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Table of contents:
1. Basics of surgery … 5
a. Some basics to start with ☺
b. Wounds (types & complications).
c. Pre-operative evaluation.
d. Post-operative complications.
e. Post-operative fever.
2. Soft tissue & skin diseases … 24
a. Cellulitis.
b. Necrotizing fasciitis.
c. Abscess.
3. Esophagus … 29
a. Anatomy review.
b. Achalasia.
c. Diffuse esophageal spasm.
d. Esophageal diverticula.
e. Esophageal ring/web.
f. Esophageal caustic injury.
g. Esophageal perforation.
h. Gastroesophageal reflux disease.
i. Esophageal cancer
j. Esophagitis.
k. Esophageal hiatal hernia.
4. GIT bleeding … 39
5. Acute abdomen … 44
6. Infections of the peritoneum … 49
7. The stomach … 53
a. Stomach & duodenum anatomy.
b. Peptic ulcer disease.
c. Complications of peptic ulcer disease.
d. Surgery in peptic ulcer disease.
e. Gastric cancer.
8. Hepatobiliary system … 62
a. Liver & gallbladder anatomy.
b. Hepatic abscess & cysts.
c. Liver tumors.
d. Gallbladder diseases.
e. Gallbladder cancer.
9. The pancreas … 78
a. Anatomy of the pancreas.
b. Acute pancreatitis.
c. Chronic pancreatitis.
d. Pancreatic cancer.
e. Islet cell tumors.
10. Hernia … 90

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11. The intestines … 104

a. Anatomy review.
b. Small bowel obstruction.
c. Acute mesenteric ischemia.
d. Chronic mesenteric ischemia.
e. Small bowel neoplasia.
f. Fistulas.
g. Ostomies & stoma.
12. The appendix … 116
13. The colon … 124
a. Anatomy of the colon.
b. Inflammatory bowel disease.
c. Diverticulosis & Diverticulitis.
d. Large bowel obstruction.
e. Colon neoplasia.
14. Rectum & Anus … 140
a. Anatomy of rectum & anal canal.
b. Anal hemorrhoidal disease.
c. Anal fissures.
d. Ano-rectal abscess.
e. Anal fistulas.
f. Pilonidal disease.
g. Anal cancer.
15. The Breast … 152
16. Neck & thyroid … 171

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Basics of
Surgery

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Basics of surgery (Introduction)

• Surgical instruments:
o For cutting & dissecting:
▪ Scalpel (‫ >> )مشرط‬available with different blade sizes (number 10 is mostly
used).
▪ Scissors:
• There is straight & curved scissors.
• Tips may be sharp-sharp, sharp-blunt, blunt-blunt.
• (1) Mayo scissors >> for tough tissues (straight or curved).
• (2) Metzenbaum scissors >> for delicate tissue (plastic surgery,
intestines).
• (3) Iris scissors >> designed for fine details, thinner than mayo (straight
or curved).
(1) • (4) Suture removal scissors >> may be straight or angled.
• (5) Bandage scissors.

(2) (3) (4) (5)

o For grasping & holding:

▪ Hemostat forceps (straight or curved):
• Used for arteries, veins, capillaries.
• It has no grooves (compared to needle holder).
• Mosquito (serrations along entire tips).
• Kelly forceps (serrations along part of tip).
▪ Thumb forceps:
• Used to hold skin & tough tissues.
• DeBakey forceps.
• Adson forceps (rat-toothed).
• Allis tissue forceps (multi-toothed).
▪ Sponge holder:
• Used to hold surgical gauze.
• Has a hole in each tip.
▪ Needle holder:
• Has a groove in the surface of its tips.
• Used to hold the suture needle.
o Retractors:
▪ Used to hook & retract edges of a wound for a better view.
▪ There is different types; Manual retractors, self-retaining retractor, Deaver
retractor, sweetheart retractor, army-navy retractor, Richardson retractor, rip
spreader.

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o Suctioning devices:
▪ Poole suction >> suctioning peritoneal fluid.
o Electrocautery (diathermy):
▪ 2 modes >> COAG & CUT (higher) mode.
▪ 2 types >> monopolar & dipolar.
▪ It can be placed on a metal instrument to transmit current for
cutting or directly used on tissue.

• Types of surgical incisions:

o Kocher incision >> right subcostal incision, usually done for open cholecystectomy.
o Midline laparotomy >> through linea alba.
o Paramedian incision >> lateral to midline.
o McBurney’s incision )gridiron incision( >> Muscle splitting technique is practices in
order to gain access to the appendix (the slanting one).
o Rocky-Davis (Lanz incision) >> also muscle splitting to gain access to appendix (the
horizontal one).
o Pfannenstiel incision >> Low transverse abdominal incision. Used for C-section,
myomectomy, prostatectomy, cystectomy.
o Groin/inguinal incision >> Over medial half of inguinal canal. Used for inguinal hernia
repair, orchidopexy, testicular cancer.
o Other incisions >> see the fig below.

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• Suturing & stitching:

o Suture is the material used to approximate tissue or ligate a blood vessel.
o Size of thread is mentioned as (number + O) in which the smaller the number, the
thicker the diameter (1-O > 3-O).
o Suture material are divided into:
▪ Absorbable or non-absorbable.
▪ Monofilament or multifilament.
▪ Synthetic or natural.
o Natural sutures (not man-made):
▪ Examples >> silk & catgut.
▪ Catgut is made from collagen fibers of the intestines of healthy cows & sheep.
▪ Useful in securing drains, but they may provoke a tissue reaction.
o Synthetic sutures (man-made):
▪ Examples >> PDS, nylon.
▪ They are more predictable & have less tissue reaction.
o Monofilament sutures (single stranded):
▪ PROS >> lower risk of infection.
▪ CONS >> they are very slippery (doctors frequently apply saline over their
gloved fingers while handling them).
o Multifilament sutures (multiple strands):
▪ PROS >> easier to handle, stronger, more secure.
▪ CONS >> higher risk of infection, organisms can collect in between strands.
o Absorbable sutures:
▪ They not need to be removed because they are dissolved by body enzymes.
▪ Often used in deep tissues & tissues that rapidly heals (bowel, stomach,
bladder).
▪ Monocryl >> monofilament, for subcuticular skin closure.
▪ PDS >> monofilament, used for abdominal wall closure, takes 6 months to
absorbed.
▪ Vicryl >> multifilament, used for bowl anastomosis & SC tissue closure.
o Non-absorbable sutures:
▪ They need to be removed & don’t get broken in order to provide long-term
support.
▪ Used for tissues that heals slowly such as fascia & tendons.
▪ Synthetic:
• Prolene >> monofilament, for arterial anastomosis.
• Polyamide/Ethilon >> monofilament, closing skin wounds.
▪ Natural:
• Silk >> multifilament, securing drains.
• Catgut >> not used as often.
o When we remove the sutures:
▪ Rapidly healing skin surfaces are removed earlier.
▪ Face, neck, & scalp are removed >5 days.
▪ Abdominal, proximal limbs & clips are removed >10 days.
▪ Distal extremities are removed >14 days.
▪ SSI are removed as soon as possible.

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• Laparoscopy (important to know):

o Generally speaking, surgeries can be divided into open surgery or other minimally
invasive surgeries (e.g. laparoscopy).
o Surgeries that can be done laparoscopically (there is a large list):
▪ Cholecystectomy.
▪ Appendectomy.
▪ Inguinal & ventral hernias.
▪ Nissen fundoplication & Bariatric surgeries.
▪ Others (morcellation & splenectomy, colostomy, bowel resection).
o Procedure steps:
▪ Peritoneal cavity is inflated with CO2:
• How? Either by open method or veress needle.
• Why? Because it’s less volatile (non-combustable) & less solubility in
blood (lower risk of gas embolism).
▪ Infra-umbilical incision >> insert the guided camera.
▪ Introduction of instruments using a trochar through small incisions known as
ports (there is different ports locations depending on the surgery).
o Advantages:
▪ Less invasive, smaller incision, less pain.
▪ Shorter duration of surgery & need of anesthesia.
▪ Shorter post-op stay (patient can directly eat – less risk of paralytic ileus).
o Disadvantages:
▪ Introduction injuries (trochar may injure the intestines & solid organs).
▪ CO2 embolus (triad of hypotension, low end tidal CO2 & mill-wheel murmur).
▪ Post-op shoulder pain (due to irritation of the diaphragm by inflated air).
▪ IVC compression (resulting in reduced venous return & cardiac output leading to
hypotension).

Pnemoperitoneum (air under diaphragm) is ideally seen on

erect CXR under the right hemidiaphragm.
If erect CXR cannot be done, a left lateral CXR can be done.
Remember that post-op you may normally find
pnemoperitoneum for up to 1 week

1. Hemostasis (Immediate Response)

Goal: Stop bleeding.
Platelets aggregate to form a clot and release factors like thrombin and fibrin to stabilize the clot.
This also releases growth factors (e.g., platelet-derived growth factor [PDGF]) that recruit cells for repair.
2. Inflammatory Phase (0–3 days)
Goal: Remove debris and fight infection.
Neutrophils and macrophages infiltrate the area to clean the wound and release cytokines, attracting
fibroblasts and keratinocytes.
3. Proliferative Phase (3–24 days)
Goal: Rebuild the tissue.
Fibroblasts produce collagen, new blood vessels form (angiogenesis), and epithelial cells migrate to cover
the wound.
4. Maturation/Remodeling Phase (21 days–1 year)
Goal: Strengthen and organize the tissue.
Collagen is remodeled from type III to type I, and the wound gains tensile strength.
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Wounds

• Stages of wound healing (Review):

o Hemostasis:
▪ Damage to endothelial lining of vessels expose the sub-endothelial collagen &
vWF which will initiate platelets drive (primary hemostasis).
▪ In addition, transient vasoconstriction & activation of coagulation cascade will
occur (secondary hemostasis).
▪ Hemostasis is impaired in:
• Patients on anti-platelets or anti-coagulation therapy.
• Liver & renal disease.
• Bleeding diasthesis.
o Inflammation:
▪ Cytokines release from damaged cells will call the leukocytes (PMNs &
macrophages).
▪ Goal is to (1) clear up cellular debris, (2) killing of bacteria.
▪ Cardinal signs of inflammation >> redness, hotness, swelling, pain.
▪ Inflammation process is impaired in >> immunocompromised patients (e.g.
AIDS, transplantation, patients on steroids or chemotherapy).
o Proliferation phase:
▪ Cells responsible for this phase are >> fibroblasts, endothelial cells, & epithelial
cells.
▪ Granulation tissue formation:
• FGF (fibroblast growth factor) stimulates nearby fibroblasts to lay down
collagen.
• Multiple growth factors (e.g. PDGF, TGF, FGF, & VEGF) stimulates the nearby
damaged vessels endothelium to grow promoting angiogenesis.
• This will result in granulation tissue (red beefy tissue).
• Small clean wounds that heal with primary intention have minimal
granulation tissue & rapid epithelialization (within 48h).
Epithelialization is prolonged ▪ Epithelialization:
by infections, necrotic tissues, • Epithelial cells from wound edges are stimulated to proliferate from the
poor vascularity, hematomas, outside into the bare granulation tissue to cover it.
seromas, too tight or loose
suturing, prolonged surgery
• This epithelium is immature; devoid of appendages (no sebaceous
time, hypothermia glands or hair follicles).
▪ Wound contraction & remodeling:
• Myofibroblasts area activated to contract the wounds in order to
approximate the edges to promote healing.
• Note that wound contraction is not the same of scar contraction which
is pathological (e.g. neck burn scar that results in torticollis).
• Remodeling occur over months to years in which the healed wound
start to regain tensile strength (but it will never be like its previous
strength).

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• Types of wound healing (important to know):

o Primary intention:
▪ Closure of a clean surgical incision or a traumatic laceration using sutures or
staples. (i.e. we effectively help the tissue to heal by stitching it, cleaning it,
covering it with dressing).
▪ Epithelialization occurs within 48h (dressing should be removed day 2 post-op).
o Secondary intention:
▪ Wound closure occur without approximating it with sutures or staples.
▪ Occur in >> (1) Patients not seeking medical care, (2) Infected wounds, (3) Very
large gaping wounds.
▪ Management:
• Wound irrigation (with saline).
• Packing the wound.
• Sterile dressing.
• Frequent re-assessment.
o Tertiary (delayed primary) intention >> The wound is left open with appropriate care
for 3-5 day, then it closed by sutures.

• Factors affecting wounds healing:

o Patients factors:
▪ Age >> elderly have less healing capability.
▪ Poor nutrition >> especially in vitamin C & A or proteins deficiencies.
▪ DM >> poor immunity & increased risk of infections.
▪ Chronic renal or liver diseases >> due to uremia & bleeding.
▪ Immunosuppression >> steroids or chemotherapy.
▪ Immunocompromised >> AIDS.
▪ Poor vascularity >> CHF, shocked patients.
o Local factors:
▪ Presence of foreign bodies.
▪ Surgical site infection.
▪ Necrotic tissue around the suture.
▪ Hematoma or seroma.
o Iatrogenic factors:
▪ Long OT time.
▪ Cold OT or hospital wards (hypothermia).
▪ Very tight or loose suturing.

• Complications of poor wound healing (important to know):

o Wound healing complications are divided in:
▪ Early >> (1) delay wound healing, (2) infections, (3) fascial dehiscence.
▪ Late >> (1) keloid & hypertrophied scars, (2) incisional hernia, (3) chronic wound
pain.
o Hypertrophic scar:
▪ Scar is raised above the level of the original wounds BUT not beyond the
margins.
▪ Regress spontaneously within months.

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o Keloid scar:
▪ Scar is raised above and beyond the margins of the original wound.
▪ Can occur with simple cuts (e.g. vaccinations or piercing of ears).
▪ Patient may have +ve family history of keloids.
▪ Locations >> ear lobules, shoulder, parasternum, back.
▪ Management:
• Note that keloid is usually difficult to treat & often recurs when
removed even worse than the first time.
• Intra-lesional steroids.
• Continuous pressure (using silicone gel sheets).
• Surgical excision (last resort, usually with adjuvant therapy).
o Fascial/wound dehiscence:
▪ Incomplete separation of wound site in which the deeper sutured layer (fascia)
have opened but the overlying layer are closed by sutures.
▪ Risk factors:
• Inadequate suture type & method (most important).
• Poor wound healing.
• Patients factors >> old age, obesity, ascites, coughing, vomiting,
increase intra-abdominal pressure.
▪ Clinical features:
• Classic salmon-colored discharge from the wound.
• Patients can present directly with complications; visceral evisceration
(burst abdomen with viscera protruding out).
▪ Complications >> paralytic ileus (prevented by warm saline), infection,
recurrence.
▪ Management:
• IV fluids + broad spectrum antibiotics (STAT).
• Sterile packing (saline soaked gauzes) & sterile dressing.
• Emergent surgery especially in evisceration.

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Types of wounds

• Non-surgical (Review):
o Closed wounds:
▪ Contusions )‫(كدمة‬:
• Blunt trauma resulting in extravasation of blood from capillaries.
• Can occur in internal organs such as brain & lung (which can result in
edema, especially in closed spaces such as cerebral contusion).
▪ Hematoma:
• Excessive internal bleeding that is clotted & slowly reabsorbed.
• May occur in any wound or surgical incision.
• Large hematomas could result in:
o Poor wound healing .
o Mass effect (e.g. airway obstruction).
o Infections or jaundice.
o Consumption of platelets.
• Management >> small hematomas can be aspirated, while large ones
may need surgical evacuation.
o Open wounds:
▪ Abrasion:
• Scraping of superficial layer of skin due to friction against hard surface.
• Requires anti-septic cleaning & non-adherent dressing.
▪ Laceration:
• Traumatic wounds with irregular, jagged edges.
• Have high risk of infection & tissue devitalization.
▪ Degloving injury:
• Stripping of skin & subcutaneous tissue from underlying fascia, injuring
its blood supply.
• Occur usually in limbs, but it can also occur in trunk & face.
• Replantation, revascularization, skin grafting, or skin flaps or even
amputation may be necessary.
▪ Penetrating wounds:
• Caused by pointed objects or high velocity objects with pointed tip.
• It may have small entry wound, but it can cause severe damage in
viscera & surrounding tissue.
▪ Bites:
• Human bites or hit to teeth >> eikenella.
• Cats & dogs >> pasteurella & rabies.
▪ Management of open wounds:
• ABCs.
• Pressure on site of bleeding.
• Assess neurovascular structures (pulses & sensations).
• Sterile dressing.
• Tetanus Ig & toxoid.
• Prophylactic antibiotics.
• Surgical debridement (if needed).

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• Surgical wounds (HIGH-YEILD):

o Clean:
▪ Any surgery that doesn’t enter the following systems; respiratory, GIT,
hepatobiliary, urogenital.
▪ Risk of SSI >> <1%.
▪ There is no need for prophylactic antibiotics (however, prophylactic antibiotics
must be given in prosthetic heart valve, arthroplasty, hernioplasty with mesh).
▪ E.g. hernias, thyroid surgery, breast surgery, vascular surgery, head surgeries.
o Clean-contaminated:
▪ Surgeries that enter the above systems with no infection or spillage.
▪ Risk of SSI >> 1-5%.
▪ Prophylactic antibiotics is needed + Dakin solution (Na hypochlorite).
▪ E.g. elective cholecystectomy, colorectal surgeries.
o Contaminated:
▪ Surgeries that enter the above systems and there is an infection or spillage.
▪ Risk of SSI >> 10-20%.
▪ Prophylactic antibiotics is needed.
▪ E.g. acute cholecystitis, uncomplicated appendicitis.
o Dirty:
▪ Trauma patient with devitalized tissue, perforated viscus, & emergent surgery.
▪ Risk of SSI >> >40%.
▪ E.g. perforated appendicitis, diverticulitis, exploratory laparotomy for abscess,
duodenal ulcer perforation, amputation of infected ulcer or foot.
o Prophylactic antibiotics:
▪ Given 30min prior to operation & once again if surgery lasts >4h.
▪ Choice of antibiotic vary according to the system.
▪ In general >> cefazolin (1st generation cephalosporin) + metronidazole.

Surgical wounds are classified into four categories:

Clean: No infection; no entry into respiratory, GI, or GU tracts (e.g., hernia repair).
Clean-Contaminated: Controlled entry into respiratory, GI, or GU tracts (e.g.,
cholecystectomy).
Contaminated: Major spillage or open, fresh wounds (e.g., bowel perforation).
Dirty/Infected: Old wounds, existing infection, or necrosis (e.g., abscess drainage).

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Pre-operative evaluation (HIGH-YEILD)

• Overview:
o Importance of pre-operative evaluation:
▪ Assess whether or not this patients is fit for surgery.
▪ Decrease the risk of complication.
▪ Prepare the patient for the surgery.
▪ Reveal in drugs allergy (important to anesthesia).
o American society of anesthesiologists (ASA) classification:
▪ ASA I >> healthy patients.
▪ ASA II >> mild to moderate systemic diseases (e.g. well controlled DM).
▪ ASA III >> severe disease process with morbidity but not incapacitating (e.g.
poor controlled DM).
▪ ASA IV >> severe disease that is a constant treat to life (e.g. CH, severe angina).
▪ ASA V >> a moribund patient who is not expected to survive without surgical
procedure (e.g. ruptured aortic aneurysm).
▪ ASA VI >> brain dead patient / organ donor patients.
o Pre-operative history:
▪ Indications of surgery.
▪ Past medical history + their medications + disease progress.
▪ Past surgical history & anesthesia problems.
▪ Medications history & Drugs allergy.
▪ Social history (smoking, drugs abuse, alcohol).
o Pre-operative examinations:
▪ General inspection:
• Assess consciousness.
• Oriented to time, place person.
• Mood (relaxed, agitated, irritated).
• Obvious distress (e.g. gasping for air, toxic appearance).
• Skin manifestations (jaundice, pallor, cyanosed, plethoric).
▪ General exam:
• Vitals (pulse, BP, RR, temperature).
• Examine specifically for reason of surgery (e.g. cardiology exam,
respiratory exam, abdominal exam).
• Lower limb exam (inspection, peripheral pulses, edema, homan’s sign,
calf tenderness).

• Pre-operative investigations & preparation:

o Standard investigations for all patients:
▪ CBC >> assess Hb & WBCs for any infections.
▪ Blood grouping & cross matching >> needed for any urgent blood transfusion.
▪ RFTs (BUN, Cr, electrolytes, eGFR) >> baseline of renal function.
▪ LFTs >> base line of liver function (most of anesthetic drugs are hepatotoxic).
▪ Coagulation profile >> assess bleeding tendency.
▪ CXR >> assess any abnormalities.
▪ ECG >> assess any arrhythmia.

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o General preparation for all patients:

▪ Consent.
▪ NPO (no water or food for at least 6-8h) + IV cannulation.
▪ DVT prophylaxis (SQ, LMWH 2h pre-op).
▪ Antibiotic prophylaxis (depending on type of surgery):
• Clean (e.g. thyroid, head, breast, cardio, extremities) >> no need.
• If not clean:
o Antibiotic prophylaxis is given 30min before surgery, another
dose must be given if the surgery lasted longer than 4h.
o Generally cefazolin is given.
o GI surgery >> cefazolin + metronidazole.
o Urology >> ciprofloxacin.
o Head & neck >> cefazolin + gentamycin.
o Special cases:
▪ Cardiology:
Fluid distribution post-op in • Patients with HF or IHD >> ask for ECHO (assess EF).
HF patients: • Patients must be evaluated by a cardiologist.
During operation, we give IV
fluids, which most of it
• Aspirin must be stopped 7 days before surgery.
moves out of the • Post-op MI (common complication in cardia disease patients):
intravascular compartment o Typically silent or can present with features of HF, Usually occur
(3rd spacing). In 2nd post-op in 2nd or 3rd post-op days.
day, the fluid redistributes
to intravascular
o Previous MI <3 months >> increase risk of post-op MI by 30%.
compartment. In most o Previous MI 3-6months >> increase risk of post-op MI by 10%.
people this doesn’t cause o Previous MI >6 months >> increase risk of post-op MI by 5%.
problems, but in patients ▪ Respiratory:
with HF this can be fatal.
• PFTs may be need in smoker patients or patients with CXR findings.
• Smoker patients needs to stop smoking for a period before surgery.
▪ Liver disease:
• In patients with cirrhosis >> CHILD’s & MELD score.
Jaundice can occur because of • Treat any underlying conditions if found before surgery (e.g. ascites).
defect in coagulation • Note that acute hepatitis is contraindicated to surgery.
synthesis in case of liver
disease. • Pre-op jaundice:
o Always evaluate for the cause before surgery.
Hepatorenal shutdown occur o We worry about bleeding tendency in vitamin K deficiency from
because of bile salt cast malabsorption (secondary to lack of biliary flow).
formation
o Give Vitamin K + antibiotics (due to infection risk) + hydration
(risk of hepato-renal shutdown).
▪ Renal failure patients >> dialyze patients within 24h prior to surgery.
▪ Sickle cell disease patients:
• History >> number of VOC & hospital admissions, blood transfusion, any
current bone pain.
• Anemia is contraindicated to surgery.
• Significant thrombocytopenia (<50,000) may need platelet transfusion.
• Biggest fear is intra-op VOC.
• Steps of pre-op preparation:
o (1) Admit on day before (2) in warm room.
o (3) Oxygenation + (4) IV fluids + (5) HbS level by electrophoresis.

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o (6) Simple blood or exchange transfusion prior to surgery.

o (7) Prophylactic antibiotics.
Patients with chronic RA
may have antlantoaxial ▪ Diabetic patients:
subluxation (C1-C2) which • Order glucose levels & HbA1c.
can result in fatal • Put patient on sliding scale (blood glucose is measured at fixed intervals
consequences during depending of the patients risk factor, and insulin injections is given
preparation of general
anesthesia, hyperflexion of according to the blood glucose level).
neck must be avoided, thus, ▪ Patients with prolonged steroids use (e.g. adrenal insufficiency, RA, SLE):
the anesthesiologist must • Increase steroid doses, then gradually tapper the dose after the surgery.
be addressed to avoid this • Complications >> adrenal crisis (fainting, Coma, hypoglycemia, fever).
▪ Patients with thyroid disease:
• Order TFTs, Ca levels.
Biggest fear is thyroid storm
intra-op (50% mortality) • Give B-blockers to decrease HR + iodine to decrease thyroid vascularity.
• Give anti-thyroid medication (e.g. neomercazole) to achieve euthyroid.
• Laryngoscopy prior to surgery & during surgery to study the vocal cords
Patients with thyroid surgeries for recurrent laryngeal nerve injury.
must be refer to ENT to check • Post-op >> a drain device (I forgot it name) is put after the surgery to
the both sides of vocal cords to
assess any previous damage to
prevent the development of hematoma which can compress the
them before surgery (medico- trachea.
legal issues) ▪ Patient with colorectal surgery:
• Bowel preparation (cleaning bowel before surgery):
o There is different protocols (e.g. drinking fluids, antibiotics).
If we where in the surgery and
o Goal is to prevent spread of colonic bacteria that can result in
we find that the bowel is not
clean, colostomy is done. Then peritonitis.
after proper cleaning of the ▪ Patients with history of DVT:
bowel, a 2nd surgery is needed • Pre-op >> anti-coagulant (LMWH) + hydration.
for the primary anastomosis
• Intra-op >> intermittent pneumatic compression OR compression
stocking OR raise the heal of patient.
• Post-op >> early ambulation & good hydration.
▪ Specific medications:
• Aspirin >> stop 5-7 days before surgery (platelets half-life).
• Warfarin >> measured by INR, stopped 3 days before surgery, start SQ
LMWH and continue post op.

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Post-operative complications (HIGH-YEILD)

• Overview:
o Post operative complications are divided into >> anesthesia & surgical.
o Anesthesia complications:
▪ Altered mental status, nausea, vomiting, jaundice, constipation.
Malignant hyperthermia ▪ Throat soreness.
occur due succinylcholine. ▪ Arrhythmia & MI.
Antidote is dantrolene ▪ Urinary retention or Anaphylactic reaction.
▪ Hyperthermia or Hypoventilation.
▪ Malignant hyperthermia (AD genetic disorder).
o General surgical complications (for any surgery):
▪ Immediate (post-op day 1):
• Primary hemorrhage >> needs replacement of blood loss & may return
to OT for exploration. May complicated to shock & renal failure.
• Basal atelectasis >> most common cause of post-op fever in POD-1.
• Surgical site infection >> only if the causative organism is streptococci
or clostridia.
▪ Early (2 days – 3 weeks):
• Mental status changes >> tired, confused, delirious that occur
secondary to anesthesia, electrolytes imbalance, dehydration.
Hypokalemia is the most • Constipation >> secondary to sedatives or paralytic ileus.
common electrolyte imbalance • Fever >> discussed later in details.
causing paralytic ileus • Reactive hemorrhage >> occur after the 3rd spaced fluid return to the
circulation & increases BP.
• Small bowel obstruction (SBO) >> due to fibrinous adhesions (most will
resolve spontaneously).
• Other >> wound hematoma or seroma, wound dehiscence.
▪ Late (months to years):
• Small bowel obstruction (SBO) >> caused mostly by adhesions.
• Incisional hernia >> can also result in SBO.
• Poor wound healing or non healing wounds.

• Post-operative respiratory failure:

o Causes:
▪ Pulmonary embolism.
▪ CO2 necrosis (in COPD patients).
▪ Atelectasis or mucous pulg.
▪ Pneumonia (infection or aspiration).
▪ Pulmonary edema (MI, HF, AKI).
▪ Narcotic overdose (respiratory depression).
o Investigations:
▪ Labs >> ABG, RFTs, cardiac enzyme, coagulation profile.
▪ Imaging/procedure >> CXR, ECG, ECHO, CT angio.
o Management:
▪ Always ABCs + Frequent monitoring.
▪ Management is directed towards the cause.

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• Aspiration pneumonia:
o Occur due to aspiration of oropharyngeal secretions.
o Chemical pneumonitis is different from aspiration pneumonia, in which chemical
pneumonitis result from aspiration of gastric contents.
o Risk factors:
▪ Being unconscious (e.g. GA or comatose patients).
▪ Absent gag reflex (stroke, MS).
▪ Seizures.
o Common affected areas:
▪ The right lung is most common affected (due to angle of the carina).
▪ Supine or prone patients >> posterior segment of upper lobe are most
commonly affected.
▪ Upright patients >> upper segment of lower lobe are commonly affected.
o Complications:
▪ Chemical pneumonitis >> ARDS, lung abscess.
▪ Aspiration pneumonia >> lung abscess, difficult to treat pneumonia.
o Management:
▪ ABCs & supplemental oxygen.
Antibiotics are given
▪ IV broad-spectrum antibiotics >> clindamycin + ciprofloxacin (fluroquinolones),
because there is high risk
of developing secondary Augmentin (beta-lactams) for 7-10 days.
infection ▪ If hospital acquired >> add vancomycin (to over MRSA) &
piperacillin/ceftazidime (to cover psudomonas).
o Prevention >> NPO prior to surgery (6-8h) & rapid sequence induction for anesthesia.

• Central line infections:

o Causes:
▪ S. Epidermis (Coagulase -ve staphylococcus).
▪ S. Aureus.
o Risk factors >> Total parenteral nutrition given through central line.
o Central line associated blood stream infection (CLABSI):
▪ Central line >2 days.
▪ +ve blood culture.
▪ No other source infection.
o Clinical features:
▪ Fever.
▪ Pus and erythema at central line insertion site.
▪ Unexplained hyperglycemia.
▪ Complications >> septicemia (altered mental status, high fever, tachycardia, low
BP).
o Management:
▪ Remove the line & send it for culture & sensitivity.
▪ Begin empirical IV antibiotics.
▪ If necessary, place a new central line at different site.

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Post-operative fever (HIGH-YEILD)

• DDx of post-operative fever:

o Wind >> basal atelectasis (POD1-2), pneumonia.
o Water >> UTI (POD3-4), urinary retention.
o Wound >> SSI (POD5-7).
o Walk >> DVT/PE (POD7-10, but can occur earlier).
o Wonder drugs >> complication of medications.
o Wonky gland >> adrenal crisis, thyroid storm.

• Basal atelectasis:
o Collapse or closure of a lung resulting in decreased or absent gas exchange.
o It’s the most common cause of post-op fever within 24h.
o Symptoms >> fever, SOB, & cough.
o Signs >> high RR & hypoxemia, difficulty in completing sentences, dullness on
percussion, reduced breath sounds over lungs, +/- crackles.
o Management:
▪ Sitting upright & early ambulation.
▪ Incentive spirometry (breath in).
▪ Chest physiotherapy.
▪ +/- bronchodilators or CPAP.

• Post-op Pneumonia:
o Occur more commonly in elderly, associated with high mortality rate.
o Symptoms >> fever, productive cough, purulent sputum, dyspnea, pleuritic chest pain.
o Signs >> toxic looking patient, increased tactile fremitus, dullness on percussion,
bronchial breathing, crackles.
o Investigations:
▪ Calculate CURB-65 score.
▪ CBC, electrolytes, BUN.
▪ Sputum culture & staining.
▪ +/- blood culture.
o Management:
▪ Always ABCs, patient need frequent monitoring.
▪ Oxygenation & IV fluids (as needed).
▪ Empirical antibiotics >> cephalosporin + azithromycin.
▪ Definitive antibiotics >> after sensitivity results.

• Post-op Pulmonary embolism:

o Definition >> PE occur when a thrombus in other region (DVT) embolize to pulmonary
vessels causing blockage of blood flow (decrease oxygenated blood to the body).
o Sources of thrombus:
▪ Lower extremity DVT (Iliofemoral DVT is the most common site).
▪ Fat embolism (long bone fractures).
▪ Air embolism (trauma or catheter insertion).

