breast pathology.
❖ MRI:
▪ Can be useful in a number of settings:
1) To distinguish scar from recurrence in women who have had
precious conservative breast therapy
2) To assess multifocality & multicentricity in lobular carcinoma
and to assess the extent of high-grade DCIS.
3) To assess response to chemotherapy
4) It’s the best imaging modality for the breast of women with
implants
5) As screening tool in high-risk women (because of family
history)

❖ Fine needle aspiration cytology (FNAC):

▪
❖ Biopsy:

44
 ▪ Is the gold standard investigation, why?
1. Gives a definitive diagnosis
2. Differentiates between in situ and invasive disease
3. Allow staining of the tumor for receptor status
4. Grading the tumor
▪ Tru-cut biopsy (core biopsy), done under local anesthesia when
there’s a deep lump. Can be done in the outpatient clinic. A
specimen taken by core biopsy:
1) Allows a definitive preoperative diagnosis
2) Differentiates between in situ and invasive disease
3) Allow the tumor to be stained for receptor status.
▪ Incisional biopsy, used in case of fungating tumors (large mass ±
ulcer)
▪ Excisional biopsy used when there’s a small lump that looks
benign. The whole mass is excised. When it’s possible it’s the best
and most reliable biopsy and provides a big enough specimen to
allow for hormone receptor staining as well.
▪ Frozen section biopsy, the specimen is frozen and slides are
prepared from the frozen blocks. A diagnosis is obtained within 20
minutes. If the result is negative the patient is woken up. If it’s
positive the surgeon proceeds with radical surgery. These
possibilities should be discussed with the patient before the
operation.
▪ Stereotactic core biopsy, (mammography guided)
▪ Biopsy from impalpable breast masses

Always remember: in any patient who presents with a breast lump or other
breast symptoms suspicious of cancer, the diagnosis should be made by Triple
assessment which includes: clinical assessment (Hx & Ex), radiological
imaging and samples taken for histopathological analysis. The positive
predictive value of this combination should exceed 99.9%.

45
 Benign breast conditions

Congenital anomalies:
▪ Athelia: absence of the nipple, very rare, usually associated with amazia
▪ Polythelia: supernumerary nipples occur anywhere along either or both
the mammary ridges. May be mistaken for a mole or a wart.
▪ Amazia: absence of the breast. Usually unilateral and often associated
with absence of the sternal portion of the pectoralis major (Poland
syndrome). It’s more common in males.
▪ Polymazia: supernumerary breast. Due to persistence of extra mammary
portions of the mammary ridges. They may function during lactation.
▪ Infantile gynecomastia: diffuse enlargement of the male breast which
may be unilateral or bilateral. It’s caused by the effect of circulating
maternal sex hormones. It’s reversible by 6 months and requires no
treatment.
▪ Mastitis of infants
▪ Diffuse hypertrophy

The nipple:
❖ Nipple retraction:
▪ May occur in puberty or later in life.
▪ Nipple retraction occurring in puberty is called simple nipple
inversion and the etiology is unknown (benign horizontal
inversion). In about 25% the condition is bilateral. Treatment is
usually unnecessary and the condition may resolve spontaneously

46
 during pregnancy or lactation. Or can be corrected by suction
devices.
▪ Slit-like retraction: may indicate duct ectasia and chronic
periductal mastitis.
▪ Circumferential retraction: may indicate an underlying
carcinoma

❖ Papilloma of the nipple:

▪ It has the same features as any cutaneous papilloma.
▪ Should be excised with a tiny disc of skin.
▪ Alternatively, the base may be tied with a ligature and the
papilloma will spontaneously fall off.

❖ Retention cyst of gland of Montgomery: these glands, situated in the

areola, secrete sebum and if they become blocked a sebaceous cyst forms.
❖ Eczema: a rare condition often bilateral. Usually associated with eczema
elsewhere on the body. It’s treated with 0.5% hydrocortisone.
❖ Paget’s disease of the nipple caused by malignant cells in the subdermal
layer and is usually associated with a carcinoma within the breast.
Clinical difference between Paget’s disease and eczema
Paget’s disease Eczema

Unilateral Commonly bilateral

Usually occurs at menopause Commonly occurs at lactation

No itching Itching

No vesicles – not oozing (dry) Vesicles – oozing

Nipple is erodes Intact nipple

Well defined Ill – defined

A breast lump may be felt No lump

No response t o eczema Tx Responds to Tx

Starts in the nipple Starts in the areola

47
❖ Discharge from the nipple:
▪ Discharge can occur from one or more lactiferous ducts.
▪ Investigations: Triple assessment
▪ Management:
 Microdochetomy (take out single duct). Indications:
1. Bloody discharge
2. Persistent discharge
 Core excision of the major ducts (Hadfield operation,
subareolar resection): the entire major duct system is
excised for histological examination. Indications:
1. The duct of origin of nipple bleeding is uncertain
2. Bleeding or discharge from multiple ducts
3. Recurrence
4. Mammary duct fistula.

It’s vital to warn the patient that she will be unable to breastfeed
after this and may experience altered nipple sensation.

48
Benign breast diseases:
❖ Breast trauma:
▪ Blunt trauma to the chest produces 2 lesions:
1. Hematoma, particularly a resolving hematoma, gives rise to
lump, which in absence of overlying bruising is difficult to
diagnose correctly unless it’s biopsied.
2. Traumatic fat necrosis usually occurs in stout, middle – aged
women. Following a blow, or even indirect violence (e.g.
contraction of pectoralis major). Presents as a cyst (that contains
thick oily fluid) or a painless lump and may mimic carcinoma
even displaying skin tethering and nipple retraction (do triple
assessment to exclude cancer)

49
❖ Acute bacterial mastitis (lactational mastitis):
▪ The most common variety of mastitis and is associated with
lactation
▪ The most common organism involved is staphylococcus aureus.
Usually after the 2nd day of life organisms form the mouth of the
suckling infant gain access through nipple cracks and opening of
the lactiferous ducts.
▪ Clinical features:
1. Stage of milk engorgement: may affect the whole or a sector
of the breast. There’s dull aching pain & persistent pyrexia.
Examination reveals enlargement and induration of the breast
but there are no physical sings of inflammation
2. Stage of acute mastitis: the pain gets worse and there’s
continuous higher pyrexia. Examination reveals diffuse
swelling, redness, induration and tenderness.
3. Stage of acute abscess, suppuration is diagnosed if:
o Pain is throbbing
o Temperature is hectic
o Physical signs get localized in the breast
o Pitting edema is elicited in the area of the skin overlying
the abscess
o Persistence of local signs of inflammation for more than
5 days or of severe systemic upset for more than 2 days
after full antibiotic treatment.
o Fluctuation is a late sign (diagnosis of abscess is not
based on it here)
4. Stage of chronic abscess

▪ Treatment:
1. Antibiotics: flucloxacillin or co-amoxiclav
2. Support of the breast, helps lessen pain and prevents edema
3. Local heat (warm fomentation) and local analgesia
4. In case of abscess formation, it’s treated by incision and
drainage under general anesthesia. Complications:
i. Inadequate drainage, leading to chronic mastitis

50
 ii. Mammary duct fistula (Zuska disease). Treated by
Hadfield operation.

- If an antibiotic is used in the presence of undrained pus an antibioma may

form. This is a large, sterile, brawny edematous swelling that takes several
weeks to resolve.
- If infection didn’t resolve within 48hrs after treatment, then repeated
aspirations under antibiotic cover is performed. This often allows resolution
without the need for an incision, and will also allow the patient to continue
breastfeeding.

❖ Mammary Duct ectasia/periductal mastitis/Plasma cell mastitis:

▪ This is dilatation of the breast ducts, which is often associated with
periductal inflammation in which round cell infiltration
predominates.
▪ It’s much more common in smokers
▪ Clinical features: (may be asymptomatic)
1. Nipple discharge: may be blood – stained, serous, creamy,
white, or yellow (simply of any color)
2. Slit – like retraction of the nipple, due to fibrosis.
3. Subareolar mass
4. abscess
▪ investigations and treatment:
o Triple assessment to rule out cancer
o Antibiotics: flucloxacillin or co-amoxiclav and
metronidazole. For non – complicated cases.
o Hadfield operation for complicated cases (presence of a
mass or recurrent condition)

❖ Fibrocystic disease of the breast:

▪ Also described by other names like Aberrations of normal
development and involution (ANDI) and fibroadenosis.
▪ More common in women aged 30 – 50 years old and is rare after
menopause (this suggests that it’s related to ovarian activity)
▪ The exact etiology is unknown. The pathogenesis involves
disturbances in the breast physiology extending from a perturbation
of normality to well-defined disease process.

51
▪ The upper outer quadrant of the breast is the commonest site of
affection.
▪ It consists essentially of 4 features that may vary in extent and
degree in any one breast:
1. Cyst formation, cysts are almost inevitable and vary in size
2. Fibrosis, replacement of the fat and elastic tissue by fibrous
tissue
3. Hyperplasia (adenosis) of epithelium in the lining of the ducts
and acini (with or without atypia)
4. Papillomatosis, the epithelial hyperplasia may be so extensive
that it results in papillomatous overgrowth within the ducts.
▪ Clinical features:
1. May be completely asymptomatic
2. A lump (often discrete), can be unilateral or bilateral
3. Mastalgia, usually a cyclical mastalgia. The pain is felt few
days premensturally and is accompanied by enlargement and
increase in the nodularity of the breast.
4. Nipple discharge may occur (usually clear or yellow)
▪ Investigations: Triple assessment to rule out cancer
▪ Treatment:
o Exclusion of malignancy and reassurance of the patient are
most important.
o Lumpy breast: firm reassurance and reviewing the patient
at a different point in the menstrual cycle (e.g. 6 weeks after
the initial visit) and often clinical signs will have resolved by
that time.
o Cysts are aspirated. A recurring cyst is excised for biopsy.
o Mastalgia:
▪ Reassurance: use pain chart if unsure if cyclical or
non-cyclical. Also allows time for reassurance to
become active.
▪ Adequate support: wearing firm bra during the day
and soft bra at night.
▪ Avoid caffeine
▪ Primrose oil one capsule every night. Better effect in
women over 40 years old than in younger women.
▪ NSAIDs

52
 ▪ For intractable symptoms: anti-gonadotropin (danazol)
or prolactin inhibitors (bromocriptine) 0.5mg/week for
6 weeks.

DDx of tender breast:

1. Cyclical mastalgia
2. Mondor’s disease (thrombophlebitis of the
superficial veins of the breast and anterior
chest wall)
3. Tietz syndrome (benign inflammation of one
or more of the costal cartilages)

❖ Breast cysts:
▪ These occur most commonly in the last decade of reproductive life
as a result of a non-integrated involution of stroma and epithelium.
They are a manifestation of fibroadenosis.
▪ They are often multiple, may be bilateral and can mimic
malignancy (do triple assessment)
▪ Large cysts distended with clear fluid may have a blue-green color
(blue-domed cysts of Bloodgood)
▪ Treatment is usually aspiration.
▪ A cyst is considered benign & requires no further treatment, if:
1) Aspirated fluid is not blood-stained
2) The mass disappear completely after aspiration leaving no
residual lump.
3) Does not recur within 2 weeks
o If one of these 3 options occurs then a core biopsy or local
excision for histological diagnosis is advisable. This will
exclude cystadenocarcinoma.

❖ Galactocoele:
▪ Usually presents as a painless, solitary, subareolar cyst during or
shortly after lactation.
▪ It contains milk and in long-standing cases its walls tend to calcify.
▪ Excision is usually needed.

53
❖ Fibroadenoma (breast mouse):
▪ The commonest breast mass of young women between the ages of
15 – 25 years.
▪ They arise from hyperplasia of a single lobule and usually grow up
to 2 – 3 cm in size. Fibroadenomas which are over 5 cm in size are
called giant fibroadenoma and they occasionally occur during
puberty.
▪ The patient present with a painless lump that is accidently
discovered. Usually small, spherical, well circumscribed. It’s
highly mobile hence the name breast mouse.
▪ Management:
1) Triple assessment to exclude carcinoma. In US and
mammography it appears as a well defined mass (surrounded by
a well-marked capsule)
2) Reassurance only: if the diagnosis is certain and the lump is not
symptomatic
3) Regular monthly breast self – examination, and seek
reassessment if the lump starts to enlarge rapidly or become
painful.
4) Excision is indicated in cases of:
▪ Suspicion of cancer (suspicious cytology)
▪ It becomes very large (>5 cm, Giant fibroadenoma)
▪ In elderly females
▪ Patient desire

❖ Phyllodes tumor:
▪ There’s a spectrum of benign (70%), to borderline (20%) to
malignant (10%) pyllodes tumors.. Previously known as serocystic
disease of Brodie or cystosarcoma phyllodes.
▪ It’s a rapidly growing tumor resembling fibroadenoma.
Microscopically, there’s a leaf-like structure, with a high mitotic
count than seen with fibroadenomas. Also, unlike fibroadenomas
(which arise from lobular component), phyllodes tumor arise from
the breast stroma.
▪ Usually occur over the age of 40 years.

54
 ▪ They present as a large, sometime massive tumor with an unevenly
bosselated surface.
▪ Occasionally, ulceration of overlying skin occurs because of
pressure necrosis.
▪ Despite their size they remain mobile on the chest wall.
▪ Malignant phyllodes tumors are considered soft tissue sarcomas,
and they tend to metastasize (very rare) via the bloodstream (to the
lungs)
▪ Investigations: triple assessment
▪ Treatment:
 Excision with a 1 cm safety margin
 Mastectomy in case of:
1) Massive tumors
2) Recurrent tumors
3) Those of malignant type.

DDx of giant breast:

1) Giant fibroadenoma
2) Phyllodes tumor
3) Gigantism

Carcinoma of the breast

• Breast cancer is the most commonly diagnosed cancer in women

worldwide (23% of total cancers)
• Most cases develop after the age of 50 with a peak at 70 years.
• It’s rare under the age of 30

55
❖ Risk factors:
1. Age, extremely rare below the age of 20 years
2. Gender, 99% of breast cancer is in women
3. Genetics, BRCA1, BRCA2 and p53. BRCA2 is associated with
male breast cancer. BRCA1 in families is also associated with
breast, ovarian and colorectal cancers.
Features suggesting familial breast cancer:
1) Age, very young at presentation
2) Male with breast cancer in the family
3) Bilateral breast cancer (a patient treated in one breast and
then after a while develops breast cancer in the other
breast).
- Screen the family members for breast cancer (MRI)

4. Diet, high alcohol intake increase the risk while caffeine decreases
the risk. Smoking hasn’t been proven to be a risk factor.
5. Endogenous estrogen exposure:
▪ Early menarche
▪ Few/no pregnancies (nulliparity)
▪ Age at first pregnancy >35 years
▪ Late menopause
▪ Postmenonpausal obesity BMI >28, due to increased
conversion of steroid hormones to estradiol in the body fat.
▪ Chronic liver disease
▪ Breastfeeding history (breastfeeding is a protective factor)
6. Exogenous estrogen exposure:
▪ Contraceptives (increased risk during use, lowers to baseline
at 10 yrs after discontinuation)
▪ Hormonal replacement therapy (HRT) for >5 yrs >age 50
years
7. History of previous breast cancer, invasive or in situ carcinoma.
8. Specific forms of benign breast change (see below)

56
❖ Types of primary breast cancer:
 In situ breast cancers (the basement membrane is not breached):
▪ Ductal carcinoma in situ (DCIS).
▪ Lobular carcinoma in situ (LCIS), tend to be multifocal
and bilateral.
DCIS LCIS

Frequency More common Less common

Bilaterality and rare Common

multicentricity
Micro-calcification Present Absent

Early detection Possible Less likely

Potential for 30 – 50% It’s a marker of

invasive cancer increased risk of
malignancy in the
same or other
breast

57
 Treatment As invasive Strict follow up
cancer, but no
axillary dissection

 Invasive breast cancer:

▪ Ductal carcinoma, the most common (78%). Classical firm
lump
▪ Lobular carcinoma (5-10%), may be bilateral and it shows
multicentricity.
▪ Mixed (both ductal & lobular features),
immunohistochemical analysis may aid in knowing the
predominant tumor using the e-cadherin antibody, which
reacts positive in lobular cancer.
▪ Medullary carcinoma (5-7%), has a well – circumscribed
border, and there’s intense infiltration by lymphocytes and
plasma cells.
▪ Mucinous (colloid) carcinoma (3%), its cells produce
abundant mucin
▪ Tubular carcinoma (2%)
▪ Papillary carcinoma (1-2%)
▪ Inflammatory carcinoma, a rare, highly aggressive cancer
that presents as a painful, swollen breast, which is warm
with cutaneous edema. This results from blockage of the
subdermal lymphatics with carcinoma cells. It involves at
least one third of the breast (DDx: Breast abscess).
Diagnosis is confirmed by biopsy.
▪ Paget’s disease of the breast, it’s an intraductal carcinoma
that reaches the skin of the nipple.

❖ The spread of breast cancer:

▪ Local spread: tends to involve the skin and to penetrate the
pectoral muscles and even the chest wall if diagnosed late.
▪ Lymphatic spread:
 Occurs primarily to the axillary lymph nodes
 Tumors in the posterior one-third of the breast are more
likely to drain to the internal mammary nodes.

58
  Involvement of supraclavicular nodes or any contralateral
lymph nodes represents advanced disease.

▪ Blood stream spread: to the lungs, bones (in order of frequency:

lumbar vertebrae, femur, thoracic vertebrae, ribs, skull) , brain and
liver.
❖ Hormone receptors:
▪ About 60% of breast cancers have estrogen receptors (ER +ve)
▪ They may also exhibit progesterone receptors (PR +ve)
▪ About 20% exhibit HER2/neu receptors, which are members of
epidermal growth factor receptors involved in cell growth
regulation.
▪ About 30% of patients are don’t have any of the receptors (Triple
negative)
▪ Overexpression of HER2/neu or triple negative indicates a worse
prognosis.

❖ Clinical features:
▪ Can be asymptomatic and detected via screening.
▪ General symptoms of cancer: weight loss, cachexia, loss of
appetite.
▪ Symptomatic local/regional disease:
o Painless breast lump or thickening, skin dimpling, breast
asymmetry, skin erythema.
o Nipple retraction (circumferential) or discharge (bloody or
serosanguinous)
o The majority of breast cancers (50%) are located in the
upper outer quadrant, as the majority of the breast’s
ductulolobular units are located in this site.
▪ Symptomatic metastatic disease:
o Bone pain & pathological fracture (bone mets)
o Breathlessness (lung mets)
o Abdominal distention, jaundice (liver mets)
o Headache, fits, personality changes (brain mets)

59
 ▪ Signs:
o Hard, irregular, ill-defined mass
o Skin tethering, caused by invasion and shortening of
ligaments of Cooper.
o Nipple retraction or discharge
o Peau d’orange sign, caused by cutaneous lymphatic
obstruction in locally advanced disease. The edematous
skin is pitted at the sites of hair follicles, sebaceous
glands, and sweat glands giving the appearance of an
orange peel.
o Axillary and supraclavicular lymph nodes: number and
mobility of palpable lymph nodes are assessed.