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o Risk factors:
▪ Prolonged embolization (after surgery).
▪ History of DVT or PE.
▪ Long bones fractures, hip/knee replacement.
▪ Age >60ys, Malignancy, Pregnancy or OCPs use.
o Symptoms:
▪ Sudden onset of dyspnea, pleuritic chest pain, hemoptysis.
▪ +/- low grade fever.
▪ +/- syncope.
▪ +/- signs of DVT (erythema, pitting edema, warmth, tenderness).
o Signs:
Hypotension, JVD, clear
▪ Vitals >> Tachypnea, tachycardia, hypoxemia.
lung sounds suggest
obstructive shock ▪ Auscultations >> clear lung sounds, prominent S2 heart sound.
▪ Shock + rapid circulatory collapse; hypotension, syncope, RHF (large PE).
o Investigations & Diagnosis:
▪ Well’s criteria:
Give 3 points for each Give 1.5 points for each Give 1 point for each
S&S of DVT in lower limb Tachycardia Hemoptysis
Prolonged immobilization (>3days)
Active malignancy or
Alternative diagnosis unlikely OR Surgery within the last month
chemotherapy
Previous history of PE or DVT
Score <4 >> low probability (start with D-dimer)
Score >4 >> high probability (start with CT angio)

▪ Best initial tests are CXR, ECG, & ABG:

• CXR >> usually normal, R/O other DDx (e.g. pneumonia, atelectasis).
S1Q3T3 pattern (suggest right • ECG >> sinus tachycardia, S1Q3T3 pattern (rare but specific).
heart strain) • ABG (Can be normal ☺):
Large S wave in lead 1, deep Q
wave & T wave inversion in lead 3
o Low PaO2 & PaCO2.
o High pH (respiratory alkalosis) due to hyperventilation &
washing out CO2.
▪ D-dimers:
• Very sensitive but not specific (high also in MI, pneumonia, CHF).
• Skip D-dimer & do CTPA in high susceptible patients.
▪ CT pulmonary angiogram (CTPA) with IV contrast (test of choice):
• IV contrast is given to visualize lung vessels & identify any blockage.
• It’s contraindicated in renal failure patients.
▪ V/Q scan:
• There will be complete inhalation but with incomplete perfusion (IV
injected labeled albumin).
• Hard to interpret with underlying lung disease (a normal CXR is needed).
▪ Doppler US >> if +ve for DVT, PE suspicious is high (-ve test doesn’t exclude PE).
▪ Pulmonary angiography (gold standard) >> Most accurate but invasive, not
done in emergent sittings.

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o Management:
▪ Emergent management:
• Always ABCs (O2 supplements in hypoxic patients, intubation or
Contraindications are active ventilation may needed).
bleeding, uncontrolled HTN, • LMWH (enoxaparin):
recent stroke o Immediate if suspecting PE (before diagnosing PE).
o Give one bolus, then IV infusion for 5-10 days.
▪ Hemodynamic unstable patients (large PE):
• ABCs & Resuscitation
• Thrombolytic >> streptokinase, t-PA (usually cannot be used post-op).
• Surgical thromboectomy >> in patients with large proximal thrombus.
▪ Long-term treatment:
• Long term anti-coagulant therapy (3-6 months) >> LMWH + warfarin is
The reason why we give heparin is given for 4-5 days until target INR is achieved (2-3). Then oral Warfarin
to counters the early effect of
is initiated for 3-6 months, monitor INR.
warfarin which result in
hypercoagulable state + bridging • Inferior vena cava filter placement:
effect until warfarin action starts o Indicated in recurrent PE, CI of anti-coagulants use, RHF.
o Complications >> Misplacement, perforation, obstruction,
thrombosis.
o Prevention of post-op DVT:
▪ Pre-op >> anti-coagulant (LMWH) + hydration.
▪ Intra-op >> intermittent pneumatic compression OR compression stocking OR
raise the heal of patient.
▪ Post-op >> early ambulation or compression stockings.

• Post-operative UTI:
o Causes:
▪ E. coli (most common).
▪ Staphylococcus saprophyticus, Klebsiella.
▪ Candida (in DM patients).
▪ Proteus enterococci & pseudomonas (nosocomial).
o Risk factors >> (1) Placement of Foley’s catheter, (2) Urinary retention, (3) Female
gender, (4) Patients with DM.
o Clinical features:
▪ Urinary symptoms >> Urinary urgency, frequency, Dysuria & Nocturia.
▪ +/- Low-grade fever.
▪ Pyelonephritis >> toxic looking patient, high-grade fever, chills, nausea &
vomiting, abdominal or flank pain.
o Investigations:
▪ CBC >> assess WBCs.
▪ Urinalysis >> +ve leukocyte esterase & nitrase.
▪ Urine culture & sensitivity testing >> identification of the organism.
▪ If suspecting pyelonephritis >> RFTs, blood cultures.
o Management:
▪ Empirical antibiotic therapy >> IV fluoroquinolone OR 3rd generation
cephalosporins OR ampicillin.
▪ Antibiotic therapy must be given for 5-7 days. Normal urine output 0.5-1
ml/kg/hr, it’s the best
indicator of tissue perfusion

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• Surgical site infection (SSI):

o Risk factors:
▪ DM, obesity, smoking.
▪ Type of surgical wound (contaminated, dirty).
o Classification:
▪ Superficial incisional (skin & subcutaneous tissue).
▪ Deep incisional (involving fascia & muscles).
▪ Organ/space SSI (abscess in organs).
o Timing & causes:
▪ Most SSI occur by POD5-7, causes include:
• S. Aureus (most common).
• E. Coli.
• Enterococcus.
• S. Epidermis.
• Pseudomonas.
▪ Early SSI occur within 24h & its typically caused by:
• Clostridia (bronze-brown weeping wound).
• Streptococci.
o Clinical features:
▪ Incisional site pain.
▪ Surrounding inflammation (erythema, warmth, swelling, tenderness).
▪ +/- purulent discharge.
▪ Complications:
• Delayed wound healing (dehiscence & hernias).
• Abscess, sepsis, fistulas, necrosis & gangrene.
o Investigation:
▪ CBC (show leukocytosis).
▪ Swab of infected site for culture & sensitivity.
▪ CT (If suspecting abscess).
o Management:
▪ Fluid rehydration & pain management.
▪ Removal of skin sutures.
▪ Wound debridement or drainage if necessary.
▪ Irrigation, packing & sterile dressing.
▪ Empirical antibiotics (augmentin & ciprofloxacin).

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Soft Tissue &

Skin Diseases

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Erysipelas >> involves the upper

superficial dermis.
• Cellulitis (HIGH-YEILD): Impetigo >> involve the epidermis.
o Defined as infection of deep dermis & SC tissue.
o Although the infected tissue is abundant with PMNs, there is usually no pus.
o Causes >> GABHS (streptococcus pyogens) & S. Aureus.
o Source of entry >> usually not identified or trivial (scratch or prick). Streptococcus mostly result in
o Clinical features: diffuse cellulitis (due to
▪ Local (usually affects lower limb > face): release of pyrolytic toxins),
while staphylococcus usually
• Signs of inflammation >> Erythema, pain, result in localized abscess
tenderness, warmth.
• Enlarged regional LNs.
• Usually it’s NOT purulent (if present, it may indicate abscess with
DDx of cellulitis
(1) Abscess or necrotizing
surrounding cellulitis).
fasciitis. ▪ Systemic >> moderate to high fever, toxic features (chills, nausea & vomiting,
(2) DVT or ruptured Baker cyst. altered mental status, tachycardia).
(3) Dermatitis & eczema. ▪ Examinations:
(4) Bone or joint infection.
• Assess signs of inflammation:
o Always start with the normal limb.
Complications of cellulitis o Inspect front & back of the limb.
(1) Thrombophlebitis. o Feel temperature (with dorsum of the hand).
(2) Osteomyelitis.
o Check for edema & measure the circumflex of swelling.
(3) Septic arthritis.
(4) Abscess. o Check for calf tenderness & assess ROM.
• Palpate for pulses (dorsalis pedis & posterior tibial).
• Examine regional LNs (usually inguinal LNs).
o Investigations & Diagnosis:
▪ Diagnosis is done clinically.
▪ History >> ask about signs of inflammation, fever, & assess risk factors (e.g. DM,
steroid therapy, HIV, chemotherapy, …etc.).
▪ CBC >> leukocytosis.
▪ ESR & CRP >> high suggesting inflammation.
▪ Glucose & HbA1c >> ordered even if the patient hasn’t has history of diabetes.
▪ RFTs >> assess diabetic nephropathy.
▪ Other tests may be orders depending on severity of disease or if suspecting
complications (blood culture, US, CT, ..etc.).
o Management:
▪ Most of the patients must be admitted, mild cases with no comorbidities can be
treated as outpatient.
▪ (1) Marker the edge of the erythema to assess response to the therapy.
▪ (2) Give IV antipyretic + hydration.
▪ (3) Leg rising (to enhance lymphatic drainage) (4) put patient on insulin sliding
scale (if uncontrolled diabetes).
▪ (5) Empirical IV antibiotic therapy (IV 3rd generation cephalosporins {cephalexin}
+ ampicillin {cloxacillin} for 7-10 days)
▪ In severe symptoms with no improvement in next 48h:
• Consider resistant bacteria (e.g. MRSA) OR abscess formation OR
incorrect diagnosis.
• Give IV broad-spectrum antibiotics; IV vancomycin + meropenum.
• R/O necrotizing fasciitis especially if pain out or proportion.

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• Necrotizing fasciitis (HIGH-YEILD):

o A deep tissue (fascia) infection that destroys muscle fascia & subcutaneous fat.
o Main risk factors >> DM, immunocompromised, peripheral vascular diseases.
o Cause:
▪ Type I >> polymicrobial (most common).
▪ Type II >> Group A streptococcus (S. Pyogens).
▪ Type III >> clostridium perfringes (Gas gangrene).
o Pathophysiology:
▪ It can gain access through a puncture wound or in a surgical wound (especially if
immunocompromised or DM). Then the infection spread rapidly through tissue
planes, causing necrosis & gas within them.
▪ The superficial tissue may appear less affected.
▪ As the infection become more necrotizing, the superficial tissue start to die & a
hemorrhagic bullae may form.
▪ It may progress rapidly resulting in sepsis, limb loss, or even death!!
o Clinical features:
▪ Classic symptoms is pain out of proportion & toxic-looking. Complications
(1) Sepsis & shock.
▪ Patients have high risk of developing sepsis & shock (2) Renal failure.
(hypotension, tachycardia, altered mental status). (3) scarring & cosmetic issues.
▪ Examinations >> the hallmark is crepitus felt on palpation. (4) Limb loss.
o Investigations & Diagnosis:
▪ Definitive diagnosis is done through exploratory surgery.
▪ Labs >> CBC, blood culture, blood glucose, HBA1c, other investigations may be
ordered as necessary.
▪ Skin or tissue culture.
▪ Imaging studies (US, CT, MRI) >> show gas in deep fascia.
o Management (medical emergency):
▪ (1) Admission + IV broad-spectrum antibiotics (meropenem + vancomycin +
clindamycin) (2) strong analgesia.
▪ Surgical exploration + wide surgical debridement are necessary.
o Fournier gangrene:
▪ A subtype of necrotizing fasciitis in which there is an acute necrotic infection of
the scrotum; penis; or perineum.
▪ It is characterized by scrotum pain and redness with rapid progression
to gangrene and sloughing of tissue.
▪ The testis is usually not involved because it has a different blood supply
compared to the scrotum.
▪ Management:
• IV broad-spectrum antibiotics + surgical debridement of the scrotum.
• Plastic surgeons are involved to cover the testis.
o Gas gangrene myonecrosis:
▪ Similar picture of necrotizing fasciitis, but it usually occur secondary to open
wounds that have beed closed off completely by occlusive dressing (good
medium for anaerobes).
▪ Cause >> anaerobic clostridium perfringes.
▪ Clinical features >> greenish/black discoloration, crepitus, foul-smelling
discharge.
▪ Management >> same as necrotizing fasciitis (clindamycin + metronidazole).

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• Abscess (HIGH-YEILD):
o Abscess is defined as localized suppurative inflammation in which there is a collection of
pus surrounded by granulation tissue.
o Pus components >> (1) cellular debris, (2) dead & live bacteria, (3) dead & alive
leukocytes (PMNs).
o Causes >> Pyogenic bacterial infection (most abundant organism is S. Aureus).
o Risk factors:
▪ DM.
▪ Type of surgical wound (dirty & contaminated wounds).
▪ Injection sites (especially in drug abusers).
▪ Foreign body.
o Route of entry:
▪ Direct abscess (wounds, scratches, abrasions).
▪ Local extension from adjacent focus (osteomyelitis).
▪ Lymphatic spread (LN itself may be infected & become an abscess).
▪ Hematogenous spread (bacteremia can gain access to tissue such as liver &
lung).
o Clinical features:
▪ Systemic symptoms:
How to examine a superficial • Fever (may be high, spiking, or intermittent).
mass or lump
(1) Inspection >> site, size,
• Anorexia, malaise, & headache.
shape, surface, skin ▪ Local symptoms:
overlying, surrounding • Throbbing pain & tenderness (may keeps patient awake at night).
tissues, check cough (check • Discharge (which may relieve the symptoms).
for hernia).
(2) Palpation >> confirm
▪ Signs:
inspection, warmth, • Signs of inflammation (erythema, warmth, swelling, tenderness).
tenderness, consistency, • Tender & fluctuating mass.
mobility, reducible, • Regional tender lymphadenopathy.
fluctuating.
(3) Asses regional LNs. ▪ Important DDx: How to test for fluctuation
(4) Percussion & • Cellulitis, furuncle, carbuncle, sebaceous cyst, (1) Put a finger on each opposing
auscultation (usually not side of the lump).
infected hematoma, soft tissue tumors. (2) Press the center of the lump to
done). • If in breast >> inflammatory breast cancer, see if it pushes against the 2
infective or congestive mastitis. fingers on the side.
o Complications of abscess:
▪ Septicemia.
▪ Fistulas or sinus formation.
▪ Rupture & drainage into body cavities.
▪ Specific complications due to related organ.
o Investigations & Diagnosis:
▪ Superficial abscess >> It’s a clinical diagnosis.
▪ Deep abscess >> imaging; CXR, US, CT.
▪ Other tests:
• CBC (may show leukocytosis with left shift).
• Discharge swab for culture & sensitivity.

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o Management:
▪ Role of antibiotics:
• Bigger abscess needs antibiotics.
• Antibiotics must be given to immunocompromised patients, DM, deep
seated abscess (intraperitoneal).
▪ Incision & drainage:
• Patients must be given appropriate sedation & analgesia.
• Done through a skin incision in the OT over the point of dependence.
• The loculi inside the abscess must be broken to ensure adequate free
drainage (ideally by hemostat).
• A cruciate incision is done in large abscess or in anorectal abscess.
• A rubber (penrose) drain may be used in large abscesses to continue
draining pus until none is retrieved.
▪ US/CT-guided percutaneous drainage:
• Done in deep abscesses in which the abscess or its drained contents
may be in dependent areas of the peritoneum.
• Large or multi-loculated pockets may require surgical drainage through
laparotomy/laparoscopy.
Generally speaking, a skin ▪ Steps after drainage:
abscess develops when pus • The cavity is usually irrigated, left opened, and packed (in large cavities).
collects in hair follicles, skin • Then it covered by dry gauze & bandage.
tissue, or under the skin
• It’s re-evaluated in 24-48h with the dressing change.
• Clinical improvement in 3 or so days indicated an adequate drainage.
o Carbuncle VS furuncles (skin abscess):
▪ Furuncle (boils):
• A skin abscess that affect the hair follicle & surrounding tissue.
• It starts as a red & tender lump, which grow & fills rapidly with pus.
▪ Carbuncle >> a collection of furuncles that join together under the skin, they
may affect deep layer resulting into scarring (presents with fever).
▪ Cause >> S. Aureus.
▪ Management >> Antibiotics (cloxacillin or cefazolin) & surgical debridement.

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Esophagus

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• Anatomy of the esophagus (Review):

o Esophagus is defined as the area from the incisor teeth to lower esophageal sphincter
(LES).
o Length >> 40cm in males, 38cm in females (length between UES & LES is 25cm in males
& 23cm in females).
o Length between UES & LES >> 25cm in males, 23cm in females.
o Histology:
▪ Mucosa >> stratified squamous non-keratinized epithelium until the LES.
▪ Submucosa >> rich of lymphatic canals that allows fast longitudinal spread of
neoplasia.
▪ Muscularis:
Only the distal 1-2cm of the • Inner circular & outer longitudinal.
esophagus is intraperitoneal • Upper 1/3 are skeletal muscles (voluntary).
(thus covered with serosa) • Middle 1/3 mixed.
• Lower 1/3 are smooth muscles (involuntary).
▪ Adventitia >> the esophagus is found in the posterior mediastinum
(retroperitoneal), absence of serosa allow fast horizontal spread of neoplasia to
neighboring tissues.
o Areas of narrowing:
▪ (1) At UES level (UES is formed by the cricopharyngeus muscle at level of C6).
▪ (2) When it crossed by arch of aorta & left main stem bronchus (level of sternal
angle, T4-T5 level, 2nd intercostal cartilage).
▪ (3) At LES level (produced by the esophageal hiatus at level of T10).
o Arterial supply:
▪ Cervical esophagus >> inferior thyroid arteries. Remember that the left vagus
▪ Thoracic esophagus >> branches from aorta. nerve is passing anterior to the
▪ Lower esophagus >> left gastric artery. esophagus in esophageal hiatus,
while the right vagus is passing
o Venous supple:
posteriorly
▪ Name of veins follows the arteries.
▪ Upper part drains into systemic circulation; azygous vein.
▪ Lower part drains into portosystemic venous system;
left gastric vein.
o Lymphatic drainage:
▪ Cervical esophagus >> cervical LNs.
▪ Thoracic esophagus >> trachea, tracheobronchial,
posterior mediastinal LNs.
▪ Lower esophagus >> left gastric & celiac LNs.
o Innervation:
▪ The esophagus contains the Miessner (submucosal) &
Auerbach (myenteric) nerve plexus that respond to
parasympathetic action (vagus nerve).
▪ Cervical esophagus >> RLN.
▪ Thoracic esophagus >> vagus nerve.

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Achalasia patients
have increased risk of
esophageal cancer
(squamous cell)
• Achalasia (HIGH-YEILD):
o Acquired motor disorder of esophageal smooth muscle in which the lower esophageal
sphincter (LES) fails to completely relax with swallowing + abnormal peristalsis of
esophageal body (damage to myenteric plexus of nerves in lower esophagus).
o Causes:
▪ Majority of cases are idiopathic.
▪ Adenocarcinoma of proximal stomach (2nd most common cause).
▪ Chagas disease (??)
o Symptoms: DDx of dysphagia
▪ Dysphagia to solid & liquids (Patients tends to eat (1) Intrinsic obstruction;
esophageal web, stricture,
Dr. Hamdy said it’s mainly slowly & drink lot of water to washout food).
achalasia, Zenker’s diverticulum.
for liquid because solid food ▪ Regurgitation of food contents (there may be recurrent (2) Extrinsic obstruction; thyroid
will pass by compression
pulmonary complications secondary to aspiration such goiter.
as lung abscess, bronchiectasis, or hemoptysis). (3) Esophageal cancer or thyroid
▪ Halitosis (foul breathing). cancer (in older patients).
o Investigations:
▪ Usually, first investigation to be ordered is barium swallow followed by upper
endoscopy.
▪ Imaging:
• Younger patients >> CXR & barium swallow (Bird beak’s sign).
• Older patients >> upper GI endoscopy (R/O cancer & take biopsy).
▪ Esophageal manometry >> to confirm the diagnosis; reveals failure of LES
relaxation & aperistalsis of esophageal body.
o Management:
▪ Lifestyle >> chew food more frequently, elevate the trunk, avoid food prior to
sleep.
▪ Medical therapy:
• Sublingual nitroglycerin & CCB (nifedipine) >> Cause relaxation of LES
(used in early disease & for short-term treatment).
• Pneumatic ballon dilatation:
o Forceful dilation of LES.
o Lower basal LES tone by disrupting the muscular ring.
o There is 5% risk of perforation.
• Injection of botulinum toxin:
o Injected into LES during endoscope, blocks cholinergic activity.
o Effective in 65% of cases, repeated procedure need to be done
every 2 years.
▪ Surgical (Heller myotomy):
• Circular muscle layer of LES is incised, reserved for patients who don’t
respond to dilation therapy.
• Anti-reflux fundoplication is usually done to prevent subsequent GERD.

Dysphagia grading:
I >> normal, no difficulty in swallowing.
II >> needs no drink water with solids.
III >> can swallow semi solid foods.
IV >> can swallow liquids.
V >> can swallow only saliva, no liquids, no solids.
VI >> cannot swallow even saliva.

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• Diffuse esophageal spasm (HIGH-YEILD):

o Non-peristaltic spontaneous contraction of the esophageal body at different point at the
same time (multiple segments of the esophagus contract simultaneously & prevent
appropriate advancement of food bolus). LES is functioning normally.
o Clinical features:
▪ Non-cardiac chest pain (mimics angina) that radiates to the jaw, arms, & back.
▪ Dysphagia to solids & liquids is common, precipitated with cold drinks.
▪ Regurgitation of food is uncommon.
o Investigations & Diagnosis:
▪ Upper GI barium swallow >> Corkscrew esophagus in active spams episodes,
although it may appear normal.
▪ Esophageal manometry (diagnostic) >> simultaneous, multihasic, repetitive
contractions that occur after swallowing, normal LES tone.
▪ +/- upper endoscopy >> R/O cancer in older patients.
o Management:
▪ There is no completely effective treatment.
▪ Medical treatment (nitrates & CCB) >> decrease amplitude of contractions.
▪ Esophagomyotomy >> controversial (until now, no surgical management have
been proven to be effective).

• Esophageal diverticula (HIGH-YEILD):

o Classification:
▪ True diverticula:
• Contains all layer of the walls.
• Mid-esophageal diverticula (rare).
• Non-esophageal examples (Meckel’s).
▪ False diverticula:
• Contains only mucosa & submucosa protruding through a defect in the
muscular layer of the wall.
• Zenker’s diverticulum.
• Non-esophageal examples (diverticulosis).
o Zenker’s diverticulum:
▪ False diverticulum in the upper esophagus.
▪ Originates from the defect in the cricopharyngeus muscle (Killian triangle).
▪ Symptoms >> soft neck swelling, dysphagia, regurgitation of food contents,
halitosis.
▪ Investigations:
• Barium swallow >> show collection of contrast in a sac.
• Endoscopy should be avoided due to risk of perforation.
• Others >> MRI, CT.
▪ Management:
• Medical treatment >> nitrate & CCB.
• Surgical:
o Considered if large >2cm or in severe symptoms.
o Myotomy or diverticulectomy (have high recurrence rate).

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• Esophageal ring/web (nice to know):

o Schatzki’s ring:
▪ Lower esophagus circumferential submucosal ring.
▪ Associated with hiatal hernia.
▪ Patient has intermittent dysphagia (mostly solids).
▪ Management >> pneumatic dilation.
o Pulmmer vinson syndrome:
▪ Caused by long-standing iron deficiency anemia.
▪ Consist of koilonychia, esophageal webs, glossitis, angular stomatitis.
▪ Management >> treat IDA + pneumatic dilation.

• Esophageal caustic injury (HIGH-YEILD):

o May be accidental (in children) or on purpose (suicide).
o Ingestion of both alkali (lyes) or acids can result in caustic injury.
o Alkalis are worse than acids, why?
▪ Alkali result in liquefactive necrosis (i.e. Continue to dissolve the mucosa)
resulting in esophageal perforation.
▪ Examples of alkali material >> oven & drain cleaners, lyes, Koh, laundry
detergents.
▪ Acid result in coagulative necrosis (i.e. limiting depth of injury), also acids burn
the mouth, so patients are more likely to not swallow.
▪ Examples of acidic material >> toilet cleaners, battery fluids, HCI for swimming
pools.
o Symptoms:
▪ (1) Oral or substernal pain.
▪ (2) Odynophagia, dysphagia, hypersalivation.
▪ (3) Hemoptysis, stridor, respiratory distress (due to laryngospasm &
laryngoedema).
o Complications:
▪ Acute:
• Esophageal perforation (could takes 1-7 days).
• Respiratory distress & laryngoedema.
▪ Chronic (strictures) >> occur in 80% of patients within 2 months.
o Management:
▪ ABCs (evaluate airway & intubate if necessary).
▪ Don’t induce vomiting & don’t try to neutralize.
▪ Endoscopy within 24h to assess burn degree.
▪ Degree of management depends on the severity & complications.
▪ Follow up is essential to assess & treat any complications.

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• Esophageal perforation (surgical emergency) (HIGH-YEILD):

o Causes: Boerhaave VS malloy-weiss
▪ Iatrogenic (most common) by endoscopy usually in Boerhaave tears are deeper (can
cervical esophagus. result in perforation), while mallory
▪ Trauma. is superficial (mucosal).
Boerhaave mostly located in left
▪ Foreign body or chemical ingestion.
lateral wall, while mallory on
▪ Boerhaave syndrome (severe vomiting & retching). posterior right lateral side
o Clinical features:
▪ Symptoms:
• Severe chest pain (may be substernal or upper Boerhaave syndrome present with
back). triad of (Mackler triad) (1) emesis,
(2) chest pain, (3) cervical
• Dyspnea & dysphagia. emphysema.
▪ Signs:
• Unstable patient.
• SQ emphysema ([Link] .
• Haman’s sign (crunching sound with heartbeat on palpating anterior
chest).
o Investigations:
▪ Generally, the history will lead you directly to the diagnosis, either there will be
lots of vomit or the patient just did endoscopy.
▪ Imaging:
• CXR:
o Pnemomediastinum.
o Widened mediastinum.
o Pleural effusion or pneumothorax (usually on left side).
o SQ emphysema.
• Gastrografin esophagogram:
o Gastrigrafin is a water-soluble contrast.
o It will show extravasation in mediastinum.
▪ Thoracocentesis (if done) >> high amylase, low pH.
o Management:
▪ ABCs.
▪ Broad-spectrum antibiotics.
▪ Massive tear >> surgical closure within 24h + drainage of mediastinum.
▪ Smaller tears >> NPO, IV PPI, IV antibiotics, close monitoring.

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• Gastroesophageal reflux disease (GERD) (HIGH-YEILD):

o Overview:
▪ Normally, LES prevent reflux of stomach content into the esophagus.
▪ Normal resting pressure of LES is 10-45 mmHg. When it decreases, gastric acid
reaches the esophagus & esophagus pH drops from 7 to 4.
▪ GERD >> defined as resting pressure of LES <10 mmHg which allows back flow of
gastric acid in the esophagus.
o Causes:
▪ Hiatal hernia (obese individuals & during pregnancy).
▪ Products that increase production of gastric acids or decreased the tone of the
lower esophageal sphincter (e.g. alcohol, spicy food, coffee, soda, tea).
o Clinical features:
▪ Symptoms occurs usually at night.
▪ Typical symptoms >> heartburn, regurgitation, waterbrash (hypersalivation).
▪ Atypical symptoms:
• Retrosternal chest pain (mimics MI).
• Dysphagia.
• Persistent coughing (morning cough).
• Halitosis (foal breath).
• Ear or nose discomfort.
• Nocturnal asthma unresponsive to asthma treatment.
▪ Symptoms suggestive of malignancy >> unintended weight loss, iron deficiency
anemia, anorexia, odynohagia (painful swallowing), upper GI bleeding
(hematemesis, coffee ground).
o Complications of GERD:
▪ All complications are diagnosed through upper endoscopy, +/- biopsy.
▪ Reflux esophagitis (most common) >> signs of erosions & ulcers during
endoscopy.
▪ Peptic stricture >> narrowing of the lumen most commonly in distal esophagus,
occur due to healing of esophageal erosions & scars.
▪ Barrett’s esophagus )chronic GERD >5ys(:
• A premalignant lesion in which normal stratified squamous epithelium
is replaced by metaplastic simple columnar epithelium.
• Patients with Barrett’s esophagus have increased risk of developing
esophageal cancer (esophageal adenocarcinoma).
• Risk factors >> male sex, white race, age >50 ys, obesity, tobacco use,
having a hiatal hernia, having 1st degree relative with esophageal
cancer.
• Diagnosis >> upper endoscopy & biopsy (metaplasia, Goblet cells,
eosinophilia).

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o Investigations & Diagnosis:

▪ Upper endoscopy & biopsy >> assess for complications & R/O malignancy.
▪ Esophageal manometry:
• Identify functional esophageal disorders (e.g. achalasia, diffuse
esophageal spasm).
• Evaluate the peristaltic function of the esophagus before a surgical
intervention for GERD.
• Measure the pressure in both upper & lower esophageal sphincters.
▪ 24h Esophageal pH monitoring (gold standard):
• Used to confirms diagnosis of GERD in patients with atypical symptoms
or in patients unresponsive to medical therapy.
• Demeester score is calculated, score >14.7 is suggestive of GERD.
o Management:
▪ Lifestyle & dietary changes (for all patients):
• Weight loss in obese patients.
• Elevate the pillow about 6 inches to prevent nocturnal GERD symptoms.
• Stop foods that increase stomach acid production.
▪ GERD without alarming symptoms:
• PPI (omeprazole) >> oral for 2 months, 30min before each meal.
• Other medical options:
o Histamine 2 receptor antagonist (H2RA) >> decrease
production of gastric acid.
o Sodium alginate (sucralfate) >> enhance mucosal healing.
Nissen’s fundoplication is a
procedure in which the
▪ Anti-reflux surgery:
gastric fundus is wrapped • Most commonly Nissen’s fundoplication, there is other types.
around the distal • Indicated in (1) failure of medical therapy, (2) patient preference,
esophagus & stitched there • (3) complications, (4) hiatal hernia.
to strengthen the lower
esophageal sphincter ▪ GERD with alarming symptoms (do endoscopy):
• If initial biopsy show no metaplasia >> upper endoscopy is repeated
after 3-5 years + PPI trial.
• If initial biopsy show metaplasia >> increase PPI dose & repeat biopsy
after 2 months of medical therapy.
• If initial biopsy show high-grade dysplasia or carcinoma >> endoscopic
resection of the esophageal mucosa & submucosa.

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• Esophageal cancer (HIGH-YEILD):

o Histological types:
▪ Squamous cell carcinoma:
Other risk factors of • More common than adenocarcinoma in developing countries.
esophageal carcinoma • Affects upper 1/3 of esophagus.
are smoking, alcohol,
• Most important risk factors >> achalasia & ingestion of hot liquids.
radiotherapy, family
history, old age ▪ Adenocarcinoma:
• More common in developed countries.
• Affect lower 1/3 of esophagus.
• Most important risk actors >> prolonged GERD & Barrett’s esophagus.
o Clinical features:
▪ Constitutional symptoms >> weight loss, fatigue, cachexia (extreme weight loss
& muscle wasting).
▪ Gradual dysphagia >> first to liquids then to solids.
▪ Symptoms of GI bleeding >> hematemesis, melena, anemia S&S.
▪ Symptoms of metastasis:
• Local invasion (coughing, stridor, hoarseness).
• Lung invasion (dyspnea, recurrent lung infections).
• Bone invasion (bone pain).
• LNs invasion (lymphadenopathy; left supraclavicular).
o Investigations:
▪ Labs >> CBC (Hb), LFTs (liver metastasis), RFTs (electrolytes & dehydration).
▪ Barium swallow may be done first.
▪ Upper endoscopy with biopsy.
▪ For staging >> endoscopic US + CT chest & abdomen.
o Management:
▪ Management depends on TNM staging.
▪ If limited to esophagus >> Surgical resection + neoadjuvant or adjuvant
Neoadjuvant = chemotherapy radiotherapy or chemotherapy.
before surgery. ▪ If advanced (i.e. go beyond muscle layer, involve local structure or LNs):
Adjuvant = chemotherapy after
surgery
• Palliative surgery, +/- adjuvant radiotherapy.
• Poor prognosis (15% 5 year survival).

• Esophagitis (nice to know):

o Causes:
▪ Infections >> candida (most common), HSV, CMV.
▪ Others:
• Reflux esophagitis & GERD.
• Eosinophilic esophagitis.
• Chemical esophagitis or Drugs (biphosphanate).
o Candida esophagitis:
▪ Always assume an esophagitis to be candidiasis (clinical diagnosis).
▪ Management >> Fluconazole. If no response, do upper endoscopy to investigate
other causes.

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o HSV esophagitis:
▪ Considered in immunocompromised patients.
▪ Diagnosis (endoscopy) >> Bunched out & small ulcers (volcano-like) & biopsy
will show giant cells, cowdry A bodies.
▪ Management >> oral acyclovir.
o CMV esophagitis:
▪ Considered in immunocompromised patients.
▪ Diagnosis (endoscopy) >> Large, linear & deeper ulcers.
▪ Management >> IV ganciclovir (poor oral absorption).

• Esophageal hiatal hernia (nice to know):

o A hernia in which an anatomical part (such as stomach) protrudes through the
esophageal hiatus of the diaphragm.
o Risk factors:
▪ Increase intra-abdominal pressure (Obesity, Pregnancy, Abdominal ascites).
▪ Aging (muscle weakness &loss of elasticity).
o Types:
▪ (type 1) The sliding hernia >> characterized by an upward dislocation of the
cardia in the posterior mediastinum.
▪ (Type 2) The rolling (paraesophageal hernia) >> characterized by an upward
dislocation of the gastric fundus, alongside a normally positioned cardia.
▪ (Type 3) the combined sliding-rolling hernia >> characterized by an upward
dislocation of both the cardia & the gastric fundus.
o Clinical features:
▪ Most patients are asymptomatic.
▪ In minority, S&S of esophageal reflux diseases or worsening of existing reflux.
▪ Complications >> GERD, reflux esophagitis, Barret’s esophagus
o Investigations & diagnosis:
▪ Most patients will present with S&S of GERD, so GERD investigations is usually
done. Other patients may present with incidental signs of hiatal hernia on CXR.
▪ Imaging methods >> barium swallow & upper endoscopy.
o Sliding esophageal hernia (type I):
▪ Herniation of gastroesophageal junction & stomach into the thoracic cavity.
▪ Account for 90% of all hiatal hernias.
▪ Can leads to reflux & esophagitis, eventually Barrett’s esophagus.
▪ Management (same as GERD):
• Medial >> antacids, PPI, head elevation.
• Surgery (only in 15% of cases):
o Indicated in severe GERD, failure of medical therapy, or
presence of complications.
o Nissen’s fundoplication is mainly done.
o Paraesophageal hiatal hernia (type II) (rare <5%):
▪ Herniation of stomach without disruption of gastroesophageal junction.
▪ Have high risk of complications (i.e. obstruction, strangulation, & hemorrhage).
▪ Management:
• Prompt surgical correction (either by laparoscopic or open approach).
• A reduction of the herniated stomach with or without fundopliction is
done.

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GIT
Bleeding
(HIGH-YEILD)

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• Causes:
o Upper GI bleeding:
▪ Refers to a bleeding above ligament of Treitz in the duodenum.
About 80% of episodes of ▪ Peptic ulcer diseases (PUD); duodenal ulcer (25%), gastric ulcer
upper GI bleeding stop (20%), gastritis (25%).
spontaneously and only ▪ Reflux esophagitis.
need supportive therapy
▪ Esophageal or gastric varices.
▪ Arteriovenous malformations.
▪ Mallory-Weiss syndrome & Dieulafoy lesions.
▪ Cancers of upper GIT (bleeding is not rapid, usually not emergency).
o Lower GI bleeding:
▪ Refers to a bleeding below ligament of Treitz in the duodenum.
▪ Any lower GI bleeding in patients over 40s is colon cancer until proven
otherwise.
▪ Diverticulosis is the most common cause of lower GI bleeding (40%).
▪ Anatomic >> diverticulosis, hemorrhoids & anal fissures, meckel’s diverticulum.
▪ Vascular >> angiodysplasia, ischemic colitis, radiation induced.
▪ Inflammatory >> infectious colitis (E. Histolytica, salmonella, shigella, C. difficle),
IBD (mainly UC).
▪ Neoplastic >> colorectal cancer & adenomatous polyps.

• Clinical features:
o Signs of volume depletion >> depending on severity & rate of blood loss.
o S&S of anemia >> fatigue, pallor, exertional dyspnea.
o Symptoms of upper GI bleeding:
▪ Hematemesis >> indicates moderate to severe bleeding that may be ongoing.
Always ask patient with GI ▪ Coffee grounds emesis >> upper GI bleeding that has already oxidized by
bleeding if they took any stomach acid, usually suggest lower rate of bleeding.
NSAIDs, aspirin, clopidogrel, ▪ Melena:
anticoagulants
• Black, tarry, liquid, foul-smelling stool.
• Suggest upper GI bleeding in 90% of cases (can be from small intestines
Note that any upper GI bleeding is or ascending colon in 10% of cases).
like having high protein meal, for • Caused by degradation of Hb by colonic bacteria, presence of melena
this reason it exacerbate hepatic
suggest that blood has remained in GIT for several hours.
encephalopathy in liver failure
patients • Note that dark stools can also result from bismuth, iron, spinach,
charcoal, licorice.
o Symptoms of lower GI bleeding:
▪ Hematochezia:
• Bright red blood per rectum that may or may not be mixed with stool.
• Suggest lower GI bleeding (typically left colon or rectum), however, it
may be present in large upper GI bleeding.
• DDx >> diverticulosis, arteriovenous malformations, hemorrhoids, &
colon cancers.

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• Investigations & Diagnosis:

o Vital signs >> decreased BP, tachycardia, or postural change in BP or HR are signs of
significant hemorrhage (however, vitals may be normal).
o Laboratory tests:
▪ CBC:
• Hb & Hct (>7-8 g/dl is acceptable in young healthy patients, >10 should
be in elderly especially with cardiac diseases).
• Low MCV suggestive of IDA.
▪ Electrolytes, BUN, Cr >> assess dehydration or renal dysfunction.
Occult means there is no ▪ LFTs, bilirubin, albumin >> assess liver function.
visible evidence & detected ▪ Coagulation profile (platelet count, PT, PTT, INR) >> R/O bleeding disorders.
by fecal occult blood test.
▪ Blood grouping & Cross-matching >> for transfusion.
▪ Stool guaiac for occult blood >> source of bleeding may be anywhere along GIT.
o If upper GI bleeding is suspected in stable patients:
▪ Upper endoscopy within 24h.
▪ Note that in hemodynamically unstable patients, a surgical and radiological
team must be nearby because endoscopy can precipitate complications (e.g.
perforation).
o If lower GI bleeding is suspected in stable patients >> colonoscopy within 24h.
o Other procedures:
▪ Bleeding scan (radionuclide scan) >> reveals bleeding even with low rate.
Doesn’t localize the lesion; only identifies continued bleeding.
▪ Arteriography >> localize the bleeding but should performed during active
bleeding, mostly used in lower GI bleeding.
▪ Exploratory laparotomy >> last resort.

• Management:
o If patient is hemodynamically unstable, resuscitation is always top priority:
▪ Supplemental oxygen.
In any case of massive GI ▪ Place 2 large-bore IV lines & give IV fluid if volume depleted (500 mL of normal
bleeding order at least 4 saline or lactated Ringer’s solution).
units of blood (PRBCs) to ▪ Draw blood for investigations.
prevent fluid overload
▪ IV PPI (promotes hemostasis & decrease risk of recurrent bleeding).
▪ Blood transfusion (in severe cases or if IV fluids are not enough).
o If patient is hemodynamically stable, give blood transfusions only in:
▪ Elderly with comorbidities or if Hb <9 g/dl.
▪ Young patients if Hb <7 g/dl.
o Indications of surgery in patients with GI bleeding:
▪ Hemodynamically unstable patients that not respond to IV fluids, transfusion,
endoscopic intervention, or correction of coagulopathies.
▪ Severe initial bleeding continued for >24hr.
▪ Visible vessel at base of ulcer (50% chance of re-bleed).
▪ Ongoing transfusion requirement (5 units within first 4-6 hours).

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o Management of upper GI bleeding:

▪ Peptic ulcer disease:
• Thermocoagulation therapy during or hemostatic clips combined with
injected epinephrine (vasospasm) during upper endoscopy.
• Treatment of peptic ulcer disease (discussed later).
▪ Esophageal varices:
• IV octreotide & IV antibiotics (ciprofloxacin or ceftriaxone).
• Variceal ligation or endoscopic sclerotherapy.
• Ballon tamponade in refractory cases.
▪ Mallory-Weiss syndrome:
• Antiemetic agent (e.g. metoclopramide).
• Endoscopic therapy with thermocoagulation, hemostatic clips, band
ligation if active bleeding.
▪ Dieulafoy lesion >> epinephrine injection with endoscopic thermocoagulation
or hemostatic clips.
o Management of lower GI bleeding:
▪ Diverticulosis:
• Colonoscopy with thermocoagulation or epinephrine injection.
• If bleeding not stopped, angiography to identify source of bleeding with
vasoconstriction medication (e.g. vasopressin) or vessel embolization.
• In refractory cases, segmental colectomy surgery.
▪ Colorectal cancer:
• Hemospray during colonoscopy.
• Cancer is treated with surgical resection or with chemotherapy.
▪ Hemorrhoids:
• Dietary & lifestyle modifications, goal is to soften the stool (more water,
Remember!! food rich in fibers).
Internal hemorrhoids bleeds
& don’t hurt. • Analgesics creams, hydrocortisone suppositories, or Sitz-baths to relieve
External hemorrhoids hurt & pain.
don’t bleed as much. • Internal hemorrhoids >> rubber band ligation.
• External hemorrhoids >> hemorrhoidectomy.
▪ Intestinal ischemia:
• Nonviable tissue >> surgery to remove ischemic part.
• Arterial occlusion >> surgical embolectomy.
• Venous thrombosis >> anticoagulant or thrombolysis therapy.
▪ Arteriovenous malformations >> endoscopic treatment with argon plasma
coagulation, thermocoagulation or homeostatic clips.

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• Esophageal varices:
o Causes:
▪ Liver cirrhosis (portal HTN; lower esophageal veins are submucosal veins).
Variceal hemorrhage has a ▪ Schistosomiasis.
higher mortality rate (30%)
▪ Liver congestion (Budd-chiari syndrome).
▪ Portal vein thrombosis.
o Clinical features:
▪ Symptoms >> massive hematemesis (fresh blood), exacerbation of hepatic
encephalopathy.
▪ Signs:
• Hemodynamic instability (tachycardia, low/orthostatic BP, pale, altered
mental status).
• Stigma of liver failure (jaundice, nail clubbing, dupytren’s contracture,
astrexis, ascites, …etc.).
o Investigations >> patients usually present with upper GI bleeding (see investigations of
upper GI bleeding).
o Management:
▪ Hemodynamic stabilization (fluids to maintain BP) (see management in upper GI
bleeding).
▪ IV octreotide + IV PPI + IV antibiotics (ceftriaxone) >> causes splanchnic
vasoconstriction & reduces portal pressure.
▪ Variceal ligation:
• Initial endoscopic treatment of choice with effective control of active
bleeding.
• Lower rate of re-bleeding more than sclerotherapy.
▪ Endoscopic sclerotherapy:
• Sclerosing substance is injected into varices during endoscopy.
• Control bleeding in 80-90% of cases.
• Up to 50% of patients may re-bleed.
▪ If massive bleeding or endoscopic therapy failure >> balloon temponade OR
TIPS.
▪ Prophylactic measures:
• Non-selective B-blockers (propranolol).
• Serial endoscopic evaluation (every 3 years).

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Acute
Abdomen
(HIGH-YIELD)

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• Overview:
o Acute abdomen is defined as any sudden, spontaneous, non-traumatic, severe
abdominal pain of <24h in duration.
o Emergency laparotomy is indicated in:
▪ Generalized peritonitis:
• Patient is unwell, lying still, with unstable vitals.
• Peritonitis is usually caused by a rupture viscus (i.e. ruptured appendix,
perforated ulcer, strangulated & necrotic hernias, bowel obstruction,
mesenteric ischemia, diverticulitis, ruptured ectopic pregnancy).
• Abdominal examinations shows >> (1) involuntary guarding with broad
rigidity, (2) diffuse abdominal pain, (3) rebound tenderness.
▪ Signs of advanced or non-improving bowel obstruction >> Unstable patient
with abdominal distention, vomiting, & obstipation.
▪ Radiological evidence of pneumoperitoneum (air under diaphragm).
▪ Uncontrolled massive or ongoing bleeding.
▪ All penetrating abdominal traumas.

• Types of pain:
o Visceral VS somatic:
▪ When the abdominal viscus is dilated, the pain is vague & dull. It usually felt in
the midline depending from where it derived embryologically (foregut >>
epigastric, midgut >> periumbilical, hindgut >> infra-umbilical).
▪ Irritation of the parietal pleura will produce pain over this specific location, the
pain will be more sharp, well-localized, & have rebound tenderness.
o Special pain characters:
▪ Referred pain (share the same origin of nerve):
• Biliary tract / right hemidiaphragm irritation >> right scapula or right
shoulder pain.
• Splenic rupture / left hemidiaphragm irritation >> left shoulder pain
(Kehr sign).
▪ Radiating pain (connected by anatomic tract):
• Acute pancreatitis >> upper back.
• Ureteric colic >> loin to groin.
▪ Migrating pain >> acute appendicitis (first vague & dull, then localized to RIF).

• Differential diagnosis abdominal pain:

o DDx of diffuse abdominal pain:
▪ GI:
• Bowel obstruction (small or large).
• Peritonitis (+ its causes).
• Mesenteric ischemia (may be LUQ or epigastric).
• Gastroenteritis.
▪ Genitourinary >> ruptured ectopic pregnancy, testicular or ovarian torsion.
▪ Cardiovascular >> AAA rupture.
▪ Endocrine >> DKA, addisonian crisis.
▪ Hematologic >> sickle cell crisis, porphyria.

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o DDx of pain by quadrant:

RUQ pain Epigastric pain LUQ pain

Liver >> hepatitis, abscess. Cardio >> inferior wall MI, AAA
biliary tract >> biliary colic, acute rupture, abdominal aorta
cholecystitis or cholangitis, dissection. GI >> splenic rupture, perforated
obstructive jaundice. Liver >> hepatitis, abscess. ulcer, diverticulitis, UC.
GI >> perforated duodenal ulcer, biliary tract >> biliary colic, acute GU >> nephrolithiasis, urolithiasis,
appendicitis in pregnancy. cholecystitis or cholangitis, pyelonephritis.
GU >> nephrolithiasis, urolithiasis, obstructive jaundice. Others >> right lower lobe
pyelonephritis. GI >> perforated duodenal or pneumonia.
Others >> right lower lobe gastric ulcer, acute pancreatitis.
pneumonia.
Acute mesenteric ischemia
RLQ pain Hypogastric pain LLQ pain
Peri-umbilical >> acute
GI >> acute appendicitis, crohn’s
appendicitis (early), acute
disease, Meckel’s diverticulitis, GI >> diverticulitis, sigmoid
pancreatitis, AAA rupture,
strangulated hernia, mesenteric volvulus, UC, pseudomembranous
gastroenteritis, IBS.
adenitis (e.g. Yersinia), colitis, fecal impaction,
Suprapubic:
intussusception, cecal volvulus, strangulated inguinal hernia.
GI >> sigmoid diverticulitis,
abdominal TB. GU >> testicular or ovarian torsion.
strangulated groin hernia.
GU >> ovarian or testicular torsion.
GU >> cystitis, acute retention.
GI >> acute mesenteric ischemia
OBS/GYN >> Mid-cycle pain (mittelscmerz), ectopic pregnancy rupture, TOA/PID, abortion, uterine pathology
(e.g. fibroid red necrosis),

• History in a patient with abdominal pain:

o History of present illness:
▪ Pain details (SOCRATES) + migration of pain.
▪ Associated symptoms of all possible systems:
• GI >> pain, distention, nausea, vomiting, anorexia, change in bowel
habits, changes in stool, etc… .
• Urinary >> dysuria, urgency, frequency, dribbling, etc.. .
• Hepatobiliary >> jaundice, change in stool or urine color, itchiness,
bleeding.
▪ Constitutional symptoms >> fever, weight loss, anorexia.
▪ History of trauma >> especially blunt trauma.
o Past history:
▪ Medical illnesses, level of control, medications.
▪ Regular medications + history of blood transfusions + history of allergy.
▪ It’s very important to ask about previous operation & the details.
▪ In females ask about menstrual & obstetric history.

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• Examinations in a patient with abdominal pain:

o General exam:
▪ Vitals (most students forget them) >> pulse, RR, temp, O2 saturation, BP.
▪ General inspection:
• Level of consciousness (conscious, awake, oriented).
• Well, unwell, toxic-looking, in pain.
• IV lines & any devices.
• Laying in bed with knee bend >> may suggest peritonitis.
▪ Eyes >> assess jaundice & pallor conjunctiva.
▪ Mouth >> assess central cyanosis.
▪ Hands >> assess palmar erythema, dupuytren contracture, sweating, clubbing,
capillary refill, pulse.
▪ Leg >> assess lower limb edema.
o GI examinations:
▪ Exposure >> from 2nd ICS to the mid-thigh.
▪ Inspection:
• First, stand at foot of the bed and assess flanks symmetry, then move to
the right side of patient.
• Shape of abdomen (scaphoid, flat, distended).
• Type of breathing (abdominothoracic in males).
• Inspect the umbilicus (inverted, everted, flat).
• Previous surgical scars or visible veins.
• Hair distribution (if shaved you must say it).
• Any obvious swellings (site, size, shape, consistency, surface, skin
overlying, special characters).
• Cough test >> ask the patient to cough 2-3 times when supine & look as
all potential hernia sites or the site which already has a hernia.
▪ Palpation:
• Always always always ask about pain before palpating. Leave the
painful area to the last.
• Superficial palpation >> Assess any masses, tenderness, rebound
tenderness, guarding, rigidity.
• Deep palpation >> for liver & spleen.
• Possible findings:
o Guarding >> diffuse guarding suggest peritonitis, while if involve
one region it may suggest diverticular abscess.
o Rebound tenderness )Blumberg’s sign( >> tenderness after
removing the hand, suggesting peritonitis.
o Murphy’s sign >> hand is placed below the right costal margin
and asked to breath in, if the patient stops breathing due to
pain, it’s a +ve sign. Usually suggest acute cholecystitis.
o McBurney’s sign >> tenderness at McBurney’s point, suggesting
appendicitis.
o Rovsing sign >> palpation of LLQ cause pain in RLQ, suggesting
appendicitis.
o Courvoisier sign >> firm & painless gallbladder, suggest
malignancy or chronic biliary tree obstruction.

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▪ Percussion:
• Normally its tympanic.
• Hyper-resonance may suggest air accumulation.
• Dullness may suggest fluid accumulation (e.g. ascites), organomegaly.
• Moderate ascites >> do shifting dullness test.
• Massive ascites >> do fluid thrill test.
▪ Auscultation:
• Normal is 2-12 medium-pitched gurgles/min.
• Decreased, high-pitched sounds may suggest obstruction or peritonitis.
• Hyperactive, medium-pitched sounds may suggest inflammation within
GI tract (e.g. gastroenteritis).
• Abdominal bruit may suggest abdominal aortic aneurysm.
▪ Ideally GI exam is finished by digital rectal exam & pelvic exam.

• Investigations:
o As a general rule; emergency surgery should not delayed in history & examinations have
clear indication to do it.
o Investigations must be directed towards the suspected cause.
o General investigations in any patient with abdominal pain:
▪ CBC >> assess leukocytosis & anemia.
▪ Electrolytes panel >> assess any disturbances (especially with vomiting).
▪ Amylase & lipase >> assess pancreatitis or perforation (amylase are high in
perforation).
▪ LFTS >> baseline + assess any abnormalities.
▪ RFTs >> baseline + assess any abnormalities.
▪ Pregnancy test >> in any childbearing aged women.
▪ Urinalysis >> if cystitis or pyelonephritis is suspected.
o Imaging:
▪ Plain radiographs (abdomen & chest X-rays):
• May show air-fluid levels or pneumoperitoneum (obstruction or
perforation).
• Kidney stones or gallstones identifications.
• Lower lobe infiltration.
▪ Ultrasound (rapid, bedside):
• Assess kidney stones, gallstones, or AAA.
• Also, it provides useful info about ectopic pregnancy, ovarian torsion,
hemoperitoneum, pancreatitis.
▪ Abdominal CT:
• Used if diagnosis remains unclear.
• Can sow signs of diverticulitis, cancers or other masses, AAA, mesenteric
ischemia.

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Infections of
the Peritoneum

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• Primary (spontaneous) peritonitis:

o Also known as spontaneous bacterial peritonitis (SBP).
o Occurs with the absence of bowel perforation.
o Mostly occur in patients with ascites in which the ascetic fluid get infected (in patients
with liver or renal failure)
o Associated with high mortality rate (20-30%), it may lead to sepsis.
o Causative organisms >> E. Coli (most common), Klebsiella, Strept. Pneumoniae.
o Clinical features >> abdominal pain, fever, vomiting, rebound tenderness, & guarding.
o Investigations & Diagnosis:
▪ Established by paracentesis (cell count, gram stain, cultures).
▪ WBC >500 & PMN >25% suggest SBP.
▪ SAAG score of >1.1g/dl.
▪ Culture-negative SBP is common.
o Management:
▪ Broad spectrum antibiotics usually IV Cefotaxime (give specific therapy if
organism is identified).
▪ Clinical improvement should be seen in 24-48h, repeat paracentesis to
document decrease in PMN.

• Secondary peritonitis:
o Causative organisms:
▪ [Link].
▪ Aerobic & anaerobic streptococci.
▪ Bacteriodis.
▪ Pneumococci, enterococcus.
o Source of organism: Note that the more distal
organs that perforate, the more
▪ Infected organs (appendicitis, diverticulitis, cholecystitis). likely severity of peritonitis (i.e.
▪ Leaking organs (perforation, leaking anastomosis, diverticulitis is more dangerous
extravasated urine bile peritonitis). than rupture appendix, which is
▪ Direct entry (from OT wound or traumatic wound). more dangerous the perforated
duodenal ulcer)
▪ Hematogenous.
o Course:
▪ After perforation, paralytic ileus occurs at first as a reflex to minimize spread.
▪ Then the omentum try to minimize the inflammation process by containing it.
▪ Then the course has 2 ways; (1) localization, (2) flaring up.
▪ Localization (abscess formation):
• At the same site of primary infection (e.g. abscess in acute appendicitis).
• At dependent zones usually in abrupt onset perforations (e.g.
subphrenic, iliac, pouch of Douglas, recto-vesical pouch).
▪ Flaring up (develops generalized peritonitis):
• Sudden perforations (peritoneum doesn’t have enough time for
defensive mechanisms).
• Persistent source of infections.
• Immunosuppressed patients.
• Extreme of ages (children & elderly).
• May complicated to septicemia, SIRS, multiple organ failure, septic
shock & death.

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o Clinical features:
▪ Acute abdominal pain + septic picture.
▪ May present with the clinical picture of the original cause.
▪ Symptoms:
• Diffuse abdominal pain that is aggravated by movements & coughing
(patient prefers to lie still).
• Abdominal distention.
• Vomiting.
• Obstipation (suggest complete bowel obstruction).
▪ Signs:
• Unwell, toxic-looking patients, lying still in bed may have altered mental
status.
• Unstable vitals; high fever, tachycardia, low BP.
• Palpation >> generalized tenderness with rebound, involuntary
guarding, rigidity.
• Auscultation >> absent bowel sounds.
o Investigations:
▪ Routine labs for acute abdomen >> CBC, RFTs, LFTs, amylase, lipase,
coagulation profile, glucose, B-hCG.
▪ Erect X-ray >> air under diaphragm suggest perforated viscus.
▪ Paracentesis >> WBCs count >200 cells/ul.
o Management:
▪ (1) ABCs + IV fluids.
▪ (2) NPO + NGT (decompress stomach) + foley catheter (monitor urine output).
▪ (3) IV analgesia.
▪ (4) IV broad spectrum antibiotics (cephalosporins + metronidazole).
▪ (5) Surgical management (when patient is stable):
• Exploratory laparotomy (midline incision).
• Specific management to the original cause (e.g. graham patching).
• Peritoneal irrigation/toileting with saline.
• Peritoneal drainage.
▪ Prognosis >> mortality rate about 40% (more with distal causes).

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• Intraperitoneal abscess:
o Localized septic peritonitis.
o Having a peritoneal abscess is better than generalized peritonitis, it means that the body
was capable to localize the infection, especially with the help of the omentum.
o Location of abscess:
▪ Primary site of the original infection.
▪ Dependent peritoneal sites:
• Subphrenic area (e.g. morrison’s pouch).
• Right iliac fossa (through right paracolic gutter).
• In the pelvis (e.g. Douglus pouch/recto-vesical).
o Causes:
▪ Right side >> acute appendicitis, cholecystitis, perforated duodenal ulcer.
▪ Left side >> perforated diverticulitis, perforated cancer of sigmoid, subphrenic
abscess.
▪ Pelvis >> PID, TOA.
▪ Abscess could develop anywhere is cases of generalized peritonitis.
o Clinical features:
▪ Symptoms:
Mesentery cyst is usually • Fluctuating or spiking high fever.
found near the umbilicus. • Pain & swelling at the affected site.
Key clinical feature that the
cyst is moving only • Nausea & vomiting.
perpendicular to the root of • +/- shoulder pain (suggesting irritation of the diaphragm).
the mesentery (i.e. moves up • Pelvic abscess may present with deep pelvic pain, diarrhea, dysuria.
& down, but not left or right) ▪ Signs:
• Tenderness & rigidity at the site of abscess.
• Mass may be palpable.
• Overlying skin may show signs of inflammation.
o Investigations:
▪ Routine labs for acute abdomen (CBC, LFTs, amylase, lipase, electrolytes, RFTs).
▪ CBC >> may show leukocytosis.
▪ Imaging >> US or CT will demonstrate the site of the abscess.
o Management:
▪ (1) IV analgesia & antibiotics.
▪ (2) US/CT guided percutaneous drainage.
▪ If (2) fails or not possible, do surgical drainage.

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The
Stomach

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• Stomach anatomy (review):

o Parts of the stomach:
▪ Cardia >> where esophagus enter.
▪ Fundus >> lies posterior to the 5th left rib in the
midclavicular plane (source of gastric bubble).
▪ Body >> Greater & lesser curvatures.
▪ Antrum >> opens up into pylorus & contains the
pyloric sphincter.
o Layers of the wall:
▪ Mucosa & submucosa >> simple columnar
epithelium.
▪ Muscular layer:
• An innermost oblique muscle layer.
• An inner circular layer.
• An outer longitudinal layer.
▪ Serosa (intraperitoneal).
o Blood supply:
▪ Arterial supply:
• Lesser curvature:
Gastroduodenal artery runs o Right gastric artery (branch from
behind 1st part of duodenum. hepatic artery).
Posterior duodenal ulcer result
o Left gastric artery (branch from celiac trunk).
in bleeding from this artery
• Greater curvature:
o Right gastroepiploic artery (branch from gastroduodenal artery).
o Left gastroepiploic artery (branch from splenic artery).
• Pylorus >> gastroduodenal artery.
• Fundus and upper body of stomach >> short posterior gastric arteries
(branch from splenic artery).
▪ Venous drainage:
• Follows arterial names & drain into the portal venous system.
Parasympathetic effect: • Pre-pyloric vein of mayo is a surgical landmark of the pylorus.
(1) Increase peristalsis. ▪ Lymphatic drainage >> follow the arteries, mostly to celiac LNs.
(2) Increase laminal secretions.
(3) Opens up sphincters.
▪ Innervation:
• Parasympathetic (vagus nerve – CN10):
o Left & right vagus become the anterior & posterior vagal trunk.
Sympathetic effects:
(1) Diminished activity of viscera. o The vagal trunks form the nerve of Laterjet, which provide
(2) Close sphincters. several small branches to the stomach (crow’s foot).
(3) Vasoconstrictor. • Sympathetic (T6-T9) >> from greater splanchnic nerve.

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• Anatomy of duodenum (review):

o The duodenum is considered as the first and shortest (25cm) part of the small
intestines. It begins at the pylorus and ends at the duodenojejunal junction.
o Histology >> characterized by having villi & submucosal Brunner’s glands (function in
protecting duodenal mucosa).
o Parts of the duodenum:
▪ 1st part (2 inches) >> Duodenal cap (first 1 inch) is the only intraperitoneal part.
▪ 2nd part (3 inches) >> where the ampulla of vater enters (marks the division
between the foregut & midgut).
▪ 3rd part (4 inches) >> crosses to the left anterior to IVC & aorta, it’s over run by
the superior mesenteric vessels.
▪ 4th part (1 inch) >> ascends to join the jejunum where it takes a sharp turn due
to ligament of Trietz.
o Arterial supply:
▪ 1st & 2nd parts >> Anterior & posterior superior pancreatoduodenal artery
(branch from gastroduodenal artery).
▪ 3rd & 4th parts >> Anterior & posterior inferior pancreatoduodenal artery
(branch from superior mesenteric artery).
o Venous drainage >> Duodenal veins which follow the arteries and drain into the hepatic
venous system.

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• Peptic ulcer disease (High-Yield):

o Defined as deep erosions in the lining of the stomach or duodenum that result in
Protective factors of inflammation of gastric or duodenal wall.
gastric mucosa
(1) Mucus secretion. o Causes:
(2) Bicarbonate secretion. ▪ Helicobacter pylori infection (gram -ve bacteria). Zollinger-Ellison syndrome
defined as a gastrinoma (gastrin-
(3) Prostaglandins (inhibit ▪ NSAIDs (inhibit prostaglandin production, which leads to secreting tumor) the are located
acid secretion).
impaired mucosal defenses). in duodenum or pancreas which
Destructive factors of ▪ Acid hyper-secretory states (Zollinger-Ellison syndrome). result in increased secretion of
gastric mucosa
(1) NSAIDs.
▪ Other risk factors >> smoking, alcohol, emotional stress, gastric acid
(2) H. Pylori (urease dietary factors (coffee, spicy food).
secretion). o Clinical features: Dyspepsia = epigastric pain
(3) Uremia.
(4) Bile reflux. ▪ Epigastric pain (aching), nausea, vomiting, early satiety, related to food, early satiety,
(5) Alcohol, smoking, weight loss. postprandial belching, & nausea.
spicy foods. ▪ May be complicated by upper GI bleeding (hematemesis).
▪ Duodenal VS Gastric ulcers:

Duodenal ulcers Gastric ulcers

Caused by increase in offensive factors
Pathogenesis Caused by decrease in defensive factors
(more gastric acid secretion)
H. Pylori infection 70-90% of cases 60-70% of cases
Type I (70%) >> lesser curvature.
Posterior duodenal ulcer >> most
Type II >> type I + duodenal ulcers.
common, gastroduodenal artery are the
Type III >> prepyloric (within 2cm of
most likely to bleed.
Location & types pylorus).
Anterior duodenal ulcer >> more likely to
Type IV >> near esophagogastric junction.
perforate to the lesser sac cavity.
Posterior wall ulcer >> may result in
Kissing ulcer >> anterior & posterior ulcers.
pancreatitis & bleeding (spelnic artery).
Age distribution In younger patients (<40) In older patients (>40)
Eating increase the pain.
Specific clinical Eating relieves pain.
Complications rates are higher.
feature Nocturnal pain is more common
Higher recurrence rate with medical therapy.
High (5-10% are malignant), do biopsy to
Malignant potential Low R/O malignancy, most common type are
adenocarcinoma

o Investigations & Diagnosis:

▪ Labs (acute abdomen) >> CBC, LFTs, amylase, lipase, RFTs, urinalysis, etc..
If patient is present with ▪ Chest & abdomen X-ray >> R/O emergency causes (air under diaphragm).
upper GI bleeding, upper ▪ Upper endoscopy (most accurate):
endoscopy must be done • Biopsies >> for H. Pylori diagnosis + R/O malignancy in gastric ulcers.
anyway
• Preferred when severe or acute bleeding is present (can perform
electrocautery of bleeding ulcers).
Zollinger-Ellison syndrome is • Malignancy findings >> raised, nodular edges, non-radiating gastric
suspected if there is
multiple ulcers. Gastrin
folds.
levels are >1000pg/mL ▪ Barium meal >> sometimes used initially, but less reliable than endoscopy.
▪ Serum gastrin measurement >> if considering Zollinger-Ellison syndrome as a
diagnosis.