❖ Staging (you must know it):

▪ The management and prognosis of breast cancer depends on the
stage of the disease.
▪ Axillary lymph nodes are the most important prognostic factor.
▪ There are 2 common systems of staging: the international TNM
staging system and the union for international cancer control
staging (UICC)

TNM staging
Primary (T) Tis: in situ cancer
T0: no primary tumor located
T1: tumor <2 cm
T2: tumor 2-5 cm
T3: tumor >5 cm
T4:
a: extension to chest wall
b: ulceration, ipsilateral satellite
nodules, peau d’orange
c: both T4a and T4b
d: inflammatory carcinoma

Nodes (N) N0: no nodal involvement

N1: mobile ipsilateral axillary nodes
N2: fixed level I/II ipsilateral axillary
nodes

60
 N3: ipsilateral level III axillary nodes
or supraclavicular nodes
Metastases (M) M0: no metastases
M1: distant metastases
Add i+ for isolated tumor cells
Add mi+ for micrometastases

UICC staging
Stage UICC Description category 5 year survival
rate (%)
I T1, N0, M0 Early breast 93
cancer
II IIA T2, N1, M0 Early breast 72
cancer
IIB T3, N0, M0 Locally
III IIIA T1-3, N1-3, M0 advanced breast 42
IIIB T4, any N, M0 cancer
IV Any T, any N, Metastatic 18
M0

❖ Investigations:
▪ Triple assessment: clinical examination, imaging and tru cut biopsy
(check investigations of the breast for more details)

❖ Treatment:
 Treatment of early breast cancer (stages I and IIA):
▪ The cutoff TNM staging for this treatment is T2N1M0.
▪ One of 2 options:
1) Conservative breast surgery (CBS):
▪ It’s a combination of surgery and radiotherapy
▪ It’s commonly referred to as a wide local excision. Wide
local excision of the tumor with a 1 cm safety margin.
▪ Indications: small tumor ≤ 4 cm, large lesions in large
breasts, solitary or multifocal lesions(lesions present in
one quadrant)
▪ Contraindications: pregnancy, extensive
microcalcificaitons, multicenteric masses as detected by
MRI.

61
 ▪ Management of the axilla: if the sentinel lymph node
is positive or the patient is N1 then do axillary lymph
nodes dissection (ALND). Removal of level I & II and, if
grossly involved, level III. An ANLD should remove 10
or more nodes.
▪ Postoperative radiotherapy: for 5 weeks.
▪ Hormonal therapy: to all receptor +ve cases. It reduces
recurrence by 40%. Tamoxifen block ER. Anastrazole is
an aromatase inhibitor that inhibits peripheral conversion
of androgen to estrogens; it’s suitable only for post-
menopausal women.
▪ Chemotherapy: in case of +ve axillary nodes, tumors >
5 cm, and hormone receptor -ve & HER2/neu +ve
tumors.
▪ Targeted therapy: for HER2/neu +ve cases. Give
trastuzamab (herceptin)

2) Modified radical mastectomy (MRM, Patey mastectomy):

▪ The breast and associated structures are dissected en bloc
and the excised mass is composed of:
o The whole breast
o A large portion of skin, the center of which
overlies the tumor but which always includes the
nipple
o All of the fat, fascia and lymph nodes of the axilla.
 The axillary vein and nerves to serratus
anterior and latissimus dorsi (the
thoracodorsal trunk) should be preserved.
▪ The intercostal brachial nerves are usually divided in this
operation and the patient should be warned about
sensation changes postoperatively.
▪ MRM indications:
1. Large tumors in smaller breasts.
2. Central tumors
3. Multifocal or multicenteirc tumor (tumors in more
than one quadrant)
4. Local recurrence

62
 5. Pregnancy (do simple mastectomy in which axillary
LN are not dissected)
6. Patient preference
▪ The wound is drained using a wide-bore suction tube.
▪ Early mobilization of the arm is encouraged and
physiotherapy help normal function to return very
quickly.
▪ Postoperative radiotherapy to the internal mammary and
supraclavicular lymph nodes, for T3 patients and for
tumors in the medial half of the breast.
▪ Adjuvant systemic therapy is given in appropriate
patients for all node +ve patients and T3 patients.
❖ Reconstructive procedures after mastectomy:
1. A synthetic implant (silicone gel implant)
2. A musculocutaneous flap: either latissmus dorsi muscle (LD flap)
or transversus abdominis flap (TRAM flap). The latter gives
excellent cosmetic results in experts’ hands.
3. Nipple reconstruction, simple and done under local anesthesia.
4. External breast prostheses that fit within the bra are the most
common method of restoring volume fill.

❖ Follow up: every 6 months for 5 years, then annually for 10 years by
mammography.

 Treatment of intermediate disease (locally advanced breast

cancer):
▪ Neoadjuvant (adjuvant therapy before surgery) allows
reduction in the tumor size and allows breast conservative
therapy instead of mastectomy in some cases.
▪ The same drugs used in the adjuvant protocol are used in
neoadjuvant treatment. After surgery theses patients will
start radiotherapy but will not take chemotherapy anymore.

 Treatment of advanced disease:

▪ The aim is palliation and improving the quality of life.
▪ This category comprises:
1) Stages III & IV UICC
2) T4 patients

63
 3) Fungating tumors
4) Ulcerations
5) Inflammatory carcinoma
6) Recurrent cases
7) Distant metastese
▪ Modalities of treatment:
1) Radiotherapy, for palliation of pain or ulceration
2) Hormone therapy, for receptor +ve patients. Tamoxifen
is not given for more than 5 years to avoid the risk of
endometrial cancer or thrombogenesis. If no response use
aromatse inhibitors.
3) Chemotherapy, the basic treatment of metastatic disease,
response rate is 60 – 70%.
4) Surgery is indicated for the following case:
 Toilet mastectomy for unpleasant
malodorous fungating tumor (the term toilet
mastectomy is used when the cancer is so
advanced and mastectomy is done only to
improve appearance and quality of life and
not done to cure the cancer)
 Internal fixation of pathological fractures
 Urgent decompression and stabilization of
the spine if a vertebral collapse causes spinal
cord compression.
5) Management of specific problems:
o Hypercalcemia: in patient with widespread bone
metastases. Patients complain of thirst, drowsiness
and constipation. The patient is dehydrated and the
serum calcium is high. Treated by correction of
dehydration with IV fluids, together with
furosemide, prednisolone and bisphosphonates
o Pathological fractures, internal fixation and
radiotherapy
o Cerebral metastases: corticosteroids +
radiotherapy

64
 o Spinal cord compression: surgical cord
decompression with stabilization + radiotherapy
o Pleural effusion: responds to systemic therapy and
chest tube drainage. If not, give cytotoxic
bleomcyin
o Liver metastases: chemotherapy.

❖ Indications of chemotherapy:
1. LN +ve
2. Triple negative tumors
3. HER2/neu +ve
4. Large tumors
5. Stage III & IV
6. Metastases
7. Lymphovascular invasion

❖ Agents used in chemotherapy:

1. First-generation regimen (CMF): Cyclophosphamide,
methotrexate and 5-fluorouracil (no longer considered adequate
adjuvant chemotherapy)
2. Modern regimens (2nd & 3rd generations): anthracycline
(doxorubicin or epirubicin) + taxanes.

❖ Phenomena resulting from lymphatic obstruction in advanced

breast cancer:
1. Peau d’orange (already mentioned)
2. Lymphedema, a complication of ALND (incidence is 5%) or
radiotherapy. Don’t do both ALND and radiotherapy as it increases
the incidence to 30%.
3. Cancer-en-cuirasse: the skin of the chest is infiltrated with
carcinoma and has been likened to a coat (cuirasse means piece of
armor covering the chest and sometimes the back). Occurs in cases
of local recurrence after mastectomy and is occasionally seen to
follow the distribution of irradiation to the chest wall.
4. Lymphangiosarcoma: a rare complication of lymphedema. It takes
the form of multiple subcutaneous nodules in the upper limb. It must
be distinguished from recurrent carcinoma of the breast. Has a poor
prognosis but some respond to cytotoxic therapy or irradiation.

65
 Diseases of the male breast

Gynecomastia:
• Generalized enlargement of the male breast. May be unilateral or
bilateral.
• Etiologies:
1. Idiopathic
2. Physiological:
▪ Infantile gynecomastia, due to circulating maternal sex
hormones
▪ Pubertal gynecomastia, asymptomatic and usually resolves
within 2 years.
▪ Senile gynecomastia, related to reduction of testicular
function.
3. Hormonal :
▪ Stilberstol therapy for prostate cancer
▪ Teratoma of the testes, anorchdism, and after castration
▪ Bronchial carcinoma and in adrenal & pituitary disease, due to
etopic hormonal production.
4. Associated with:
▪ Leprosy, due to bilateral testicular atrophy
▪ Chronic liver failure, due to failure to metabolize estrogens.
▪ Klinefelter syndrome, 47XXY trisomy.
• Treatment:
o Most cases require no treatment. Reassurance may be sufficient
o Persistent gynecomastia causing embarrassment is treated
surgically by mastectomy (with preservation of the areola and
nipple) or liposuction.

Carcinoma of the male breast:

▪ Very rare (0.5% of cases)
▪ Predisposing factors: gynecomastia and excess endogenous or exogenous
estrogen.
▪ It tends to present as a lump and most commonly an infiltrating ductal
carcinoma.
▪ Treatment: MRM with chemotherapy and tamoxifen postoperatively
▪ Has a worse prognosis than female breast cancer.

66
GASTROINTESTINAL TRACT
SURGERY

HERNIA
Hernia is an abnormal protrusion of an organ or viscous usually within a
peritoneal sac through defect in the abdominal wall.

❖ Anatomy of the hernia:

Skin – subcutaneous tissue – deep fascia – muscles – transverse fascia – parietal
peritoneum – visceral peritoneum – viscous

❖ Aetiology :
- Congenital causes :
• Un-obliterated processus vaginalis → congenital inguinal hernia
• Un-obliterated physiological umbilical hernia→ congenital
umbilical hernia
- Acquired causes:
• Increased intra-abdominal pressure: due to
Chronic cough - chronic constipation ”straining”

67
 Obesity - heavy work - pregnancy - splenomegaly

Ascites or tumor

• Weak abdominal wall:

Obesity - pregnancy - previous surgical scar
Damaged nerve supply - smoking “ it decrease collagen”
❖ Components:
1- Sac : is a peritoneal pouch which have neck, body and tail
2- Contents : it could be any abdominal organ except the pancreas (
omentum and intestine are the most common)
➢ Special contents:
- Richter’s hernia : contain part of the bowel circumference , common in
the femoral hernia *
- Littre’s hernia : contain meckel’s diverticulum
- Maydl’s (W) hernia: contain 2 loops of intestine while the intermediate
loop lie in the peritoneal cavity.
- Urinary bladder : in inguinal and femoral hernia
3- Coverings
❖ Natural History Of The Hernia:
- Reducible
- Irreducible → due to adhesions between the sac and the contents or
overcrowding ( needs urgent surgery within 2 wks)
- Obstructed hernia : presents with colicky pain
- Strangulated hernia : present with continuous pain due to ischemia , on
examination it is tender and tense.
Veins will be obstructed at first → leading to edema → increase pressue
→ arterial flow will be impaired→ ischemia.
❖ Complications:
1- Irreducibility 4- inflammation
2- Obstruction 5- torsion of the omentum
3- Strangulation 6- hydrocele of hernia sac
❖ Inguinal Hernia: 2 types
1- Direct 2- indirect
Inguinal ligament (between the anterior superior iliac spine and the pubic
tubercle) is the floor of inguinal hernia.

Inguinal canal in males transmit:

68
 - spermatic cord: which contain (testicular artery & vein and ductus
deferns)
- Ilio-inguinal nerve
*deep inguinal ring is lateral to the inferior epigastric artery

*inguinal triangle (Hesselbach triangle): Boundaries

- Medially : rectus abdominis - Superiolaterally: inferior epigastric

artery

- inferiorly: inguinal ligament

- If the hernia directly emerge through the triangle → direct inguinal

hernia
- If it emerge lateral to the artery→ enter the deep ring , go through the
inguinal canal to the superficial ring → indirect inguinal hernia
- So the sac of indirect inguinal hernia is attached to the spermatic cord
• Indirect inguinal hernia:
- Common in children , it goes to the scrotum
- On examination : - can’t feel the spermatic cord on the affected site
-you can feel both testis
- Strangulation is more common than in direct hernia

• Direct inguinal hernia:

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 - Common in adults
- Usually bilateral
- Donesn’t reach the scrotum
*the best way to differentiate between the two types is intra-operatively:

The landmark is inferior epigastric artery:

Medial to it: direct / lateral to it: indirect

*Special forms:

- Bantalon hernia: direct and indirect inguinal hernia at the same time on the
same side

- Inflammatory hernia: contain inflammatory components

❖ Femoral Hernia:
- Femoral ring is very small opening in the thigh
- Risk of strangulation is high, so it is urgent hernia
- More common in females with recurrent pregnancies
- DD: for femoral swelling
• Femoral hernia
• Femoral artery aneurysm
• Saphena varices “varicosity of saphenous vein”
• Lymph node
*injury to the ilio-inguinal nerve during appendectomy can lead to direct
inguinal hernia.

*how to differentiate femoral / inguinal hernia?

- inguinal hernia: sac is above and medial to pubic tubercle

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- femoral hernia: sac is below and lateral to pubic tubercle

❖ Umbilical Hernia:
- Common in children “congenital”
- Defect in umbilical ring
- Role of 3: - 3% of live birth
Incidence 3 out of 1000
Treated at age of 3 years
- Strangulation is not common
- Treatment: anatomical repair

❖ Para-umbilical Hernia:
- Above the umbilical → sad face
- Below umbilical → smile face
- Treatment: mesh repair

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 ❖ Epigastric Hernia:
- Hernia through linea alba
- Between xyhpoid process and umbilicus
- Common in obese females
- Treated by anatomical repair
❖ Strangulated hernia:
• Management :
- Admission
- Resuscitation
- NPO
- Iv fluids and electrolytes
- Iv antibiotics
- Analgesia
- NG tube
- Urinary catheter
- Follow up and monitoring

❖ Surgical treatment of hernia:

1- Herniotomy:
- Open the sac, inspect the contents
- Reduction of the contents
- Excision of the sac and close the defect
2- Herniorrhaphy:
- Same above steps
- Muscle repair using non-absorbable suture (nilon, protein) to stimulate
fibrous tissue formation
3- Hernioplasty:
- Herniotomy + mesh repair (synthetic material = polypropylene)
- Commonly used nowadays
❖ Complications of hernia repair:
• Immediate : bleeding
• Early :
- infection “ after 72 hrs

- Hematoma : with inguinal hernia, it appear in the scrotum” scrotal

hematoma” which may progress to abscess → treated by aspiration

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 - Ilio-inguinal nerve injury→ numbness in abdomen and thigh
• Late:
- Testis atrophy: due to injury to testicular artery
*Truss : is a belt used for patients who are unfit for surgery.

* difference between hernia contents;

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* Strangulated hernia on examination:

- Tense - Tender

- irreducible - no cough impulse

* intestinal obstruction don’t occur with:

- omentum

- richter’s hernia

- littre’s hernia

* Sliding hernia: viscus (bladder; cecum; sigmoid) forms part of the wall of the
heria sac.

Common in : longstanding gernia / old males

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Diseases of the Esophagus
Gastro-esophageal reflux disease (GERD):
▪ Occasional episodes of gastro-esophageal reflux are common in health.
Reflux is normally followed by esophageal peristaltic waves which clear
the gullet, alkaline saliva neutralizes residual acid, and symptoms do not
occur.
▪ GERD develops when the esophageal mucosa is exposed to
gastroduodenal contents for prolonged periods of time.

▪ Etiologies:
1) Lower esophageal sphincter hypotension
2) Sliding hiatus hernia, because the pressure gradient between the
abdominal and thoracic cavity that normally pinches the hiatus is lost.
3) Delayed esophageal clearance (loss of esophageal peristaltic activity)
4) Defective gastric emptying
5) Increased intra-abdominal pressure, pregnancy & obesity
6) Gastric acid hypersecretion
7) Alcohol, smoking
8) Drugs (TCA, anticholinergics, nitrates)
9) Surgery in achalasia, as a complication
10) Systemic sclerosis

▪ Symptoms:
 Esophageal:
1) Heartburn, which is increased after meals, leaning forward,
stooping or straining, and relieved by antacids.
2) Acid brash due to regurgitation of acid or bile
3) Waterbrash; increased salivation due to reflex salivary gland
stimulation by the acid.
4) Odynophagia, due to esophagitis or ulceration

 Extra-esophageal:
1) Nocturnal asthma,
2) Atypical chest pain (DDx angina)

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 3) Chronic bronchitis
4) Acid laryngitis (presents with hoarseness, throat clearing)
5) Sinusitis

▪ Complications:
1) Esophagitis, presents as odynophagia
2) Benign (peptic) stricture, due to fibrosis and presents as dysphagia
which is worse for solids than for liquids. Diagnosis by endoscopy and
treatment by endoscopic balloon dilatation or bouginage + long term
therapy with PPIs.
3) Iron – deficiency anemia, due to insidious blood loss form long –
standing esophagitis or bleeding from erosion of the neck of hiatus
hernia sac (Cameron lesion). Fe2+ deficiency anemia should always
raise suspicion to colorectal cancer even if esophagitis & hiatus hernia
are present.
4) Gastric volvulus, due to twisting of a massive intrathoracic hiatus
hernia upon its self. Patient presents with severe chest pain, vomiting
and dysphagia. Diagnosis by CXR (air bubble in the chest) and
Barium swallow. Surgery is usually advised after nasogastric
decompression.
5) Barrett’s esophagus, it’s a pre – malignant condition where the
epithelium of the lower third of the esophagus is replaced by columnar
epithelium with areas of intestinal metaplasia.

▪ Diagnosis:
- Indications for endoscopy:
• Age > 55 years
• Symptoms > 4 weeks or persistent symptoms despite treatment
• Dysphagia
• Relapsing symptoms
• Weight loss
If endoscopy is negative then consider 24hr esophageal pH monitoring.
- 24hr esophageal pH monitoring is the gold standard test for
diagnosis.

▪ Treatment:
• Life style modification:

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 ✓ Weight loss
✓ Elevation of the bed head
✓ Avoidance of late meals, alcohol and smoking
✓ Avoidance of drugs that worsen the symptoms (nitrates,
anticholinergics, CCB)
• Drugs: Antacids or PPIs (e.g. lansoprazole). PPIs improve
symptoms and aid in healing of the esophagus, so they are the
drugs of choice.
• Surgery: Laparoscopic Nissen fundoplication in case of sever
GERD (confirm by pH-monitoring/manometry) if drugs are not
working, or if patients are intolerant to PPIs. The aim of the
surgery is to ↑resting lower esophageal sphincter pressure. Other
options:
▪ laparoscopic insertion of a magnetic bead
band
▪ Radio – frequency induced hypertrophy.

Barrett’s esophagus:
▪ It’s a pre – malignant condition in which normal squamous epithelium of
the lower esophagus is replaced by columnar epithelium (columnar lined
oesophagus, CLO) with areas of intestinal metaplasia as a result of
chronic GERD. This intestinal metaplasia looks velvety.
▪ It’s a major risk factor for esophageal adenocarcinoma (GERD → reflux
esophagitis → Barrett’s esophagus → dysplasia → adenocarcinoma)
▪ Treatment: (depends on dysplasia grade, so do biopsy first)
 In case of No/low – risk dysplasia: First line ttt is high dose of
PPIs for 8 – 12 weeks, then re – endoscopy.
 In case of High – risk dysplasia: cryotherapy (offers the most
promising results) or endoscopic resection.

Motility disorders:

1) Achalasia of the esophagus:

▪ Failure of esophageal peristalsis and of relaxation of lower
oesophageal sphincter (LOS) due to degenerative loss of ganglia from
Auerbach's plexus i.e. LOS contracted, oesophagus above dilated.