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▪ H. Pylori Diagnosis:
• Endoscopic biopsy (gold standard) >> Giemsa stain or biopsy urease
test.
• Stool antigen test >> high sensitivity, easy, good Both urea breath test & stool
for screening. antigen test have false -ve result if
the patient is taking PPI, bismuth, or
• Urea breath test: antibiotics. So before doing these
o Highly sensitive & specific. tests make sure that the patient is
o Documents active infection & help to not taking any medications
assess the result of antibiotic therapy.
• Serology (low specificity) >> Presence of H. Pylori antibodies doesn’t
necessary indicates active infection.
o Management:
▪ Lifestyle & supportive measure:
Majority of PUD patients • Discontinue aspirin & NSAIDs.
can be successfully treated • Restrict alcohol use, stop smoking, decrease emotional stress.
by curing [Link] infection,
avoidance of NSAIDs,
• Avoid eating before bedtimes.
appropriate use of anti- ▪ Acid suppression therapy:
secretory drugs • PPI (omeprazole):
o 1st line, most effective agent.
o Blocks H+/K+ ATPase pump directly in parietal cell membrane.
Note that acid suppression
• H2 receptor blockers (cimetidine/rantidine) >> Blocks histamine-based
agents can be discontinues
after 4-6 weeks in patients parietal cell acid secretion.
with uncomplicated ulcers • Antacids (aluminum hydroxide / calcium carbonate) >> used as
who are asymptomatic. adjunctive therapy & symptomatic relief.
Patients with risk of ▪ H. Pylori eradication therapy:
recurrence may benefit from
maintenance therapy • Triple therapy:
o PPI + amoxicillin + clarithromycin.
o Metronidazole is used instead of amoxicillin if patient has
penicillin allergy.
o Given for 14 days.
• Quadruple therapy:
o PPI + bismuth + metronidazole + tetracycline.
o Indicated in patients with risk factors of macrolide resistance.
o Given for 7 days.
▪ Surgery in PUD >> relatively uncommon nowadays, discussed later.

Clinical notes ☺

While describe any ulcer you have to cover

(1) Base (under the floor).
(2) Floor.
(3) Edges.
(4) Margin (around the edges).

Examples of ulcers:
Slopping >> healing & venous ulcers.
Punched out >> traumatic, syphilitic, ischemic, trophic.
Undermined >> TB, decubitus (bed sores).
Everted >> squamous cell cancer.
Rolled >> basal cell cancer.

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• Complications of peptic ulcer disease (High-Yield):

o GI bleeding:
▪ PUD is the most common cause of upper GI bleeding.
▪ Duodenal ulcer is the most common (from gastroduodenal artery).
▪ Clinical features:
• Slow bleeding >> show signs of IDA, coffee grounds vomit, melena.
• Rapid & severe bleeding >> present with hematemesis or melena.
▪ Diagnosis >> Upper GI endoscopy (diagnostic & therapeutic).
▪ Management:
• Acute slow bleeding is usually stops spontaneously due to clot
Re-bleeding risk based on ulcer formation.
base finding (highest to lowest): • (1) ABCs, 2 large IV bore needles, draw bloods, give IV fluids, blood
(1) Visible vessel. transfusion if necessary.
(2) Clot. • (2) NPO, NGT for suctioning.
(3) Pinpoint bleeding.
(4) Clean base. • (3) IV PPI + IV antibiotics.
• If bleeding is controlled & patient is stable >> do endoscopy within
24h.
• If bleeding is uncontrolled or patient is unstable >> urgent endoscope.
• Ulcers with high re-bleeding risk >> do surgical hemostasis with sutures
or pyloroplasty.
o Gastric outlet obstruction:
▪ Generally, this complication is less common nowadays due to early presentation
& use of PPIs.
▪ Common with duodenal ulcers & type III gastric ulcer (pyloric antrum).
▪ Clinical features:
• Nausea & vomiting (poorly digested food).
In gastric outlet obstruction, • GERD symptoms.
paradoxical aciduria will develop • Epigastric fullness & distention, early satiety, Weight loss.
due to metabolic alkalosis
• Examination >> succession splash (when shaking the abdomen, +/-
visible peristalsis).
▪ Diagnosis:
• Barium swallow & upper endoscopy.
• Electrolytes panel & ABG >> hypochloremic, hypokalemic metabolic
alkalosis + hyponatremia.
• Saline load test >> empty stomach with a nasogastric tube, then added
750ml saline, aspirate after 30min, test is +ve is aspirate >400ml.
▪ Management:
• Initially management >> nasogastric suction, replace electrolytes &
volume deficits, supplement nutrition.
• Surgery (pyloroplasty) >> necessary in 75% of patients.

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o Perforation:
Note that the pain may develop
▪ Occur usually in anterior duodenal ulcer & gastric ulcers. in RLQ if draining fluid tracks
▪ Clinical features: down the right paracolic gutter
• Acute, severe epigastric pain (may become diffuse) (Valentino’s sign) which usually
which worsened by movement & respiration. misdiagnosed as acute
appendicitis
• Signs of peritonitis (fever, etc..).
• Hemodynamic instability (tachycardia, tachypnea).
• Can progress into sepsis & death if not treated early.
▪ Examinations:
• Inspection >> patient looks ill, lying still, shallow rapid breathing.
• Auscultation >> absent bowel sound.
• Palpation >> epigastric tenderness, involuntary guarding, broad-like
rigidity.
• Percussion >> very painful.
▪ Diagnosis:
• Upright CXR:
o Free air under diaphragm (enough to suggest perforation).
o If upright CXR is not possible, do left lateral decubitus CXR.
• CT >> most sensitive test in detecting free abdominal air.
▪ Management (Emergent surgery):
• ABCs (airway, IV fluids, blood collection).
Why we use omentum? Because • IV antibiotics + IV PPI.
the edges of the perforated ulcer • Emergency laparotomy (upper med-line incision): Surgery should be done early &
are necrotic & very friable (primary
o Graham patching (close the perforation fast to prevent the
suturing will be useless), thus the
omentum is placed over the using a piece of omentum). conversation of chemical
perforation & suture further away o Peritoneal toileting/irrigation. peritonitis to septic peritonitis
from the edge o Close abdomen with drain inserted.
• Perform definitive ulcer operation (e.g. highly selective vagotomy or
truncal vagotomy).

• Surgery in peptic ulcer disease:

o Goal of surgery >> reduction of gastric acid secretion + excision
of the ulcer.
o Indications:
▪ Refractory of treatment (12 weeks failure).
▪ Cancer possibility.
▪ Complications (Gastric outlet obstruction, perforated
ulcer, hemorrhagic features).
o Duodenal ulcers >> highly selective vagotomy (high recurrence
rate), +/- ulcer excision.
o Gastric ulcers:
▪ Type I >> ulcer excision + Bilroth I (distal gastrectomy + gastroduodenostomy).
Only type II & III needs ▪ Type II & III >> ulcer excision + truncal vagotomy + pyloroplasty (drainage).
truncal vagotomy, because
▪ Type IV >> ulcer excision + Bilroth II (distal gastrectomy + gastrojejunostomy).
they are associated with acid
hypersecretion

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o Complications of surgery:
▪ Nutritional disturbances >> mainly vitamin B12 & iron.
▪ Marginal ulcer:
• Ulcers that occur on stumps or anastomosis
• Mostly related to incomplete vagotomy.
• Clinical features >> Patient will present with PUD symptoms again.
• Investigations >> endoscopy will confirm the diagnosis.
• Management >> PPI trial + re-operation may be considered.
▪ Post-vagotomy diarrhea >> occur in many patients, improve with time.
▪ Dumping syndrome:
• Unregulated movement of gastric contents from stomach to small
intestines (i.e. movement occur very quickly; hyperosmolar solutions
enters small bowel).
• Clinical features:
o May be early (5-15min post-prandial) or late (2-4h).
o GI symptoms >> nausea, vomiting, diarrhea, flatus, blenching.
o Vasomotor symptoms >> tachycardia, palpitations, flushing,
diaphoresis, dizziness.
o Late >> hypoglycemia.
• Management >> dietary modification, small frequent meals that is low
in carbs & high in proteins + avoid fluids with meals.
▪ Afferent (or efferent) loop syndrome:
• Afferent limb of a Bilroth II gets obstructed or dilated fr any reason (e.g.
kinking, angulation, volvulus, adhesions).
• Clinical features:
o Post-prandial RUQ pain + abdominal fullness.
o Bilious vomiting that alleviates symptoms.
o Steatorrhea.
• Investigations:
o US >> show dilated afferent loop.
o Barium meal >> enters the afferent loop.
• Management >> surgical revision (e.g. do Bilroth I or roux-en-Y).
▪ Biliary gastritis (reflux gastritis):
• Bile enters the stomach & irritates the mucosa.
• Clinical features >> Bilious vomiting with gastritis symptoms.
• Diagnosis >> by endoscopy.
• Management >> revision surgery is indicated.

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• Gastric cancer (High-Yield):

H. Pylori is a risk factor for both
o Gastric cancer is the 4th most common cancer worldwide. adenocarcinoma & lymphoma
o Histological types: (MCQ question ☺)
▪ Adenocarcinoma (95%).
▪ Lymphoma (4%).
▪ GIST (1%).
o Gross types:
▪ Polypoid.
▪ Ulcerative (25-50%); sharp nodular margins, non-radiating gastric folds.
▪ Superficial spreading (best prognosis).
▪ Linitis plastic (thick wall, lack of gastric folds).
o Adenocarcinoma of the stomach:
▪ Risk factors:
• Non-modifiable >> Age >60ys, male gender, family history of gastric
cancer.
• Environmental >> H. Pylori infection, Smoking, Diets high in smoked
foods (nitrites), alcohol, NSAIDs.
• Inherited >> Familial adenomatous polyposis (FAP), Pernicious anemia
(auto-antibodies), lynch syndrome.
▪ Clinical features:
• Patients often presents late with vague symptoms (anorexia,
weight loss, dyspepsia).
• Bleeding related symptoms (melena, hematemesis, anemia).
• Signs >> Transmitted pulsating non-expansile epigastric
masses, ascites, hepatomegally, acanthosis nigricans.
• Metastatic features:
o Hard, enlarged left supraclavicular LN (Virchow/Troisier sign).
o Sister Mary Joseph nodule (periumbilical metastatic nodule due
to intraperitoneal seeding).
o Krukenbug tumor (metastasis to bilateral ovaries resulting in
large ovarian cyst mass).
The most common site of o Seborrheic heratosis on back (lesar-Trelat sign).
metastasis is liver followed
o Pseudomyxoma peritonei (malignant ascites).
by the peritoneum
o Blumer’s shelf (digital rectal exam shows mass in pouch of
Douglas or recto-vesical pouch).
▪ Investigations:
• Routine labs >> CBC, electrolytes, LFTs, RFTs, occult blood, etc.. .
• Imaging >> US & Barium meal.
• Tumor markers (not specific) >> CEA (carcino-embbryonic antigen), CA-19-9.
• Diagnosis & staging >> endoscopy with biopsies + abdomeno-pelvic CT
scan.
▪ Management:
• Early >> radical subtotal gastrectomy, +/- neoadjuvant chemotherapy.
• Late >> cisplatin-based chemotherapy + palliative surgery.
• Prognosis >> poor with high recurrence rates, cure rate with surgery is
low.
Drugs like 5-FU, cisplatin, and epirubicin are commonly used.

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Hepatobiliary
system

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Liver & gallbladder anatomy (Review)

• Liver anatomy:
o The liver is the largest solid organ in the body, it fills the right
hypochondrium & epigastric regions.
o Surface anatomy:
▪ Point A >> right 5th rib in mid-clavicular line.
▪ Point B >> left 6th rib below the nipple.
▪ Point C >> right lowest point of costal margin.
o Liver surfaces:
▪ Parietal (diaphragmatic) surface (superior & anterior):
• Related to the diaphragm + part of anterior abdominal wall.
• Covered by visceral peritoneum )Glisson’s capsule( except for the bare
area.
• Ligaments to know >> coronal ligament, falciform ligament, ligamentum
hepatic teres (remnant of fetal umbilical vein).
▪ Visceral surface (inferior & posterior):
• Left side >> anterior surface of stomach.
• Right side >> gallbladder, right kidney, right colonic flexure.
• Posteriorly >> IVC (retroperitoneal) & gallbladder.
• Fissures of visceral surface (H shape): Ligamentum venosum is
o Right sagittal fissure >> fossa of gallbladder the remnant of ductus
venosus
(anteriorly), IVC groove (posteriorly).
o Left sagittal fissure >> round ligament
(anteriorly) & ligamentum venosus (posteriorly).
o Transverse fissure >> porta hepatis.
o Lobes of the liver:
▪ Anatomical (by falciform ligament):
• Big right lobe.
• Small left lobe.
• Caudate lobe (associated with IVC).
• Quadrate lobe (associated with gallbladder).
▪ Division depending on blood supply >> Cantile line, an
imaginary vertical line at the level of SVC & gallbladder.
▪ Segments of the liver >> Arranged into clockwise pattern prom posterior to
[Link] are 8 segments on total, segment 1 is the caudate.
o Hilum of the liver:
▪ The portal triad runs in the hepatoduodenal ligament (free border of lesser
omentum).
▪ Portal triad includes:
• Hepatic portal vein (posteriorly) >> formed by fusion of splenic & SMV
(behind the pancreas neck).
• Hepatic artery proper (anteriorly) >> arise from celiac trunk.
• Common bile duct (anteriorly).
▪ The portal triad divid to right & left branches when they approaching the hilum,
the entry point is called porta hepatis.

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o Hepatic blood supply:

▪ Hepatic portal vein >> supply 75% of liver blood (supplies 50% of O2).
▪ Hepatic artery (branch of celiac trunk) >> supply 25% of liver blood (supplies
50% of O2).
o Venous drainage >> The whole liver is draining into hepatic vein which enters the IVC.
o Lymphatic drainage:
▪ Diaphragmatic surface >> phrenic LNs.
▪ Visceral surface >> hepatic LNs, celiac LNs, cisterna chyli – thoracic duct.

• Anatomy of gallbladder:
o A pear-shaped organ that lies in the gallbladder fossa.
o The peritoneum completely surrounds the gallbladder & binds it to the liver.
o Parts:
▪ Fundus & infundibulum (Hartmann’s pouch).
Boundaries: ▪ The gallbladder connects to the liver directly by the way of the Ducts of Lushka.
Medial: Common hepatic duct. o Murphy point:
Inferior: Cystic duct. ▪ A surface landmark of the fundus of gallbladder.
Superior: Inferior surface of the
liver. ▪ Right subcostal border at the level of mid-clavicular line (L1)
Contents: o Cystohepatic triangle:
Cystic artery: The primary artery
supplying the gallbladder, which ▪ Border include the liver, cystic duct, & common bile duct.
is commonly ligated during a ▪ The cystic artery crosses through this triangle.
cholecystectomy. o Calot’s triangle:
Cystic lymph node (of Lund):
Important for lymphatic drainage ▪ Smaller part of the cystohepatic triangle.
of the gallbladder. ▪ Boundaries are CBD (medially), cystic artery (superiorly), cystic duct (laterally).
Lymphatics and connective
tissue. o Arterial supply >> cystic artery (branch from right hepatic artery).
o Venous drainage >> cystic vein (drain into portal vein).
o Lymphatic drainage >> celiac LNs.

• Biliary tree:
o The biliary tree is composed of:
▪ Cancaliculi (smallest part).
Spiral valve of Heister ▪ Canals of Hering (lined with cholangiocytes).
Found in the proximal
mucosa of cystic duct near
▪ Bile ductules.
the attachment of of ▪ Right & left hepatic ducts.
common hepatic duct ▪ Common hepatic duct.
▪ Cystic duct (contains spiral valves of Heister).
▪ Common bile duct.
o Common bile duct (CBD):
▪ Formed in the lesser omentum by union of cystic & common hepatic duct.
▪ Then it comes in contact with the main pancreatic duct forming the
hepatopancreatic ampulla (ampulla of Vater).
▪ The Vater ampulla opens in the duodenum though the major duodenal papilla
which is controlled by hepatopancreatic sphincter (sphincter of Oddi).
▪ Parts >> supraduodenal, retroduodenal, pancreatic, intramural.

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• Overview of hepatobiliary investigation & procedures:

o Liver function tests (LFTs):
▪ Aminotransferases (ALT & AST) >> high levels suggest liver damage, ALT is
more sensitive & specific than AST for liver damage.
▪ Alkaline phosphatase (ALK-P):
• Not specific to liver, also found in bone, gut, & placenta.
• ALK-P is elevated when there is obstruction to bile flow (e.g. cholestasis)
in any part of biliary tree. Normal levels makes cholestasis unlikely.
• If ALK-P is high >> measure GGT to make sure that the elevation is
hepatic in origin. If GGT is normal, consider pregnancy or bone disease.
▪ Gamma glutamyl transferase (GGT):
• Used to confirm that ALK-P elevation is due tp hepatic cause.
• GGT is elevated in cholestatic disease.
o Ultrasound:
▪ The best imaging tool fo gallbladder visualization.
▪ Most stones are cholesterol stones that can be visible on US.
▪ Can look into the proximal CBD & cystic duct, but not the retroduodenal part.
▪ Can indirectly tell you about distal obstruction by seeing dilated proximal ducts.
o Cholangiography (visualizing the bile duct):
▪ Forms:
• ERCP.
• Intra-op cholangiogram (IOC).
• Precutaneous transhepatic cholangiography (PTC).
▪ Endoscopic retrograde cholangiopabcreatography (ERCP):
• Often done with sphincterotomy (papillotomy).
• It have diagnostic & therapeutic role:
o CBD stone removal (using basket or stent).
o Cholangitis decompression.
o Choledochal cyst removal (type III).
• Complications >> mainly iatrogenic acute pancreatitis (1%).
o Hepatobiliary imino-diacetic acid (HIDA) scan:
▪ RBCs tagged with Technetium 99 is injected IV.
▪ This will be taken by liver & then to CBD which spilled to duodenum.
▪ Timed photographs are taken to assess the uptake process (can estimate
gallbladder ejection fraction).
▪ Absent uptake suggest dysfunction or blockage.

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Hepatic abscess (HIGH-YEILD)

• Overview:
o Causes >> pyogenic, amebic, fungal (rare).
o Route of entry:
▪ Direct spread (biliary tract infection, portal spread, site of trauma).
▪ Systemic spread (hematogenous).

• Pyogenic (bacterial) abscess:

o Common organisms >> polymicrobial, [Link], proteus, klebsiella (Gram -ve).
o Common sources:
▪ Ascending cholangitis (most common).
▪ Portal vein (diverticulitis or appendicitis).
▪ Sepsis.
o Clinical features (not specific, suggestive of liver disease): Hepatic abscess usually affects
▪ Signs of toxemia (fever, chills, septic-like picture). right lobe more than the left,
▪ RUQ pain & jaundice. left lobe abscess have risk to
▪ S&S of pleural effusion (SOB, stony dullness). rupture into the peritoneum
▪ Examinations >> tender hepatomegally.
o Investigations: Note that any abscess in the liver may
▪ CBC >> leukocytosis. produce local effect to the right lower
▪ CRP & ESR >> elevated. pleura. Thus, patients may presents with
S&S of pleural effusion (e.g. dyspnea,
▪ LFTs >> elevated. reduced tactile fremitus, stony dullness)
▪ Hepatitis serology >> R/O viral hepatitis.
▪ Urinalysis + culture >> R/O kidneys problems.
▪ Imaging:
• RUQ US >> liver & kidney is examined, it can show the abscess
(Pyogenic abscess tend to be small and multiple).
• CT abdomen & chest >> may show right sided pleural effusions as an
effect of liver abscess.
o Management:
▪ IV broad spectrum antibiotics >> ceftriaxone + metronidazole (4-6 wks).
▪ CT / US guided percutaneous drainage >> drain is sent for culture & sensitivity
testing, then change antibiotics to appropriate.
▪ Operative drainage >> refractory to therapy or if multiple abscesses.

• Amebic abscess:
o Caused by Entamoeba histolytica.
o Source >> Feco-oral route (E. Histolytica causes bloody diarrhea, flask-shaped intestinal
ulcers, then it gains access to portal circulation).
o Risk factors >> immigrants, male homosexuals, traveling to endemic areas (e.g. India,
Africa).
o Clinical features:
▪ Fever (not too high with no chills, patient is less toxic).
▪ RUQ pain.
▪ +/- History of bloody diarrhea.
▪ Examinations >> tender hepatomegally.

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o Investigations >> Same as above + Serology for E. Histolytica.

o Management:
▪ IV metronidazole (DOC). Drainage classically described
▪ CT / US guided percutaneous drainage is done only if: to be achovy paste like,
because it elicits liquefactive
• Refractory to metronidazole.
necrosis (it is sterile)
• Peritoneal rupture risk.
• Co-infection.

E. Multilocaris has
• Hydatid cyst:
alveolar involvement &
o Causes >> echinococcus granulosus or multilocaris (tabeworm – parasite). it’s difficult to treat
o Source:
▪ Infected animal feces (feco-oral) by ingestion of infected vegges with excreta.
▪ Definitive host is dog (pass in dog stool).
▪ Intermediate host (sheep). Humans are considered as accidental
▪ Accidental host (humans). hosts because when they ingest the
eggs the cyst is forms in the humans,
o Risk factors >> Exposure to infected animals, immigrants. reproducing asexually to creat
o Clinical features: daughter cysts. These daughter cysts
▪ Most common location is the right lobe periphery. cannot infect other people, because
▪ Patients may be asymptomatic (found incidentally). they need to eat the egg.
▪ Liver disease symptoms (RUQ pain).
The growth rate is
▪ Respiratory symptoms (alveolar cysts) & CNS symptoms (brain cyst).
slow, 2-3cm a year
▪ Examinations >> hepatomegally + hydatid thrill on palpation (rare but
pathognomonic).
▪ Complications of liver cyst:
• Rupture (most important, result in fatal anaphylaxis).
• Cholangitis (cyst obstruct the bile duct).
• Secondary infections.
o Investigation:
▪ Labs:
• CBC >> eosinophilia.
• LFTs >> assess liver function.
• Serology >> anti-echinococcus IgG Ab.
▪ Liver US (virtually diagnostic):
Layer of Hydatid cyst • Snowflake sign (hydatid sand).
Ectocyst >> body reaction.
Endocyst >> active layer
• Double-line sign.
• Outline is calcified (suggest necrosis).
▪ CT >> multiple, multilobulated cyst, filled with fluid.
o Management (surgical):
▪ Albendazole:
Corticosteroids & • Given for 7 days pre-op & for 1 month post-op.
antihistamine can be given
pre-op to ↓ risk of • Monitor WBCs & LFTs.
hypersensitivity reactions ▪ Biggest fear & concern is that any spillage during surgery can result in fatal
anaphylaxis. Thus, always have IV/IM epinephrine prepared during surgery.
▪ Surgical resection:
• Needs good visualization.
• Scolicidal agent is injected (20% hypertonic saline) to kill daughter cysts.
We need to be very careful to • There is risk of residual cysts implanting during the surgery.
protect ourselves & the patients
body from dropping cysts. So,
we drape the body with
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Liver tumors

• Important points that you must know (HIGH-YEILD):

o The most common benign liver tumor is Cavernous hemangioma.
o The most common primary malignant liver tumor is Hepatocellular carcinoma (HCC).
o The most common liver malignancy overall is metastasis from colorectal tumor,
followed by lung & then the breast.

• Benign liver tumors (nice to know):

o Cavernous hemangioma:
▪ Symptoms >> patients are asymptomatic or present with S&S of liver disease
(RUQ pain, bleeding, jaundice).
▪ Signs >> hepatomegally + RUQ bruit (bloody tumor).
▪ Investigations:
• Labs >> CBC (thrombocytopenia), LFTs.
• Imaging >> liver US & CT with contrast (homogenous, hyperechoic
mass).
• Biopsy >> contraindicated because it may result in fatal hemorrhage.
▪ Management:
• Asymptomatic >> monitoring with serial US.
• Symptomatic >> surgical resection.
o Hepatocellular adenoma:
▪ Benign proliferation of hepatocytes without bile ducts.
▪ Risk factors >> OCP use, anabolic steroids, glycogen storage diseases.
▪ Typical patient is a women of childbearing age.
▪ Symptoms >> RUQ pain, fullness.
▪ Signs >> RUQ tenderness, +/- mass.
▪ Investigations:
• Labs >> CBC, LFTs.
• Imaging >> liver US & CT with contrast (solitary, well-demarcated
heterogenous mass)
▪ Management:
• In all cases, stop OCPSs & anabolic steroids.
• If asymptomatic & small (<5cm) >> monitoring.
• If symptomatic or big (>5cm) >> surgical resection.

• Hepatocellular carcinoma (HCC) (nice to know):

o Also known as hepatoma.
o It’s the most common primary malignant liver cancer. The most common malignancy in
the liver overall is metastatic.
o Epidemiology >> affects male more than females, age 50-60s. The commonest one is colorectal
o Risk factors: cancer, followed by lung &
▪ Liver Cirrhosis (5% of cirrhosis patients develop HCC): breast cancer
• Chronic viral hepatitis (HCV, HBV).
• Alcoholic cirrhosis.
• Genetic diseases (hemochromatosis, Wilson’s disease).
▪ Others >> smoking, carbon tetrachlorides, liver flukes (shistosoma), aflatoxins
(aspergillus fumigatus).

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o Clinical features (suggestive of liver disease):

▪ Symptoms >> RUQ pain, Weight loss, Symptoms of polycythemia (headache,
vision disturbances).
▪ Signs:
• Signs of portal HTN & liver failure.
• RUQ bruit (high vascular tumor).
• Tender hepatomegally & Splenomegaly.
o Investigation & Diagnosis:
▪ Labs >> CBC, LFTs, AFP.
▪ Imaging >> liver US & CT.
▪ CT/US guided liver biopsy >> for definitive diagnosis.
o Management:
▪ If early & non-cirrhotic >> Lobectomy with wide margins (either left or right to
Unresectable tumors have the cantlie line).
very poor prognosis ▪ Liver transplant, only in:
• Cirrhotic patient, Non-resection candidate.
• No LNs involvement or vascular involvement.
• Fulfills Milan criteria (1 site <5cm OR 3 sites but <3cm).

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Gallbladder diseases (HIGH-YEILD)

• Cholelithiasis (Gallstones): Supersaturation = abnormal

o Pathophysiology >> Imbalance between components of bile bile salt / cholesterol ratio
which result in less bile or
(supersaturation) + Biliary stasis.
high cholesterol
o Risk factors:
▪ (5Fs) Female, Fat, Fertile, Forty, Flatulent.
Patients with gallstones have ▪ Obesity or rapid weight loss.
increased risk of developing ▪ Hyperlipidemia.
gallbladder cancer
▪ Hemolytic anemias (e.g. SCD) or CD.
▪ Terminal ileum resection (low enterohepatic circulation).
o Types of stones:
▪ Cholesterol stones (most common – 80%):
• Non-pigmented stones.
• Bile supersaturation with cholesterol, especially in patients with obesity,
rich fatty meals.
▪ Bilirubin stones (15%):
• Pigmented stones (15% of these stones are calcified to appear on
radiographs).
• Occur in patients with hemolysis (e.g. SCD), which a lot of unconjugated
bilirubin get conjugated.
• Ca bilirubinate >> black stones.
• Infected bilirubin stones >> brown stones.
▪ Ca oxalate stones >> found in Crohn’s disease patients.
o Clinical features:
▪ Asymptomatic (risk of symptoms is 1%/year) >> most patients (80%) don’t
have symptoms & they are identified incidentally on imaging.
▪ Symptomatic gallstones (biliary colic):
While taking history all of the • RUQ (colicky) pain that lasts for 1-3h.
following must assessed:
(1) Gallstone symptoms.
• The pain is steady with episodes of increased severity.
(2) GI symptoms (history of PUD, • The pain is aggravated by fatty meals (CCK result in gallbladder
reflux, bowel movements). contraction against blockage).
(3) Liver symptoms (jaundice,
itchiness, pale stools, dark urine). • The pain may radiates to right shoulder or inferior scapula (Boas sign)
(4) GU symptoms (dark urine, due to irritation of diaphragm (phrenic nerve)
dysuria).
(5) Respiratory (cough, SOB).
• The pain may be associated with nausea & vomiting.
(6) Cardiac (chest pain, sweating, • It’s not a true colic (they have a persistent background pain that is
arm pain). increased from time to time).
▪ Complicated gallstones (patient presenting with complications):
• Choledocholithiasis (obstructive jaundice).
• Acute calculous cholecystitis.
• Ascending cholangitis.
• Acute pancreatitis (gallstone pancreatitis).
• Mucocele (stole impaction leading to mucus accumulation).
• Empyema (infection of mucocele).
• Mirrizi syndrome (external compression of CBD by large stone in cystic
duct).
• Gallstone ileus (S&S of bowel obstruction).

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o Investigations & Diagnosis:

▪ Labs (of acute abdomen):
• CBC >> assess WBCs (biliary colic VS acute cholecystitis).
• LFTs >> R/O hepatitis.
• Amylase + lipase >> R/O acute pancreatitis.
• RFTs >> R/O renal causes.
• Urinalysis >> R/O UTI & stones.
▪ Imaging:
• Gallbladder US:
o Patients must be fasting (fill gallbladder).
o Assess gall bladder & proximal CBD for stone, if it’s dilated, this
indicated distal CBD stone.
• CXR >> R/O pneumonia.
o Management:
▪ Asymptomatic patient >> no treatment. Ursodeoxycholic acid my
Patient can be discharge ▪ Mild symptoms >> analgesia, lifestyle changes. help is dissolving the stones
after vitals & appetite ▪ Severe symptoms or complication:
improvement +
• Analgesia (morphine + anti-emetic + buscopan).
tolerating oral food
• Pre-op IV broad-spectrum antibiotics (considered as clean-
contaminated surgery) + laparoscopic cholecystectomy.
o Cholecystectomy:
▪ Indications:
• Severely symptomatic Gallstones.
• Asymptomatic in special populations (SCD, pediatrics,
immunocompromised, DM, large stones, porcelain gallbladder).
• Complicated gallstones.
▪ Safety considerations:
• The gallbladder lies on liver visceral surface, with the cystic artery &
duct exposed.
• Calot (Ludig) node lies in between the artery & duct.
▪ Laparoscopic ports (trochar) sites:
• 1st >> infra-umbilical (fo camera).
• 2nd >> RUQ (for assistant; to hold gallbladder in place).
• 3rd >> LUQ (for surgeon).
▪ For surgical incision >> Kocher incision (right hypochondrium).
▪ Steps of cholecystectomy:
• Achieve critical view of safety; free the cystic duct & artery from
adhesions & hold fundus of gallbladder.
• Staple & then ligate the cystic artery & duct.
• Free gallbladder from liver bed.
• Pull the gallbladder out through the umbilical trochar.
• Highest likelihood of damage is to the right branch of the hepatic artery.
• Gallbladder tissue is sent for histopathology.

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▪ Complications of cholecystectomy:
• Laparoscopic complications (introduction injury, air embolism, low BP).
• Specific:
o Damage to right hepatic artery or damage to CBD (most feared).
o Retained stones (small stones are missed & enter the CBD
leading to post-op RUQ pain & obstructive jaundice).
o Bile leakage & peritonitis (always a bag is used to pull out the
gallbladder).

• Choledocholithiasis:
o A complications of gallstones, in which there is a stone in the common bile duct (CBD).
o Clinical features:
▪ Biliary colic symptoms. Pruritus occur due to
▪ Cholestasis (obstructive jaundice, pale stools, dark urine, accumulation of bile salts &
pruritus, bleeding tendency). irritation of nerve endings
▪ Complications >> pancreatitis, cholangitis.
o Investigations & Diagnosis:
▪ Labs >> LFTs will show cholestatic disease pattern (high ALK-P & GGT + high
conjugated bilirubin).
▪ Imaging:
• US >> assess proximal CBD for stones, if it’s dilated, consider a distal
stone.
• ERCP >> diagnostic & therapeutic.
o Management:
▪ (1) ERCP-guided sphincterotomy & basket retrieval of stone.
▪ (2) If fails, open surgery; CBD exploration & removal of stones + intra-operative
cholangiogram & T-tube placement to drain bile.
▪ (3) Interval cholecystectomy (after normalization of LFTs).

• Acute calculous cholecystitis:

o Defined as inflammation of gallbladder wall due to obstruction of cystic duct by stones
(not infection), occur in 10% of patients with gallstones.
o Clinical features:
▪ Symptoms:
DDx • Steady, severe, sharp RUQ pain:
(1) Cholangitis. o Unlike colic, it lasts >3-6h & mostly localized.
(2) Pancreatitis.
(3) Hepatic abscess, hepatitis.
o May have referred pain to right shoulder or scapula.
(4) Perforated duodenal ulcer. o Increased with fatty meals.
(5) Acute appendicitis o Associated with nausea & vomiting.
(retrocecal appendix). • Biliary tract obstruction signs >> jaundice, pruritus, clay-colored stool,
(6) Pyelonephritis or renal
dark urine.
stones.
(7) Lower lobe pneumonia. ▪ Signs:
• RUQ tenderness (+/- rebound).
• +ve Murphy’s sign (inspiratory arrest when RUQ is palpated during
inspiration) ([Link]
• Palpable tender gallbladder (33% of patients).
• Low Grade fever (VS Cholangitis which is more toxic).

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▪ Compilations:
Mechanism of cholecystenteric
• Generally, same as gallstones complications. fistula formation
• Mucocele or empyema of the gallbladder. The omentum try to limit the
• Perforation & bile peritonitis. infection by covering the
gallbladder, which will result in
• Cholecystenteric fistula (result in gallstone ileus).
approximating the intestine to the
• Risk of Gallbladder cancer. gallbladder
o Investigations & Diagnosis:
▪ Labs (of acute abdomen):
• CBC >> leukocytosis.
• LFTs >> assess liver function.
• Amylase & lipase >> R/O pancreatitis.
• Urinalysis >> R/O pyelonephritis.
• +/- Others >> RFTs, electrolytes panel.
▪ Imaging:
• CXR >> R/O lung causes, assess air-under diaphragm.
• RUQ US (required for diagnosis):
o Enlarged bladder & wall thickness (>4mm).
o Peri-cholecystic fluid.
o Stone in cystic duct.
o Sonographic murphy’s sign (painful US exam).
• CT scan >> more sensitive than US identifying complications (e.g.
perforation, abscess, pancreatitis).
• HIDA scan >> not routinely done, used if US is non-conclusive, it will
show non-filling gallbladder.
o Management:
▪ Conservative management:
• (1) Hydration & bowel rest (NPO) to prevent stimulation of CCK which
increase gallbladder contractility.
• (2) IV broad-spectrum antibiotics (3rd generation cephalosporins +
metronidazole).
• (3) IV analgesia (morphine + buscopan + anti-emetic).
• (4) Correction of electrolytes abnormalities.
▪ If present within 48-72h >> urgent laparoscopic cholecystectomy OR open
cholecystectomy (if complicated).
▪ If presents >72h:
• Continue conservative management + interval cholecystectomy (>6
weeks), because the tissue will be very friable, inflamed, & adhesive,
making the surgery very difficult.
• If patient deteriorate, do surgery in any case, either cholecystectomy or
percutaneous cholecysteostomy tube (drainage of gallbladder).

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• Acalculous cholecystitis:
o Cholecystitis, but on imaging there is no stones (rare).
o Risk factors (biliary stasis or hypoperfusion):
▪ ICU patients (NPO & on TPN).
▪ Hospitalized patient with prolonged post-op stay.
▪ Dehydration.
o Clinical features & investigations >> same as acute cholecystitis, however, there is no
evidence of stones on US, biliary sludge may be seen.
o Management >> urgent cholecystectomy.

• Gallstone Ileus:
o A small bowel obstruction at the ileocecal valve by a gallstone received through the
duodenum by a cholecystoenteric fistula (size >2cm).
o Clinical features:
▪ Symptoms >> SBO symptoms; abdominal pain & distention, bilious vomiting,
constipation.
▪ Signs >> abdominal distention & tenderness, hyperactive bowel sounds.
o Investigations (same as SBO):
▪ Erect AXR:
• Air-fluid levels (step-ladder pattern).
• Distal compression beyond ileocecal valve.
• Pneumobilia (air in biliary tree).
▪ Supine AXR >> air is collected centrally.
▪ CT abdomen >> it will show pneumobilia, the fistula, & the stone.
o Management:
▪ Same management steps as any SBO.
▪ Exploratory laparotomy:
• Enterotomy with tone removal by milking.
• If stable, do cholecystectomy + fistulectomy at the same time.
• If unstable, arrange for interval cholecystectomy.

• Acute (ascending) cholangitis:

o Defined as bacterial infection (due to biliary stasis) of the biliary tract proximal to an
obstruction in the CBD
o It’s a potentially life threatening & requires emergent management (mortality 50%).
o Causes:
▪ Intraluminal >> choledocholithiasis (most common cause), biliary stenting.
▪ Intramural >> Strictures (post-ERCP), cancer or choledochal cyst.
▪ Extra-luminal >> Mirrizi syndrome, Cancer of head of pancreas, Pancreatic
pseudocyst.
o Causative organism:
▪ E. Coli (most common).
▪ Others >> Klebsiella, Proteus, Enterobacter, Pseudomonas, enterococcus.

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Charcot’s triad
(1) RUQ pain.
(2) Fever, chills.
(3) Jaundice.
o Clinical features: Reynold’s triad
▪ Symptoms: (1) Charcot’s triad.
(2) Altered mental status.
• RUQ pain.
(3) Low BP.
• Nausea & vomiting.
• High-grade Fever + chills.
• Cholestasis symptoms; jaundice, dark urine, pale stools, pruritus.
▪ Signs >> Unstable, toxic looking patients (tachycardia, high fever, low BP,
dehydrated) + Jaundice.
▪ Complications >> the most serious complications is hepatic abscess.
o Investigations:
▪ Stabilization of patient is a priority, then precedes to investigations.
▪ Labs:
• CBC >> leukocytosis.
• CRP & ESR >> high.
• LFTs >> cholstatic pattern (high ALK-P, GTT, direct bilirubin).
• Electrolytes panel >> assess any disturbances.
• Urinalysis >> R/O pyelonephritis.
• Amylase & lipase >> R/O pancreatitis.
• Blood culture >> usually +ve (septic picture).
▪ Imaging:
• RUQ US (best initial):
o Dilated CBD system + it may show the obstruction.
o Gallbladder contains many stones.
o R/O any extrinsic causes.
• ERCP (diagnostic, therapeutic, modality of choice):
o Usually done after stabilization of patient.
o If patients fulfills Charcot’s triad, do it directly.
o Obstruction is identified + pus may be seen oozing from the
ampulla.
o It may be suppurative (needs decompression) or non-
suppurative.
o Management:
▪ ABCs >> IV fluid resuscitation, draw blood for investigations, NPO.
▪ IV analgesia & IV antibiotics >> cephalosporins + metronidazole (70-80% may
respond to antibiotics, still, we must identify the cause).
▪ Definitive treatment:
• ERCP-guided sphincterotomy & decompression + Stone extraction + pus
drainage.
• If ERCP fails >> do percutaneous drainage (PTC).
• If PTC fails >> do open surgery; CBD exploration + intra-op T tube
insertion.
• Interval cholecystectomy must be done.

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Gallbladder cancer (nice to know)

• Gallbladder cancer:
o Most common type is adenocarcinoma, rare, occur in <1% of patients with gallstones.
o Risk factors:
▪ Gallstones.
▪ Cholecystoenteric fistulas. Any patient with calcified gallbladder
▪ Procelain gallbladder (50% risk of pancreas). needs cholecystectomy due to high
▪ Typhoid carrier. risk of gallbladder cancer
o Clinical features:
▪ Most common location is gallbladder fundus.
▪ Patients tends to be asymptomatic until late stages.
▪ Constitutional symptoms; weight loss, fever.
▪ Hepatobiliary symptoms; RUQ mass, RUQ pain, jaundice.
▪ Gallbladder cancer have an early metastasis to the liver.
o Investigations >> CBC, LFTs, US, ERCP.
o Management:
▪ Involving mucosa only >> open cholecystectomy.
▪ Beyond mucosa >> open radical cholecystectomy (removal of gallbladder,
related liver lobes, LN dissection), +/- chemotherapy.
▪ Don’t remove it laparoscopy, because it may result in tumor implants in the
trochar site.
▪ Prognosis is very poor; 5% 5-years survival, because most of patients are
diagnosed late.

• Cholangiocarcinoma:
o Adenocarcinoma of bile ducts (cholangiocytes).
o Risk factors:
▪ Choledocal cysts.
▪ Primary sclerosing cholangitis (PSC).
▪ Liver flukes (clonorchiasis).
o Clinical features:
▪ Typical location is at the bifurcation of hepatic ducts (proximal ducts).
▪ Constitutional symptoms; weight loss & fever.
▪ Cholangitis-like picture.
▪ Cholestasis symptoms; dark urine, pale stools, jaundice, pruritus.
▪ RUQ swelling.
o Investigations >> US, CT, ERCP biopsy.
o Management:
▪ Proximal >> resection + roux-en-Y anastomosis.
▪ Distal >> Whipple procedure.

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• Other Information (nice to know):

o Role of bile:
▪ Composition of bile:
• (1) Bile salts & acids (50%):
o Function in fat emulsification to allow for more surface area to
absorb in the small intestines in form of micelles.
o Vitamins ADEK are fat-soluble vitamins that need adequate bile
for absorption.
• (2) Phospholipids (40%) >> licithin.
• (3) Bile pigments (conjugated bilirubin).
• (4) Cholesterol.
▪ Most of bile is reabsorbed in the terminal ileum (95%) (entero-hepatic
circulation).
▪ Gallbladder contracts in response to cholecystokinin (CCK) which is released by
duodenal cells secondary to intra-luminal dietary fats & AAs (contraction against
a blocking stone result in biliary colic).
▪ Principles of bile stones:
• Most common is cholesterol supersaturation & precipitation
(cholesterol stones).
• In patients with chronic hemolysis, supersaturation is with bilirubin
(resulting in bilirubin or pigmented black stones).
• If pigmented stones get infected, brown stones develop.
• In case of CD, calcium oxalate tones develops.
o Jaundice:
▪ Yellow discoloration as a result of elevated bilirubin (>2.5-3.5 g/dL).
▪ First location of jaundice is under the tongue (not practical) followed by sclera.
▪ Causes of hyperbilirubinemia:
• Pre-hepatic (lemon-yellow) >> hemolysis, Gilbert & criggler Najjar
syndromes.
• Hepatic (mixed) >> hepatitis, alcoholic cirrhosis, liver toxicity.
• Post-hepatic (olive green):
o Cholestasis (obstructive jaundice).
o Patients develops jaundice, pale stools, dark colored urine,
pruritus, xanthomas, nausea & vomiting.
o Causes >> choledocholithiasis, PSC, PBC, choledochal cysts,
cancer of head of pancreas.
▪ Causes of obstructive jaundice:
• Proximal:
o Cholangiocarcinoma.
o Lymphadenopathy.
o Sclerosing cholangitis.
• Distal:
o Choledocholithiasis & ascending cholangitis.
o Pancreatic head cancer.
o Pancreatic pseudocyst.
o Pancreatitis.

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The
Pancreas

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Anatomy of the Pancreas (review)

• Pancreas development (embryology review):

o The pancreas develops from the foregut (endoderm) at the level of the duodenum.
o It first appears as a ventral & a dorsal bud, then the ventral bud turn to fuse with the
dorsal bud.
o Ventral bud >> forms the uncinate process + the inferior part of the head + the proximal
part of the main pancreatic duct.
o Dorsal bud >> the rest of the pancreas + the rest of the pancreatic duct.

o Abnormalities:
▪ Pancreatic divisum:
• The most common congenital anomaly of the pancreas.
• Improper infusion resulting in the main pancreatic duct draining into the
accessory duct (which is too small).
• As a result:
o The main pancreatic duct drains a small portion of the head.
o The rest of pancreas drain into the minor sphincter.
• May lead to chronic pancreatitis with acute or chronic episodes.
▪ Annular pancreas:
• Malrotation of the ventral bud resulting in a ring o pancreatic tissue
around the duodenum.
• It’s a cause of duodenal obstruction (DDx of duodenal atresia).

• Anatomy of the pancreas:

o The pancreas is a retroperitoneal organ, except for the tail which is intraperitoneal (lies
within the splenorenal ligament).
o It’s located posteriorly to the stomach, between the duodenum on the right & the
spleen on the left.
o Parts:
▪ Head & uncinate process (behind superior mesenteric vessels).
▪ Neck (overlies the superior mesenteric vessels).
▪ Body (overlies the superior mesenteric vessels).
▪ Tail (closely related to the hilum of the spleen, abundant of islets cells of
Langerhans).

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o Pancreatic ducts:
▪ The main pancreas duct starts from the tail and run through the parenchyma to
the head where it turns inferiorly and merges with the bile duct.
▪ Both main pancreatic duct & bile duct fuse together to form a short, dilated
hepatopancreatic ampulla.
▪ The accessory pancreatic duct drains the uncinate process & the inferior part of
the head & opens in the minor duodenal papilla.

o Arterial supply:
▪ Splenic artery (A branch from the celiac trunk,
Also supply the stomach
runs on the superior rim of the pancreas).
through the short gastric
arteries & left ▪ Anterior & posterior superior pancreatoduodenal
gastroepiploic artery artery (branch from gastroduodenal artery).
▪ Anterior & posterior inferior pancreatoduodenal
artery (branch from SMA).
o Venous drainage >> pancreatic veins drains in splenic
vein into the hepatic portal vein.

• Physiology:
o Pancreas endocrine function:
▪ Insulin from beta cells.
▪ Glucagon from alpha cells.
▪ Somatostatin from delta cells.
▪ VIP.
o Pancreas exocrine function:
▪ Production of lipase, amylase, trypsin, proteases.
▪ All these enzymes are secreted in inactivated from, they are activated by
enterokinases that are present in the duodenum.

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Acute pancreatitis (HIGH-YEILD)

• Overview:
o Defined as auto-digestion of the pancreas due to premature activation of pancreatic
enzymes.
o Causes (I GET SMASHED):
▪ Idiopathic.
The most common causes are ▪ Gallstones blocking ampulla of Vater (40%).
gallstones, alcohol, idiopathic ▪ Ethanol abuse (40%).
▪ Trauma (most common in children). Mild-moderate >> most common & respond well to
▪ Steroids. treatment.
▪ Mumps virus. Severe acute (necrotizing pancreatitis) >> occur in
▪ Autoimmune diseases. 25% of patients, has significant mortality &
morbidity.
▪ Scorpion sting.
▪ Hypertriglycerideemia & Hypercalcemia.
▪ ERCP (as a procedure complication).
▪ Drugs (NRTIs, valporate, etc..).
o Pathophysiology:
▪ There is a premature activation of pancreatic enzymes which will result in auto-
digestion of the tissue.
▪ Lipase breakdown fat in omentum & peritoneum releasing free Fas.
▪ Free Fats combines with Ca (resulting in hypocalcemia) causing fat
saponification (fat necrosis & chalky white spots on pancreas).
▪ Other enzyme may digest tissues, blood vessels & result in cytokine release
leading to other complications.

• Clinical features:
o Symptoms: DDx
▪ Severe epigastric pain that radiates to the back, worsen (1) Perforated duodenal ulcer.
when supine & after meals, relived by sitting or leaning (2) Acute mesenteric ischemia.
forward. (3) Cholangitis or cholecystitis.
(4) AAA rupture.
▪ Nausea, vomiting, anorexia. (5) Inferior wall MI.
o Signs:
▪ Low-grade fever.
▪ Epigastric tenderness (+/- guarding) & abdominal distention.
▪ Absent bowel sounds.
o In severe disease:
▪ Hypovolemic shock (tachypnea, tachycardia, hypotension).
▪ SIRS (systemic inflammatory response syndrome) >> hypovolemic shock + fever.
o In hemorrhagic pancreatitis:
▪ Cullen sign (periumbilical ecchymoses).
Extra-intestinal manifestations
▪ Grey-Turner sign (flanks ecchymoses). of acute pancreatitis
▪ Fox sign (ecchymosis of inguinal ligament). (1) Uveitis.
(2) Pleural effusion or ARDS.
(3) Shock.

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• Investigations & Diagnosis:

Acute pancreatitis diagnosis is
o Diagnosis is clinical, investigations are done to R/O other causes usually made clinical, laboratory
& to provide more evidence of diagnosis. studies is supportive, CT is
o Labs & imaging of acute abdomen is usually done. confirmatory
o Labs:
▪ CBC >> leukocytosis, low HB in hemorrhagic pancreatitis.
▪ Blood typing & crossmatching >> for possible blood transfusion.
▪ Amylase & lipase:
• Both are elevated (must be >3 normal limit).
ECG is important to be done
• Lipase is more specific, rises earlier, stays longer.
to monitor arrhythmia due to
hypocalcemia • High amylase may be found in perforated GI viscus, ruptured ectopic
pregnancy, renal failure, DKA.
▪ Electrolytes panel & ABG >> Hypocalcemia, acidosis, low Mg (in alcohol cases).
▪ Glucose >> assess hypo/hyperglycemia.
▪ RFTs >> high BUN (due to hypovolemic shock).
▪ Coagulation profile >> assess possible risk of DIC.
▪ LFTs >> R/O hepatic causes, AST may be elevated.
▪ LDH >> for Ranson’s criteria.
▪ CRP >> measured after 48h, if >150 , it indicates poor prognosis.
o Imaging:
▪ The main purpose of imaging is to R/O other causes of acute abdomen, in
The best initial imaging addition, patients with acute pancreatitis mostly will be normal in early disease
modality for uncomplicated,
(<72h).
stable patients with suspected
acute pancreatitis is ▪ Supine & erect AXR (normal in early diseases):
abdominal US. • R/O other causes of acute abdomen, assess air under diaphragm.
The best initial imaging • Sentinel loop sign (the adjacent duodenum has adynamic ileus).
modality for complicated,
unstable cases with suspected
• Colon cut-off sign (absent air in the splenic flexure).
acute pancreatitis is ▪ Abdominal US (normal in early disease):
abdominal CT scan with • Helpful in identifying gallstones (gallstone pancreatitis).
contrast. • It’s not very helpful in diagnosing acute pancreatitis in early disease, it
may show enlarged, hypoechoic pancreas.
▪ CT scan with contrast (normal in early disease):
• Used mainly to assess pancreatitis severity + assess any complications.
• May used in rare cases if diagnosis is not clear initially, it may show (1)
Edematous pancreas, (2) Severe fat stranding around pancreas, (3) Peri-
pancreatic fluid collection.
o Prognostic criteria )Ranson’s Criteria(:
▪ >3 needs ICU admission.
▪ 0-2 >> <5% mortality.
▪ 3-4 >> 15% mortality.
▪ 5-6 >> 40% mortality.
▪ >7 >> 100% mortality.

Ca HOBBS 48 hrs post Admission

Calcium 2mmol/L
Hematocrit fall>10%
02 < 60mmHg
BUN increase>1.79mmol/L
Base deficit>4mEq/L
Sequestered fluid>6L
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• Management:
o Mild acute pancreatitis:
▪ Bowel rest (NPO) >> Goal is to rest the pancreas, give TPN or naso-jejunal tube
feeding. Oral nutrition can be started within 24hr in mild cases.
▪ Pain control >> opioids (Fentanyl & meperidine) is preferred over morphine
(increase sphincter of Oddi pressure).
▪ Aggressive IV fluids & monitoring:
• Insert 2 large pore IV lines + Foley’s catheter (normal urine output is 1-
Generally, antibiotics is not 2ml/Kg/hour).
indicated in acute • Patients will have severe intravascular volume depletion due to
pancreatitis, except in
infective necrotic pancreatitis
vomiting & 3rd spacing.
• Balanced crystalloids (lactated Ringer solution) are superior to normal
saline (normal saline can result in hyperchloremic metabolic acidosis
that will stimulate the pancreas, thus, worsening the condition).
• Correct any electrolytes abnormalities.
o Severe acute pancreatitis:
▪ Admission to ICU.
When acute episodes
▪ Early enteral nutrition in first 72h is advised through nasojejunal tube.
resolves, CT scan must be
done in all patients to look ▪ If not resolved in few days, supplemental parenteral nutrition should be started.
for complications ▪ If >30% of pancreas is necrosed, IV antibiotics must be started (imipenem or
meropenum).
o In Gallstone pancreatitis:
▪ All patients must do cholecystectomy.
There is very high
morbidity & mortality ▪ In mild pancreatitis >> same time of admission.
rate if cholecystectomy ▪ Severe pancreatitis >> interval cholecystectomy after patient is stable (after 6
is done in severe weeks).
pancreatitis cases. ▪ ERCP >> may be done if the stone is stuck into the ampulla of vater.
o Debridement Surgery is indicated in:
▪ Hemorrhagic pancreatitis.
▪ Infected necrotizing pancreatitis (fever, unresolved pancreatitis symptoms,
sepsis).
▪ Complicated pseudocysts (i.e. rupture risk, hemorrhage, infection, gastric outlet
obstruction).

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• Complications of acute pancreatitis:

o Pancreatic pseudocysts:
▪ Encapsulated fluids collection that develops weeks to months after an acute
DDx [Link] a true cyst, it lacks an epithelial lining.
(1) Pancreatic abscess. ▪ Causes >> acute pancreatitis, chronic pancreatitis, trauma.
(2) Tumors (if no history of ▪ Types >> communicating & non-communicating.
pancreatitis.
▪ Clinical features:
• Unresolved pain +/- epigastric mass.
• Features of obstructive jaundice.
• Features of gastric outlet obstruction.
▪ Diagnosis >> CT scan or US.
▪ Management (50% will resolve spontaneously):
Surgical cysts drainage • It’s important to wait for around 6 weeks before deciding to drain (the
We join cyst to nearby organ to wall will become mature & strong enough to hold structures).
drain (i.e cystogastrostomy,
• If cysts <5cm >> only observation (no drainage).
cystoduodenostomy, in tail we
resect in along with the cyst). • If cysts >5cm or symptomatic >> drainage either percutaneously or
surgically.
▪ Complications of untreated pseudocysts:
A biopsy is taken during
drainage to R/O cystic
• Rupture, fistula, infection.
carcinoma • Gastric outlet obstruction.
• Hemorrhage into cyst.
• Pancreatic ascites.
o Pancreatic abscess (not very common):
▪ Causes >> usually gram -ve ([Link], klebsiella, proteus).
▪ Clinical features >> persistent fever, +/- epigastric mass.
▪ Investigations >> CT imaging, fine needle aspiration (culture & sensitivity).
▪ Management:
• IV Broad spectrum antibiotics (cephalosporins + metronidazole).
• CT/US guided percutaneous drainage.
• If not possible do operative drainage.
o Other possible complications:
▪ Sterile Pancreatic necrosis >> 50% of cases will resole spontaneously, however,
infection may develop (do CT-guided percutaneous aspiration with Gram
stain/culture).
▪ Infected Pancreatic necrosis >> Result in multiple organ failure in 50% of cases.
Surgical debridement & antibiotics are indicated.
▪ Adult respiratory distress syndrome >> life-threatening complication that occur
due release of inflammatory mediators & trypsin activity.
▪ DIC >> inflammation activates coagulation cascade.
▪ Pleural effusion
▪ Pancreatic ascites.

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Chronic pancreatitis (HIGH-YEILD)

• Overview:
o Persistent inflammation of the pancreas resulting in irreversible parenchymal fibrosis,
destruction, & calcification.
o The endocrine & exocrine functions of the pancreas are impaired.
o Causes:
▪ Chronic alcoholism (most common cause, 70% of cases).
▪ Other causes >> CF, idiopathic, pancreatic congenital anomalies.
• Clinical features:
o Can be asymptomatic for a long time.
o Severe pain in the epigastrium:
▪ Recurrent or persistent (may be confused with PUD, chronic mesenteric angina).
▪ Radiates to back in 50% of patients.
▪ Often accompanied by nausea & vomiting.
▪ Aggravated by drinking alcohol or eating.
o Exocrine insufficiency >> fat malabsorption (steatorrhea & weight loss).
o Endocrine insufficiency >> glucose intolerance & DM (polyuria, polydipsia).
o Complications:
▪ Narcotic addiction (most common).
▪ Diabetes mellitus / impaired glucose tolerance.
▪ Malabsorption / steatorrhea / vitamin B12 deficiency (due to pancreatic
exocrine insufficiency – late manifestation).
▪ Splenic vein thrombosis (resulting in gastric varices).
▪ Pseudocyst formation & pancreatic ductal dilation.
▪ CBD obstruction (secondary to fibrosis on head of pancreas).
▪ Increased risk of pancreatic carcinoma (2%).
• Investigations & Diagnosis:
o Labs (generally, same as acute abdomen, not useful in diagnosis):
▪ CBC >> assess any infections.
▪ Amylase & lipase >> R/O acute pancreatitis, usually normal in chronic
pancreatitis.
▪ LFTs >> R/O liver causes, assess any cholestasis.
▪ Random blood glucose & GGT >> assess development of DM.
▪ 72h fecal fat analysis:
• Assess fat malabsorption.
• Qualitative (fat globules, meat fibers).
• Quantitative (elastase-1).
▪ Secretin stimulation test >> measure the ability of pancreas to respond to
secretin (i.e. measure digestive function of the pancreas).
o CT scan (best in diagnosis):
▪ Calcifications on pancreas is the classic sign (mild cases may not be detectable,
MRCP = Magnetic resonance
cholangiopancreatography
so normal CT doesn’t exclude the diagnosis).
▪ MRCP is alternative non-invasive technique.
o Abdominal radiographs >> presence of pancreatic calcifications is 95% specific, but is
found only in 30% of cases.
o ERCP (gold standard) >> not routinely done (invasive).

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• Management:
o Nonoperative management:
▪ Lifestyle >> alcohol cessation, frequent, small-volume, low-fat meals may
improve abdominal pain.
▪ Pain control >> Narcotic (opioids) analgesics.
▪ Pancreatic enzyme & H2 blockers (given together):
• Pancreatic enzymes inhibit CCK release, thus inhibiting pancreatic
secretion after meals.
• H2 blockers inhibit gastric acid secretion, preventing degradation of
pancreatic enzymes.
▪ Insulin therapy >> if DM developed.
o Surgery:
▪ Indication:
• Persistent pain.
• Biliary obstruction.
• Complicated pseudocysts.
▪ Celiac plexus block (for pain control).
▪ Pancreaticojejunostomy (most common).
▪ Pancreatic resection (distal pancreatectomy, Whipple procedure).

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Cases (Acute & Chronic pancreatitis)

• A 40 yo female presented with an epigastric pain of 2 days duration radiating to the back with
high lipase and amylase. Ultrasound showed a stone in the common bile duct.
o This is a case of biliary pancreatitis, treat the patient just like the treatment of any
pancreatitis with ERCP and laparoscopic cholecystectomy after 6 weeks.

• A 40 yo female presented with a severe epigastric pain radiating to the back with nausea and
vomiting, U/S showed bulky head of pancreas. The patient had several attacks of such pain
before she also has recurrent kidney stones. No evidence of gallstones.
o Check the patient Ca+ levels, if the levels were high then check for the PTH levels
(hyperparathyroidism). To confirm hyperparathyroidism do U/S and sestamibi scan. She
probably had the recurrent attacks of pancreatitis due to hypercalcemia which is caused
by primary hyperparathyroidism.

• A 50 year old alcoholic male presented with severe epigastric radiating to the back with high
lipase and amylase. Normal U/S, CT showed dilated head of pancreas, Ca+ normal. You
stabilized the patient and at night the patient was very disoriented.
o Delirium tremens due to alcohol withdrawal. Treat the patient with thiamin and
benzodiazepines to prevent Wernicke encephalopathy which is caused by thiamin
deficiency.

• A 40-year-old female presented with epigastric pain high lipase amylase all tests were
negative (U/S, Ca+, lipids)
o You have to rule out autoimmune pancreatitis with an endoscopic U/S guided biopsy
(with show lymphocytic infiltration) treat her with steroids if you confirmed the
diagnosis.

• A 9 year old male presents with on and off epigastric pain radiating to the back.
o Congenital pancreatitis (divisum) diagnosis with MRCP.

• A 30 year old female had a history of acute pancreatitis 2 months ago and now she presents
with a mass and early satiety.
o Pancreatic pseudocyst; it’s a collection of pancreatic fluid surrounded by a wall with no
epithelium. Diagnosed with CT scan, in most patients the pseudocyst will resolve
spontaneously within 6 weeks.

• A patient presented with alcoholic pancreatitis and was shifted to ICU, CT scan showed
pancreatic necrosis, his WBC counts were high and he had fever.
o This is a case of necrotizing pancreatitis, treat the patient with broad spectrum
antibiotic then do a CT guided aspiration of pancreatic fluid and send for culture. If the
patient developed an abscess as a complication of necrotizing pancreatitis wait for 2-3
weeks to see the area of demarcation and then resect the affected area.

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Pancreatic cancer (HIGH-YEILD)

• Overview:
o The most common type is adenocarcinoma from the exocrine pancreas.
o 2/3rd occur in the head of the pancreas, which considered better from cancer in the tail,
Why? Because patients present early with signs of biliary obstruction.
o Risk factors >> smoking (3 times more risk), alcohol use, chronic pancreatitis, DM.

• Clinical features:
o Symptoms: DDx
▪ Constitutional (weight loss in 90% of cases). (1) Other intra-abdominal
▪ Chronic epigastric pain (75% of cases). malignancies.
▪ Painless jaundice. (2) Chronic pancreatitis.
(3) pancreatic pseudocysts.
▪ Gastric outlet obstruction (non-bilious vomiting, early satiety).
o Signs (may be normal):
▪ Palpable painless gallbladder if tumor is in the head (Courvoisier’s sign).
▪ Migratory thrombophlebitis (trousseau syndrome – mostly in case of tail/body).
▪ Splenomegaly & ascites.
▪ Virchow’s node or Sister Mary Joseph nodule.

• Investigations & Diagnosis:

o Routine labs >> CBC, RFTs, LFTs, electrolytes, coagulation profile, amylase & lipase.
o Tumor markers >> CEA & CA 19-9.
o Imaging:
▪ CT with contrast >> double duct sign.
▪ ERCP with biopsy >> if peri-ampullary.