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▪ Infection with trypanosoma cruzi in Chagas disease causes a
syndrome that is clinically indistinguishable from achalasia.
▪ It’s a rare disease affecting 1:100000 people.
▪ Usually develops in middle life but can occur at any age.
▪ Achalasia predisposes to squamous carcinoma of the esophagus.
▪ Clinical features:
1. Dysphagia of BOTH solids and liquids. A long – standing
dysphagia for both solids and liquids suggests a functional (as
in achalasia) rather than mechanical cause of the dysphagia.
2. Vague chest pain, due to esophageal spasm
3. Nocturnal cough, due to nocturnal pulmonary aspiration of the
esophageal contents.
4. Heartburn does not occur because the closed LOS prevents
gastro – esophageal reflux.

▪ Investigations:
 Esophageal manometry: the gold standard test for
achalasia. It confirms the high-pressure, non-relaxing LOS
with poor contractility of the esophageal body (atonic
esophagus)
 Barium swallow: shows gross dilatation of the proximal
esophagus with smooth tapered narrowing of the lower
esophagus (typical bird’s peak appearance).
 Endoscopy: should always be done, why? Because carcinoma
of the cardia can mimic the presentation and radiological &
manometric features of achalasia (pseudo-achalasia)

▪ Treatment:
• Heller’s myotomy + anti-reflux procedure (e.g. partial
fundoplication), it’s extremely effective.
• Balloon dilatation
• Endoscopically directed injection of botulinum toxin, but
relapse is common. Reserved for the frail or elderly patient in
whom invasive procedures pose a high risk

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 • Other drugs (CCBs & nitrates), of no use because of their side
effects.

Extra notes:
Other diseases that can be diagnosed by manometry (Systemic sclerosis & diffuse
esophageal spasm)
▪ Systemic sclerosis:
• Either limited systemic sclerosis (CREST syndrome, 80%) or
diffuse (20%)

• CREST Syndrome:
• Calcinosis: calcified nodules in skin
• Raynaud’s phenomena
• Esophageal motility disorder
• Sclerodactily
• Telangiectasia
o On manometry: absent peristalsis + decreased LES
tone (note the difference between it and achalasia on
manometry).

▪ Diffuse esophageal spasm:

• “Arrhythmia of the esophagus”

• Chest pain due to sudden contractures (DDx: angina)

• Corkscrew appearance on barium swallow
• On manometry: abnormal contractures (may be normal
during episodes).

2) Pharyngeal pouch (esophageal diverticulae):

▪ Pharyngeal pouch is a posterior-medial herniation through Killian ‘s
dehiscence (the triangular area in the wall of the pharynx between
the thyropharyngeus and cricopharyngeus muscles)
▪ More common in elderly men
▪ Symptoms:
• Dysphagia is the prominent feature. It occurs after a few
swallow as the pouch fills with food
• Gurgling sound on swallowing
• Halitosis

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 • Regurgitation at night when patient is recumbent, may cause
cough and aspiration pneumonia.
▪ Treatment: surgical excision of the pouch & cricopharyngeal
myotomy.

Tumors of the esophagus

Leiomyoma is the most common benign tumor of the esophagus.

Carcinoma of the esophagus:
• Adenocarcinoma:
▪ The most common type
▪ Occurs in the lower (distal) third of the esophagus
▪ Predisposing factors are GERD & Barrett’s esophagus
• Squamous cell carcinoma:
▪ Occurs in the upper and middle thirds of the esophagus
▪ Predisposing risk factor: Achalasia, smoking, alcohol excess, hot
tea, tobacco, Plummer-Vinson syndrome, post-cricoid web, tylosis
(familial hyperkeratosis of palms and soles)
• Clinical features:
1) Dysphagia, progressive and painless, initially for solids then liquids.
2) Weight loss, is often extreme.
3) Chest pain or hoarseness suggest mediastinal invasion
4) Fistulation between the esophagus and the trachea or bronchial tree
leads to coughing after swallowing, pneumonia and pleural
effusion..
• Investigations:
▪ Upper GI endoscopy with cytology and biopsy is the investigation
of choice.
▪ Barium swallow: ‘shouldered’ stricture.
• Treatment:
▪ Surgery: the treatment of choice if the tumor is operable.
▪ Palliative care: when the disease is extensive and inoperable (70%
of cases). Treatment is based upon relief of dysphagia and pain
(palliation can be offered using radiotherapy, chemotherapy or with
the insertion of a stent for symptoms of dysphagia

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STOMACH

✓ Investigations:
- Barium meal
- OGD: oesophago-gastro-duodenoscopy
- EUS: Endoscopic Ultrasound
- CT and MRI

❖ H.pylori

it may cause
- peptic ulcer
-Gastric lymphoma (MALTOMA)
-Chronic Gastritis type B
(chronic gastritis type A : autoimmune gastritis = pernicious anemia)
Sites of Peptic Ulcer:
✓ Lesser curvature of the stomach
✓ First part of the duodenum
✓ Lower esophagus
✓ Jejunum in cases of Gastrojejunal anastomosis after ulcer surgery
✓ Ileum : Meckel’s diverticulum containing ectopic gastric mucosa
“remember rule of 2→ it contains 2 types of tissues Gastric and
pancreatic

Mechanism of peptic ulcer:

✓ Defect in the protective mechanisms “Mucosa” -→ occurs in gastric
ulcers
✓ Over-secretion of acid → in duodenal ulcers

Exacerbating factors in peptic ulcer:

✓ Stress: Curling ulcer with burn
Cushing ulcer with head trauma
✓ Smoking
✓ Alcohol
✓ NSAIDs

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 ✓ Steroids
✓ Hyperparathyroidism
✓ Zollinger-Ellison Syndrome
✓ Blood group “O”

Clinical Features:
✓ Duodenal ulcer

Hunger pain relieved by food

Anterior duodenal ulcer tend to perforate, while the posterior duodenal ulcer
tends to bleed because the gastroduodenal artery lies behind the duodenum.
✓ Gastric ulcer:

Pain after meals relieved by vomiting

Wt loss because the patients tends to avoid eating due to pain
✓ Other features:
✓ Nausea and vomiting
✓ Iron deficiency anemia
✓ Epigastric tenderness
✓ Haematemesis or malena
✓ Healing by fibrosis → acquired pyloric stenosis

Diagnosis of peptic ulcer:

✓ General investigations
✓ Stool Ag test
✓ Urea breath test
✓ Serum gastrin level “ if zollinger-Ellison is suspected”
✓ OGD and biopsy → diagnostic

Management :
✓ Life style modification
✓ Medical treatment:
✓ Anti-acids ; relieve the pain but are of limited value
✓ Proton pump inhibitors; reduce acid secretions
✓ Eradication therapy for H.pylori ;
Either triple therapy “ PPI + clarithromycin+ metronidazole or
amoxicillin”
Or Quadrable therapy “PPI+ bisthmus + tetracycline + metro”
✓ Surgery : indicated in
✓ Failure of medical treatment

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 ✓ Complications :haemorrhage , perforation, pyloric stenosis
✓ Intractable pain interfere with the patient life and daily activities

Types of surgery:
✓ In the past: vagotomy and drainage, highly selective vagotomy
✓ Nowadays:
- pyloroplasty with oversewing of bleeding duodenal ulcer
- partial gastrectomy for bleeding gastric ulcer

Types of partial gastrectomy:

Complications of Gastrectomy:
1- Diarrhea after each meal : codeine phosphate and small dry meals may
help, Less after selective vagotomy
2- Dumping :

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 Early dumping: the patient develop hypotension after meals due to
sequestration of fluids in the intestine caused by the osmotic effect of the
food
Late dumping: hypoglycemia 1 to 3 hrs after meals, → food goes directly
into intestine → rapid absorption and rapid increase in blood glucose →
high insulin secretion → insulin have long half-life it decrease slowly
causing hypoglycemia
3- Epidastric fullness
4- Recurrence of ulcer: Zollinger-Ellison and hypercalcemia should be
excluded
5- Gallstones : vagotomy may cause bile stasis
6- Anemia: iron deficiency anemia due to reduced Hcl
And megaloblastic anemia with total Gastrectomy due to loss of intrinsic
factor
7- Wt loss
8- Steatorrhea due to poor mixing of food with enzymes
9- Bolus obstruction
10- Risk of gastric carcinoma.

• Clinical presentation of perforated peptic ulcer:

Sudden onset of sharp stabbing localized severe epigastric pain “chemical

peritonitis”
The the pain disappear “dilution of acid and omentum reaction” and reappear
again as generalized abdominal pain with guarding and fever “bacterial
peritonitis”
Later on the pain concentrate on the right iliac fossa → the fluid and pus will
collect in the right iliac fossa by the action of gravity (DDx acute appendicitis)
On examination:
✓ Rigidity, guarding and tenderness
✓ Loss of liver dullness and resonant percussion → air under diaphragm

Investigations:
✓ Erect X-ray : air under the right diaphragm ( left diaphragm is not
considered because stomach on the left normally contain air)
✓ CT scan
✓ Serum amylase to exclude acute pancreatitis

DDx of air under Diaphragm:

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 1- Perforated viscus
2- Post-operative “especially laproscopic operations”
3- Sub-phrenic abcess
4- Trauma
5- Other causes

Management :
1- Admission and resucitation
NPO antibiotics
Iv fluids NG tube
Analgesia Catheter for fluid monitoring
2- Emergency laproscopy : suction and peritoneal lavage
3- If perforation at stomach:
✓ Suture and reinforcement with omental patch
✓ Injectable PPI and continue orally after surgery
✓ Upper GI endoscopy after 6 wks to make sure that ulcer heals completely

Complications of Peptic Ulcer:

1- Perforation
2- Bleeding
3- Healing by fibrosis → Pyloric stenosis
• Gastric outlet obstruction: presents as
✓ projectile non-bilious vomiting
✓ dehydration
✓ hypochloremia “loss of HCl
✓ hypokalemia
✓ paradoxical acid urea

On Examination:
✓ abdomen is distended
✓ visible peristalsis→ more reliable in children
✓ on auscultation: splash sound

Investigations:
✓ endoscopy - Barium meal

Management:
✓ NG-tube and suction
✓ Correction of electrolyte imbalance
✓ Pyloroplasty or Gastro-jejenostomy+ vagotomy

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 ❖ Gastric Carcinoma:

Associated with:
✓ High socioeconomic status - Gastrectomy
✓ Chronic Gastritis type A
✓ gastro-jejenostomy due to biliary reflux
✓ Blood group A
✓ Smoking and alcohol
✓ Diet : low fiber, more nitrate and nitrite
✓ Adenomatous polyps
• Signs :
✓ Early satiety → early sign
✓ Epigastric pain + alarm symptoms
✓ Lymphadenopathy :
Supraclavicular: Virchow node
Para-umblical : sister mary jousif
• Macroscopic types of the cancer;

Polyp , ulcer and diffuse “linitis plastic”

• TNM Stagging:

T1 : cancer involve the mucosa and submucosa

T2 : the muscular layer
T3 : serosa
T4 : adjacent organs
N0 : no lymphatic involvement
N1 : < 7
N2 : 7 to 15
N3 : > 15
M0 : No metastasis
M1 : distant metastasis
• Spread by:
✓ Local invasion: to the duodenum, pancreas , spleen
✓ Lymphatics
✓ Blood : to the liver
• Management :
✓ If the patient presents early treatment will be curative surgery

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 • Distal tumor: Billroth type 2 ( duodenal stump + Gastrojejunostomy +
vagatomy)
• Proximal tumor : Rouex-Y operation → ( total gastrectomy +
splenectomy + radical lymphadenoctomy + distal pancreatectomy +
oesophago-jejunostomy and duodenal stump)
• If the tumor is in the cardiac part patient presents with dysphagia
Palliative management : feeding jejunostomy
• If the tumor is advanced and distally causing gastric outlet obstruction →
gastro-jejunostomy
• Gastric cancer can spread to the ovaries via transcoelomic route →
krukenberg tumor

❖ Zollinger –Ellison Syndrome:

✓ Gastrinoma
✓ Multiple gastric ulcers resistant to treatment
✓ 40% are malignant
✓ Part of MEN 1 “Multiple Endocrine Neoplasia type 1”

Investigations:
✓ Fasting Serum gastrin level
✓ CT scan
✓ Angiography

Management :
✓ Excision if liver mets not occur
✓ If tumor is advanced: - PPI to control acid
-total gastrectomy “rarely”

❖ GIST “Gastro-intestinal Stromal Tumor”

✓ Vary from benign to high grade malignant

✓ Present as : - epigastric discomfort - indigestion
-hematemesis or malena

- investigations : OGD and CT scan

- Management : surgical excision
Imatinib “tyrosine kinase inhibitor”

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• Other causes of Hematemesis:
✓ Oesophageal varices → Portal HTN
✓ Mallory-weiss syndrome
✓ Gastric carcinoma
✓ Portal hypertension gastropathy
✓ Aorto-enteric Fistula
✓ Bleeding disorders
✓ Drugs : steroids, NSAID, Anticoagulants
• Management of hematemesis:
✓ ABC
✓ Two wide bore cannula
• Blood sample for :CBC, Blood grouping and cross-matching,
coagulation profile
• Iv fluids → Ringer lactate
✓ Monitor the vital signs : pulse, BP, CVP, UOP
✓ NG-tube :
• to remove blood from the stomach ; if blood remain in the stomach
this will result in high ammonia production which will lead to
encephalopathy
• and to estimate the blood loss
✓ to stop the bleeding :
• Endoscopy :
Sclerotherapy
Rubber band ligation
TIPS: Trans-jugular -Intra-hepatic Porto-systemic shunt
• Sengstaken tube + vasopressin
• complications of Sengstaken tube:
✓ Aspiration pneumonia “the most common”
✓ Mucosal necrosis
✓ Prophylaxis : give B-Blockers
✓ Indications for surgical intervention:
✓ Massive uncontrolled bleeding
✓ Re-bleeding
✓ More than 4 units bleed in 24hrs unless the cause is varices.

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 Small and Large Bowel
❖ Carcinoid Syndrome:
Is benign tumor arising from entero-chromaffin cells in the intestine .
The most common sites are terminal ileum and appendix
Macroscopically it appears as yellowish mass.
It secrete serotonin → leads to systemic symptoms ( hot flashes ,
Diarrhea , wheeze)
Carcinoid tumor + systemic symptoms = Carcinoid syndrome
Metastasis mostly to the lung and liver
It also can arise in the lung and anywhere in the GIT
• Diagnosis:
- CT scan
- 5-Hydroxyindole Acetic Acid in the urine (metabolite of
serotonin)
• Treatment:
If <1 cm → local resection
If >1cm → extensive resection “right hemi- colectomy = removal
of the terminal ileum, appendix, cecum, ascending and part of
transverse colon”
If there is liver mets → resect the liver mets

❖ Angiodysplasia:
Angio = blood vessels
Dysplasia = abnormal
Angiodysplasia is capillary hemangioma arise in the bowel wall
It usually arise in the ascending colon and cecum
It is usually submucosal , if you do colonoscopy you may not find the
lesion

• Presenting complain: rectal bleeding and malena

Usually it associated with aortic stenosis and von-will-brand disease

• Investigations:
- Colonoscopy - CT scan with Contrast
- Mesenteric Angiography “the best”

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 • Treatment:
- If seen on colonoscopy → laiser, diathermy, cautery
- If bleeding is massive→ surgical resection

It can be congenital or acquired

o Congenital: called Meckel’s diverticulim

usually single
Arise from the ileum
Involve the full thickness of the bowel wall
✓ The Rule of 2:
- In 2% of people
- 2 inch in length
- 2 feet from ileocecal valve
- 2 types of tissues “ gastric / pancreatic”
- 2 common complications “ inflammation and perforation/ rectal
bleeding”
In the presence of inflammation it called Meckle’s diverticulitis and it
presents with para-umbilical pain that shifted to Right iliac fossa (DDx :
Appendicitis)

If not treated → perforation → peritonitis

One of the commonest causes of massive rectal bleeding in children

✓ Diagnosis:
Meckel’s technetium scan
✓ Management:
- If inflamed or impend to perforate do excision and anastomosis
- If discovered accidently during another surgery remove it if:
It was longer than 5 cm
Has wide base > 2 cm
Multiple diverticula also can arise from jejunum causing mal-absorption “not
common”

✓ Complications:
- Intussusception
- Intestinal obstruction by congenital bands

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 o Acquired “Diverticulosis”:
90% involve the sigmoid colon
multiple
Arise from colon
Only mucosa
Acute diverticulitis presents as:

- Severe abdominal pain in the left iliac fossa

- Guarding , rigidity, and tenderness
- Palpable sigmoid colon
- Rebound tenderness
It is similar to acute appendicitis so it called “ Left-sided appendicitis”

✓ Diagnosis:
US
CT scan
Barium enema “ saw-teeth appearance”

✓ Management:
Mainly conservative
- Admission , NPO
- NG Tube
- Analgesia
- Antibiotics → cephalosporin + flagyl
- IV fluids
- Monitoring
✓ Complications:
1- Perforation:
- Release of feces will lead to fecal peritonitis
- Mortality is very high
- Management:
Laparotomy → peritoneal lavage → resect the area of
perforation and do colostomy
2- Chronic inflammation : leads to formation of fistula
- External fistula
- Colo-vesical fistula: between the colon and urinary bladder ,
patient will complain of :

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 Fecolurea and pneumaturea “bubbles in the urine”
3- Massive rectal bleeding:
Diverticulosis is the most common cause of massive rectal bleeding in
adults.

Diverticular disease + GERD+ Gallstones = Saint’s triad

❖Chronic illnesses;
disease of relapse and remission
1. Crohns disease:
Can affect all the tract from mouth to anal canal sparing the rectum
• Mouth ……aphthus ulcer
• Esophagus …..stricture
• Intestine ……commonest site ;(ulcer, stricture, granuloma)
• Large bowel….rectal bleeding
• Anus …..fistula, abcess.
*note:
- characterized by skip lesion ; so difficult to control by surgery.
- affect all layers (trans mural)
2. Ulceritve Colitis (smoking is protective ):
* Affect colon only specially rectum
* cause multiple ulcer in mucosa and multiple abscess in the sub mucosa (crypt
abscess ) , inflammatory pseudo polyps .
* do not affect the mussels and serosa
* can be controlled by surgery
* can affect the ileum , causing back wash ileitis
* presentation:
- bloody mucoid diarrhea
-painful deification
- sense of incomplete evacuation …..similar to rectal cancer

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 ✓ Complication of IBD:
1. medical:
✓ extra intestinal manifestations;
- iritis , scleritis , uveitis
- erythema nodosum , byoderma gangrenosum
- ankylosing spondylitis
- primary sclerosing cholangitis , auto immune hepatitis .
2. surgical :
1- perforation ---→ mainly with Ulcerative colitis
2- massive rectal bleeding --→ with ulcerative colitis
3- intestinal obstruction --→ with crohns disease
4- abdominal masses and adhesions ---→ crohns
DD. of right iliac fossa masses:
✓ crohns disease
✓ appendicular mass
✓ Ca of the cecum
✓ abdominal TB
✓ ovarian pathology
✓ psoas abscess
✓ pelvic kidney , transplanted third kidney
✓ un descended testes….. examine scrotum
5- malabsorption …crohns
6- cancer :
Ulcerative colitis is a precancerous condition
metaplasia( need follow up with colonoscopy ) --→ low grade dysplasia
(do laser diathermy, cautery ) --→ high grade dysplasia(prophylactic
colectomy ) --→ neoplasia .
7- toxic mega colon :
is an emergency complication of ulcerative colitis (pt , present to the
casualty w/ severe abdominal pain ,distention , pt is toxic ill and febrile

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 ,O/E abdomen is hyper resonant . on A Xray dilation o large bowel and
rectum ) managed conservatively and serial x- ray monitoring.