• Management:
o Most patients are diagnosed when tumor is non-resectable .
o Conservative management >> analgesia, hydration, electrolytes correction, etc.. .
o Localized tumors:
▪ Cancer of pancreatic head >> Whipple procedure, pancreatico-duodenectomy +
duodeno-duodenostomy.
▪ Body / tail cancer >> distal or near total pancreatectomy.
▪ Post-op chemotherapy.
Whipple procedure removes:
o Non-resectable cases (palliative care):
▪ Pancreatic cancer considered non-resectable if: Head of the pancreas
Duodenum
• Vascular involvement (SMA, hepatic artery). Gallbladder
• Liver metastasis. Distal bile duct
Distal stomach (optional in pylorus-
• Peritoneal implants. preserving Whipple)
• Malignant ascites. Nearby lymph nodes

• Distal LN involvement.
• Distant metastasis.
▪ Relieve pain >> pain killers & ablation of celiac plexuses.
▪ Relieve of biliary obstruction >> ERCP stenting or surgery.
▪ Relieve duodenal obstruction >> bypass procedure.
Reconstruction
Pancreaticojejunostomy: Attaches the remaining pancreas to the small intestine.
Hepaticojejunostomy: Reconnects the bile duct to the small intestine.
Gastrojejunostomy: Reattaches the stomach to the small intestine, if the pylorus was removed.

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Islet cells Tumors (Extra – not important)

• Insulinoma:
o Most common type of islet cell tumors (beta cells).
o 90% are benign (compared to other tumors of islet cells).
o Associated with MEN-I.
o Clinical features:
▪ Typical patient >> obese patient with hypoglycemia.
Always suspect factitious ▪ Symptoms of hypoglycemia:
insulin in any patient with
• Neurological symptoms; altered mental status, confusion, seizures.
hypoglycemia
• Sympathetic over-stimulation symptoms; diaphoresis, anxious, tremors,
tachycardia.
o Investigations: Whipple triad
▪ Fasting Blood glucose >> low. (1) Symptoms of hypoglycemia.
▪ Fasting blood insulin >> high. (2) Evidence of low blood
▪ C-peptide >> high (it will be low in factitious cases). glucose (<50mg/dL).
Diazoxide (inhibits (3) Improvement of symptoms
insulin release)
▪ CT abdomen >> shows mass in the liver. after eating.
o Management >> Surgical resection of tumor (90% curative).

• Gastrinoma (Zollinger-Ellison):
o 2nd most common type of islet cells tumor.
o 90% occur in gastrinoma triangle.
o They are slow growing, but 60% are malignant.
o Clinical features >> PUD refractory to standard management.
o Investigations:
▪ Upper Endoscopy >> multiple ulcers in different sites.
▪ Serum Gastrin levels >> >1000pg/ml
o Management >> PPI + surgical resection + chemotherapy.

• VIPoma:
o VIP >> vasoactive intestinal peptide.
o Most are malignant & metastasize early to LNs.
o Clinical features:
▪ Triad of watery diarrhea, hypokalemia, achlorhydria.
▪ Hypokalemia symptoms; constipation, polyuria, arrhythmias.
o Investigations >> high VIP levels (>1800 pg/ml).
o Management >> surgical resection, chemotherapy, octreotide (symptomatic control).

• Glucagonoma:
o Alpha-cells tumor, most are malignant & usually metastasize to liver.
o Clinical features:
▪ Hyperglycemia.
▪ Weight loss (no glycogen build up).
▪ Necrolytic migratory erythema (psoriatic-like rash with serpiginous red borders
over lower limb & trunk).
o Investigations >> high fasting glucagon level, skin biopsy of NME.
o Management >> surgical resection, chemotherapy, octreotide.

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Hernia

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• Anatomy of abdominal wall (review):

o Layers of the anterior abdominal wall:
▪ (1) Skin.
▪ (2) Fatty superficial fascia (Camper’s fascia).
▪ (3) Deep membranous fascia (Scarpa’s fascia –
becomes Colles fascia in perineum).
▪ (4) External oblique muscle (aponeurosis).
▪ (5) Internal oblique muscle.
▪ (6) Transversalis muscle.
▪ (7) Transversalis fascia.
▪ (8) Parietal peritoneum.
o Muscles of the abdominal wall (total 5 muscles):
▪ External oblique muscle (superficial):
• Contains the superficial inguinal ring.
• It’s inferior border folded backward forming the inguinal ligament.
▪ Internal oblique (intermediate):
• Conjoint tendon >> formed by the lower part of the internal oblique
aponeurosis + transversus abdominis aponeurosis.
• Lies immediately behind the superficial inguinal ring.
▪ Transversus abdominis (innermost muscle).
▪ Rectus abdominis >> most of it enclosed by the rectus sheath.
▪ Pyramidalis muscle >> a small triangular muscle that lies in the rectus sheath
anterior to the inferior part of rectus abdominis (present in 80% of population).

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o Rectus sheath:
▪ Formed by interlaced aponeuroses of the flat
abdominal muscles (all 3).
▪ The rectus sheath is meet in the center to form the
linea alba.
▪ The linea alba can be separated in a condition called
diastasis (divarication) recti which is most commonly
occur in multiparous women.
o Peritoneal folds:
▪ The internal surface of the abdominal wall is covered by transversalis fascia,
variable amount of Extraperitoneal fat and parietal peritoneum.
▪ Median umbilical fold:
• Extends from the apex of urinary bladder to the umbilicus.
• Contains the median umbilical ligament (remnant of urachus).
▪ Two medial umbilical folds >> contain the medial umbilical ligaments (remnants
of umbilical arteries).
▪ Two lateral umbilical folds:
If hernia occurs lateral to
this fold, it’s indirect • Contain the inferior epigastric vessels that will run medially towards the
If hernia occurs medial to rectus sheaths.
this fold, it’s direct • This is a key anatomical landmark that differentiates direct & indirect
inguinal hernia.

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• Inguinal region anatomy (review):

o Important landmarks:
▪ Inguinal ligament:
• It’s the thickened inferior most part of the external oblique aponeurosis.
• Originated from ASIS & inserted into pubic tubercle.
• It form the floor of the inguinal canal.
• Midpoint of the inguinal ligament >> the deep inguinal ring lies about
1inch above it.
▪ Pubic tubercle:
• Important landmark in which the superficial inguinal ring lies above it.
• Identified clinically by asking the patient to adduct their thigh against
resistance, & then follow the adductor longus muscle to its attachment
at the pubic tubercle (this technique is mainly for obese individuals).
▪ Mid-inguinal point >> The half way in between the ASIS & pubic symphysis (not
pubic tubercle). It’s at this point the femoral artery pulse can be felt.

o Inguinal canal:
▪ It’s an oblique canal that runs over the medial half of the inguinal ligament, run
inferomedialy between the deep & superficial inguinal rings (around 4cm).
▪ It transmits contents from the abdomen into the scrotum/labia.
▪ Boundaries:
• Anterior wall >> external oblique aponeurosis (medial 2/3) & internal
oblique aponeurosis (lateral 1/3).
• Posterior wall >> conjoint tendon (medially) & transversalis fascia
(laterally).
• Roof >> internal oblique & transversus abdominis arching fibers.
• Floor >> inguinal ligament & lacunar ligament.
▪ Deep (internal) inguinal ring:
• The internal opening of the canal that begins in the transversalis fascia.
• Anatomically located 1inch above the midpoint of the inguinal ligament.
• The transversalis fascia itself is pulled along the course of the canal to
form the internal spermatic fascia.
• Inferior epigastric vessels are lie medial to it.
• Note that the inguinal branch of ilioinguinal nerve doesn’t enter through
it.

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▪ Superficial (external) inguinal ring >> It’s a triangular opening in the external
oblique aponeurosis above the pubic tubercle which allows the contents of the
canal to exit & enter the scrotum/labia.
▪ Contents of the inguinal canal in females >> Round ligament of the uterus +
Ilioinguinal nerve.
▪ Contents of the inguinal canal in males (spermatic cord):
• The wall of spermatic cord from inside to outside:
o Internal spermatic fascia (from transversalis fascia).
o Cremasteric fascia (from internal oblique muscle).
o External spermatic fascia (external oblique aponeurosis).
• Contents of the spermatic cord (rule of 3):
o 3 nerves >> genital branch of the genitofemoral nerve +
cremasteric nerve + ilioinguinal nerve.
o 3 arteries >> testicular artery + artery to vas deferens +
cremasteric artery.
o 3 veins >> cremasteric vein + vein of vas deferens +
pampiniform plexus.
o 2 structures >> lymphatics + vas deference .
o Hasselbach inguinal triangle boundaries:
▪ Medially >> rectus abdominis muscle.
▪ Laterally >> inferior epigastric vessels.
▪ Inferiorly >> inguinal ligament.
▪ Any weakness in this un-reinforced wall (from old age usually) makes it the most
common site of direct inguinal hernia.
o Important nerves to know:
▪ L1 gives rise to (Both runs along the psoas major muscle):
• Iliohypogastric nerve.
• Ilioinguinal nerve:
o Runs along the spermatic cord through the superficial ring, but
not the deep ring (it doesn’t supply any of its contents).
o Supply sensations of (1) base of the penis, (2) lateral scrotum,
(3) medial thigh, (4) mons pubis & labia majora (in females).
o It may be injured in hernia repair surgeries resulting in loss of
sensations.
▪ L2 give rise to Genitofemoral nerve:
• Genital branch:
o Runs within the spermatic cord (passes through the deep &
superficial ring).
o Supply (1) cremasteric muscle (responsible for cremasteric
reflex), (2) part of the skin of the scrotum, (3) mons pubis &
labia majora in females.
• Femoral branch >> runs beneath inguinal ligament to supply area of
skin in the thigh.

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Embryology (review)
• In utero, the gonads develop in the high posterior abdominal wall & then pulled down into their final position by the
gubernaculum.
• As the testis in males approach the anterior abdominal wall, an invagination of the wall forms right in front of it,
guiding the ways down for it. This is known as processus vaginalis, which normally disappear by the time the baby is
born, leaving behind a tunica vaginalis in the scrotum.
• A patent processus vaginalis is the leading cause of indirect inguinal hernia, which is the most common type of
hernias in males & females.
• If processus vaginalis not fully disappeared, a tiny communication between the peritoneum & tunica vaginalis can
result in hydrocele.
• Testis arterial supply >> testicular artery (from abdominal aorta).
• Testis venous drainage:
o Right testes drains into IVC directly.
o Left testes drains into left renal vein (more likely to develop varicocele do to the perpendicular fashion).
• Lymphatic drainage:
o The testis into the para-aortic LNs.
o Scrotum into the superficial inguinal LNs.

• Femoral triangle (Review):

o Femoral triangle is a subfascial space in the anterior, superior third of the thigh.
o Boundaries:
▪ Superior >> inguinal ligament.
▪ Medial side >> adductor longus.
▪ Lateral side >> Sartorius.
▪ Floor >> iliopsoas laterally & pectineus medially.
o Contents of the femoral triangle (lateral to medial):
▪ Femoral nerve.
▪ Femoral artery (continuation of external iliac artery below inguinal ligament).
▪ Femoral vein (it will receive the great saphenous vein in the saphenous ring).
▪ Femoral canal, site of possible femoral hernia. It has a tight neck, so hernia
contents are likely to incarcerated.
▪ Lymphatics; deep inguinal LNs (cloquet’ nodes).
o Femoral sheath:
▪ A fascial tube that passes deep to the inguinal ligament & enclose the proximal
parts of femoral vessels & form the femoral canal.
▪ It’s formed by the inferior prolongation of transversalis & iliopsoas fascia.
▪ Compartments:
• Lateral >> contain femoral artery.
• Intermediate >> contain femoral vein.
• Medial (femoral canal) >> contains lymphatics & fat.
o Femoral canal:
▪ It present underneath the inguinal ligament & extends distally to the level of
saphenous opening.
▪ Allows the femoral vein to expand when the venous return is increased.
▪ Borders:
• Anteriorly>> inguinal ligament.
• Medially >> lacuna ligament.
• Posteriorly >> cooper’s ligament.
• Laterally >> femoral vein.

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• Overview of hernia (High-Yield):

o Definition of hernia >> protrusion of a viscus or a part of viscus, which could be
congenital or acquired through a defect in a cavity in which it’s contained.
o Important terminology:
▪ Hernial sac >> the peritoneal reflection that contains the contents of the hernia.
▪ Contents of a hernial sac >> most commonly small intestinal loop, but can be
omentum, ovaries, fallopian tube, etc.. .
o Epidemiology:
▪ 10% of population have hernias.
▪ Male:female ratio is 7:1.
▪ Age distribution:
• Neonates (usually congenital).
• Early adulthood (weight lifting).
• Elderly (muscle wall weakness).
o Risk factors:
▪ Old age >> result in weak abdominal wall muscles.
▪ Increased intra-abdominal pressure:
• Chronic cough (e.g. in COPD).
• Chronic constipation, colon cancer, BPH.
• Multiparity or pregnancy.
• Ascites & peritoneal dialysis.
• Heavy weight lifting.
▪ Previous surgical incisions >> important to ask about previous surgeries.
▪ Smoking.
o Types based on condition of hernia:
▪ External hernia >> the sac protrudes completely through the abdominal wall
The smaller wall defects are (e.g. inguinal & femoral hernias).
worse in which the viscus is ▪ Internal hernia >> the sac is within the visceral cavity (e.g. diaphragmatic
more likely to strangulate
hernias, hiatal hernia, brainstem hernia).
▪ Intra-parietal hernia >> the sac is contained within the abdominal wall (e.g.
spigelian hernia).
▪ Reducible hernia >> Hernia that can pushed back into it’s orifice, either
spontaneously (lying back) or by pushing it physically.
▪ Irreducible hernia:
• Regardless of method, hernia cannot be pushed back.
• Possible complications:
o Incarcerated (asymptomatic trapping).
o Obstructed (patients develops SBO).
o Strangulated (ischemia begins to develop).
Note that not all strangulated ▪ Strangulated hernia (emergency):
hernia must be obstructed. If • Occur due to to closed loop obstruction that progresses to ischemia &
it contains omentum it can
then necrosis of the segment trapped in hernia.
strangulate alone or if this is
Ritchter’s hernia (strangulated • There is increased intraluminal pressure, impeding venous drainage &
without obstruction) then arterial supply.
• Complications >> necrosis, perforation, peritonitis, sepsis, death.

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o Types based on location:

▪ Inguinal hernia >> can be direct or indirect.
Most common types ▪ Pantaloon hernia >> direct & indirect occur together.
(1) Indirect inguinal hernia ▪ Femoral hernia >> in femoral canal.
(50%) in males & females.
(2) Direct inguinal hernia
▪ Sliding hernia >> when hernia SAC wall consist of part of the herniated viscus.
(25%). ▪ Spigelial hernia >> hernia through the linea semilunaris of rectus abdominis
(3) Femoral hernia (5%) muscle.
mostly in females. ▪ Richter’s hernia:
• Only part of the wall of the involved viscus is within the hernia sac.
• It may strangulate without obstruction.
• Occurs in femoral & obturator hernias.
▪ Incisional hernia >> hernia occur at sites of previous abdominal incisions.
▪ Umbilical hernia >> hernia through the umbilical ring, usually congenital (down
syndrome, congenital hypothyroidism).
▪ Para-umbilical hernia:
• Hernia that occurs near the umbilicus (above or below).
• Usually occurring in adults in cases of massive ascites, pregnancy or
multiparity, obesity.
▪ Lumbar hernia >> Occurs in the posterior abdominal wall in between the
muscles.
▪ Littre’s hernia >> Hernial sac contains meckel’s diverticulum.
▪ Amyand’s hernia >> inguinal hernia that contains the appendix.
▪ De Garengeot’s hernia >> femoral hernial sac contains appendix.
▪ Maydl’s hernia >> W-shaped intestinal loop hernia, the part of this loop that
remains within the abdominal cavity may have been strangulated & may be
missed.
▪ Esophageal hiatal hernia >> discussed in details in esophageal notes.
▪ Congenital diaphragmatic hernia:
• In utero herniation of abdominal contents through defect in diaphragm
into the chest.
• Posterior (Bochdalem) is the most common, anterior (Morgagni) is less
common.

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• History taking of hernia (highlighted):

o Chief complaint + duration >> usually lump with or without pain.
o History of present illness:
▪ (1) History of lump:
• When did you first notice the lump (onset)?
• What makes you notice the lump (swelling or pain)?
• Ask about progression of size.
• With or without pain (apply SOCRATES if pain is present)?
• Aggravating or reliving factors (standing, straining, etc..)?
• Reducible or not?
• Any other swellings?
• Previous history of the same condition?
• History of trauma.
▪ (2) Associated symptoms (R/O other DDx):
• GI >> nausea, anorexia, vomiting, abdominal pain, diarrhea,
constipation, passing flatus or not.
• Resp >> cough, SOB (R/O lower lobe pneumonia).
• Biliary >> yellowish discoloration, any change in urine or stool color.
• Constitutional symptoms >> weight loss, fever.
▪ (3) Assess any hernia complications >> mainly small bowel obstruction
(Abdominal pain, vomiting, & constipation).
o Past medical history:
▪ Assess risk factors:
• Ask about chronic cough & chronic lung disease.
• Ask about chronic constipation or straining.
• Ask about pregnancies in females.
• Ask about weight lifting in young patients.
▪ Medical illnesses & their treatment, controlled or not.
▪ Previous operations (may suggest incisional hernia).
▪ Medications & allergy.
▪ History of blood transfusions.
o Family history >> same as always, anybody with the same problem.
o Social history >> smoking, IV drugs.
o Differential diagnosis:

DDx of Inguinal mass DDx of Inguinoscrotal swelling

DDx of Scrotal swelling (pure)
(1) Inguinal hernia (indirect, direct). (1) Indirect inguinal hernia.
(1) Epididymitis, orchitis, epididymal cyst.
(2) Superficial inguinal lymphadenopathy (in (2) Testicular torsion.
(2) Hydrocele/hematocele/spermatocele.
children). (3) Varicocele (bags of worms).
(3) Testicular torsion.
(3) Lipoma, sebaceous cyst, or abscess. (4) Encysted hydrocele.
(4) Testicular cancer.
(4) Hematoma or seroma. (5) Lipoma in cord.
(5) Cryptorchidism (undescended testis) or (6) Undescended or ectopic testis.
ectopic testis (in children).
(6) Saphenous vrix (in females). DDx of lymphadenopathy
(7) Femoral artery aneurysm. (1) Inflammation (local infection, TB,
(8) Sarcoma. sarcoidosis).
(9) Psoas abscess. (2) Neoplasia (lymphoma).
(3) Infiltration (metastatic disease, malignant
melanoma).

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• Clinical examinations of a patient with hernia (Abdominal examination):

o See acute abdomen notes for full abdominal examinations details.
o (1) General exam:
▪ Vitals (most students forget them) >> pulse, RR, temp, O2 saturation, BP.
▪ General inspection >> Level of consciousness (conscious, awake, oriented), well,
unwell, toxic-looking, in pain, IV lines & any devices.
▪ Eyes >> assess jaundice & pallor conjunctiva.
▪ Mouth >> assess central cyanosis.
▪ Leg >> assess lower limb edema.
o (2) Abdominal examination:
▪ Exposure >>2nd inter-costal space to the mid-thigh.
▪ Inspection:
• First stand on the lend of the bed & assess flanks symmetry.
• Assess shape of abdomen, type of breathing, previous scars, visible
veins, obvious masses, hair distribution.
• Cough test >> ask the patient to cough 2-3 times when supine & look as
all potential hernia sites or the site which already has a hernia.
▪ Palpation & percussion:
• Ask for pain, leave the painful site or hernia site for the end.
Deep palpation & organ • Ask the patient to raise his shoulder or to raise his lower limb in order
palpation/percussion doesn’t have a
to flex the abdominal muscles:
role in hernia examinations but may
done as a full abdominal examination o If the swelling increase in size >> it’s superficial (e.g. lipoma).
o If the swelling fades away >> it’s deep.
o If the swelling stays the same >> it may be a desmoid tumor of
Note that we cannot confirm the muscle.
type of hernia only by • Palpating the hernia & scrotum:
examinations, it’s only confirmed
intra-operatively in relation to o Warmth & tenderness.
inferior epigastric vessels o Shape & borders.
o Consistency:
▪ Soft & elastic >> gut.
Standing position is a key ▪ Doughy & granular >> omentum.
examination point that all examiners ▪ Tense & tender >> strangulated.
want to see you doing it.
There is 2 option:
o Cough impulse (expansile).
(1) Do abdominal examination, then o Palpate the scrotum (index finger & thumb) to check for scrotal
stand and do hernia & scrotal mass & do a scrotal neck test.
examination. o +/- percuss over the hernia (dull = omentum, resonant = gut).
(2) Ask the patient to stand from the
• Deep inguinal ring (patient must be standing):
start, inspect, palpate, & do hernia
tests. Then ask patient to lie down & o Ask the patient to reduce the hernia (only if it’s reducible).
do abdominal examination. o Press over the deep inguinal ring & ask the patient to cough.
o In direct inguinal hernia >> the swelling will return, usually
medial to your finger.
o In indirect inguinal hernia >> the swelling doesn’t return, but
instead you will feel a cough impulse beneath your finger.
▪ Auscultation:
• Check for bowel sounds (absent, high-pitched, normal).
• Bowel sounds over the swelling (present, bruit?).
• Renal arteries & abdominal aorta for bruit.

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• Inguinal hernia (High-Yield):

o Indirect inguinal hernia (lateral to inferior epigastric vessels):
▪ The most common type of hernia in both males & females.
Generally, inguinal hernias ▪ Most important cause >> patent processus vaginalis (congenital).
are more common in right ▪ Types:
side because the left testes
descends earlier
• Incomplete >> bubonocele (in cord), funicular (at external ring).
• Complete >> in testes.
▪ 1/3rd of cases are bilateral. How to differentiate between inguinal &
▪ Non-trapped indirect hernias can be reduced. femoral hernia clinically? By relation to
▪ Silk-glove sign (pediatrics) >> A special sign of pubic tubercle.
thickened spermatic cord suggesting indirect
Inguinal hernia >> above & medially.
inguinal hernia. Femoral hernia >> below & laterally.
o Direct inguinal hernia (medial to inferior epigastric
vessel):
▪ Passes through hasselbach’s triangle & through the superficial ring only.
▪ Occur almost exclusively in older patients (usually smoker males).
▪ It has a wide neck (uncommon to strangulate).
▪ Common to be bilateral.
▪ Most of direct hernias are irreducible (because the wall is weakened).

• Femoral hernia (High-Yield):

o Occur through the femoral canal (below inguinal crease &
inguinal ligament).
o More common in females (80%) due to wide pelvis.
o Right side is more common than the left.
o It has a tight neck (high risk on incarceration & Strangulation).

• Umbilical hernia (High-Yield):

o It’s often congenital & occurs in infants, especially in down
syndrome, congenital hypothyroidism, premature infants.
o Management is rarely needed as most of the time it resolves
spontaneously by 2-3ys.
o Surgical correction is needed in:
▪ Persistent, should be corrected before entering school (>4ys of age).
▪ Disfiguring.
▪ >2cm or complicated.

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• Clinical features & investigations (High-Yield):

o Symptoms:
▪ Swelling (most common presenting symptom):
• Usually intermittent & painless, or persistent if incarcerated.
• Size increase with coughing, crying (infants), lifting heavy objects,
standing, straining.
• May be reduced spontaneously or manually (if not trapped).
▪ Pain:
• Patients may have dull, discomforting dragging pain at site of hernia.
• Worse at end of the day, when patient lies down or when reduced.
▪ Strangulation symptoms:
• Most common type to strangulate is femoral followed by para-umbilical
hernia.
• Acute colicky abdominal pain, maximal at site of inguinal strangulated
hernia, which doesn’t reduce.
• Signs of SBO (abdominal distention & pain, vomiting, obstipation).
• +/- Signs of peritonitis or perforation (shock, altered mental status,
diffuse abdominal pain).
o Signs >> Swelling with visible or palpable expansile cough impulse that increase in size
or appears while standing.
o Investigations:
▪ Diagnosis is usually done clinically.
▪ Radiological investigations are only done if the patient is obese or complications
are suspected.
▪ Acute abdomen labs may be done if the patient is present with acute abdomen.
▪ Standard pre-op workup is necessary.

• Management (High-Yield):
o Management of risk factors >> any underlying cause or risk factors must be treated &
controlled to prevent recurrence of future hernias.
o Herniotomy (opening of hernial sac):
▪ Done with a groin incision (incised structure are skin, superficial fascia, external
Herniotomy is usually oblique aponeurosis).
sufficient in young, muscular ▪ The spermatic cord is opened up & the contents of the inguinal canal are
individuals & in children
identified and separated.
▪ The hernia sac is identified, freed, opened, & its contents are studied.
▪ The contents is reduced back to its original location, the neck is ligated, the sac
is reduced.
o Hernioplasty (tension-free repair):
▪ Use of synthetic structures to repair the defect in the abdominal wall.
▪ It’s the method of choice in modern day (low recurrence rate).
▪ Process >> flat sterile mesh patch is placed over weakened muscle opening &
stitched into the surrounding tissue. The mesh will increase the
fibroblastic activity leading to fibrosis & strengthen of muscles. Although hernia repair is
▪ Done either by anterior approach (Lichtenstein’s repair) or considered clean surgery,
use of mesh warrants the
posterior approach. administration of
prophylactic antibiotics

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Darn Technique: Non-absorbable

sutures (e.g., polypropylene) are
used in a weaving fashion to
create a mesh-like layer over the
weakened area of the inguinal
o Herniorraphy (old school): canal.
▪ Use of local structures to repair the abdominal wall defect.
▪ Process:
• (1) A long incision is done over the hernia.
• (2) Herniated tissue is pushed back & the hernia sac is removed.
• (3) Edges of healthy muscles are stitched together.
▪ Methods:
• Bassini’s repair >> using incurved part of inguinal ligament.
• Shouldice repair >> double breasting of transveraslis fascia.
• Cooper’s/McVay repair >> using copper ligament.
o Strangulated hernia management (emergency):
▪ ABCs, NPO + NGT.
▪ IV analgesia + IV antibiotics.
▪ Surgery >> open the hernia, drain any secretions, assess bowel viability,
reduction of hernia & closure.
o Laparoscopy indications >> recurrence or bilateral hernia.

• Complications of hernia repair surgery (High-Yield):

o General >> anesthesia complications.
o Local >> wound infection, hematoma, seroma, wound dehiscence.
o Specific to hernia repair:
▪ Recurrence of hernia (especially in herniorrhaphy).
▪ Injury to vas deference.
▪ Injury to ilioinguinal nerve.
▪ Entrapment of ilioinguinal nerve.
▪ Injury to testicular artery.
o Clinical scenarios:
▪ (1) You’ve done a surgery on a 70 year old male in the morning and at night he
complained of pain in the suprapubic area. What do you suspect?
• Urinary retention, can be secondary to BPH
• Management >> catheter
▪ (2) Patient came to your clinic weeks after surgical repair of hernia
complaining of loss of sensation in the medial thigh and lateral scrotum. What
do you suspect?
• Injury to the ilioingunial nerve
▪ (3) Post-surgical patient came with chronic pain after hernia repair (>3
months), What do you suspect?
• Entrapment of the ilioingunial nerve (chronic pain syndrome).
• Diagnosis >> MRI.
• Management >> cut the nerve
▪ (4) A 30-year-old male patient complained of severe testicular pain after
hernia repair what do you suspect?
• Injury to the testicular artery.
• Diagnosis >> duplex ultrasound (no perfusion will be detected).
• Management >> orchiectomy.
• Complications (if not removed) >> antibodies can be formed against it if
the affected testicle was not removed.

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• Saphena varix (nice to know):

o A dilation of saphenous vein at its junction with the femoral vein in the groin.
o Associate with varicose veins.
o Clinical features:
▪ Patient usually present with inguinal swelling that usually mistaken for femoral
hernia.
▪ Reducible swelling in groin, a cough impulse may be found, disappears when
patient lies down.
o Diagnosis >> duplex US.
o Management >> Surgical disconnection & ligation of the saphenofemoral junction.

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The
Intestines

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Anatomy of the small Intestines

• Embryology (review):
o The digestive tract is developed from the primitive gut (endoderm):
▪ Foregut >> give rise to esophagus, stomach, & duodenum until the ampulla of
Vater. It also gives rise to the accessory organs such as pancreas, liver,
gallbladder, & spleen.
▪ Midgut >> from the 2nd part of the duodenum up to 2/3rd of the transverse
colon.
▪ Hindgut >> from the 2/3rd of the transverse colon to the dentate (pectinate)
line.
▪ Beyond the pectinate line, the ectoderm gives rise to the anal canal (stratified
squamous non-keratinized epithelium).
o Physiological herniation & rotation of the midgut:
▪ Physiological herniation >> as a result of the rapid elongation of the cephalic
limb + expansion of liver, the abdominal cavity temporarily becomes too small
to contain all the intestinal loops. Thus, they enter the extra-embryonic cavity in
the umbilical cords.
▪ Rotation >> The primary intestinal loops rotate around an axis formed by SMA
(counterclockwise 270 degree rotation).
▪ Retraction of herniated loops >> returning of the herniated bowel to its normal
site.
▪ Abnormalities:
• Omphalocele >> herniation of abdominal viscera due to failure of the
bowel to return.
• Vitelline duct abnormalities >> result in Meckel’s diverticulum, vitelline
cyst, vitelline fistula.
• Gut rotation defects >> malrotation, reversed rotation.

• Anatomy of small intestines (review):

o Function of the small intestines >> digestion & absorption of nutrients.
o Histology:
▪ Mucosa >> contains plicae circulares & villi (simple columnar epithelium with
brush borders with goblet cells).
▪ Submucosa >> contains larger blood & lymph vessels + submucosal nerve
plexus.
▪ Muscularis >> internal circular & external longitudinal.
▪ Serosa.
▪ Important notes:
• Histology (jej) >> characterized by having only villi with glands.
• Histology (ile):
o Characterized by having villi + Peyer’s patches & M cells.
o Peyer’s patches >> lymphoid nodules in the ileum which
hypertrophy in response to gut bacteria or viral infections.

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Radiologically, the small

intestines are centrally
o Parts of small intestines: distributed & differentiated by
▪ Duodenum >> discussed in pancreas notes. their small caliber, high number
▪ Jejunum VS ileum: of loops, & vulvae conniventes

o Arterial supply >> superior mesenteric artery (SMA).

o Venous drainage >> superior mesenteric vein (SMV).
o Lymphatic drainage (lacteals) >> superior mesenteric LNs.
o Innervation:
▪ Sympathetic (T8-T10) >> (1) reduce secretions & motility (2) vasoconstrictor.
▪ Parasympathetic (vagal trunk) >> increase secretion & motility.

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Small bowel Obstruction (HIGH-YEILD)

• Overview:
o Risk factors:
▪ Previous abdominal operations (most important).
▪ Hernia.
▪ IBD (especially Crohn’s).
▪ Ingested foreign body. Types of bezoars:
▪ History of cholecystitis or cholelithiasis (gallstone ileus). (1) Trichobezoars (hair)
(2) Phytobezoars (veggis)
o Most common causes >> (1) Adhesions, (2) Incarcerated hernia, (3) Pharmacobezoars (meds)
(3) Malignancy or cancer. (4) Lactobezoars (concentrated
o Classification: milk formula in neonates)
▪ Mechanical obstruction:
• Intraluminal >> bezoars, foreign bodies, gallstone ileus, intussusception.
• Intramural >> Crohn’s diseases, malignancy, radiation stricture.
• Extraluminal >> adhesions (especially previous operations),
incarcerated small bowel hernias, volvulus.
▪ Functional obstruction (Paralytic ileus) >> peritonitis, post-op, electrolyte
disturbances (hypercalcemia, hypokalemia).
o Types of obstruction:
▪ Incomplete:
• Only a portion of lumen is occluded.
• Patient can pass gas & some fluids.
▪ Complete:
• Lumen is completely occluded.
• Progress faster, no passage at all (obstipation).
▪ Closed loop:
• Obstruction occur at 2 points (proximal & distal).
• Require emergency surgery.
• Occurs in incarcerated hernia, torsion, adhesions, Volvulus.
o Pathophysiology:
▪ (1) Obstruction result in proximal fluid-air collection & distal compression.
▪ (2) Increased intestinal activity (peristalsis) to overcome the obstruction (i.e.
contraction against a block tube) will result in colicky pain (early).
▪ (3) As a result, there will be increased bowel wall edema, intraluminal contents
& pressure.
▪ (4) All these will result in disruption of venous, then arterial circulation.
▪ (5) Finally, ischemia & necrosis will occur. It may complicated by perforation
(peritonitis, septicemia, & shock).

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• Clinical features of SBO:

o Symptoms:
▪ Colicky abdominal pain (diffuse or central).
▪ Abdominal distention.
▪ Nausea & vomiting (bilious vomiting suggesting proximal obstruction to ampulla
of vater).
▪ Constipation (pass gas) or obstipation (no pass at all).
o Signs:
▪ General >> Unstable patients (unwell, altered mental status, fever, dehydrated,
Virgin abdomen means that tachycardia, hypotension).
the patient has no previous ▪ Inspection >> Abdominal distention, visible peristalsis, previous operation scars.
operations (consider need of
▪ Auscultation >> Hyperactive bowel sounds (high-pitched tinkling) OR absent
emergency surgery)
bowel sounds in paralytic ileus.
▪ Palpation >> abdominal rigidity, guarding (strangulation or peritonitis).
▪ Digital rectal exam >> empty rectum.

• Investigations & Diagnosis:

o Routine labs (of acute abdomen):
▪ CBC (assess infections & Hb for possible surgery), +/- Blood culture if septic.
▪ Blood typing & cross matching (need for surgery).
▪ RFTs & electrolytes panel (baseline + assess dehydration).
▪ Amylase + lipase (R/O pancreatitis).
▪ Blood glucose & lactate.
o Imaging & procedures:
▪ Plain X-ray (abdomen & chest):
• Erect X-ray >> show air-fluid levels + air under diaphragm (suggesting
perforation) (significant if at least 3 air fluid levels found).
• Supine X-ray:
o Assess location of obstruction.
o SBO will show dilated bowel loops centrally that have valvulae
conniventes + Absent air in colon or distal to obstruction.
o In case of paralytic ileus, the whole small & large intestines will
be filled with air.
▪ CT abdomen & pelvis:
• Useful in showing transition point, possible causes, & confirm X-ray
findings.
• Pneumobilia (air in biliary tree) highly suggesting gallstone ileus
(gallstones >2cm may be found stuck if the ileocecal valve).

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• Management:
o (1) ABCs (IV fluids, foley’s catheter to monitor urine output).
o (2) NPO + NGT (gastric decompression).
o (3) IV analgesia + antibiotics (metronidazole + cephalosporin).
o (4) Conservative management (only if adhesions is suspected):
▪ Tried in patient with history of abdominopelvic surgery.
▪ 80% of adhesions will resolve spontaneously.
▪ 48h of surveillance of vitals, symptoms, labs, & imaging.
▪ If condition deteriorates or develop complications, do urgent surgery.
o (5) Surgical management:
▪ Goals >> (1) exploration & treatment of underlying cause, (2) assess bowel
viability, (3) toileting or irrigation if needed.
▪ Emergency surgery indications:
• Evidence of strangulation.
• Complete SBO.
• Perforation of peritonitis.
• Medical/conservative management failure.
▪ Exploratory laparotomy (midline incision) is preferred.
▪ Adhesions >> lysis of adhesions.
▪ Hernia >> herniotomy or herniorraphy.
Bowel viability factors:
▪ Crohn’s diseases >> stricturoplasty. (1) Pink/Red color (black is necrotic).
▪ Bezoars or gallstone ileus >> removal. (2) Mesenteric pulsations are present.
▪ Volvulus >> reduction. (3) Peristalsis is present.
(4) Bleeds on cut surfaces.
(5) IV fluorescein assessment with
Wood’s lamp (fluoresces = viable).
(6) Doppler assessment of arterial flow.
(7) 2nd look in 24h if still questionable.
NON-viable bowel needs resection +
end-to-end primary anastomosis

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Acute Mesenteric ischemia

• Overview:
o Mesenteric ischemia is basically an arterial blockage (the same way in the whole body,
e.g. acute ischemic limb).
o In any ischemia, you must consider is it Acute or chronic ?
▪ Acute blockage >> there is no time for collateral circulation to develop, thus,
ischemic changes occur quickly.
▪ Chronic blockage >> there is enough time for collateral circulation to develop,
thus ischemic changes worsens over period of time.
o Acute mesenteric ischemia usually affects SMA.
o Causes:
▪ Arterial:
• Embolus (most common 50%; AF, post-MI, endocarditis septic emboli).
• Thrombosis (15-25%).
• Vasospasm (occur in hypovolemia or by vasopressor medications).
▪ Venous >> mostly thrombosis & hypercoagulable state.
o Pathophysiology:
▪ Ischemia to the bowel results in necrosis, because most of the arteries are end
arteries.
▪ Mucosa is the first to get affected.
▪ Mucosal sloughing & bleeding occurs in 3h of ischemia.
▪ Infarction occur after 6h of ischemia.

• Clinical features:
o Symptoms:
▪ Acute abdominal pain >> severe pain (out of proportion), diffuse, colicky, could
be epigastric or mid-abdominal.
▪ Others >> nausea, vomiting, & diarrhea.
o Signs:
▪ Patient may be unstable (tachycardia, tachypnea, dehydrated).
▪ Irregularly irregular pulse suggest AF.
▪ Patients with late presentation may present with signs of peritonitis & SBO.

• Investigations & Diagnosis: You must R/O acute mesenteric

o Routine labs for acute abdomen. ischemia in any patient present
o Electrolytes panel & ABG >> metabolic acidosis. with acute abdomen with
metabolic acidosis
o Imaging:
▪ CT angiography.
▪ Mesenteric angiography (best tool, invasive, diagnostic & therapeutic).

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• Management:
o (1) ABCs (IV fluid resuscitation, correct acidosis & electrolytes imbalances).
o (2) NPO & NGT (gastric decompression).
o (3) IV antibiotics + IV PPI + IV analgesics.
o (4) Anti-coagulation (heparin).
o If there is signs of peritonitis or perforation:
▪ Do emergent exploratory laparotomy.
▪ Intra-operative embolectomy or thrombectomy.
▪ If fails, by pass or stent techniques.
▪ Resect any non-viable bowel, if unsure, close and arrange for a second look
laparotomy.
o If there is no need for emergent laparotomy:
▪ Mesenteric angiography.
▪ If suspecting vasospasm >> papaverine infusion (vasodilator).
▪ If suspecting thrombosis >> catheter directed thrombolytic therapy.
▪ If suspecting embolism >> embolectomy.
▪ Successful of management should be monitored by imaging techniques. If
management fails or signs of bowel non-viability, proceed to laparotomy.

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Chronic mesenteric ischemia

• Overview:
o Episodic intestinal hypoperfusion that doesn’t lead to infarction, there is enough time
for collaterals to develop.
o Causes:
▪ Arterial ischemia (most common); atherosclerosis, low CO states such as HF.
▪ Venous thrombosis.
▪ Vasculitis.
o Risk factors:
▪ Any risk factors of atherosclerosis (modifiable or non-modifiable).
▪ Smoking.
▪ Thrombophilias.
▪ Arcuate ligament syndrome (narrowing of celiac vessels via extrinsic
compression by median arcuate ligament).

• Clinical assessment & management:

o Symptoms:
▪ Post-prandial abdominal pain (angina), the pain is dull or cramps.
▪ Weight loss (due to food avoidance fearing of pain).
o Signs >> usually normal with no findings.
o Investigations:
▪ Labs (assess risk factors) Big DDx is intra-
abdominal malignancy
• Lipids profile.
(i.e. pain, weight loss)
• Coagulation profile.
• Blood glucose & HBA1c.
▪ Imaging >> CT angiography & mesenteric arteriography.
o Management:
▪ Treat any risk factors accordingly >> statins, stop smoking, control sugar, etc.. .
▪ Arterial disease (re-vascularization) >> percutaneous transluminal angiography
or bypass grafting.
▪ Venous >> anticoagulation therapy.

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Small bowel neoplasia (Nice to Know)

• Overview:
o Benign (adenoma – 35%):
▪ Most commonly found in the duodenum.
▪ Most common cause of intussusception in adults.
▪ Should be excised endoscopically.
o Malignant:
▪ Adenocarcinoma (most common, most common site is in duodenum).
▪ Carcinoid tumor.
▪ GIST.
▪ Lymphoma.
o Management (general):
▪ Treatment of malignant bowel tumors involves wide resection of involved
segment with LNs dissection.
▪ Duodenal lesions may need Whipple procedure.

• Carcinoid tumor:
o A malignant tumor that arise from enterochromaffin cells.
o Most common site is appendix tip > small intestines > rectum.
o Patients may be symptomatic or presents with S&S of acute appendicitis or SBO.
o Clinical features:
▪ Most patients are asymptomatic (slow growing tumor).
▪ Symptoms >> vague abdominal pain, intermediate obstruction in 25% of
patients.
▪ Carcinoid syndrome (found in 10% of patients):
• Occur due production of serotonin, bradykinin, tryptophan.
• These metabolite deprive the body from vitamin B3 (niacin) resulting in
pellagra.
• Pellagra symptoms >> confusion, flushing, nausea, decrease appetite,
watery diarrhea, wheezing.
▪ Metastasis to liver, right heart valves, & lung is all possible.
o Investigations & diagnosis:
▪ Most patients are found incidentally with radiographs or appendectomy or SBO.
▪ In carcinoid syndrome >> urinary 5-HIAA (24h collection) + plasma
chromogranin A. (5-hydroxyindoleacetic acid)
o Management:
▪ Medical >> serotonin antagonist (cyproheptadine), octreotide.
▪ Surgical:
• If <2m do appendectomy alone.
• If >2cm or involve the base of appendix do right hemicolectomy.

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Fistulas

• Overview:
o Definition >> an abnormal connection between 2 epithelial surfaces.
o Sinus >> connection to one epithelial surface from a closed cavity.
o Factors that keep a patent fistula:
▪ High-output fistulas (>500ml/day).
▪ Intestinal destruction.
▪ Short fistulas.
▪ Foreign bodies (pricible of gastrostomy & jejunostomy).
▪ Infections (abscess of fistula).
▪ Epithelialization (principle of stomas).
▪ Neoplasia.
▪ Distal obstruction of the fistula.
o Clinical diseases that cause fistulas:
▪ Diverticulitis (most common).
▪ Crohn’s disease.
▪ Colorectal cancers.
▪ Radiations & radiotherapy.
▪ Cholecystitis (cholecystoenteric fistula).

• Colovesical fistula (most common):

o Causes >> Usually occur due to diverticulitis.
o Clinical features >> recurrent UTIs, foul-smelling urine, pneumaturia, fecauria.
o Complications >> pyelonephritis & renal failure.
o Investigations:
▪ Urinalysis (show presence of stool & colon microorganism).
▪ Cystoscopy & barium enema (barium enema contrast will appear in the
bladder).
o Management >> surgical segmental colon resection & anastomosis.

• Enterocutaneous fistulas:
o Causes >> anastomotic leak, colon or bowel injury (e.g. diverticulitis, perforation), CD,
abscess.
o Complications:
▪ High output (>500ml/day).
▪ Malnutrition.
▪ Skin irritation (develop secondary SCC).
o Investigations >> CT or fistulogram.
o Management:
▪ Bowel rest >> NPO & TPN (50% of fistulas will close spontaneously).
▪ Treat the underlying cause >> drain any abscess, manage CD.
▪ If refractory cases >> surgical resection of affected bowel segment.

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Ostomies & Stomas (HIGH-YEILD)

• Ostomies & Stomas:

o Definition >> as unnatural connection to an epithelial surface (i.e. man-made fistula).
o Done mostly to GIT to the skin or to other GIT lumen.
o Gastrostomy or jejunostomy:
▪ In both, we use a tube to connect the organ to the skin.
▪ The tube elicits a foreign body reaction, keeping the connection patent.
▪ If the tube is removed, the connection will close in matters of hours.
o Colostomy & ileostomy:
▪ Generally, stomas on right side is ileostomy, while stomas in left side is
colostomy.
▪ Indications >> feeding, lavage, decompression, diversion.
▪ Types:
• End colostomy >> proximal end of colon is brought to the skin.
• Mucous fistula >> distal end of colon brought up to the skin (for
decompression).
• Hartmann’s pouch >> end colostomy with the distal blind ended pouch
left inside the body.
• Loop colostomy >> large loop of colon is brought out, cut open, with
both ends sewed to the skin (there will be 2 openings).
• Ileal conduit >> ileal segment is resected , then connected to the skin &
both ureters (a type of ureter diversion after cystectomy).
▪ Complications:
• Local >> skin irritation, infection, ischemia.
• Structural:
o Parastomal hernia or prolapse of stoma.
o Stoma retraction.
o Stoma obstruction or stenosis.
• Systemic >> electrolyte disturbances, dehydration, malabsorption.

Ileostomy VS colostomy
Ileostomy:
• Mostly in right side.
• Watery liquid stool & liquid containing enzymes.
• High discharge frequency.
• They have sprout, odor, & have more risk of fluid/electrolytes disturbances.

Colostomy:
• Mostly in left side.
• Solid & hard stools.
• Low discharge frequency.
• More odor with NO sprout.

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General Management Principles

a) Stabilization
Control infection:
Drain abscesses.
Administer antibiotics as needed.
Correct electrolyte imbalances: Especially in enterocutaneous fistulas with high fluid loss.
Nutritional support:
Enteral or parenteral nutrition may be required, especially for gastrointestinal fistulas.
b) Identification and Monitoring
Imaging studies like:
MRI or CT scans (fistulogram) to assess complexity.
Endoscopy for internal fistulas.
Measure output in high-output fistulas (e.g., >500 mL/day in enterocutaneous fistulas).
c) Medical Management
Address underlying conditions (e.g., inflammatory bowel disease).
Reduce output in gastrointestinal fistulas:
Use agents like octreotide to decrease secretion.
Proton pump inhibitors (PPIs) for gastric fistulas.
d) Conservative Management
Some fistulas (especially simple, low-output) heal spontaneously with:
Adequate drainage.

The
Nutritional support.
Avoidance of further trauma.
3. Surgical Management
Indications:
Failure of conservative treatment.
Complications (e.g., abscess, sepsis).
Persistent high-output fistulas.
Procedures:
Fistulotomy: Opening and flattening the fistula (common in anal fistulas).
Fistulectomy: Complete removal of the fistula tract.

Appendix
Seton placement: For complex anal fistulas, to allow drainage while promoting healing.
Reconstruction: For large or complex fistulas (e.g., flap surgeries for rectovaginal fistulas).

SNAP for Fistula Management

S: Sepsis Control
Drain abscesses and treat infections with antibiotics.
N: Nutritional Support
Provide enteral or parenteral nutrition as needed, especially for gastrointestinal fistulas.
A: Anatomy Identification
Use imaging (CT, MRI, or fistulograms) or endoscopy to locate and assess the fistula.
P: Plan for Closure
Allow time for spontaneous healing if appropriate or plan surgical intervention for complex or non-healing fistulas.

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Anatomy of the appendix (Review)

• Anatomy of the appendix:

o The appendix extends from the postero-medial aspect of the cecum inferior to the
ileocecal junction.
o It has a short triangular mesentery called meso-appendix (derived from terminal ileum
mesentery).
o Histology >> considered as a lymphoid tissue (may play an immunological role).
o Size >> 6-9cm.
o McBurney point >> it’s the surface marker for the base of the appendix, it’s the 2/3rd
the way from the umbilicus to the right ASIS.
o Position of appendix:
▪ Retrocecal (44% - most common) (11 0’clock).
▪ Subcecal (24%) (6 o’clock).
▪ Post-ileal (14%).
▪ Pelvic (9%).
▪ Paracecal (6%).
▪ Pre-ileal.
o Arterial supply >> appendicular artery (branch from ileocecal artery which is a terminal
branch of SMA).
o Venus drainage >> ileocecal vein (drain into SMV).
o Lymphatic drainage >> ileocecal LNs to superior mesenteric LNs.

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Acute appendicitis

• Overview:
o It’s the most common cause of acute abdomen that requires surgery (always on top of
your differentials of acute abdomen).
o Epidemiology:
▪ Peak age group is 10-30ys (thus, it’s usually misdiagnosed in young children,
pregnant women, elderly patients).
▪ Occur more in males than females.
▪ Incidence of perforation:
• By 24h 25%.
• By 36h 50%.
• By 48h 75%.
o Pathophysiology:
▪ (1) luminal obstruction at the base of appendix by lymphoid hyperplasia (in
young patients) OR fecolith, OR carcinoid tumor (in older patient).
▪ (2) There will be increased intraluminal secretions & pressure beyond this
obstruction (with peristalsis against obstruction).
▪ (3) Venous drainage impairment (due to low BP and it’s thin muscle wall).
▪ (4) Arterial impairment (mucosal, then whole wall ischemia).
▪ (5) Wall edema, inflammation, & invasion by luminal bacteria ([Link], B.
Fragalis).
▪ (6) Complications occur in unrecognized early (discussed later).
• Necrosis, perforation, peritonitis, sepsis.
• Appendicular mass (phlegmon).
• Appendicular abscess.

• Clinical features:
DDx of RLQ pain
o Symptoms: GI:
▪ Acute RLQ pain (usually comes <24h): 1. Acute appendicitis.
• Initially the pain is periumbilical & then 2.
3.
CD.
Meckel’s diverticulitis.
If pain precedes the vomiting,
migrates to RLQ (represent irritation of 4. Mesenteric adenitis (in
consider acute appendicitis.
If vomiting precedes the pain, parietal peritoneum). children).
5. Gastroenteritis (especially
consider other causes • The pain is severe, steadily increasing, worse Yersinia).
by movement or coughing. 6. Perforated duodenal ulcer
▪ Nausea & vomiting. (Valentino’s sign).
7. Strangulated hernia.
In pediatrics, they mostly will ▪ Anorexia (most sensitive symptom). 8. Colon cancer (old patients).
present with persistent ▪ Fever (low or high grade). 9. Intussusception & cecal
periumbilical pain, and in most volvulus.
of the cases it will be ▪ +/- Dysuria (inflamed appendix may irritates the GU:
perforated at time of diagnosis. bladder). 1. Testicular or ovarian torsion.
▪ +/- Constipation or diarrhea (inflamed appendix may 2. Ruptured ectopic pregnancy.
3. Red necrosis of leiomyoma,
irritates the rectum). PID (females).
▪ Rupture appendix >> diffuse abdominal pain, signs of 4. Urolithiasis.
peritonitis (involuntary guarding). 5. UTIs or pyelonephritis.

In history taking, always ask about:

(1) GI symptoms in general.
(2) GU symptoms in males (scrotal swelling).
(3) GU in females (pregnancy, bleeding).
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o Signs & examinations:

▪ General inspection >> patient appears in pain, lying
still in the bed, fearful of examinations. Note that, rectocele appendicitis
▪ Vitals >> +/- fever & tachycardia. can have -ve rebound tenderness,
▪ Palpation >> RLQ tenderness (sensitive) & rebound but instead they may have flank
tenderness
tenderness (not necessarily on McBurney point).
▪ Special signs:
• Rovsing’s sign >> palpating the LLQ result in pain felt in RLQ.
• Iliopsoas sign >> RLQ pain with extension of right thigh suggesting
retrocecal appendix.
• Obturator sign >> RLQ pain with internal rotation of right thigh
suggesting pelvic appendix or abscess.
▪ Digital rectal exam:
• Not routinely done, but should be done if suspecting rupture cases.
• Pain during exam suggest pelvic appendicitis, peritoneal abscess, fluid
collection in pouch of Douglas or recto-vesical pouch.
▪ Signs of peritonitis (rupture cases):
• Unwell patient, toxic-looking, in severe pain, +/- hemodynamic
instability.
• Diffuse abdominal pain tenderness.
• Involuntary guarding & rigidity.
• Site of maximal tenderness + rebound tenderness at RLQ.
• Investigations & Diagnosis:
o Acute appendicitis is a clinical diagnosis, we need investigations to (1) help confirming
the diagnosis, (2) R/O other causes of acute abdomen, (3) pre-op assessment.
o Labs:
▪ CBC:
• Leukocytosis with left shift (PMN predominance).
• >18,000 WBCs cont may suggest perforation or abscess.
▪ Blood typing & cross matching >> as pre-op assessment.
▪ Urinalysis (dipstick & microscopy):
• Pyuria (may suggest UTI, however, it can present in acute appendicitis
due to irritation of the bladder).
• Crystals or RBCs (suggest stones).
▪ B-hCG (in all females) >> assess pregnancy & help R/O other causes.
▪ Electrolytes panel >> assess any disturbances.
▪ Other acute abdomen labs if needed.
o Imaging:
▪ Imaging is unnecessary & shouldn’t delay treatment.
▪ Ultrasound:
• Done in all women of childbearing age.
• Very helpful in R/O gynecological diseases.
• Findings on graded compression US of acute appendicitis:
o Widened lumen & closed loop.
o Edematous wall & surrounding fluid collection.
o Non-compressible appendix (compressible is either ruptured or
normal).

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CT Scan (Computed Tomography) of the Abdomen and Pelvis:

Investigation of choice for most adults.
Highly sensitive and specific (90–98%).
Identifies appendiceal inflammation, abscess, or perforation.

▪ AXR (erect):
• Usually done routinely, no significance in acute appendicitis.
DDx of fecalith • Possible findings that may suggest acute appendicitis:
(1) Appendicitis. o Fecalith (<5%); highly suggestive of appendicitis.
(2) Uroliths. o Scoliosis aways from right side.
(3) Phleboliths. o Loss of psoas shadow.
(4) Mesenteric LN calcification.
• Can detect complications or R/O other diseases such as air
under diaphragm (perforation), or SBO signs.

• Management (non-complicated):
o Prerequisites:
▪ No signs of peritonitis.
▪ No imaging findings of advanced bowel obstruction or perforation.
▪ Patient presented within 24-48h, not delayed.
o (1) Initial steps:
▪ Admit the patient + insert IV cannula to collect blood.
▪ NPO + IV fluids + IV analgesia.
o (2) Pre-op IV antibiotics:
▪ Usually metronidazole + cephalosporins.
▪ Give one dose 1h before surgery, +/- another dose after 6 hours.
▪ Antibiotics doesn’t need to continue beyond the 1st post-op day.
o (3) Urgent appendectomy:
▪ Must be done on the same day (risk of perforation in <24h is 25%), especially in
high risk populations (e.g. children, elderly, pregnant women).
▪ Details of surgery >> Considered as contaminated surgery. May be done open
surgery or laparoscopy.
▪ Open surgery >> Gridiron (oblique) or Lanz (horizontal) incision is used.
o Post-op care:
▪ Patient is continued on IV fluids & analgesics (24h coverage).
▪ The wound is dressed & left to heal.
▪ Patient is NPO until passing gas & bowel sound are heard (paralytic ileus is
expected immediately post-op). Then give clear liquids, soap, then solid food.
▪ Post-op diarrhea & DRE tenderness might indicated spillage from surgery (intra-
peritoneal pus or abscess).
▪ Patients are usually discharged on the 2nd post-op day.
o Follow up:
▪ 5th day post-op >> inspect for signs of SSI, if present remove the suture & treat
accordingly. If no SSI keep the sutures.
▪ 10th day post-op >> the suture is removed in the health center.
▪ Follow up appointment at the surgery clinic to discuss the results of the
pathology report.

Important, common scenario that may happed during the surgery

If the appendix appears normal grossly
laparoscopic Vs. open (1) Expand the incision in order to look for other causes
Laparoscopy is preferred because of A. CD or meckel’s diverticulum in ileocecal area.
less adhesion, easier, faster recovery, B. Mesenteric adenitis in the mesentery.
C. Ovaries & tube in females.
and only will keep patient NPO post
D. Perforated duodenal ulcer (worst scenario).
op until he is fully awake (VS till (2) If CD findings are found (e.g. creeping fat), assess the base of appendix.
passing stool in open) (3) If it’s involved with CD lesions don’t do any thing, close the abdomen,
arrange for colonoscopy with biopsy for diagnosis of CD.
(4) If nothing is found or the base of the appendix is normal, just remove the
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• Appendicitis in special populations:

o Appendicitis need specific attention in (1) pediatric age group, (2) pregnant women,
(3) elderly.
o We worry about there populations due to:
▪ They usually have atypical presentation, thus diagnosis may be delayed.
▪ Faster rate for progression & complications.
o Pediatric age group:
▪ They have underdeveloped omentum.
▪ Have difficulty to communicate symptoms.
▪ Low index of suspicion among physicians.
▪ The most sensitive symptom in pediatric age group is persistent RUQ pain.
▪ Faster progression, 80% of patients may present with features of perforation.
o Pregnant women:
▪ Acute appendicitis considered as the most common surgical emergency in
pregnant women.
▪ The appendix is shifted to the RUQ due to the gravid uterus .
▪ Atypical presentation:
• RUQ pain (instead of RLQ).
• Nausea & vomiting (confused with nausea & vomiting of pregnancy).
• Other DDx are highly considered (e.g. ectopic pregnancy, miscarriage).
▪ Investigations >> US is the most helpful tool.
▪ Management (if appendicitis):
• Laparoscopic or open surgery are equally safe in 1st & 2nd trimester.
• The surgery must be done anyway, there is high risk of mother & fetus
mortality if ruptured or perforate.
o Elderly patients:
▪ 50% of death from appendicitis occurs in the elderly age group (due to
increased comorbidities & impaired immunity).
▪ There is usually a delay of diagnosis due to there are investigated for other
causes.

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• Complications of appendicitis & their management:

o The most important complications are >> (1) perforation & peritonitis, (2) appendicular
mass, (3) appendicular abscess.
o Perforated appendicitis with peritonitis (surgical emergency):
▪ Presentation:
• Signs & symptoms suggestive of appendicitis.
• Signs & symptoms suggestive of peritonitis (diffuse abdominal pain,
abdominal distention, toxic patients, unstable vitals, generalized
tenderness on palpation with rebound, involuntary guarding).
▪ Investigations shouldn’t delay the surgery (mortality rate >5%).
▪ Management:
• ABCs (2 large IV bore needles to collect blood for investigations, IV
fluids).
• Pre-op IV antibiotics (metronidazole + cephalosporins) + IV analgesia.
• Surgery (done immediately):
o (1) Appendectomy (laparoscopic or open), +/- laparotomy
(consent should be obtained from patients for possible convert
to an open laparotomy if needed).
o (2) Peritoneal irrigation & toileting.
o (3) A peritoneal drain can be placed.
o (4) Wound is closed by secondary or tertiary intention because
of high risk of SSI.
o Post-op antibiotics >> IV metronidazole + cephalosporins for 3-
7 days or even more.
o Appendicular mass:
▪ Pathophysiology:
• A ruptured appendix may be localized by the omentum (protective
mechanism represents the success of body to isolate the danger).
• This inflammatory mass may represent the phlegmon, which can resolve
or progress to an abscess.
▪ Presentation:
• Patients usually presents late (>4 days).
• Symptoms of appendicitis is present but without signs of peritonitis
(patient is stable).
• A palpable mass is present in the RLQ, but the patient is clinically
satisfactory & no features of an abscess is present.
▪ Diagnosis >> mainly by US, in refractory case, CT can be done.
▪ Management (Ochsner-Sherren regimen):
• It’s an non-operative program, because surgery may be technically
Signs of improvement difficult at this point due to adhesions with surrounding organs.
(1) Stable vitals. • (1) IV fluids + IV antibiotics (metronidazole + cephalosporins) + IV
(2) Decreased tenderness. analgesia.
(3) Decreased mass size. • (2) NPO + TPN (if needed) + foley’s catheter (monitor urine output).
(4) Improvement inn appetite.
(5) Normalization of CRP & • (3) The mass is marked with a skin pencil (monitor change in size).
WBCs count. • (4) Patients vitals, symptoms, CBC, & CRP are frequently monitored.
• Do urgent surgery if there is deterioration or complications developed.
• Interval appendectomy is done 6-12 weeks later.

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o Appendicular abscess:
▪ Pathophysiology:
Contained perforation, • A perforated appendix was localized by the omentum & then an
then phlegmon, then
abscess
inflammatory mass developed.
• This initial non-inflammatory mass is known as phlegmon.
▪ Presentation:
• Patients usually presents late (>4 days).
• Sick or toxic looking patient.
• High, spiking fever, tachycardia.
• RLQ tender mass, +/- overlying skin changing (redness, warmth).
• The abscess is classically fluctuant.
• Rectal examination >> pain indicates presence of pus or abscess in the
recto-uterine or recto-vesical pouches.
▪ Investigations:
• US or CT >> show appendiceal abscess with echogenic mass.
• Imaging is necessary in order to determine the location, size of the
abscess & look or any potential pockets.
▪ Management:
• ABCs.
• IV antibiotics (metronidazole + cephalosporins) + IV analgesia.
• CT or US guided percutaneous drainage or surgical drainage (a drain is
left & the wound is left to heal by tertiary intention).
• IV antibiotics are continued for 10-14 days (IV until afebrile, then oral).
• Interval appendectomy in 6-12 weeks later.

• Appendiceal tumors:
o Types:
▪ Mucinous adenocarcinoma (most common).
▪ Carcinoid tumor (2nd most common).
o Presentation >>ًpatient either presents with appendicitis or SBO.
o Management:
▪ <2cm >> appendictomy.
▪ >2cm or involving the base of appendix >> right hemicolectomy.

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The Colon
Retroperitoneal organs
Mnemonic: SAD PUCKER
S: Suprarenal (adrenal) glands
A: Aorta and IVC
D: Duodenum (second to fourth parts)
P: Pancreas (except the tail)
U: Ureters
C: Colon (ascending and descending)
K: Kidneys
E: Esophagus (thoracic part)
R: Rectum (mid and upper parts)

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Anatomy of the Colon (Review)

• Anatomy of the colon:

o Function:
▪ Right side >> water, electrolytes absorption, & forming stool.
▪ Left side >> housing of fecal matter with mucus secretion.
o Histology >> it contains no glands or villi.
o Colon characteristics:
▪ Much larger caliber.
▪ Tinea coli >> outer longitudinal layer of muscle in colon that is divided into 3
columns of muscles & meet at the base of the appendix.
▪ Haustrations >> externally visible curvatures due to contracted tinea coli.
▪ Fat appendages (epiploic appendix) >> small fat-filled projections of colon.
▪ Radiological features:
• Peripherally located.
• Large caliber filled with air & feces.
• Haustrations.
• Air in the rectum can be seen centrally above the level of pubic
symphysis (absent air suggest proximal obstruction).
o Parts of the colon:
▪ Cecum (1st part):
• Lies in the right inguinal fossa.
• Entirely covered by peritoneum but it has no mesentery (Predispose to
cecal volvulus is kids).
▪ Appendix:
• Mobile appendage arising from the cecum at a fixed point (the base of
the appendix).
• The position of the appendix is different from one person to another.
• The base of the appendix is identified intra-operatively as the point at
which all 3 tinea coli unite (McBurney point).
• Histologically it’s very lymphoid in nature.
The great omentum ▪ Ascending colon >> retroperitoneal (covered by peritoneal anteriorly & on
(policeman of the abdomen) sides).
It has very important role ▪ Transverse colon:
during inflammation & • Intraperitoneal.
perforation, it adheres to the
area to contain it + protect • Left colic flexure (splenic flexure) is more superior & less mobile than
the peritoneum. the right one. It’s located below the left kidney & attached to the
diaphragm by phrenicocolic ligament.
▪ Descending colon >> Retroperitoneal.
▪ Sigmoid colon:
• Intraperitoneal.
• The sigmoid colon mesentery is S shaped & predisposes this part of the
colon to volvulus.
• Left ureter & left common iliac artery lie retroperitoneal posterior to
the apex of the root of the sigmoid mesocolon.