✓ Investigation:
General : CBC: anemia, proteins (low).
Specific:
✓ Barium enema (loss of haustration in ulcerative colitis)
✓ colonoscopy , sigmoidoscopy(reach splenic flexure)
✓ biopsy for suspected cancer.

✓ Management:
- medical management if pt is stable and no cancerous change
(Aminosalysilates (mesalamine) ,corticosteroids orally or topically)
- In acute crisis (emergency) give methylprednisolone IV.
-crohn fistula give infliximab.
- If medical treatment fail the condition complicated go for surgery mainly in
ulcerative colitis.
✓ Indications:
1-failure of medical management to control disease.
2-Development of complication (toxic mega colon , cancer , perforation)
3- Long standing pan colitis with biopsy show dysplasia.
4-Stricture formation.
A- Total colectomy with ileo- rectal anastomosis(pt will have persistent
diarrhea) or ileostomy+ rectal stum
B- panproctolectomy : colon +rectal with ileoanal anastomosis.

❖Colo -rectal cancer:

• Colon cancer, Rectal cancer , Anal cancer.
• Five years survival is improving nowadays
• Risk factors divided in to:

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 1. Acquired:
dietary factors ( low fibers ,nitrates, increased animal fats) , and smoking
2.Hereditary:
hereditary polyposis and hereditary non polyposis.
a) Hereditary polyposis;
* can be adenomatous, hamartomatus ,inflammatory
*polyp can be villous , tubular or tubule villus(the only precancerous)
- Solitary villous adenoma : is a polyp develop into cancer by “adenoma
carcinoma sequence”
- FAP “Familial Adenomatous Polyposis”:
> 100 polyps
Due to mutation in chromosome 5
If detected early do Prophylactic colectomy
✓
b) Hereditary non polyposis;
Related to specific genes; BRCA, ABC, P53
Others; ulcerative colitis, utero colic anastomosis
❖ Pathology:
75% of cancers in the left site
• Gross Types:
✓ Annular type; constricting cancer ,(stricture /narrowing) is the
commonest in the left side.
✓ Ulcerative type , right sided.
✓ Tubular type
✓ Cauliflower like polyploidy , in the cecum.
all types are adenocarcinoma arise from columnar epithelium.
• Presentation:
depends on the side and type of cancer
✓ left sided tumors :
- Intestinal obstruction,

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 - Change in bowel habits ,
- Rarely fresh rectal bleeding mixed with stool
✓ Right sided tumors;
- Melena
- Iron deficiency anemia in elderly.
✓ Rectal tumors;
-Rectal bleeding
-tinsmus
-in advance stages ;mass and intestinal obstruction.
• Examinations:
General : pallor ,Virchow node , jaundice, inguinal lymph nodes
Abdominal : distention ,palpable mass , palpable liver, Ascites
PR: may feel mass , lymph node, blood.

• Spread;
1. Direct “local spread “:
• to the wall and neighboring cecum and small intestine, Then to organs;
Transvers colon -→ to the stomach (casing gastro colonic fistula , and the
pt, present with fecal vomiting)
• Ascending and descending colons >>to the ureter and lead to renal failure
• Sigmoid -→ to bladder casing colo- vesical fistula and the patient present
with hematuria , fecal urea.
2. lymphatic , superior and inferior mesenteric lymph nodes 40% of cases.
3. blood, mainly to the liver.
4. trans peritoneal, casing nodules and ascites.
• Staging;
1. TNM staging ;
T:
T1; invades in to the sub mucosa T2; in to mucosa

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 T3; to sub serosa T4; serosa and other organ
N:
N0 : no lymph node N1: 1-2 nodes
N2: 3or more
M:
M0 ; no metastasis M1; metastasis

2. DUKES staging ;(‫( مهم يحفظ‬

A) tumor confined to the wall = 90% five years survival
B) invade the wall and spread to organs =70% five years survival
C) spread to lymph node = 40% five years survival
D) metastasis via blood = 10% five years survival

• Investigations;
1. General investigations ; look for anemia
2. Tumor markers ; prognostic rather than diagnostic.
3. Barium enema ;( contrast radiograph) ; apple core sign
4. PR-→ sigmoidoscopy -→ colonoscopy ---→biopsy
(* Note ; synchronized tumors 5% of cases -→ arise at same time , while
metachronized tumors arise at different times)
5. LFT , abdominal US , CT, IVU ,CXR for mets .
6. MRI / endorectal US ; to assess depth of invasion.
• Treatment;
Duck A& B aim of ttt is curative .
✓ Surgery:
Colonic surgery require bowel preparation ;
- Mechanical preparation ; phosphate enema

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 - Chemical preparation; laxative ( lactulose) ; antibiotics (neomycin
,flagyl ) ; receive fluids only 2-3 days before surgery.
✓ In case of obstruction ;( emergency operation ) :do on table lavage ,
resection and anastomosis.
✓ In elective operations , inspect for ; liver mets , ascites : contra -
indicate surgery.
✓ Right hemi colectomy and ileo- colic anastomosis
✓ Transvers colectomy.
✓ In left side ; resection and anastomosis , in emergency operations do
colostomy then anastomosis.
✓ In advance cases ; chemo radiotherapy --→ C5 flurouracil +folenic
acid

• Complications ;
1. intestinal obstruction in 20% of left side tumors (due to a) smaller lumen of
left colon ,b)stock tend to be solid , c) carcinoma tend to be of stenosing type).
2.perforation ; entero colic or vasico colic fistulas.
3.bleeding ; mainly chronic
4.complications of spread ; jaundice , ascites , liver failure , rectal cancer
common in males ,cecum on females.
• Treatment ( ‫;)القصر العيني‬
Surgery is the main treatment
✓ Radical resection for operable cases
✓ Tumor resection for non operable.
Treatment depends on ;
✓ Whether present with acute obstruction or not
* note ; acute obstruction do tumor resection + colostomy+ later
anastomosis.
✓ Tumor is operable or not
➢ Inoperable tumors ;: liver mets , peritoneal nodules , fixation to important
irremovable structures --→ do palliative resection ; remove only tumor.

➢ Operable cases : No obstruction

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Elective radical resection → include ; removal of the tumor segment +
lymphatic drainage + ligation and division of the blood vessels at their origin+
ileotransvese anastomosis.
A) Cecal tumors → right hemi colectomy + ileocolic and right colic vessels
divided at origin +ileo transvers anastomosis.
B) Ascending colon tumors → extended right hemi colectomy (at the junction
of right 2/3 and left 1/3 of the colon)+ above vessels and middle colic vessels .
C) Transvers colon → transvers colectomy + middle colic vessel removal
D) left colon → left hemi colectomy + inferior mesenteric vessels divided at
their origin.
E) Sigmoid → sigmoid colectomy + sigmoid vessels.
F) Upper 1/3 of the rectum tumors → anterior restorative resection ( anterior
mesenteric artery divided +sigmoid and upper half of the rectum removal +
restore bowel continuity )
G) Lower 1/3 of the rectum → abdomino perineal resection ; as above on (F)+
whole rectum + anal canal+ terminal colostomy.
H) Middle 1/3 rectum tumors , same as (G).

✓ worse prognostic factors:

1- Young age at presentation
2-Colonic obstruction or anastomosis
3-Blood vessels or lymphatic invasion
4-Liver or distal mets
5- Aneuploidy

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Intestinal obstruction

Intestine is a tube which have proximal and distal parts .

Causes of intestinal obstructions are :-

• Exta-mural cause
• Intramural cause
• Intra-lumenal cause
1. Extramural cause :- AHIV
i. Adhesions ( the most common cause)
ii. Hernia
iii. Intussueptions
iv. Volvuls
1. Adhesions :-

Adhesions is the most common cause of small intestinal obstruction in young

patients .
Adhesion is fibrous tissue that formed Frome :-
• Previous surgery
• Peritonitis
2. Hernia :-

Can be external hernia or internal hernia

Internal hernia :-
-retrocecal recess -epiplotic foramane intrapment ( EFE)

3. Intusepsion :-
The proximal segment of the bowel invaginate in the distal segement due to
excessive peristalsis , the led point (the origin of peristalsis) it can be:-
-Lymph node “ the commonest in intestine “
-Appendix
-Meckel’s diverticulitis .
□Note :
-Lymph node: arise inside the lumen of intestine ,common in winter in children
(5-10 months) with URTI ; because children with tonsillitis swallow their sputum.
-intusepsion in elderly (60-70 years) led point may be tumour
- if appendix is the lead point -→ this lead to ileocolic or ileocecal intussception
(the ileum enter the cecum )

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- if it is meckle’s diverticulum -→ ileo-ileal intussception
- if tumor → colo-colic intussception.

4. Volvulus:-
Twisting of the bowl around its mesentery .
This can obstruct the blood vessels that supply the bowel .
It occurs due to :- (predisposing factors)
1. Bowel is overloaded : chronic constipation .
2. Adhesion at the apex of sigmoid loop
3. Narrow base of sigmoid mesentery.
4. Redundant mesentery ie; abnormally long .
90% 0ccurs in sigmoid colon, it’s disease of elderly

B. Intra-mural causes :-
1-Tumours :-
“ in elderly “ ,( old pt. With intestinal obstruction ; volvulus or tumour)
It can be benign malignant or lymphoma .
2- strictures:-
-Crohn’s disease -TB of the bowel -radiation
C. Intra-luminal causes :-
1. Gallstone ileus
2. Worms ; Ascaris
3. Froing body.
➢ Gallstones ; obstruct the narrowest part of ileum which is 2 feet from ileo-
cecal junction , it reach the ileum leading to chronic cholycystitis then
fistula “ cholycysto-entric fistula”

✓ Clinical picture :-

1.Colicy abdominal pain “on and off pain”

2. Vomiting
3. Absolute constipation
4.distension
- the proximal part of the intestine become dilated by food, gas , secretions and
fluid sequestration and the distal part is collapsed .
-Orders of symptoms differs :-
●small bowel :- start with vomiting “ileo-vomiting” pain around the umbilicus
(because bowel is part of the midget) pic. Umbilical pain, pt. Continue passing
stool , constipation occurs later .
●large bowel :- start with early constipation, distension colicky lower abdominal
pain ( because it’s part of hindgut ) then vomiting lately.
- in large bowel distension is obvious .

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- in ER : pt. is in pain , dehydrated because of fluid sequestration “3ed space
loss , 4-5L can be lost” , lethargy , dry tongue , dry mucus membrane ,sunken
eyes ,rapid weak pulse ,hypotensive .

❖ On examinations:-
➢ inspection and palpation :-
Abdomen is distended with visible peristalsis, tender look for previous
surgery and hernia
➢ percussion:-
Resonant, hyper-resonant (tympanic abdomen)
➢ Auscultation :-
Bowel sounds are exaggerated. “normal is 3-5 B.S/M”
➢ Rectal examination :-
Rectum is collapsed .
➢ absolute constipation even no flatus ( in cancer and some types of hernia
and gallstones ileus constipation is not absolute )

➢ Specific clinical features :-

●Intusussception; child present with colicky abdominal pain , episodic

screaming attacks , drawing the leg to the abdomen, current jelly stool ie; “stool
+ mucus”.
When examining the bowel :-
One side of the abdomen is empty right ilea fossa sign de Dance , left side bulging
or mass sausage shaped mass , on PR bloody meconium in 60% of cases or head
of intusscepsion can be felt .
●Volvulus:-
in elderly recurrent attacks of bowel obs.

❖ Complications of intestinal obstruction :-

1. Hypo-volumic shock .
2. Strangulation and ischemia.
3. Electrolytes disturbances (mainly hyperkalemia) and renal failure
4. Septic shock and peritonitis .
❖ Diagnosis :-

Mainly depends on : abdominal X rays “erect and supine”

-supine =air (gas) - erect= air fluid levels .
How to differentiate small/large bowel obstruction on X rays :-
●small bowel :- 1- air fluid level central on X rays

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 2- valvulae conniventes (circular mucosal folds)
3- cecum is collapsed
●large bowel :- 1. air fluid level is peripheral 2. Haustre of large bowel seen on
X ray 3. Cecum is dilated .
Note:- any normal person on X ray has 3air fluid levels :-
1. Stomach 2. First part of the duodenum 3. Cecum
So if it’s > than 3 it’s abnormal .
● intussepsion :-
1- blood : anaemia
2- Baruime enema : clue sign
3- Abdominal U/S : Target sign
●volvulus :-
diagnosed by X rays inverted U sign coffee bean sing .
●Gallstone ileus :
on x-ray you will find Regler triad :
1. Right iliac fossa opacity.
2. Central air fluid level + valvulae conniventes-→ small bowel obstructions.
3. Air in biliary tree( pnemo-bilia)-→ cholycysto-entric fistula.
• Closed-loop obstruction :-
It occurs In case of colon obstruction with competent ileocecal valve where rising
pressure in the closed proximal colon cause perforation of the cecum.
❖ Treatment :-
1. Resuscitation:-
1. Admission
2. NPO
3. IV fluid (Ringer)
4. Antibiotics.
5. Analgesia.
6. NG tube “for1- fluid suction to prevent aspiration ;2-it can
relive obs. In case of adhesions “
7. Catheterization . Urinary catheter.
– adhesive obs management is conservative for 72 h ( up to 2 weeks if pt is
managed in ICU) if not improved go for surgery
2. Surgery :
●Adhesion : adheso-lysis
●intususscpsions :
- Milking: head of the intussception is squeezed backward from the containing
colon.
- In early cases reduction by hydrostatic effect of barium enema
Look for sign of ischemia MBCPPC.
• Mobility
• Bleeding

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 • Color (pink)
• Pressure in
• Peritoneum
• consistency
➢ if Bowel is dead do Re-secsion and anastamosis
• intussception in elderly : Re-secsion and anastamosis +histopathology
• Volvulus :- un twisting + sigmoidopexy -> old procedure
Resection + anastamosis / colostomy -> new
• Gallstone ileus :- enterotomy ,remove the stone
Fistula -> plan for elective surgery .
➢ For GI surgery pt. Should fast until you hear bowel sound
➢ If pt. Complain of symptoms of obstruction after surgery -> paralytic
ileus.
➢ Paralytic ileus :- in small bowel
Non mechanical obstruction :-
• All the bowel is dilated .
• PR : rectum is full with stool .
• Management is conservative :- fasting ,IV fluid , antibiotics ,
electrolyte balance , walking .
➢ Mesenteric ischemia :-
Can present as intestinal obstruction .
- Acute abdomen
- Can be acute or chronic
- -mainly occurs in small bowel “superior
Mesenteric artery “ supply all mid gut till part of
transverse colon .
- Cause of acute obstruction :-
thromboembolism “pt. With arrhythmia AF “
- Pt. Present with sever abdominal pain ,
continous para amblical and abdomen is very
tender , blood in stool .
✓ Investigation :-

1. Doppler
2. Mesenteric angiography
3. Emergency CT abdomen
✓ Management:-

1. Admission
2. Resucitasion -> IV + heparin
3. Surgery -> emobloectomy “if bowel is alive”
If bowel is dead you have to leave 1m or more of the bowel

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complication :-
A. “short bowel syndrome if bowel <1m malabsorption “
B. entero-cutanous fistula .
➢ Treatment of short bowel syndrome :-
➢ TPA by central line , it has complications :-
1. Line complications ; sepsis bleeding , pneumothorax ,hemothorax
2. Complication of the solution :- hyper-insulinism ->hypoglycaemia
3. Gallstone formation -> due to bile stasis .
• Chronic ischemia :- due to atherosclerosis
- Patient present with post – prandial angina
(Claudication)
- Management = aspirin or clopidogrel
❖ Strangulation:-

Is suspected by:-
1. Toxic pt. ,tachycardia ,fever ,leucocytosis .
2. Evidence of blood loss ,pallor hypotension.
3. Pain not relieved by NG suction ”ischemic pain” .
4. Marked tenderness ,rebound tenderness , rigidity.
✓ Treatment :-

Conservative or surgery
✓ Conservative :-
1. Adhesion : IV drip and NG suction.
2. Ileo cecal intussusception:- hydrostatic effect of barium enema .
3. Volvulus : rectal tube passed through sigmodoscope .
❖ Paralytic ileus :-

Aetiology :-
1. Reflex inhibition of intestinal motility after abdominal operation ,
spine fracture , retro-peritonel haemorrhage (sympathetic over Act)
2. Metabolic abnormalities : hypokalemia ,DKA ,uremia ,
3. Peritonitis : direct toxic effect on nerve plexus
4. Drugs : anti cholonergic ,TCA
✓ Clinical pic :-

- Symptoms : distension, absolute constipation

,effortless vomiting, no colicky pain .
- Sign : silent abdomen “no bowel sound “

Acute Appendicitis

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Acute appendicitis is the most common cause of acute abdomen in young ad
ults ( school age -10years)

The appendix arise from the cecum , the mesoappendix containta blood supply ,
no rule of 2 ,it's a midgut organ ( referred pain T10 sympathetic system ) , the b
ase of the appendix 2 cm distal to ileocecal valve .

Position: => tail position

-retrocecal (most common) -> the tip of theappendicitis behind the cecum
-pelvic -> close to rectum / bladder /female uterus
-paracecal
-subcecal
-paraileal -> either periileal ( in front of the ileum ) or postileal ( behind the ile
um )
-subhepatic ->radiate to the right hypochondriac area ( long tail behind the liv
er .

❖ Pathophysiology =>

1/obstruction of the appendix lumen .

i- lymphoid tissue enlargement -> children / history of URTI (recurrent viral i
nfection ) / following by swollen of the sputum -> irritation & enlargement of ly
mphoid tissue of the appendix -> 2-Sequence of inflammation
Vein compression -> swelling -> oedema -> bacteria -> appendicular artery co
mpression ( which is end artery ) -> gangrenous/necrosis -> acute perforation (
at the tip of the appendix ) / peritonitis
ii-tumor in the cecum -> compress the appendix -> c/f ( above 40yrs , typical f
eature of appendicitis)
iii-fecolith -> stool cause perforation in the base of the appendix
iv-warm -> ascaris

❖ Clinical features:

Start by central periumblical colicky abdominal pain ( bcuz it’s organ of mid
gut )

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-anorexia / fever
-nausea or vomiting once or twice (vomiting is a protective mechanism due to
pyloric spasm ) , when inflammation involve the peritoneum shifting of pain
to the right iliac fossa ( and periumblical pain disappear )
-diarrhea and urinary symptoms =pelvic appendicitis ( tender PR)

O/E: slight fever ,tachycardia ,flushed face , fetor oris ,furrowed tounge (is
seen also in melkerson rossenthal syndrome which is one of the causes of fa
cial palsy ) , smelly mouth and coated tongue ( bcuz put don’t eat )
Abdomen:
1/tenderness in the right iliac fossa (Mcburney's point where the base of the
appendix located ) -> is the junction btw medial 2/3 & lateral 1/3 btw the umbli
cus and anterior superior iliac spine .

2/Rebound tenderness the pain increase when u left ur hand from his abdomin
al -not mandatory-) , guarding (voluntary ) , rigidity (involuntary ) (wall can't
be indented)

3/Point sign(finger in Mcburney's point) => the pt point exactly to the point o
f the pain by one finger

4/Rovsing sign (pushing air) => palpate the left iliac fossa then the pt may feel
pain on the right iliac fossa

5/Psoas sign= retrocecal appendix =extension of the hip causes pain

6/Obturator sign=pelvic appendix =flexion and internal rotation of hip

7-Fever +rigidity +high TWBC =perforation

▲/▲ : -diverticulitis
-meckel's diverticulitis
-ureteric colic ( stone in right ureter )
-ectopic pregnancy ( history of amenorrhea)
Other gyne conditions ( e.g. Salphingitis / ovarianschist accident - torsi
on/ rupture / haemorrhage - )
-mesenteric lymphadenitis
-yersinia enterocolitis

✓ Note : Mechel’s diverticulitis

- tube like an appendix arise from the terminal ileum

- Not attach to mesentry ( Amesentry )

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- Rule of 2 :
2% of people affected a round the world /
2 Inch in length (5cm) /
2 ft from appendix (30cm) /
2 types of ectopic tissue (e.g. Gastric and pancreatic tissue ) /
2 complication ( bleeding / inflammation , perforation , ulceration )
- same clinical feature as appendicitis ( periumblical abdominal pain -> shifting
to the Rt iliac fossa
-ttt : resection

Alvarado score: if > 7 = appendicitis , if 10 = perforation

Symptoms:
-shifting to the right iliac fossa pain 1
-anorexia 1
-nausea/vomiting 1
Signs:
-tenderness in the right iliac fossa 2
-rebound tenderness (+ve ) 1
-high temperature 1
Lab:
-leuckocytosis 2
-leukocyte shift ( segmented neutrophil in PBF ) 1

Tx: resuscitation of acute Abdomin =appeniciectoomy

Treatment of acute appendicitis is acute appendiciectomy

US only in females to exclude gyn. Conditions ( if the female is pregnant & th
e inflamed appendix close to the uterus -> can induce preterm labor )

The 1st step in theatre after GA is to examine the abdomen looking for app
endicular massn (u can feel the mass bcuz of muscle relaxation) =contraindica
tion for surgery ( wake up the patient)

incision: at Mcburney point

1/gridirioon incision -> vertical incision / if there is other DD ( perforated pepti
c ulcer ) or subhepatic appendicitis .
2/lanz incision -> transverse incision / the best ( cosmetic - healing wise )
** Morison incision -> extended gridirioon incision .

Appendiccular abscess:
More than 3 days patient develop swinging fever +mass

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Dx: US , CT scan
Tx: antibiotic and drainage

Appendicular mass: ( hard mass)

The omentum rapped around an inflammed appendix and cecum which lead to fi
brosis .
Tx: is conservative iv fluids , antibiotic (IV -5days- then oral - 4-6days-) , foll
ow up , after making it
If opened immediately will lead to bleeding / resection sedum and part of the bo
wel .
Decrease in size ( inflammatory mass which can resolve) => elective appendic
ectomy after 4-6 weeks called (interval appendicectomy )

Complications of appendicitis:
1-adhesions = intestinal obstruction = subinfertility = ectopic pregnancy (tu
bal opstruction)
2-intraabdoominal abscess
3-fistula to the skin /fecal fistula
4-Jaundice ,multiple liver abscess (abscess drain by portal vein and affect the
liver )
5-Peritonitis
6-Indirect inguinal hernia ( due to loss of integrity of ilioinguinal canal bcuz of
injured ilioinguinal nerve intraoperatively )
7-Urine retention ( bcuz of the pain )

Hemorrhoids

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-it dilated anal cushions
-anal cushion (normal mucosal tissue in the anal canal at position 3,7,11 o’clock)
Type;
1-primary (true) hemorrhoids: from anal cushion at 3,7,11 o’clock.
2-secondary hemorrhoids: any dilation in any area other than (3, 7, 11).
3-false hemorrhoids: perianal hemorrhoids.
Cause:-
-constipation
-HTN
-pelvic mass (rectal, uterus, pregnancy).
Main complication:
-rectal bleeding (fresh, after deification, painless)
-itching
Grade:
-grade 1: bleed only
-grad 2: bleed and prolapsed and return spontaneously
-grad3: prolapsed and require manual reduction
-grad 4: bleed and prolapsed permanently.
Examination:
-general, abdomen, PR
-proctoscopy
- Sigmoidocopy: to exclude other lesion
-colonscopy: if there is any doubt

Complication:
-strangulation (painful)
-infection, abscess formation
Treatment:
-Grad 1, 2: -conservative management, high fiber diet, laxative
- Sclerotherapy: injection of STDs (Na tetraethyl sulphat)
-band ligation
Grad 3, 4:
-surgical haemorrhaedectomy
Complication of haemorrhaedectomy:
1-stricture and anal stenosis
2-acute retention of urine
3-haemrrhage and infection
DD of painful anal condition:
1-anal fissure 2-anal abscess
3-thrombosed hemorrhoids
4-perianal hematoma
5-rectal prolapsed 6-IBS

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7-proctalgia fugues
8-anal polyps and carcinoma

Perianal abscess:-
-internal sphincter : arise from muscle of rectum
-external sphincter: from pelvic floor (levator ani muscle)

Common side of abscess:

-perianal abscess (subcutaneous abscess)
-ischiorectal abscess (between skin and levator ani muscle)
-sub-mucosal abscess
-Supra-levator abscess (inter-sphincter)
Complication:
-Fistula-in-ano
Treatment of abscess:
-surgical drainage: curciate incision under GA
-AB in diabetic or immunocompromised

Fistula:
-may due TB, cancer, radiation, crohn, IBD
Type:
-Trans-shincteric
-Inter –shincteric
-Extra-shincteric
Presentation:
-opening near anal opening
-discharging pus, blood, mucous, and fecal material
Investigation:
-fistulogram: injection of die x-ray
-MRI
-endo anal US
Treatment:
-fistulotomy
-fistulectomy
Lower GI bleeding (massive)
1-diverticular disease :most common cause
2-upper GI bleeding
3-angiodyspasia
4-IBD
How to manage:
1-resustation:ABc

111
 -two wide bore cannula
-blood sample for investigation
-IV fluid :ringer lactate or blood
2-raiological image
3-upper or lower GI endoscopy
*if bleeding is life threaten you can go for surgery: coloctomy
Upper GI endoscopy: O G D(,esophagus, gastric,deudenum)
Lower GI endoscopy: until the cecum
Small intestine visualize by capsule endoscopy
-in emergency can do :a-exploration surgery b-on table enterstomy

112
Gall Bladder

Gall bladder Liver

↓ ↓
Cystic duct right and left hepatic duct
↓
Common hepatic duct

Common bile duct

nd
Open in 2 part of duodenum (ampulla of patter)
Guarded by sphincter of oddi

- stones when formed for the first time in the gall bladder they may cause
inflammation → acute cholecystitis “i.e. acute inflammation of the gall
bladder” → in this case of stone it is best called 1- acute calcular
cholecystitis
- 2- Acute Acalcular cholecystitis:
due to:
- biliary stasis
- direct infection by salmonella or ascaris worms
- Major Burn
- long time fasting, TPN.
management: antibiotics
- stones can present without inflammation in which case it’s called Gall
Stones
- Stones are most commonly due to:
1. Cholesterol stones: mostly in females, fatty, fertile lady “i.e. has
estrogen”, 40s in age
2. Pigment stones: present with hemorrhagic anemia in young children
3. Mixed stones
✓ COMPLAIN of acute cholecystitis patient:
- acute abdomen: right hyponchondrial or epigastric pain, radiate to the
scapula, DULL inflammatory pain, aggravated by fatty food due to
cholecystokinin hormone
- fever, vomiting
- NO Jaundice as flow of bile to intestine is not interrupted

113
 ✓ ON EXAMINATION
- Murphy’s sign: Press hand on hypochondrial are and ask patient to take deep
breath→ patient feel tenderness → this is because with breathing diaphragm
is pushed downward and so gall bladder comes near to your hand.
- Boa’s sign: hyperesthesia of right scapula
- Zachary cope’s sign: right hypochondrial fullness
✓ INVESTIGATION
- Abdominal US (confirmative):
*multiple hyper-echoic masses are seen in gall bladder + acoustic shadow
*thickness of wall: thick if edematous , thin if bladder is distended
- X-ray: is helpful in case of renal stones only! BUT it may show calcification
in gall bladder stones
- HIDA scan: if not uptaked by gall bladder then the gall bladder is either
inflamed or absent
✓ MANAGEMANT
- RESUCITATION: regarding the antibiotics give 2nd generation
cephalosporin + flagin
- IF patient became good and no pain and signs –ve (i.e. no inflammation now
but the stones existed) → discharge on antibiotics and return after 4-6 wks
for elective cholecystectomy
- IF no improvement by conservative management and the fever is increasing
(swinging) → then there is abscess [empyema of gall bladder] → drain by
cholecystoscopy
- If not detected then it can develop to perforation “biliary peritonitis” →
management by laparotomy: lavage and wash + remove gall bladder
- Also, during management in hospital: gall bladder may be distended but
without fever “mucocele” → this is palpable and mx is by removal.
- Overall, if pt is not improving→ do emergency cholecystectomy
- If pt did not return for elective cholecystectomy he will later on experience
recurrent attacks of pain –with the same description of above pain- which
will result in a shrunken and fibrosed gall bladder → i.e Chronic
cholecystitis “acute on chronic pain”
- If stone goes down to cystic duct or neck of gall bladder it will result in
CHOLICKY pain “i.e. impacted stone”→ managed by removal of gall
bladder and tying the cystic duct proximal to the CBD.
So the complication of acute cholycystitis are: Empyema, biliary peritonitis,
mucocele, chronic cholecystitis, impacted stone
✓ SURGERY “Cholecystectomy”

114
- Can be either open or laparoscopic cholecystectomy
- Open cholecystectomy scar is 2 cm bellow the costal margin [Kocher
incision]
- Laparoscopic: the pore will be 3 pores
✓ Suprumblical
✓ right hypochondrial area,
✓ epigastric area
- Advantages of laproscopic surgery:
✓ less risk of bleeding and infection
✓ less risk of adhesions , incisional hernia , scar
✓ short hospital stay (less risk of DVT, hospital acquired infection)
- Disadvantages:
✓ Techniqally difficult
✓ More risk of visceral injury
✓ May fail, so we need to do open surgery

- Contraindications of laparoscopic surgery:

✓ Pregnancy
✓ Ascites
✓ Abdominal distention
✓ non-virgin abdomen “i.e. history of previous operations”

- The side effects of scar: bleeding, adhesion, infection, cosmetic, pain,

incisional hernia, risks of hospital admission
- Complication of Colecystectomy:
✓ Common complications
✓ Injury to common bile duct → stricture → leading to sclerosing
cholangitis which will lead to liver cirrhosis (the most serious
complication)
- Jaundice after surgery is explained by :
✓ Injury to common bile duct
✓ Retained stone

Obstructive Jaundice
- Jaundice is yellow discoloration of tissue due to deposition of >2 g/dl
bilirubin (obstructive jaundice is surgical jaundice: dark urine + bale stole +
itching + yellow sclera)

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- CAUSES “use the mnemonic 3S”
Stricture Space occupying
Stone
benign Malignant lesion
Whether coming trauma Cholangiocarcinoma CA of head of
from above or (CA of CBD) pancreas
formed denovo
Inflammation CA of ampulla
(ascending (periampulary
cholangitis) carcinoma
which occur on
top of jaundice

- In case of stone; jaundice is painful intermittent. While in case of CA head

of pancreas; it’s painless progressive although in late stages it can become
painful.
• INVESTIGATION
1- General :
✓ CBC: ↓Hg (anemic)
bleeding tendency as there is deficiency in vitamin K which fat
based and so Is absorbed via bile (note: the other fat soluble vitamins are
not affected as they have storage in body)
✓ Coagulation profile: PT, PTT
✓ RFT and Electrolyte and → the patient is at risk for dehydration →
hepatorenal syndrome → Renal failure
✓ WBC: increased as the patient may suffer from sepsis due to ascending
cholangitis
✓ So the Complications of Jaundice:
Bleeding tendency
Hepato-renal syndrome
Ascending cholangitis
Hepatic encephalopathy
2- LFT:
- check bilirubin: ↑total, ↑direct, while the indirect might be lightly
increased
- check enzymes: Alkaline phosphatase increased (very high) , GGT is
also increased
3- Abdominal US “initial test but NOT confirmative”: will show the gall
bladder and the CBD

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 *CBD is dilated proximally while the distal part is collapsed “indicating
obstruction”
4- ERCP “ Endoscopic Retrograde Cholangio-pancreatography”:
✓ “Diagnostic Role”: a test where a dye flows through the bile duct to
gallbladder and the pancreas → a filling defect indicate the presence of
stones
- diagnose stones and tumor of pancreas
-Can take biopsy from the tumor

✓ Therapeutic role:
- Stone→ sphinctrotomy and dormia basket extraction of the stone
- In case of Tumor: put stent to keep the duct patent as tumor obstruct from
outside.
*complications:
- injury or perforation
- infection “ascending cholangitis or acute pancreatitis”
- bleeding “as the patient already has bleeding tendency”

5- MRCP “Magnetic resonance Cholangio-pancreatography”

It relapse the diagnostic role of ERCP
The Best diagnostic
has no complications. Has no therapeutic role.

If stone management by ERCP Failed: due to presence of multiple

stones or large stone→ DO open surgery to remove the gall bladder and
cystic duct “cholecystectomy” + exploration of CBD + put a T-tube to
maintain it open and prevent stricture → leave the tube for 10 days
Before removal of the tube → inject dye and do X-ray “T-tube
Cholangiogram” if the dye reach intestine the tube is patent, if not →
do T-tube Choledochoscope to remove the stone.

If cancer is found on ERCP: put a stent and take a biopsy → after that follow
it by CT abdomen to stage the cancer: if early stage do curative management
by surgery, if late stage do palliative therapy.
6- Patient should take vitamin K for bleeding tendency + Antibiotic for
infection + fluids for hepatorenal syndrome + doing bowel preparation
her hepatic encephalopathy
Ascending Cholangitis

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 7- Inflammation occurring on top of obstructive jaundice
8- Charcot’s Triad of fever and rigors + jaundice + Abdominal pain
9- Give antibiotic aggressively to prevent against sepsis or encephalopathy
→ rare

Stricture
10- If due to cholangocarcinoma resulting from primary
sclerosing cholangitis then it has a poor prognosis
11- Management by hapatico-jugenostomy

Pancreas

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Its retroperitoneal organ.
Exocrine/endocrine organ. Has acnie that secret enzymes in the 2 nd part of the
duodenum. Islets of Langerhans cell that secret insulin.

❖ Acute Pancreatitis:
➢ Causes

GET-SMASHD
G: Gall stone
E: Ethanol (alcohol). It’s the most common cause of recurrent pancreatitis.
T: Toxin & drug (Na valproate) & infection (mumps).
S: Surgery & ERCP
M: Metabolic ( Ca²⁺).
A: Autoimmune.
S: Snake or Scorpion bite
H: Hypothermia
D: Duodenal obstruction.
Gall stone and alcohol are the commonest cause of acute pancreatitis.
In gall stone disease the stone obstruct the common bile duct in ampulla. So the
enzyme can’t get out from pancreas lead to autoimmune digestion and sever
inflammation…it’s a treatable cause. It is common in middle age & elderly.
➢ Presentation:

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Sudden sever epigastric pain, which is progressive. (DDx: Perforated peptic
ulcer), the pain is radiated to the back, relive by leaning forward associated with
nausea, sweating & repetitive vomiting hypovolemia
➢ O/E:

Ill Pt, lie still, shallow breathing, rapid pulse, cyanosed (; circulatory collapse).
Abdomen: pt. looked jaundice (G.S), temp. subnormal or raised (39.5), ascites &
the abdomen is tender and there is guarding and sign of hemorrhagic pancreatitis
(Cullen sign & Grey Turner sign).
➢ Types of pancreatitis:
1. Mild edematous pancreatitis.
2. Sever hemorrhagic necrotizing pancreatitis 2signs:
1. Cullen sign (ecchymosis around the umbilicus)
2. Grey Turner sign (ecchymosis in the flank), its due to extravasation of
blood stained pancreatic juice in to retroperitoneal tissues.
➢ Investigation:
1. Serum amylase/lipase: which decrease in 2-3 days, while in urine is still
high.
DDx Raised serum amylase:
Impaired renal excretion
• Renal failure∗
• Macroamylasaemia (amylase not cleared by
kidneys owing to complexing or protein binding)
Salivary gland disease
• Salivary calculi
• Parotitis
Metabolic causes
• Severe diabetic ketoacidosis∗
• Acute alcoholic intoxication
• Morphine administration (causing sphincter of Oddi
spasm5)
Abdominal causes
• Acute pancreatitis∗
• Perforated peptic ulcer
• Acute cholecystitis
• Intestinal obstruction
• Afferent loop obstruction following partial
gastrectomy
• Ruptured abdominal aortic aneurysm
• Ruptured ectopic pregnancy
• Mesenteric infarction
• Trauma, open or blunt
2. FBC: moderate leukocytosis+ anemia in severe cases
3. Blood glucose: high in 15% of the cases.
4. High serum bilirubin

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 5. ABG: hypoxia in severe cases.
6. Serum Ca²⁺: decrease; saponification.
7. Erect CXR: to exclude air under the right side of the diaphragm, to
exclude perforation.
8. CT confirm pancreatitis if amylase is normal& done if pt. is stable.
9. ECG: diminish T wave or arrhythmia.
10.US: in GS...dilated choledochilithiasis & show enlarge pancreas.
11.ERCP: if pt. jaundice & not stable.
12.Abdominal X-ray: not direct helpful. Sentinel sign (gas inside the
jejunum) & Colon cut-off sign, renal halo sign, pancreatic calcifications.
➢ Management:

Scoring of acute pancreatitis:

There are many scoring system: Ranson scoring system, Apatchy scoring
system & Glasgow.
Glasgow scoring system:
PANCREAS
P: PaO2<8kp.
A: Age>55yr.
N: Neutrophils: WBC>15*10⁹/l.
C: Ca²⁺<2mml/L.
R: Renal urea 16mmol
E: Enzyme LDH >600
A: Albumin <32g/dl.
S: Sugar >10mmol.
If more than 3 of the criteria Sever pancreatitis & need for admission to ICU.
Both a raise in CRP (>140mg/L) and non-perfusion of areas of the pancreas on
contrast-enhanced CT also predict a poor prognosis.
➢ Steps of resuscitation:
1. Admission to ICU.
2. NPO.
3. NGT.
4. IV Fluid.
5. Catheter.
6. Broad spectrum AB (Meropenum &Ibiepenum).
7. Monitoring.
8. May need O2.
9. Analgesia: Pethiden, avoid morphine; cause sphincter spasm.
➢ Role of Surgery:

It depend on the condition (complication).

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 ➢ Complication:
1. Systemic complication:
Pancreatitis → release of inflammatory mediator that affect all the body →
RDS, Respiratory Failure 1, Renal failure, Sepsis, Multiple organ failure
Ca²⁺; it precipitate in the pancreas and the omintum and fused with fat
Saponification.
Mg, albumin.
2. Local complication:
1. Localize necrosis → do necrozoctomy.
2. If necrosis not treated → pus collection → Pancreatic Abscess →
need drainage.
3. If abscess not treated→ leak of fluid rich amylase in front of the
pancreas → Pancreatic Pseudo cyst (fluid collection in the lesser sac,
which is a place between the pancreas and the stomach). The abdomen
become distended Mx if in CT there is increase in size, it may rupture and
the pt. die.
1. You can drain it by aspiration through:
a. Percuteanously
b. ERCP
c. Open surgery (Stomach Get Out) by opening the anterior wall of
the stomach and then pass through the posterior wall to reach the site
of the cyst and let it train inside the stomach by maintaining the
posterior wall patent and close the anterior wall of the
stomach…Cysto-Gastrostomy.
2. Or mange it conservatively.

4. Pancreatic ascites the ascites rich of amylase and if the leakage continue
Pleural effusion

❖ Chronic pancreatitis:

Scenario: Middle aged alcoholic male.

The alcoholic man start to develop fibrosis which cause pressure atrophy to
the acini and the duct become dilated due to obstruction.
➢ Clinical features:

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 1. Asymptomatic and discovered on CT.
2. Recurrent epigastric pain like that pain of acute pancreatitis, which
radiated to the back. The pt. develop malabsorption ;fibrosis the
pancreatic enzyme can’t get out
3. So pt. complain of steatorrhea.
4. The endocrine part of the pancreas may also affected and the pt. present
with DM.
5. OBSTRUCTIVE JUNDICE.
Some pt. develop chronic pancreatitis following Acute Pancreatitis or Cystic
Fibrosis.
➢ Investigation:
1. Serum amylase .
2. MRCP : show ductal changes.
3. CT: shrunk fibrosed, atrophic pancreas.
4. EUS: Standard for examination of the head of the pancreas& aspiration.
5. Abdominal X-ray: if any calcification in the biliary calculi.
6. Stool examination: deffency in pancreatic enzyme (trypsin, amylase
&lipase).

➢ Management:

Supportive:
1. Analgesia for the pain, and you should treat the analgesic miss use.
2. Oral pancreatic enzyme for malabsorption.
3. Insulin for the diabetic pt.
Pancreatic transplantation in severe cases.
Surgery:
1. If very frequent or the pt. develop sever pain.
2. Pancreatic duct is dilated partial pancreatectomy.

❖ CA of the pancreas:
➢ Risk factors:

- age >65
- black
- Family history
- smoking, alcoholism

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- male.

➢ Pathology:

1. Ductal adenocarcinoma
2. Cystic tumor (cystadenocarcinoma) commoner in females.
Can be in the body (25%), tail (15%) or in the head of the pancreas (65%).

➢ Presentation:

If the tumor at the head the pt. present with painless progressive jaundice;
compression of the bile duct. Associated with wt. loss, poor appetite &in
advance cases painful jaundice.
The CA pain also radiated to the back and decrease by lining forward.
Recent history of diabetes will appear.
Virchow LN in advance case.
Migratory thrombophelipitis may develop.

➢ Abdominal O\E:

Mass in the abdomen it could be: 1. tumor. 2. Liver as part of mets. 3. Gall
bladder; dilatation; the obstruction in the CBD, IT WELL BE PALPABLE
according to Courvoisier Law: in a jaundiced patient if you feel the
gallbladder palpable the cause of jaundice is un likely to be due to stone.
In the stone the GB become shrunken & fibrosed, while in CA of the head of
the pancreas the GB is healthy. Exception to the law: DE novo stone in CBD
not from the GB.

➢ INVESTIGATION:
1. Tumor marker: CA19.9 elevated
2. If pt. Jaundice: do CBC, LFT, and RFT.
3. Abdominal US: use for detection in the CBD &GB.
4. ERCP: it use to visualize the obstruction, & if you can treat the pt. you
can use it, but if you think that the pt. in the advance stage do MRCP.
5. CT: staging, take biopsy, put stent.
6. Occult blood: Silver stool from periampular bleeding.

➢ Management:
✓ Surgery:
If tumor is early &no LN involved.
➢ Spread:

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1. Local: CBD, duodenum, portal vein, superior mesenteric vein(thrombosis
or heamorrg), IVC( bilateral LL edema), stomach ( gastric out let
obstruction), colon, small intestine, spleen
2. Lymphatic: Porta hepatus LN, pancreatic LN, splenic LN.
3. Blood: liver
4. Transcoelomic: with peritoneal seeding & ascites.

➢ Whipple operation:

(pancreatico-duodonectomy)
We take the head of the pancreas + 2nd part of the duodenum.
Then we connect the stomach & pancreas & bile duct to the jejeunum (Gastro-
jejonstomy, Pancreatico-jejonstomy, choledoco-jejonostomy).
If tumor is advance: send the pt. to chemotherapy & manage pt. with palliative
ttt( for jaundice IV fluid, vit K, laxative & AB for ascending cholangitis).

➢ Palliative surgery:

Triple bypass: -gastroenterostomy

-choledojejenostomy
-entero-enterostomy : prevent food going up into the
gallbladder .
Or put a stent (expensive).
Whipple operation

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 ➢ Other pancreatic tumors:

Insolinoma:
Whipple triad:
When pt. fast he develop symptoms of hypoglycemia & when measure the
blood gluc. Found it to be low & so he take glucose & the symptoms decrease.

➢ Investigation:
- Blood glucose
- C-peptide: to exclude exogenous cause.
- localization → CT abdomen , EUS, laproscopy
✓ Glucagonoma:
- Over production of glucagon & the sugar will be high + purple skin rash.
✓ Gastrinoma:
- Produce gastrin multiple peptic ulcer (Zolinger Illson Syndrome) its un
healing ulcer.
✓ VIPoma:
- Tumor that secret VIP:over motility of the intestine diarrhea &
hypokalemia.

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 • NOTE:

Tumor that develop in the head of the pancreas is better than that of the tail
cuz pt. with tumor of the head will present early with jaundice,while in tail
tumor present late with pain.
If the tumor in the tail distal pancreatectomy + spleenectomy.

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 SUB-SPECIALITIES

Pediatric surgery

Fluids in neonates D5% +0.45%NS 120-150ml/kg/day+10mmol K/500ml

Child at birth =Hx of polyhdramnios
▲/▲ 1.esophageal atresia
2. Duodenal atresia
3. Congenital pyloric stenosis

❖ Esophageal Artesia:

Most common type is blind proximal pouch +distal TEF “Tracheo-esophageal

Fistula”
• Clinical picture:
Soon after birth child develop frothy saliva, regurgitation, chocking
,cyanosis ,Hx of polyhdromnios during pregnancy
• Investigations:
-pass NG tube =arrest
CXR=coiled tube
Esophogram(water soluble) and brochoscopy fistula resuscitation =Rt
thoracotomy

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 • TReatment:
surgery ligate fistula +divide it + end to end anastmosis of esophagus

❖ Duodenal Artesia :

Bilious vomiting ,Hx of polyhydramnios

Investigation :Abdoominal xray (double buble sign)
Tx: duodenal-dudenostomy (side to side)

❖ Congenital pyloric stenosis(IHPS):

M: F 4:1
First born male
There is familial tendency
Projectile nonbilious vomiting ,hypokalemic hypochloremic metabolic alkalosis
O/E: visible peristalsis from Lt to Rt (test feed)
Inx: US (>4mm) or Barium meal =string sign
Tx: FRPM ” Fredt Ramstedt Pyloromyotomy”
❖ Small bowel atresia:
- Single or multiple.
- Obstructing or appelpeel atresia (bowel distal to atresia called
mesenteric remenant).
- Clinical pic:
Bilious vomiting
Abdominal distention
Visible peristalsis
- Rx: resuscitation
resection + end-end anastmosis
- 6 weeks rotation, 10 weeks return back.

❖ Malrotation of the midgut (volvolus neonatorum):

- Abnormalities:
1. Dudenojuojenal junction on the right of midline.
2. Cecum
3. Small narrow base of the mesentry → risk of volvulus → risk of
strangulation
4. Peritoneal band called Ladd band →canned duodenum to the posterior
abdominal wall (pull DJ junction to Rt midline & caecum to center
+ volvolus)

129
- Clinical pic:
Bilious vomiting
Abdominal distention
rectal bleeding >> strangulation.
- Dx
1. US to abdomen: relation between mesenteric artery to mesenteric vien.
2. AXR: double bubble sign
3. Contrast study (barium >> diagnostic)
- Rx:
Resuscitation
Ladd operation:
a. Untwist the volvoulus + return bowel loops.
b. Remove dead bowel
c. Dilate root of mesentry
d. Divide ladd band
e. Remove the appendix as prophylaxis. >> cecum will lie at LUQ.

❖ Meconium ileus (cystic fibrosis):

- DDx of failing to pass meconium at birth:
Meconium ileus
Imperforate anus,
Hirschsprung disease.
- Very thick meconium which cause intestinal obstruction → distended
abdomen & history of no passage of meconium + empty rectum.
- Dx:
AXR: dilated bowel.
Cystic Fibrosis screen.
Water soluble enema.
- Rx: hypertonic saline or gastrograffin washout of the meconium.
If failed or in complication (perforation, obstruction): resection,
ileostomy and anastmosis.
- Compilcation of perforation is called meconium peritonitis.

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 ❖ Anorectal malformation:
- Imperforate anus.
- Fistula:
a. High defect:
Rectobulbar fistula
Rectoprostatic fistula
Persistent cloaca > poorly developed sphincter complex.
b. Lower defect:
Rectoperimeal fistula
Rectovestibular fistula
With developed sphincter complex
- Most common: rectobulbar & rectovestibular.
- Clinical picture:
Infant fail to pass meconium + bilious vomiting + abdominal distention +
imperforate anus ( )
- Inv.:
a. Lateral shot through prone radiograph: coin test.
b. MRI
- Rx: Resuscitation + defunctioning divided colostomy
Lower defect: anoplasty ± fistula …..
High defect: posterior sagital anorectoplasty

❖ NEC (necrotizing enterocolitis):

- Associated with: preterm baby, Hirchuspurg disease
- Ischemia + bacterial infection of the bowel > pt develops abdominal
distention + bilious vomiting + bloody mucoid diarrhea > risk of systemic
septicemia.
- AXR: Pnematosis intestinalis (intaluminal gas) >> gas in bowel wall.
Stool culture: C.difficle.
- Rx:
Resuscitation (conservative) >> NPO, NG suction, rectal washout, IV
antibiotics, TPN >> failed, perforation >> laprotomy (remove necrotic
bowel > temporal ileostomy > anastmosis later on).
- Mostly in preterm 40 – 100%

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 ❖ Diaphragmatic hernia:
Hernia may occur through:
1- Foramen of Bochdalek (defect in pleuroperitoneal canal, left
posteriolateal, most common 90%)
2- Foramen of Morgagni ( between xiphoid process and costal margin,
anteriorly )
3- Deficiency in central tendon
4- Congenitally large esophageal hiatus
- Abdominal content are in the chest → lung hypoplasia → respiratory
failure and death ( respiratory distress)
➢ Symptoms and Signs:
Displaced apex beat
bowel sound in the chest
scaphoid abdomen.
- Dx: AXR + CXR
- Rx:
respiratoy and circulatory support
close the defect (suture / put mesh)
- Complication: respiratory failure.

❖ Hirchurpurg disease:
- Aganglionosis (absence of ganglion) of the rectum
- Associated with down syndrome.
- 75% affect the rectum, rest colon 20%.
- Dilatation of the proximal bowel.
- Clinical picture:
Failure to pass meconium in newborn
Constipation and Abdominal distention
O/E: gush of stool on PR
- Complication:
Necrotizing Entero-Colitis
recurrence
- Dx:
AXR
barium enema (3 zones: dilated zone , transitional zone, collapsed zone)
Rectal biopsy: hypertrophied nerves, loss of ganglia
- Rx:

132
 resuscitation
pull through operation at age 3-6 months → following temporal
colostomy.
- 3 stages operation: (Soave endorectal pull through operation)
defunctioning loop colostomy + biopsy
Pull through at 3-6 months
Closure of the colostomy 3-4 weeks later
- Prognosis: 75% of children gain normal bowel control later on.

❖ Intussusception
- Invagination of one bowel into another.
- Complication: strangulation and gangrene.
80% ileocecal
Can be: cdocolic, ileo-ileo cecal
- Clinical pic.:
Infant 5-10 month → colicky abdominal pain + drowing up legs toward
abdomen + screaming + currant jelly rectal bleeding (blood + mucus)
- O/E: abdomen sausage shape, empty Rt iliac fossa
PR: apex of intussusceptions, bleeding
- Inv.:
US → target sign
Coiled spring → B.enema
- Rx:
Resuscitation
reduction > air (peunomatic) reduction or Hydrostatic reduction by
enema
Surgery: milking → resection and deep bowel anastmosis.

❖ Necrotizing Entero-colitis:
Ischemic disorder of newborn intestine
Most common in premature infants
➢ Etiology:
Infection
Hypoxia
Umbilical artery cannulation
➢ Risk factors:

133
 Prematurity
NASIDs
Enteral feeding
Cow milk
Diabetic mother
➢ Symptoms and signs:
Diarrhea, blood and mucus per rectum
Abdominal distension , bilious vomiting
Erythema on abdominal wall
➢ Investigations;
-AXR: distended bowel with fluid level
Diagnostic sign “pneumatosis intestinalis” is intra-mural gas
indicates bowel wall necrosis.
Free gas indicates perforation
➢ Management:
1- Resuscitation : Iv fluids, NG tube, TPN, broad spectrum
antibiotics
2- Laparotomy: indications
Perforation
Failure of medical treatment
Erythema of abdominal wall.
❖ Abdominal wall Defects:
➢ Gastroschisis:
- Defect in abdominal wall adjacent to Umbilicus.
- It is isolated deformity , no associated abnormalities.
- Diagnosis is obvious at birth , and patient is dehydrated.
✓ Management:
- Cover with normal saline gauze
- Sialo-bag suturing to abdominal wall
- Primary closure after decompressing the gut and return it to peritoneal
cavity.
- Longterm TPN until GI motility return to normal.

➢ Exomphalos: “Omphalocele”
- Opening is at the umbilicus, there is a sac cover the visceral protrution.
- May associated with chromosomal abnormalities, heart defects, GU
malformations..

134
✓ Management;
- Primary closure or
- Staged repair for large defects , using silastic sheet.

➢ Neck lumps in children DDx:

a. Brachial cyst: ant. to sternomastoid (contains cholesterol crystals)
b. Thyroglossal cyst: more with tongue protrusion
c. Cystic hygroma: post. triangle, jugular lymph sac remenants
→excision. Good prognosis.

135
Skin
❖ Neurofibromatosis :
Neuro-cutaneous syndrome, problem in nerve and skin.
It is autosomal dominant disorder of a gene locate in chromosome 17 ( in
type I ) and chromosome 22 ( in type II ).
➢ Types :
Type I (also called von Recklinghausen’s disease ) and type II
➢ Characteristics :
• Disfiguring multiple Neurofibromatosis through the whole body . On
examination -> firm and painless nodules.
• Cafe-au-lait (black spots) :
more than 5 in type I ( more Disfiguring) and less than 5 in type II ( less
Disfiguring).
• Eye nodules (lisch nodules) : melanocytic hamartoma in iris .p
• High blood pressure due to renal artery stenosis and/or
pheochromocytoma .
• Both type causes benign condition but any one of them has a chance to
convert to neurofibrosarcoma. Type II can cause acoustic neuroma (
vestibular shwanoma) in which patient come complaining of vertigo
,tinnitus and deafness .
• Orthopaedic association: scoliosis and pseudo arthrosis ( in the middle of
the shaft feel ....like fracture).
Management : No treatment
Surgical resection if one or two

❖ Abnormal scars
2 types : keloid and hypertrophic scar .
• Hypertrophic :
Arise from wound , trauma.. with the wound margin.
Can resolve spontaneously .

136
 •keloid :
Arise from wound or trauma or Spontaneous
Most commonly hormonal, in African.
It goes beyond wound margin .
No resolution/ high recurrence type.
Most common sites ; chest ,neck , shoulder (deltoid )
➢ Management:
Small keloid → steroid injection (anti healing)
Large keloid →intra lesional excision ( from inside sparing the boundaries)
+ steroid injection. If large area use skin graft
Other methods: LASER/ cryotherapy

❖ Skin infection
1. Impetigo:
Caused by staphylococci (most common) or streptococci species.
Cause yellowish material (honey colour discharge) in a vesicle.
Can spread easily to surgeons ( contagious).
Dx : swab for culture and sensitivity.
Rx : give antibiotics.

2. Cellulitis :
Caused by streptococci (most commonly) followed by staphylococci .
C/F : swelling, pain , tenderness ,redness, hotness . ( D.D : DVT ,
abscess-> try to aspirate if pus then it is abscess, bone inflammation ->
osteomyelitis )
➢ Management:
Antibiotics + elevation of the leg + monitoring (limb circumference) .

3. Necrotizing fascitis :
- Serious inflammation, polymicrobial infection (synergistic infection) ;
eg: E.coli , gram -ve , Pseudomonas, anaerobic bacteria .in some times

137
 there is gas formation as spreading inflammation below the skin (
redness , erythema)
-In immune compromised patient.
-Rx : broad spectrum antibiotics + debridement .

4. paranychia :
Collection of pus bellow the nail .
Rx : incision and drainage , remove the nail

5. Hidradenitis suppurativa :
Inflammation of apocrine sweat glands
Sweat glands of 2 types: Apocrine (in axilla/groin) and Eccrine (most of the
body ).
Osce : pus formation in the axilla, discharging .
➢ Management: drainage + antibiotics.

❖ Skin ulcers
1. Malignancy (non-healing) ulcer
2. Neuropathic ulcer ( in foot )
3. Venous (medially )
4. Ischemic ( laterally )
5. Trauma .

On examination: examin
1. The edge :
• spotting ulcer ( small) in Ischemic and Venous ulcer .
• Pounch out ulcer : in bed sores and syphilis.
• Undermining ulcer (the pocket) in TB .
• Fungating ulcer : in squamous cell carcinoma
• Rolled rdge : in basal cell carcinoma

138
139
2. The floor ( base ) : it can be muscle, bone or granulation tissue ( in
inflammatory cell with fibrosis, when scratches it bleed )
3. The discharge: serous ,bloody or cellular (pus).

❖ Tumors of the skin:

➢ Benign ( haemangioma , lipoma ,neurofibroma, dermood cyst ,
sebaceous cyst ,ganglion , mole or navus or malignant ( basal cell

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carcinoma most common, squamous cell carcinoma 2nd most common
, malignant melanoma 75% mortality rate )

➢ BENIGN TUMORS:
1. Haemangioma :
- Benign tumor of the skin , arises from epithelium of the blood
vessels .
- At birth it appears as a patch then enlarge as a swelling
(comprisable lump) ( DD : Haemangioma, aneurysm,varicose vein
)( of you press it will empty or Disappear. )
- 60% in head and neck, may resolve spontaneously until cause
problems:
1. Psychological effect ( trauma to the patient)
2. Disfiguring: close to the eye causing visual field problems,
close to the nose causing breathing obstruction,hemolysis.
3. Bleeding from it can be fatal .

2. Dermoid cyst :
Cyst beneath the skin ( from dermis)
Still cover with epiderms
➢ Causes :
A. Congenital : sequestration dermoid ( do x-ray skull or CT
before excison to exclude meningiocele ) best example :
external anngular dermoid (commonly in outer angle of
the eye ) and mid line dermoid ( middle face ) .
B. Aquired : come with patient with high rate of trauma ( )
common on fingers .
Treatment : excision because it is a mobile lump not attach
to the skin .
On examination; lump or cyst with positive cross
fluctuations test ( cross fluctuations in all directions is
needed to be positive .

3. Sebaceous cyst :
- Obstruction of the sebaceous duct of the gland.
- It is the only gland that secret by holocrine .

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- Result in acne → if prolonged it causes cyst
- Attach to the skin ( from epiderms)
- Commonly in axilla , face , scrotum , scalp .
- Multiple sebaceous cyst is called garnar syndrome.
- On examination:
Positive cross fluctuation test
Punctun ( spot) present in 50% of patients .
Sebum become dry ( sebaceous horn )
- Treatment : excision by electrical incision , open around the cyst ,
take it out and suture.
-
4. Lipoma :
• tumor of the fat , it may be subcutaneous (in skin ) subperiosteal
( bone ) sub meningeal or sub mucus .
• common in females.
•commn site is the back
•may be multiple as in dercum’s syndrome ( resembles
neurofibromatosis , painless ) .
•usually soft lobulated lump that is slebarry edge, painful and
tender in examination.
•treatment: surgical excision.

5. Ganglion :
Swelling that arise from the tendon sheeth and containing synovial
fluid.
It is A cyst ( positive fluctuation test ) ( and positive
translumination test )
Wrist is the commen side
Treatment: is by sugical excison in blood less field by using
tourniquet( 09 mins is the maximum time) under general anesthesia

6. Mole ( navus) :
- Abnormal accumulation of melanocytes ( black in color) .
- Of many types :
A. Intradermal navus
B. Junctional navus
C. Compound navus
D. Halo navus : premalignent condition can change to
malignant melanoma ( when there is change in size , shape

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 become irregular, variable colours, satallite lesiones i.e
surroundby small lesiones, Bleeding)
- May be Disfiguring and itching .
- Treatment: excision and biopsy to exclude malignancy.
➢ Malignant Tumor :
• Risk factors:
1. UV radiation .
2. Long exposure to sun light
3. Arsenic compounds ( BCC).
4. Chronic ulcer or burn scar (SCC)
5. Navus & HPV ( melanoma)
6. Albinus people
7. Tobacco smoking and irradiation
8. Premalignent conditions
9. Epiderma pigmentosa

➢ Basal cell carcinoma:

No spread by LN or blood(the best tumor)
Starts as nodule→ ulcer→ wound with rolled edge.
Painless lesion.
Sometimes maybe pigmented (black) ;so DDx: Malignant melanoma
Commonly in a triangle between, mouth and nose.
Can invade deeply till the bone(rodentulcer)
Ttt:plastic surgery: Wide local excision with free margins>0.5cm--
1cm then put a graft.

➢ Squamous cell carcinoma:

Risk factors are radiation and sunlight.
Common on scalp and forehead ,painless ulcer with everted fungated
edges.
Spread TO LN and blood occur but rarely.
ttt:wide local excision with free margins in 0.5--1cm even up to 2 cm.

➢ Malignant Melanoma:
Rare 0.5% with high mortality rate 75 %

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 In elderly people due to exposure to sun light.
• Types are related to the area:
1- leg : acral melanoma in the sole of the foot.
2- under nail : subangual melanoma.
3- Face: in cheeks, vertigo malignant Melanoma
4- Nodular melanoma : nodular shape occurs anywhere.
5- Superficial spreading melanoma...flat and invading deep.
It has tendency to spread by LN and blood to liver, lungs and brain.
So examine the LN if+ve → poor prognosis.

➢ Surgery: Wide local excision with free margins if 2 cm or less then put
agraft.
➢ Staging: with clark staging system.
The depth is the most important
- Stage1:epidermis.
- Stage2:papillary dermis.
- Stage3:junction between papillary dermis and reticular dermis.
- Stage4:reticular dermis.
- Stage5:subcutaneous tissue.

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 ❖ Skin Grafts:
- Wound closure either primary, secondary or tertiary.
- Large defect→ due to debridment,burn and trauma by:
- Graft : skin transpor from site to site (vascular recipient area).
- Or flab: move the structure from the donor site with it's blood
supply

➢ Types of grafts:
1- Partial skin thickness : all epidermis with part of the dermis.
2- Full skin thickness : all epidermis with dermis .Donor sites are; thighs
and post auricular skin.
Graft should be avoided in areas of fluid collection(hematoma and
seroma),infection sepsis With pseudomoneus, group A strep. And
MRSA.*Infection is an absolute contraindication for graft.
Do mishing of the graft so not to expend the blood supply.
Flab:it's a skin with bone (osteocutaneous), muscle(myocutaneous),
fascia(fasciocutaneous) Or any other tissue.
➢ Types of flab:
1- Local flab: in breast using latismusdorsi muscle.
2- Free flab: from area to another distal area that is a vascular e.g bone and
cartilage.

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Urology
❖ Hydronephrosis:
Dilatation of renal pelvis and calyceal system due to obstruction

➢ Causes:

1/ stone
2/stricture
3/prostatic enlargement
4/tumor

- Bilateral hydronephrosis if the obstruction in bladder, urethra and prostate

- Unilateral if the obstruction in the ureter
- Hydronephrosis causes atrophy to renal tissue (urine bag kidney) and lead to
permanent renal failure (esp if bilateral )
- it is painful plus palpable kidney on examination
And the patient will have symptoms of lower urinary tract symptoms it is divided
in to tow types:

1/Irretative (storage symptoms) 2/obstructive (voiding symptoms)

Dysuria Hesitancy
Frequency Poor stream
Urgency Post micturition Dripping
Urge incontinence Sense of incomplete evacuation

The irretative is common with infection ;inflammation and stones (bladder cause
)
The obstructive is more with prostate and uretheral stricture

➢ Investigations :

1/ abdominal ultra sound

2/IVU(intravenous urogram)
3/ x ray (KUB)
4/ RFT

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 ➢ Management:

1/ Treat the cause

2/ US Guided drainage: - PCN (percutaneous nephrostomy )

- Suprapubic cystostomy
- Ureteric / urethral

3/ Nephrostomy if severe.

❖Stones:-

➢ Causes:

1. Infection
2. Stasis due to obstruction
3. Dehydration
4. Metabolic disorder ( hypercalcemia)
5. Cysteine and Oxalate disorder ( GIT cyst, diverticulum)

➢ Types of stones :

1\calcium oxalate stone (most common) its sharp so cause hematuria

2\calcium phosphate stone
3/uric acid stone
4\cysteine stone
All stone are radio opaque except uric acid stone is radio lucent in x ray( so do
IVU or US)
➢ Clinical symptoms of stone:

1/Asymptomatic
2/Episodes of loin pain
3/Hematuria
4/If stone obstruct renal pelvis or ureter→ colicky pain(on and off pain radiated
from loin to groin)
*Stone in kidney cause loin pain or stapping pain
*The bladder stone and renal pelvic stone called obstructive stones

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 ➢ Investigation :

1/xray K U B
2/Ultra sound
3/CT K U B ( better; give you size and density of stone)

➢ Treatment:
- Depends on the site, size and density of stone:

1/if it smaller than0.5 give diuretics and increase the amount of water
consumption daily if there is pain give analgesia
2/if it 0.5cm to 2cm give patient shock waves to destroy the stone by using ESWL
(Extracorporal shockwave lithotripsy) and put double J stent to pass fragmented
stone to prevent ureteric obstruction
✓ Side effects of ESWL: faliure and embolus
✓ Contra indication of ESWL:
1- pregnancy.
2- Aortic aneurysm
3- Stone > 2cm
4- Bleeding tendency
5- Sepsis

3/ If the stone is >2cm : do surgery (- lithotomy)

Kidney : nephrolithotomy
Pelvis: pyelolithotomy
Ureter: Uretero-lithotomy
Bladder: vesico-lithotomy

✓ percutaneous nephrolithotomy
✓ Cystoscopic uretherolithotomy for ureteric stone (put dormia basket)

➢ Byelonephrosis:

it is collection of bus inside the kidney

kidney is palpable
there is fever & pain
Treatment: PCN

➢ perinephric abscess:

the bus is surrounding the kidney from out side

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peatient is complain of swinging fever and increase liability to sepsis
trearted by : PCN

Renal cancer
❖ Renal cell Ca:

Called hyper nephroma (Grawitz tumor).

More common in old age male, smoker can also be genetic.
It can be cystic( contain fluid and surrounded by pseudo capsule) or it solid tumor.
➢ Clinical presentation :

Triad of : loin pain , loin mass and painless total hematuria.

➢ Spread:
- Locally: to ureter, renal vein, inferior vena cava or aorta
- Lymphatic: Para aortic lymph node
- Metastasis: to bone , lung ( canoon ball)
- It can spread to liver ,stomach, spleen

➢ Paraneoplastic:
- Renin→ HTN
- Parathyroid hormone:→hypercalcemia
- Erythropoietin→ polythycemia

✓ If there is old age patient with varicocele in the left side mainely
(abnormal dailation of testes veines) this suggests renal cancer( because
testicular vein on left side drain to renal vein ) so do US.

➢ Investigation
- Ultrasound (capsulated)
- CT
- Biopsy is Contraindicated (dissimination of malignant cells)

➢ Management

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Radical nephroureterectomy +/- Chemotherapy

❖ Transitional cell cancer of The ureter and renal pelvis

Patient will have painless total hematurea

It has high risk of recuerrence in the bladder

➢ Investigation:

1/I V U(filling defect )

2/CT K U B for the ureter

➢ Treatment

Nephrourethrectomy +part of the bladder

High recurrence follow up with cystoscopy ( at 3 month, 6 month then every year)

❖Renal trauma
Uncommon
Patient complain of hematurea a and subcapsular hematoma
➢ Five Grades;
- Grade 1 : Sub-capsular Hematoma
- Grade 2: minor laceration
- Grade 3: major laceration in medulla
- Grade 4 : major laceration to hilum
- Grade 5 : avulsion
➢ Treatment:
90 % respond to conservative treatment

❖Ureteric injury
Trauma or iatrogenic
it will make agap so no connection beween the kidney and bladder
➢ Treatment:

1/ if the gap is small repair it

2/ if it large mobilization for the bladder( gwar slap)
3/auto transplantation by using renal artery and vein to make the connection

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5/also we can use P C N
6/nephrectomy
Urinary bladder
❖ Ectopia vesicae (bladder extrophy):
child was born with open abdomen and bladder is open and urine is come out
- associates with
- epispadias
- imperfectly descended testis
- rectal prolapse
- Umblical , inguinal hernia
- wide separation of symphysis pubis + waddling gate.
- congenital heart diseases you have to do ECHO cardio gram.

➢ Treatment :

first 24 hrs(to prevent fibrosis) approximation and suturing + urinary catheter till
healing(10 days)

❖Bladder trauma:
If it is distended the urine will dripple in the peritoneum (intrapretoneal
rupture20%(urinary peritonitis))
If the bladder is not distended the urine will dripple out of peritoneum extra
peritoneal rupture (most common).
➢ Clinical presentation:

1/severe hypogastric pain

2/distended abdomen
3/ no desire of mectiurition
4/ heamaturea
➢ Investigation:

1/US
2/CT scan
3/ high blood urea ( urine in peritoneum)

➢ Treatment:

1/By labrotomy : repair the damage and catheterization

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2/ peritoneal lavage
*exclude pelvic fracture
❖ Urine retention:
➢ Elderly male:

1/BPH
2/CA prostate
3/uretheral stricture

➢ Young male:

1/urerthral stricture
2/impacted urethral stone
3/ neurogenic ( e.g cord injury)
If female:
Commonly neurogenic bladder , stone or cord injury
➢ child:

1/posterior urethral valve

2/phymosis and paraphymosis

Usually predisposed by constipation, pain, anesethsia ,surgery or UTI

➢ Clinically: bladder is distended and dull on percussion in acute and
chronic retention but there is pain and tenderness in acute retention

➢ Treatment:
✓ Treat underlying cause
✓ catheterization:
- 2way catheter
- 3way cathrter use for bladder irrigation (patient with heamaturea)
to prevent clot which cause retention.
- supra pubic cystostomy for Pt with urethral stricture.
Contraindicated if Pt has previous abdominal surgery or you dont
know the organ (bladder ) exactly; in this situation do open surgery
to put the catheter.
✓ steps for catheterization:
1- wash your hands use gloves
2- use antisepetic for ganitalia
3- use local anesethatic(zylocaine gel)

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 4- hold the penis at right angel to patient body and insert catheter smoothly
(if any resistance stop)
5- inflate the cuff with saline
6- connect the catheter with urine bag

✓ Indications of 2 way catheter :

1/urine retention patient

2/comatose patient
3/pre operative patient
4/trauma patient
5/peatient with fracture
6/ICU Patient.
7/ monitor urine out put
8/ inject drug to the bladder
✓ Complication of urinary catheter:

Trauma, infection, stricture

❖ Vasical (bladder) stone:

Either primary or secondary.
Secondary from kidney
Primary developed in bladder.
More in male specially in children
➢ Present with

1/recurrence UTI
2/lower urinary tract symptoms
3/painful terminal hematourea
4/ scratch (children)
➢ Investigation:

1/ultra sound
2/x rays
3/KUB
➢ Treatment:
1- If < 2 cm: cystscopic litholapaxy
2- > 2 cm : open vesicolithotomy

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 ❖ Bladder cancer:
- Manily transitional cell cancer (TCC)
- Mainly in men
➢ Cause by:
- Smoking : TCC
- Chronic Inflammation (Schistosoma hematopium/ stones) :
squamous cell cancer
- Congenital anomaly of bladder : adenocarcinoma
➢ Stages of the cancer :by TNM
1- carcinoma insitue
2- superficial tumor not invasive
3- invasive tumor invade the muscle
➢ Clinical feature:
pain less and total hematureia
➢ Investigation:
1- cystoscopy+biopsy (gold standard)
2- CT
3- MRI
➢ Treatment:
1- transurethral resection and inject the area by BCG vaccine(induce
fibrosis) if the tumor is not invasive.
2- if the tumor is invasive will do radical cystectomy or radiotherapy.and do
urinary diversion by using:
- Temporal: catheter , PCN or double J stent
- Permanent: illiostomy or uretrosigmoidoscopy (SE; infection,
psychological problem, metabolic disturbance) or illium pouch

❖ Benign prostatic hyperplasia :

It is arise from medial zoon
➢ Patient will suffer from :
1- lower urinary tract symptoms
2- urine retention (acute or chronic)
3- chronic renal failure

O/E : bladder palpable and dull percussion

When you do PR you will found:

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 -Prostate enlarge ,smooth , midline sulcus, you can reach upper
border and move mucosa.
➢ Investigation:
- Trans-rectal US
- PSA(normal less than 0.4ng/dl if very high do trans rectal US
guided biobsy)
- RFT

➢ Treatment:
✓ Medical:
1- Alpha blocker
2- 5 alpha reductase inhibiters (phenasteride) it is hormonal antagonist.
✓ Surgical:
- Indications for surgery:
1- recurrent urine retention
2- patient with hydronephrosis
3- if medical treatment failed
4- if the patient having lower urinary tract symptoms
5- hematuria
6- renal impairment
- Surgical treatment is by
1- using endoscope called transeuretheral resection of the prostate.
2- or by direct open called transvasical prostatectomy.(ideal)
3- retro pubic prostatectomy.
4- preneial*
➢ Complication:
- Urinary incontinence
- retrograde ejaculation (Sexual dysfunction)→Subfertility
- impotence (erectile dysfunction)

❖ prostatic cancer :
- CA of the prostate is arise from the prepheral zoon.
- And it take along time to compress the urethra until it become
advance so for that it have adifficult treatment.
- It is the most common cancer in male after 60years .

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 - It is 90% adenocarcinoma.
- Score from 2to10 (Gleason Score)
➢ Symptoms:
1- asymptomatic
2- lower urinary tract symptoms
3- acute retention
4- chronic retention
5- chronic renal failure
6- may come with symptoms of metaestesis the comm.
Metes is bone (vertebra).
7- weight loss
8- loss of appetite
- In PR : you will find the tumor hard nodular no midline sulcus and
can not move mucosa and can't reach upper border
➢ Stageing:T N M
- T1& T2 (early) :the aim of treatment is cureative
- T3,T4 (advance): the aim of treatment is palliative
➢ The spread:
1- local spead: ureter, bladder , rectum
2- lymph: para aortic lymph node
3- blood: bone (vertebra)
➢ Investigation:
1- prostate specific antigen if it more than4 there is risk of cancer so will
take piobsy, ,if it more than 35 that mean metastesis.
Also use in follow up.
2- take piobsy by transrectal US guided biopsy
3- general investigation
4- screening for Mets
➢ Treatment:
- If the patient isT1,T2 the treatment is radical prostatectomy or
radiotherapy
- T3,T4: the aim of treatment is:
palitive by subcapsular orcidectomy (to decrease testosterone)
radiotherapy
anti-androgen ; abiraterone acetate
- The complication of surgery (100%) :
1- sexeual dysfunction

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 2- incontinence of urine

Urethra
❖ Posterior uretheral valves
- It is congenital anomaly
- Child present with urine retention
- the mother had oligo-hydrominous during pregnancy.
- The child will have papable bladder and dull in precussion.
➢ Investigation:
- Prenatal US (oligohydrominous)
- Voiding cystourethrogram (MCUG)
➢ Treatment:
- Valvotomy ( Endoscopic transurethral resection of the valve )

- If not treated child will have vesico-ureteric reflux and kidney is

dilated with hydronephrosis and renal failure
- diagnosis of vesicoureteric reflux by MCUG .
- Mx: ureter Reimplantation

❖ Uretheral hypospaides
- Opening of urethra not in normal site ( in the lower 3rd of the
shaft)
- It is common congenital anomalis it occure in 1from 200 child
- It can be :
1- glandular
2- coronal between the gland and shaft
3- penile
4- scrotal
5- perineal found closed to the anal canal.
- It can be associated with curved penis
- Circumcision is Contraindicated because fore skin is needed in
repair
➢ Treatment: repair

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➢ Complication of repair:fistula formation (btw urethra and skin)
- It may associated with bladder extrophy.
❖ Phymosis
- Common conditions in pediatric urology lead to urine retention.
- Failure of Retraction of penile skin
- This mean the skin of the penis is closed the opening.
- So the treatment is by Circumcision.
❖ Para phymosis
- Penile skin retracted and failed to go back
- The skin will compress the shaft of the penis and it will stop the
venous return.
- So this is painful the child is crying and the penis is swellowing .
- Also treatment is Circumcision

❖ Trauma:
- The urethrea in male about 20 cm so it will have chance the injury
more than female.
- Composed of 3 parts: Prostatic urethra, membranous urethra and
bulbar urethra
- Common site for injury: membranous urethra ( with pelvic
fracture) and bulbar urethra with direct trauma.
- The membranous urethra injury is just like bladder rupture patient
present with hematurea , abdominal destention and no desire for
mecturition.
- Bulbar urethra injured with direct trauma pt present with urine
retention ,blood drop from urethral meatus and butterfly brushing
in preneium.
➢ Investigation: asending cystourethrogram and PR (find high rising
prostate)
➢ Treatment is by:
superapubic catheter
And surgical repair
➢ Complication is: stricture
Urine retention, sexual dysfunction
Incontinence

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 ❖ Uretheral stricture:
- fibrosis of urethra
- Causes:
trauma (membranous urethra)
STD ( discharge) (bulbar urethra) ).
Iatrogenic
- Patient having urine retention and lower urinary tract symptoms.
➢ Investigation :
- Ascending urethrogram (find narrowing in urethra).
- MCUG.
➢ Treatment :
- By cystoscopy do visualize internal urethrotomy(VIU).
- It has risk of recurrence.
- If VIU not effective do uterhroplasty( graft from buccal mucosa).

❖ Congenital anomalies of the testes:

➢ D.D of empty scrotum:

1- Undesended testes
2- Ectopic testes
3- Rectectil testes
4- Testicular agenesis
➢ Undesended testes:
- Testes arrested in the pathway of the descend in:
1- Posterior Abdominal wall
2- Deep inguinal ring
3- inguinal canal
4- Superfacial inguinal ring
- The ideal investigation to search for testes is laporoscopy
➢ Treatment:
- Orcidopexy , if you find testis unhealthy do orcidectomy.
➢ Complications of undesended testes:
1- precancerous condition

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 2- infertility.
3- trauma and hemorrhage
- If testes are undesended bilateral >> cryptoorcidism ( you need to
do karyotyping)
➢ Ectopic testes:
- outside pathway (eg in perineium, thigh) . Search for it by
laproscopy
➢ Rectectile testes:
- active cremartric reflex ( move from scrotoum to inguinal canal
and vis versa) . Has risk of torsion.
➢ Testicular agenesis
- The testes did not formed

❖ Acute scrotum:
- Is a sudden scrotal pain bring pt to emergency can be due to:
1- torsion
2- acute epidedemorchitis
3- strangulated scrotal hernia(indirect hernia)
➢ Testicular torsion:
- top surgical emergency(stop blood supply)
- can be spontaneous specially in teenagers or congenital ( bell
clapper deformity)
- It can occur in neonates.
- It is serious problem if un treated immediately because testis die
within 6 Hours .
- The patient come with sudden scrotal pain very severe ischemic
pain and tenderness increase with scrotal elevation.
✓ Investigation:
- doppler ultra sound if not available → exploration for both testis to
assess viability
✓ Treatment :
- By surgery resolve the torsion (untwisting) and assess viability if
dead →orchidectomy
- 160160If healthy→bilateral orcidopexy

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➢ Epidedimorchitis :

- scrotal pain with fever

- pain decrease with scrotal elevation ,
- can find hydrocele .
- Tratment: analgesia and antibiotics

❖ Benign scrotal swelling :

- Hydrocele, varicocele, epidedimal cyst , tumor
➢ Varicocele:
- Dilated veins around the testes .
- Mainly occur in the left side because the left testicular vein is
drain in the left renal vein.
- Palpable as bag of warm
- Disappeared with lying down and appear with standing
• Varicocele have grades :
1- grade1varicocele: the dilated vein not palpable but
detected with doppler
2- gread 2: the dilated vein is palpable when the patient
is standing only,
3- gread 3: palpable even when the patient is laying flat
- The main problem in varicocele is pain it is very painful the other
problem is subfertility due to increase the tempreture of the both
testes.
- You have to do semin analysis: if there is risk of subfertility do
surgery if not conservative management with analgesia and scrotal
elevation
➢ Hydrocele:
- Abnormal fluid accumulation in tunica vaginalis.
- O/E : cant feel the testis
Positive fluctuation test
Positive translumination
1- Primary (vaginal) hydrocele:(most common)
- idiopathic, in elderly

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 - Management: Lord operation, Jabuody operation.
2- Secondary: due to tumor, trauma, infection
a. Diagnosis of hydrocele is clinical
✓ Investigation:
b. Scrotal Ultrasound ( search for the cause)
3- Infantile hyderocele:
- The processes vaginalies is obliterated but open just above tonica.
Fluid accumulation in tonica vaginalies and part of processes
vaginalies
4- Congenital hydrocele:
- Less than 1 year
- Patent processes vaginalies. the fluid come from the abdomen to
the scrotum when the child is standing an empty when the child is
lying down .
5- Hydrocele of the cord:
- Tunica is normal but part of it is open ,so fluid is not around the
testis but in the cord
✓ Diagnosis is clinically
✓ Treatment of hydrocele:
- Aspiration ( but recurrence is high)
- Surgery: eversion of sac ( jaboulay operation)
- Or ligation (lord operation)

❖ Epididemal cyst:
- +ve translumination test
- Normal spermatic cord
- Cause pain and can lead to subfertility
- If the cyst contain sprems we called it spermatocele and
translumonation test is -ve.
✓ Treatment : by surgery excision.

Testicular tumors

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 ✓ Type: seminoma, teratoma, mixed and choriocarcinoma and lymphoma
1- seminoma : small, spread by lymphatic
,radiosensitive, tumor marker is LDH
2- teratoma :spread by blood and Respond to
chemotherapy, tumor marker is AFP (alpha
fetoprotein)
3- Choriocarcinoma and lymphoma are radiosensitive

- Testis lymph drain to paraaortic lymph node

- The patient come with heaviness or tumor in the scortum, pain or
Mets in lung, bone .
✓ Stageing :
- Stage1 : the tumor inside the scortum .
- Stage2: the spread to paraaortic lymph nodes below diaphragm.
- Stage3: the spread to paraaortic lymph nodes above the
diaphragum.
- Stage4: blood metastesis
✓ Investigation:
1- Scrotal ultra sound
2- Tumor marker alpha fetoprotein(teratoma) and
LDH(seminoma) hCG ( choriocarcinoma)
✓ Treatment:

- Take all testis +biobsy by inguinal incision (not scrotal) and send to
histopathology
- if you did scrotal incision the Ca will spread to inguinal LN
- Cure is 80%

Vascular diseases

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 ✓ Divided into 3:

1-arterial 2-venous

3-lymphatic

❖ Arterial vascular diseases:

Either: 1-acute 2-chronic

3-acute on chronic

❖ The blood supply of the lower limb:

Aorta bifurcates into left and right common iliac arteries then external and
internal iliac arteries. The external iliac artery gives the femoral artery and the
femoral gives the popliteal artery.

The popliteal artery has 3 branches:

1- anterior tibial artery, at the level of medial malleolus it’s become dorsalis
pedi’s artery
2- poerterior tibial artery 3- peroneal artery

❖ Occlusion of 2 or more of the above 3 arteries result in acute limb ischemia.

❖ Acute limb ischemia:

✓ The cause is an embolus. The source:

1- Atrial fibrillation (arrhythmia) embolus

2- Abdominal aortic aneurysm (blood stasis forms mural thrombus that
shoot an embolus to lower limb vessels)

✓ Presentation:

6 Ps:

1-pain (continuous) 2-parasthesia

3-paralysis 4-perishing (cold)

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5-pulsless (most important) 6-pallor

❖ If the patient presents with the 6 Ps + has had chronic peripheral vascular
disease this called acute on chronic

✓ Work up for acute limb ischemia:

❖ You have 6 hours from the start of the symptoms to save the leg or it will
end up in amputation
1- BP measurement and cardiovascular examination
2- Abdominal examination for AAA
3- Analgesia: morphine \
4- IV unfractionated heparin (rapid onset of action) 100 unit/kg
5- Doppler US or angiography
6- Emergency embolectomy by Fogarty catheter.

✓ Emergency Embolectomy procedure:

Arteriotomy hole in the proximal arterial wall and pass the catheter through the
embolus, then inflate the balloon and pull the catheter.

❖ If the limb is already dead and gangrenous don’t try Embolectomy because it
will result in reperfusion injury.
❖ The dead tissue release K, myoglobin and toxic metabolites. If it enters the
circulation can lead to renal impairment.

❖ Chronic limb ischemia

The patient has already atherosclerosis (systemic disease)

Risk factors for atherosclerosis:

1-old 2-smoker

3-HTN 4-DM

5-hperlipidemia 6-alchoholic

7-lack of exercise 8-family history

✓ Atherosclerosis affects:

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1-heart 2-brain 3-limb

❖ Chronic limb ischemia:

Gradual narrowing of the artery and there in no pain except with excretion. The
pain is in the muscle group distal to the narrowing.

❖ If the atheroma in the femoral artery then the pain in the calf muscle
❖ If the atheroma in the aorta or the iliac the pain in the thigh
The pain is bilateral aggravated by excretion so the patient forced to stop
walking to relive the pain (intermittent claudication). If the patient stop
walking after special distance and the pain is constant this called claudication
distance.

Claudication distance:

Either:

1-increase = improvement due to formation of collateral vessels (angiogenesis).

There is no need for intervention

2-decrease = not forming collaterals and the patient ma y have pain at rest

✓ Critical limb ischemia has 3 signs:

1- resting pain
2- painful ischemic ulcer in the lateral malleolus (white base ulcer)
3- gangerene in the toes (ABPI < 0.3)
✓ Other features:
1- cold limb
2- brittle nails
3- venous guttering (collapsing venous grooves)
4- callus formation in the skin (scaly skin)
✓ Work up for chronic limb ischemia:

1- CVS + Abdominal examination (IHD + AAA)

2- Limb examination (look for the above signs)
3- Investigations: general
1-CBC 2-RFT 3-LFT
4-lipid profile 5-coagulation profile
6-ECG CXR ECHO
7-abdominal US for AAA

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 ✓ Specific Investigations:
1- hand held Doppler device HHDD
Apply gel in the areas of anterior & posterior tibial pulses and listen to
the blood flow.
HHDD help to measure ankle brachial pressure index (ABPI)
- ABPI = systolic ankle pressure/ brachial pressure see
✓ ABPI:

Normal 1

Mild <0.9

Moderate <0.7

Severe <0.5

Critical limb ischemia <0.3

2- Duplex scan (screen US) to see the blood flow

3- the gold standard investigation is Angiography

Conventional angiography is obsolete now:

Arteriotomoy and inject dye then imaging

✓ Draw backs of conventional angiography (Complications):

1-injury artery 2-dissection

3-haematoma 4-bleeding

5-renal toxicity 6-anaphylactic reaction from the dye

To overcome this do CT angiography CTA or MR angiography MRA (more

advanced)

✓ WHY Angiography:

Exactly the site, degree of obstruction and the presence of collaterals

✓ Management of chronic limb ischemia:

1-treat the patient

Control DM- HTN- IHD

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2-life style modification

3-if chronic intermittent claudication give ASA, clopidogril, statin

4-angioplasty balloon dilatation + stent

5-bypass graft: long saphenous vein or Dacron graft

Femro-popliteal bypass

Aorto-femoral bypass

Femro-femoral bypass

Axillo-femoral bypass

❖ Gangrene:
- macroscopic & microscopic death of tissues
- Black- pulseless- no sensation
- 3 types: dry- wet – gas
- Rx: toilet debridement without anaesthesia
• dry gangrene: there is demarcation line between the healthy and
the dead tissue
• wet gangrene: no line of demarcation (emergency)
• gas gangrene: caused by Cl.perfiringes. Offensive severe
necrosis with crepitation’s. Its ascending infections 1 cm/hour
- Gas gangrene is top emergency because the infection will ascend to
the pelvis (Fournier’s gangrene) or may invade the trunk.

❖ Amputation :
✓ Level of amputation:

1-above knee 2-gritti strokes through knee

3-below knee 4-through ankle (Symes)

5-toes amputation (V shape amputation/ Ray amputation)

✓ Indications For mputation:

- Dead limb: dry gangrene
- Deadly limb: the life of the patient may be threatened if the limb is
retained.

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 • Severe cellulitis
• Necrotizing fasciitis
• Bone tumor
✓ Dead loss: the affected limb may be considered inferior to an artificial
limb or no limb at all, so amputation can improve quality of life.
• lymphedema,
• RTA (totally destroyed limb),
• mycetoma
✓ Complications of amputation:
1- Complications due to operation : pain, infection,
bleeding, hematoma
2- Contracture in the joints
3- Psychological complications: depression
4- Complications of immobilization
5- Phantom limb: persistent pain sensation in the
amputed limb
6- neuroma: healing of nerve endings by fibrosis. Lead to
formation of very painfull subcutaneous mass at the
end of the stump
To avoid neuroma cut the nerve under tension
7- flap necrosis: skin & muscle directly on bone leading
to pressure necrosis and ulceration
✓ Most common cause of limb amputation in Sudan is diabetic septic foot.

❖ Aneurysm:

Abnormal dilatation of an artery more than double its diameter

(e.g.: Aorta normal diameter 2cm

AAA is when the diameter >4cm)

✓ Causes:

1-atherosclerosis 2-congential

3-infections (syphilis)

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 ✓ Types: 1-fusiform 2-saccular
❖ Abdominal aortic aneurysm AAA:

If diameter >4cm, but a symptomatic. Follow up every 6 months using

Abdominal US.

✓ Indications for surgery:

A- if symptoms developed

1-pain 2-urniary frequency due to pressure on

bladder

3-thrombosis & embolization (acute limb ischemia)

4-impending rupture

- If the aneurysm ruptured mortality is 50%

- If the aneurysm not ruptured mortality is 5%

B- diameter >5.5 cm even without complications

C- dilatation of >1cm per year
✓ Surgeries: Open surgery or Stent
- Open surgery:
- Clamp the aorta and put Dacron graft inside the aorta then cover the graft
with aorta (aneurysm sac), to avoid aorto-eneteric fistula (present with
hematemesis)
❖ AV fistula:

Abnormal connections between artery and vein

✓ Causes:

1-iatrogenic most common, dialysis patient

2-congenital 3-trauma (stab wound)

✓ Examination of fistula:

- On inspection: scar/ mass/dilated veins

- On palpation: thrills, palpable mass
- On auscultation: bruits

✓ Complications of AV fistula:

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 1- shifting blood from artery to vein so increase the venous return resulting
in hyper dynamic circulation and heart failure (especially with congenital
AV fistula)
2- ischemia distal to the fistula (steal syndrome)
3- rupture (most serious) cause massive bleeding and death especially in
renal failure patients
✓ Management of AV fistula complications is by ligation or embolization.
✓ DDx of AV fistula is pulsatile neck lump

1-carotid aneurysm

2-carotid body (chemoreceptors) tumor

❖ Subclavian steal syndrome SSS:

Syncopial attack and fainting following use of upper limb.

Subclavian artery gives vertebral to the brain

SSS is the stenosis of subclavian artery before the origin of vertebral artery, so
only during use of the upper limb the blood supply to the brain stopped.

❖ Varicose veins:
✓ Superficial veins:

1-long saphenous vein from medial malleolus drain into the femoral vein

2-short saphenous from lateral malleolus drain into the popliteal vein

✓ Deep veins:

1-anterior tibial vein 2-posterior tibial vein

3-peroneal vein

Deep veins drain into popliteal, from popliteal to femoral, and to iliac, and iliac
drain into the inferior vena cava

✓ There are connections between deep and superficial systems:

1-saphenofemoral junction between the long saphenous and femoral system

2-saphenopopliteal junction between the short saphenous and popliteal system

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3-small connections called perforators

The connections guarded by one way valves which prevent the flow of blood
from the deep to the superficial system

✓ Varicose veins: are abnormally tortious elongated superficial veins due to

valve incompetence
✓ Causes:

1-hereditary 2-long standing occupation

3-pelvic mass or pregnancy (due to increase the pressure inside the pelvis
cause the back flow of blood from the deep to the superficial system)

4-DVT (obstruction of flow from deep system leading to back flow to the
superficial system)

5-AV fistula

✓ Clinical features:

- Itchy
- Break through the skin
- Venous ulcer: painless in the medial malleolus, red base (because of the
congestion of blood)
- Skin pigmentation due to hemosiderin deposition
- Lipodermatosclerosis (thickening of the sclerosis of the skin)
- Superficial thrombophlebitis
- rupture bleeding (most serious)
❖ varicose vein at the saphenofemoral junction form cyst called saphena varix
(DDx: 1-lipoma 2-hernia)

✓ Clinical test for varicose is tourniquet test

✓ Investigations:
1- doppler
2- duplex
3- venography or varicography
✓ Treatment:
1- stocking grade 2 (grade 1 for cosmetic surgery, grade 3 for lymphedema)
2- sclerotherapy injection of STDs (sodium tetra diethyl sulfate)

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 3- surgery: ligation of the valve – evulsions of the perforators – stripping of
the superficial veins
➢ Complications of surgical management:
1- saphenous nerve injury
2- recurrence of the varicose
- Complications of venous ulcers is Marjolin’s ulcer (premalignant) can
become squamous cell carcinoma
➢ Treatment of venous ulcer:
- 4 layers compression bandage and follow up every 2 weeks
- If the ulcer not healing suspect squamous cell carcinoma, do incision
biopsy.
- (+ve) excision of the ulcer and slain graft.
➢ Neuropathic ulcer
- In Diabetic patient of patients with peripheral neuropathy, found in the
sole of the foot

❖ Deep vein thrombosis DVT:

➢ Virchow triad:

1-stasis 2-endothelial injury

3-hyercoalguble state

➢ Risk factors:
1- obese patient undergoing abdominoplevic or orthopedic surgery
2- immonility
3- pregnancy - use of contraceptives
4- congenital hemophilia (deficiency of protein C, protein S and ant-
thrombin III)
5- heart failure – Nephrotic syndrome

➢ Clinical features:

- unilateral leg pain

- swelling
- red, shiny skin
- pitting edema

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 - dilated veins
- hotness

➢ DDx:

1-cellulitis 2-congenital AV fistula

3-ruptured backer’s cyst

➢ Diagnosis:

1-duplex or venography (gold standard is Duplex)

2-D-diamer

➢ Complications:
1- Pulmonary embolism
2- varicose vein + venous ulcer due to chronic venous insufficiency (in this
situation removal of the varicose vein is contraindicated, only treat the
DVT). This called post phlebitis syndrome.

➢ DVT probability: Wells score system

1- bedridden >3days
2- paralysis, paresis, casting
3- active malignancy
4- recent surgery
5- dilated veins
6- pitting edema
7- tenderness of the whole leg
8- swelling in entire leg
9- diameter of leg >3cm compared to the other leg

❖ 3-9 high probability

➢ Management:
1- unfactinated bolus IV heparin 80 units/kg and maintenance 15 units/kg
2- change to warfarin if INR 2-3 for at least 6 months
3- if recurrence warfarin for life, do screening for hypercoagulabilty
- followup: APPT , INR

❖ Diabetic septic foot:

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 ➢ Triad:
1- poorly controlled diabetes mellitus
2- foot neuropathy (chronic ischemia of the limb lead to wound or ulcer)
3- sepsis: infected wound, redness, pus offensive cellulitis

➢ Work up for diabetic septic foot:

1- Assess the patient general condition: CVS , Renal
2- General investigations:
- CBC
- RFT
- Random blood glucose
- HBA1c
3- Admission, start insulin, dietary support , blood transfusion if needed
4- treat the comorbidities
➢ Causes:
A- Neuropathic
- In the sole and pressure areas.
- Signs: numbness, loss of sensation, and Charcot joint deformity.
B- Ischemic
- Painful, white base ulcer in the lateral malleolus.
- Signs are: pale, hairless, absent pulse, callus formation, brittle nails and
ABPI <0.9
➢ Management according to the cause:

If neuropathic:

- Foot care (inspection and daily cleaning, nails cutting)

- Gabapentin for pain
- Vitamin B12
If ischemic:

- Asprin / clopidogril + statin

- Duplex or angiography and consult vascular surgeon to perform balloon
dilatation angioplasty or bypass graft
For infections:

- Swab for culture and sensitivity

- Give broad spectrum antibiotics

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 ❖ Lymphedema:

Unilateral swollen leg due to lymphatic obstruction

➢ Causes:
1- Congenital lymphedema : Meig’s syndrome,.Lymphedema tarda
2- acquired: filariasis, W. Bancrofi, surgical removal of lymph nodes, turner
syndrome, yellow nail syndrome, radiation

➢ Grading of lymphedema:

Grade I: pitting edema, disappear on elevation

Grade II: non pitting edema, doesn’t disappear on elevation

Grade III: skin thickening, you can’t pinch the skin

➢ Complications:

1- difficulty walking
2- cellulitis (staph/strep)
3- precancerous (lymphangioma, lymphangio sarcoma)

➢ Investigations: lymphangiography
➢ Treatment: multidisciplinary and supportive

1- analgesia
2- antibiotics
3- grade III stocking
4- if very advance amputation

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