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o Arterial supply:
▪ Superior mesenteric artery (SMA):
• Gives rise to (1) right colic artery, (2) middle colic artery, (3) ileocolic
The most watershed zones is artery.
the splenic flexure &
rectosigmoid colon • Cecum >> ileocolic artery (terminal branch of SMA).
• Appendix >> appendicular artery (terminal branch of ileocolic artery).
• Ascending colon >> right colic artery.
• Transverse colon >> middle colic artery + anastomosis of right & left
colic artery.
▪ Inferior mesenteric artery (IMA):
• Gives rise to (1) left colic artery, (2) sigmoid artery.
• Descending & sigmoid colon >> left colic artery + sigmoid artery.
• Rectosigmoid colon >> anastomosis by IMA & superior rectal artery.
▪ Marginal artery >> an anastomosis of all branches of the arteries that supplies
the colon.
o Venous drainage:
▪ Cecum, appendix, ascending, & transverse colon >> SMV.
▪ Descending & sigmoid colon >> IMV.
o Lymphatic drainage:
▪ Follows the arterial supply through mesenteric lymph nodes to the origin of the
major arteries (e.g. SM lymph nodes, IM lymph nodes).
▪ Mesenteric adenitis may present as abdominal pain and or mass.
o Innervation:
▪ Parasympathetic:
• Simulate peristalsis & secretions.
• Anterior & posterior vagus trunks (celiac plexus) >> supply the
intestines all the way down to the splenic flexure.
• Pelvic splanchnic nerves (S2-S4) >> supply the rest of the colon.
▪ Sympathetic:
• Slows down motility & secretion.
• Greater, lesser, & least splanchnic nerves (thoracolumbar sympathetic
nerves).

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Inflammatory bowel diseases

• Overview:
o Definition >> idiopathic chronic systemic inflammatory condition associated with
autoimmune, environmental, & genetic factors whose effect mainly fall on the GIT.
o Risk factors >> Family history, Smoking (worse CD, better UC), Male gender.
o Crohn’s disease )CD(:
▪ A chronic transmural inflammatory disease that can affect any part of the GI
tract (mouth to anus), but most commonly involves the ileocecum.
▪ Distribution >> Terminal ileum & cecum (40%), Small intestines (30%), Colon
(25%), Rarely other parts (stomach, mouth, esophagus).
▪ Symptoms:
• Chronic watery diarrhea (>4weeks) (not bloody as UC, but it can be).
• Abdominal pain (RIF pain that may be misdiagnosed as acute
appendicitis).
• Recurrent oral ulcers, +/- dysphagia.
▪ Extra-GI manifestations:
• Constitutional (weight loss, low grade fever, fatigue).
• Joint symptoms (migratory mono-articular seronegative arthritis).
• Eye symptoms (Episcleritis & uveitis).
• Skin symptoms (clubbing, erythema nodosum).
▪ Complications:
• Malabsorption:
DDx of chronic diarrhea + abdominal o Megaloblastic anemia (vitamin B12).
pain o Recurrent cholelithiasis & nephrolithiasis (Ca oxalate stones).
(1) IBD (CD or UC).
(2) IBS.
o Malnutrition of fat-soluble vitamins (ADEK).
(3) Infectious colitis (salmonella, • Strictures & SBO:
shigela, yersinia, clostridium difficile). o Most common indication of surgery.
(4) Colon cancer. o Initially due to edema & spams of bowel.
(5) Diverticular disease (painless
bleeding).
o Later due to scarring & thickening of bowel (chronic narrowing).
(6) Ischemic or radiation colitis. • Fistula formation >> enteroenteric, enterovesical, enterocutaneous.
(7) Endometriosis in females. • Peri-anal disease >> anorectal abscess, fistulas, fissures.
• Colon cancer & toxic megacolon >> not as much as UC.
o Ulcerative colitis (UC):
▪ UC is a chronic inflammatory disease of the colon or rectal mucosa.
▪ Distribution >> Proctiits (rectum alone), Proctosigmoiditis, Distal colitis
(descending colon), Extensive colitis (transverse colon), Pancolitis, Backwash
ileitis (involving the terminal ileum).
▪ Symptoms:
• Chronic diarrhea (>4weeks), usually bloody (hematochezia).
• Colicky abdominal pain (usually LLQ) + Tenesmus.
▪ Extra-GI manifestations:
• Constitutional (weight loss, low grade fever, fatigue).
• Joint & eye symptoms same CD.
• Skin manifestations (pyoderma gangrenosum, clubbing).
• Hepatobiliary (obstructive jaundice – primary sclerosing cholangitis).
• Venous or arterial thromboembolism (with active disease & pancolitis).

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▪ Complications:
• Massive lower GI bleeding, electrolytes disturbances, dehydration.
• Chronic bleeding & IDA.
• Toxic megacolon & colonic perforation.
• Colorectal cancer.

• Investigations & diagnosis:

o Labs:
▪ CBC >> assess anemia & infections.
▪ ESR & CRP >> suggestive active inflammation.
▪ LFTs >> baseline, R/O liver disease.
▪ Stool analysis >> ova, parasite, microscopy, culture.
o Ileocolonoscopy (IBD only diagnosed by biopsy):
▪ Crohn’s:
• Transmural inflammation with skip lesions.
• Aphthous ulcers (terminal ileum is the hallmark location).
• Cobblestone appearance, creeping mesenteric fat, & fibrosis.
• Histology >> Non-ceseating granulomas.
▪ Ulcerative colitis:
• Circumferential inflammation or ulceration that is continuous.
• Mucosa are so friable & can bleed with touching.
• On histology >> inflammation confined to mucosa & submucosa, crypts
abscess.
o Imaging (mainly for complications):
▪ CT with contrast >> Identify affected areas, strictures, fibrosis.
▪ Barium enema >> string sign in CD, lead-pipe sign & pseudopolyp in UC.
• Management:
o Medical management:
▪ Acute (for flares) >> steroids.
▪ Disease-modifying agents:
• 5-ASA (mesalamine).
• Immunosuppressants (azathioprine, mercaptopurine).
• Biologics (infliximab).
o Surgical management (typically for complications):
▪ Crohn’s disease:
Important notes • Generally, surgical options are feared because of the high recurrence
(1) CD may be misdiagnosed as
acute appendicitis, however intra-
risk + risk of fistulas.
op, the appendix may appear • SBO & strictures >> stricturoplasty.
normal, so we will remove it to • Ano-rectal abscess >> percutaneous or surgical drainage.
prevent diagnostic confusion in the
future, unless the base of appendix • Enteric fistulas >> NPO, fistulectomy.
is involved with CD (increase the risk • Acute appendicitis (as DDx) > appendectomy is only done if the base of
of fistulas).
(2) IF the appendix is normal,
the appendix is not infected by CD.
explore the area, & if the findings is ▪ Ulcerative colitis:
suggestive for CD, don’t touch it,
• Often done if medical management fails or if there are complications.
close up, arrange for colonoscopy &
biopsy. • UC is generally more responsive to surgical treatment (low recurrence
(3) Sometimes terminal ileitis is rate).
seen but with no other features if
CD (this could be the patient’s 1 st • Procto-colectomy with ileostomy.
presentation of CD).

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o Comparison between UC & Crohn’s:

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Diverticulosis & diverticulitis

• Diverticulosis:
o Diverticulosis defined as out-pouching along the wall of a hollow
structure. It’s caused by increased intra-luminal pressure in which inner
layer of colon bulges through the focal area of weakness in the colon.
o The most common location is the sigmoid colon. However, it can occur
any where.
o Types:
▪ True diverticula >> all layer a involved (e.g. mickle diverticula).
▪ False diverticula >> only mucosa & submucosa (more common).
o Risk factors:
▪ Old age (>70ys), family history.
▪ Low fiber diets & chronic constipation.
▪ +ve family history.
o Clinical features:
▪ Usually asymptomatic (70-80%) & discovered incidentally or if complications
occur (mainly Diverticulitis).
▪ Vague LLQ discomfort, bloating, flatulence, constipation or diarrhea may be
present.
o Complications:
▪ Painless rectal bleeding (40%):
• Usually clinically insignificant & stops spontaneously.
• In 5% of patients, the bleeding is severe & some present with
hypovolemia signs.
• Colonoscopy may be performed to locate the site of bleeding & for
management (e.g. epinephrine injection, thermocoagulation).
• Other management measures >> angiography, embolization, segmental
colectomy.
▪ Diverticulitis (25%) >> discussed below.
o Investigative methods >> Barium enema (test of choice, show out-pouching), Contrast
CT, Colonoscopy.
o Management:
▪ High-fiber food (e.g. bran - ‫ >> )نخالة‬increase stool bulk.
▪ Psyllium (‫ >> )اليافًقشورًالسيليلوم‬if patient cannot tolerate bran.
▪ Patients must be instructed when to seek care (e.g. in cases of bleeding or
symptoms of diverticulitis).
▪ 90% of cases will imporve with conservative treatment.

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• Diverticulitis:
o A complication of diverticulosis in which there is Inflammation or infection of
diverticula.
o Pathophysiology:
▪ Blockage of the diverticula results in increased intra-luminal pressure, mostly
due to food o fecal impaction, which result eventually in bacterial colonization.
▪ This can result into inflammation, edema, ischemia & necrosis.
▪ Outcomes:
• Micro-perforation which contained by the omentum resulting in
phlegmon, abscess, or fistulas.
• Macro-perforation resulting in peritonitis.
• Chronic diverticulitis resulting in strictures & large LBO.
o Clinical features (same as acute appendicitis but on the left side):
▪ Symptoms:
DDx of severe LLQ pain • Fever & LLQ pain.
(1) Acute diverticulitis. • Anorexia, constipation or diarrhea, vomiting.
(2) Colon cancer ▪ Signs >> Fever, LLQ tenderness with rebound.
complications.
▪ Complications:
(3) Colitis (UC, ischemic
colitis, pseudomembranous • Abscess formation (palpable tender abdominal mass, spiking fever).
colitis). • Colo-vesical fistula (dysuria, bubbles in urine, fecal masses in urine).
(4) Sigmoid volvulus. • Large bowel obstruction (due to chronic inflammation – distention,
(5) Strangulated inguinal
vomiting, obstipation).
hernia.
• Free colonic perforation (uncommon but dangerous resulting into
peritonitis).
o Investigations & Diagnosis:
▪ Labs (+/- of acute abdomen):
• CBC >> leukocytosis.
• RFTs & electrolytes >> assess kidney function & electrolytes
disturbances (especially in diarrhea).
• Stool culture & microscopy >> R/O infectious diarrhea.
• Urine analysis >> sterile pyuria (due to nearby inflammation).
• LFTs & amylase >> R/O other causes for abdominal pain.
▪ Imaging:
• CT scan with contrast (test of choice) >> reveal a swollen, edematous
bowel wall, assess other complications (abscess, fistulas).
Barium enema & colonoscopy
• Abdominal radiograph >> exclude other potential causes of LLQ pain,
is done in follow up to R/O R/O obstruction (air-fluid levels & distention), perforation (air under
malignancy (after 4-6 weeks) diaphragm).
• Note that barium enema & colonoscopy are contraindicated in acute
diverticulitis due to the risk of perforation.
o Management:
▪ Uncomplicated diverticulitis:
• Bowel rest (NPO), IV fluids, analgesia (non-opioid).
• Oral antibiotics (7-10 days) >> metronidazole + ciprofloxacin.
• In severely ill patients >> IV metronidazole + IV ciprofloxacin + IV fluids
+ pain killer.
• Symptoms persist >4 days >> surgery, resection of involved area.

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▪ Complicated diverticulitis (Hinchey staging):

• (I) Phlegmon or small abscess >> IV antibiotics, +/- draining.
Indications of surgery in • (II) Large abscess >> CT/US guided percutaneous drainage + IV
diverticulitis
(1) Unstable patients with signs of
antibiotics + elective surgery to remove diverticula.
peritonitis. • (II) Fistulas >> surgical closure + IV antibiotics.
(2) Hinchey stage III or IV. • (III) Purulent Peritonitis (6% mortality):
(3) Complicated diverticulitis. o Peritoneal irrigation & toileting.
(4) Immunocompromised patients.
(5) After several attacks (>3 attacks).
o Hartmann procedure (sigmoid colectomy with proximal
(6) Failed medical Rx colostomy).
(7) Inability to R/O cancer. o Colostomy is reversal (re-anastomosis in 3-6 months).
• (IV) Feculent peritonitis (35% mortality) >> same as above.
▪ Follow up >> necessary after 4-6 weeks for colonoscopy to R/O malignancy.

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Large bowel obstruction

• Overview:
o Most common causes:
▪ Colorectal adenocarcinoma (65%).
▪ Complicated diverticulitis; scarring & strictures (20%).
▪ Sigmoid volvulus or IBD (5%).
o Causes:
▪ Mechanical:
• Intra-luminal >> constipation, foreign body.
• Intra-mural >> adenocarcinoma, diverticulitis scarring, IBD strictures,
radiation stricture.
• Extra-mural >> volvulus, adhesions, hernias.
▪ Functional >> ogilvie syndrome.
o Clinical features:
▪ Symptoms:
• Colicky abdominal pain.
• Abdominal distention.
• Nausea & vomiting (less marked).
• Obstipation (early).
▪ Signs:
• Abdominal distention.
• Hyperactive bowel sounds.
• Rectal exam may show empty rectum.
o Investigations:
▪ Routine labs for acute abdomen.
▪ Erect AXR >> air-fluid levels, distended proximal colon, absent air in rectum.
▪ Supine AXR >> picture-frame appearance.
o Managemnet (general):
▪ ABCs + NPO + NGT (gastric decompression), IV broad spectrum antibiotics.
▪ Specific treatment of underlying cause.
▪ Enemas for fecal disimpaction.
▪ Surgical correction of obstruction.

• Volvulus:
o Defined as rotation of a segment of the intestine around its mesenteric axis resulting in
closed loop obstruction.
o It’s the 3rd most common cause of LBO.
o Risk factors:
Presence of free air & ▪ Age >70.
pneumatosis can ▪ High fiber diet (-_-).
indicate necrotic ▪ Chronic constipation or Laxative abuse.
bowel ▪ Pregnancy.
o Presentation >> typically in elderly patients with S&S of LBO.
o Investigations:
▪ AXR >> coffee-bean or omega loop sign.
Examples of volvuli ▪ Sigmoidoscopy >> diagnostic & theraputic.
(1) Sigmoid volvulus (75%).
(2) Cecal volvulus (25%).
(3) Midgut volvulus (pediatrics).
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o Management:
▪ Sigmoid volvulus:
• Non-operative >> Sigmoidoscopic decompression followed by rectal
tube insertion (high RR, plan for future elective surgery).
• Operative:
o Untwisting of involved segment.
o Involved segment is studied for viability, if non-viable,
Hartamann procedure may be done.
▪ Cecal volvulus (always surgical):
• Untwisting of involved segment.
• Involved segment is studied for viability, if non-viable, right
hemicolectomy & ileotransverse anastomosis may be required.

• Ogilvie syndrome:
o A functional obstruction of the colon, in which the colon is massively dilated on imaging,
but a mechanical cause is not identified.
o Typically occur in Bedridden or institutionalized patients, may be related to some drugs
(e.g. anti-cholinergic or opioids).
o Presentation >> S&S of LBO with marked abdominal distention & less abdominal pain.
o Investigations >> LBO (AXR, colonoscopy).
o Management:
▪ ABCs, NPO, NGT decompression.
▪ LGIT decompression >> rectal tube, colonoscopy, cholinergic drugs
(neostigmine), surgery.

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Colon neoplasia

• Benign colon tumors (polyps):

o Histological types:
▪ Adenomatous (pre-malignant):
• Tubular (75%).
• Tubulovillous (15%).
• Villous (10% - most dangerous).
▪ Non-adenomatous (no malignant potential):
• Hyperplastic polyp (most common type overall).
• Inflammatory polyp / pseudopolyps.
• Juvenile polyps.
• Hamartomatous.
o Gross morphology:
▪ Sessile (flat) >> more dangerous, more difficult to resect.
▪ Pedunculated >> has a stalk (‫)متدلدل‬.
o Malignant potential of any colon polyp is determined by: Familial adenomatous polyposis (FAP)
▪ Size of >2cm is more likely. is an inherited disorder characterized
▪ Sessile shape is more likely than the pedunculated. by a thousands of polyps & have 100%
risk of colon cancer
▪ Histological type; villous > tubulovillous > tubular.
▪ Severe atypia.
o Clinical features:
▪ Patient could be asymptomatic & found incidentally.
▪ Change in bowel habits (diarrhea or constipation or even LBO).
▪ Mucus discharge with perianal discomfort.
▪ Hematochezia or melena indicating bleeding.
o Diagnosis is done mainly by colonoscopy (diagnostic & therapeutic):
▪ Study entire colon.
▪ Polypectomy (as management) & sending the biopsy to histopathology lab.
o Management:
▪ Polypectomy.
▪ Follow up patients with adenomatous polyp (within 3 years).
▪ If FAP, offer prophylactic colectomy OR annual screening.

• Colorectal cancer (CRC):

o Epidemiology:
▪ It’s the 3rd most common cancer & cancer-related mortality in men & women.
▪ Age group >> risk begins to rise >50s, peak is 60-79s.
o Risk factors:
▪ Male gender.
▪ Age >50s.
▪ Family history (1st degree) or personal previous history of adenoma or CRC.
▪ IBD (UC > CD).
▪ Inherited syndromes (discussed later).
▪ Low fiber diet & Smoking.

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o Pathogenesis:
▪ Adenoma-carcinoma sequence (80%):
• Patients has 1 APC mutation already & the other mutation occur
sporadically (1st hit).
• Mucosa at risk >> Proto-oncogene mutation, KRAS mutation or loss of
DCC gene (occur within 2-5 years).
• Uncontrolled proliferation (adenomatous polyps) >> p53 (2nd hit)
within 2-5 years.
• CRC >> occur eventually nearly at the 10 year.
▪ Microsatellite instability pathway:
• Related to mismatch repair genes (hMSH2, hMLH1).
• There is increased number of short base repair repeats.
• Results in lynch syndrome (15% of sporadic cases of CRC).
o Colon cancer screening:
▪ For normal individual, screening is offered from 50s up to 75s:
• Colonoscopy every 10 years.
• Sigmoidoscopy every 5 years.
• Fecal occult blood yearly.
▪ For individuals with 1st degree relative with CRC >> Screening is offered at 40s
or 10 years younger then the age of diagnosis of the relative.
o Clinical features:
▪ Most common site of colon cancer >> sigmoid > rectum > cecum > ascending &
transverse colon.
▪ Most patient are asymptomatic until late stages (that’s why we do screening).
▪ Symptoms:
• Constitutional symptoms >> weight loss & anorexia.
• Right-sided cancers (bleeds) >> Occult blood loss & melena.
Complications of CRC • Left-sided cancers (obstruct):
(1) Local invasion of peritoneum
with seeding. o Reduced stool caliber (pencil-shaped).
(2) Metastasis. o Change in bowel habits (constipation, encopresis).
(3) Lower GI bleeding & anemia. o LBO S&S (abdominal distention, cramping abdominal pain,
(4) Fistulas. obstipation).
(5) Perforations.
o +/- hematochezia.
• Rectal cancer >> hematochezia, tenesmus, rectal mass.
▪ Signs >> Usually none, mass may be felt.
o Investigations & Diagnosis: Metastasis of CRC
▪ As a general rule, cancers must diagnosed by biopsy. (1) Liver (most common).
▪ Routine labs: (2) Bones.
(3) Lungs.
• CBC (microcytic anemia).
• RFTs & LFTs (as a baseline).
• Occult blood test.
• Tumor markers (CEA, CA 19-9 for follow up not diagnosis).
▪ Barium enema >> may show apple-core appearance.
▪ Colonoscopy with biopsy >> the entire colon is studied lesions can present at
different sites at the same time (synchronous), biopsy confirms the diagnosis.
▪ CT of chest, abdomen & pelvis >> for staging.
▪ Transrectal/endorectal US or pelvic MRI >> assess depth of cancer invasion.

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o Staging of CRC (TNM staging):

▪ TNM staging:

▪ Duke’s stages:
• Stage I >> T1-T2 (minimally invasive).
• Stage II >> T1-T4 without N or M (locally invasive).
• Stage III >> N1-N2 (with LNs involvement).
• Stage IV >> M1 (distant metastasis).
o Management:
▪ Treatment options:
• (1) Surgical resection:
o Bowel preparation must be done before surgery.
o Involved segment is removed with wide margins (2-5cm of
healthy tissues) + related LNs + all vessels and mesentery.
• (2) Radiotherapy OR Chemotherapy.
▪ By stages:
• Stage I & II >> surgical resection with LN dissection.
• Stage III >> surgical resection with LNs dissection + adjuvant
chemotherapy.
• Stage IV >> palliative care.
▪ Rectal cancer:
• Neoadjuvant radiotherapy (5-FU) + surgical resection.
LAR >> low anterior resection • Proximal cancer (>4cm from anal verge) >> LAR + TME + colo-anal
TME >> total meso-rectal excision anastomosis.
APR >> abdomino-perineal resection • Distal cancers (<4cm from anal verge) >> APR + TME + permanent
colostomy + closure of anus.
• Complications >> Incontinence, urinary & sexual dysfunction,
How to differentiate between
permeant and temporary anastomotic leak, stricture formation.
colostomy? We examine the ▪ Metastasis (liver) >> lobectomy of affected lobe.
The first thing to assess in a
anus, if it’s closed, it’s ▪ Follow up: colostomy is ischemia or
permanent colostomy. • There is 80% recurrence within 2 years. change in color (must be assed
• Every 3 months for 2 years. during the first 24h)
• Every 6 months for the next 2 years.
• Annually thereon.
• In every visit order the following:
o Assess patient history & perform abdominal examinations.
o CBC + CEA + stool guaiac.
o Colonoscopy (yearly).
o CXR (every 6 months).

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• Inherited syndromes with increased risk of CRC:

o Familial adenomatous polyposis (FAB):
▪ An AD inherited disease.
▪ Mutation:
• Adenomatous polyposis coli (APC) gene (a tumor suppressor gene).
• Located on Ch-5.
• As a result, 100s-1000s of adenomatous polyps develop early in lifetime
(late adolescence).
• There is 100% risk of developing CRC.
▪ Screening >> we offer screening at age 10 years old.
▪ Management >> Prophylactic proctocolectomy with ileostomy or ileorectal
anastomosis is offered.
o Gardner syndrome (AD disease) >> Patients present with adenomatous polyposis +
osteomas (mainly in skull) + sebaceous cysts + Desmond tumor (managed as FAP)
o Turcot’s syndrome )AD disease) >> adenomatous polyposis + CNS tumors
(glioblastomas, medullablastomas).
o Lynch syndrome:
▪ Also known as hereditary non-polyposis coli CRC (HNPCC).
▪ Develops using microsatellite instability pathway (not adenoma-carcinoma
sequence).
▪ Lynch I >> right sided colon cancer.
▪ Lynch II >> colon cancer + risk of other cancers (endometrial, ovarian, breast).
o Peutz-legher syndrome (AD disease) >> Patients develop hamartomatous polyps of the
entire GIT + melanotic pigmentations of face, lips, oral mucosa, & palm.

• Pseudomembranous colitis:
o Antibiotic-associated colitis (death of normal flora) resulting in growth of C. Difficile.
o May occur with clindamycin, ampicillin, cephalosporins prolonged use.
o Clinical features >> watery diarrhea, crampy abdominal pain.
o Complications >> toxic megacolon, perforation, anasarca.
o Diagnosis >> identification of C. Difficile toxins in stool, sigmoidoscopy.
o Management:
▪ Stop offending antibiotic if possible.
▪ Metronidazole (DOC) or vancomycin.
▪ Cholestryramin to improve diarrhea.

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Rectum &
Anus

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• Anatomy of the rectum (review):

o Important points:
▪ The rectosigmoid junction lies at level of S3 vertebra.
rd
The lower 1/3 attached ▪ The terminal part of the rectum bends sharply in a
anteriorly to denonvillier’s fascia, posterior direction forming anorectal flexure due to the
& posteriorly to retrosacral fascia puborectalis muscle.
)Waldeyer’s fascia(
▪ The rectum has a continuous layer of longitudinal muscles,
which is tenia coli widening to cover the whole rectum.
o Main function >> storage of feces (thus, it has very high pressure +
it’s full of bacteria).
o The peritoneum is reflected from the rectum to:
▪ Posterior wall of bladder (rectovesical pouch in men).
▪ Posterior fornix of the vagina (rectouterine pouch in women).
▪ Lateral reflection forming para-rectal fossa in both sexes.
o Arterial supply:
▪ Proximal part >> superior rectal artery (branch from IMA).
▪ Middle & inferior parts >> middle rectal artery (branch from inferior vesicle in
male & uterine artery in females).
o Venous drainage:
▪ Drained by superior, middle and inferior rectal veins.
▪ Superior rectal vein drain into portal venous system.
▪ Middle & inferior drain into systemic circulation.
▪ The vein are form the internal & external rectal venous plexuses.
o Lymphatic drainage:
▪ Superior half >> para-rectal LNs.
▪ Inferior half >> sacral & internal iliac LNs.
o Innervation:
▪ Sympathetic >> lumbar splanchnic nerves &
hypogastric plexus.
▪ Parasympathetic >> pelvic splanchnic nerves
(S2-S3).

• The anal canal:

o It’s the terminal part of the large intestines that extends
from the pelvic diaphragm to the anus.
o Anal columns (of Morgagni):
▪ Arise from the dentate line.
▪ Contains terminal branches of superior rectal arteries & veins.
▪ Inferior ends of these columns are joined by the anal valves.
▪ Between the columns there is anal sinuses (crypts) that contain mucous glands.

The pelvic floor is formed by >> puborectalis,

pubococcygeus, iliococcygeus
These muscles are somatic & helps keeping the
pelvic contents in their places (weakness result
in vaginal or rectal prolapse)

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o Anal sphincters:
▪ External anal sphincter (voluntary):
• Has 3 parts; subcutaneous, superficial, deep.
• Supplied by inferior anal nerve (S4).
• Contribute 20% of resting contraction pressure & 100% of the voluntary
pressure.
▪ Internal anal sphincter (involuntary):
• It’s a thickening of the circular muscles layer.
• Contribute 80% of the resting contraction pressure.
• Contraction >> sympathetic fibers (superior rectal & hypogastric
plexus).
• Relaxation >> parasympathetic fibers.
o The dentate (pectinate) line:
▪ It’s the division between the rectum & the anal canal.
▪ It represent the transition between the endoderm (hindgut) to ectoderm.
▪ Above the dentate line (ectoderm) >> there is simple columnar epithelium.
▪ Below the dentate line (endoderm) >> there is stratified non-keratinized
squamous epithelium.
▪ Note that, the white line of Hilton, which is much lower, represent the anal
verge, where non-keratinized epithelium becomes keratinized.
o Vasculature of anal canal:
Arterial supply * Venous drainage ** Lymphatic drainage
Superior part Superior rectal vein (drain Inferior mesenteric LNs (para-aortic
Superior rectal artery (branch from IMA)
(above dentate) into IMV – portal system) LNs)
Inferior part Inferior rectal artery (branch from Inferior rectal vein (drain Inguinal or internal iliac LNs ☺
(below dentate) internal pudendal artery – internal iliac) into caval venous system). Superficial inguinal below white line

* Note that the middle rectal a. assist the blood supply to the anal canal by forming anastomosis with the
superior & inferior rectal arteries.
** There is communication between the internal & external plexus.
o Innervation:
▪ Above dentate line:
• Sensation goes back with sympathetic fibers.
• Involuntary autonomic supply:
o Sympathetic >> promotes increased tone & reduce peristalsis.
o Parasympathetic (pelvic splanchnic) >> promotes peristalsis &
relaxation of tone .
▪ Below dentate line:
• Sensations goes back with parasympathetic.
• Somatic nerves supply voluntary sphincter through inferior anal nerve
(pudendal nerve).

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Anal hemorrhoidal disease (HIGH-YEILD)

• Overview:
o Hemorrhoidal disease is an enlargement of the submucosal venous (hemorrhoidal)
plexus in the anus or rectum, in which they may protrude into the lumen or prolapse
downwards.
o It’s a very common condition that affects males & females equally. Hemorrhoids as a term is normal
o Risk factors (anything cause straining): (the venous plexus are called
▪ Old age. hemorrhoid), but the abnormal
▪ Chronic constipation & straining. dilation is pathological & we call it
hemorrhoidal disease
▪ Prolonged sitting.
▪ Increased pelvic pressure (e.g. pregnancy, ascites, cancer).
▪ Portal HTN & liver diseases.
o Common locations (anal cushion areas):
▪ Right anterior (11:00).
▪ Right posterior (7:00).
▪ Left lateral (3:00).
o Classification:
▪ Internal hemorrhoids >> above dentate line, painless.
▪ External hemorrhoids >> below dentate line, painful.
▪ Mixed >> both internal & external.

• Clinical features & Diagnosis:

o Symptoms (non-acute):
▪ 40% of patients are asymptomatic.
Complications of ▪ Hemorrhoidal bleeding (PR hematochezia):
hemorrhoidal disease • Usually painless following bowel movements.
(1) Hemorrhage (bright
• Patients may describe it as drips into toilet bowl or coats the stool.
red blood by rectum).
(2) Thrombosis. • Rarely develops anemia.
(3) Strangulation. ▪ Mucous discharge >> staining of underwear with peri-anal pruritus & irritation.
(4) Fibrosis. ▪ Sensation of fullness in perianal area >> only in prolapsed hemorrhoids.
(5) Infection.
▪ Constipation >> most patients presents with chronic constipation (they are
aware that the constipation is the cause).
o Acute hemorrhoidal attack:
▪ Represents thrombosed external hemorrhoids.
▪ Excruciating peri-anal pain of acute onset for 2-3 days.
▪ Patient is unable to sit.
▪ On examination, there is palpable & tender peri-anal lump.
o Signs & examinations:
▪ Direct visualization >> By naked eye or through anoscope.
▪ Digit rectal exam:
• Must be done to R/O cancer.
• Non-complicated hemorrhoids are compressible during DRE & you
won’t feel them.

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▪ Internal hemorrhoids degrees:

• I >> protrudes, no prolapse.
• II >> prolapse only during straining with spontaneous reduction
• III >> prolapse & require manual reduction.
• IV >> prolapse but cannot be reduced + pain if thrombosed.
o Investigations & diagnosis:
▪ It’s a clinical diagnosis.
▪ In prolonged cases, keep in mind other DDx (cancer, IBD, portal HTN).

• Management:
o Medical (95%):
▪ Lifestyle changes >> high fiber diet, hydration, avoid straining, anal hygiene.
▪ Sitz bath >> principle is to add salts that will cause an osmotic shift to relieve
the swelling of veins.
▪ Topical agents >> steroids, +/- lidocaine gels (procto-glyvenol).
▪ Medications >> laxatives, venoconstrictors (Daflon), analgesics (NSAIDs).
o Surgical – hemorrhoidectomy (rarely needed):
▪ Closed (office-based) >> Rubber-band ligation,
infrared cauterization, laser coagulation,
sclerotherapy.
▪ Open hemorrhoidectomy:
• Surgical excision, requires 2-4 weeks of
recovery.
• Offered in severe cases (III or IV) or in
refractory cases or in acute thrombosis (within 24-72h).
• Complications:
o Exsanguination (pooling of blood).
o Pelvic infection.
o Incontinence.
o Anal stricture.

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Anal fissures (HIGH-YEILD)

• Overview:
o Anal fissure is a painful linear tears in the anal mucosa below the dentate line.
o Causes:
▪ Chronic constipation.
▪ Hyperactive sphincter (i.e. many bowel movements).
▪ Crohn’s Disease.
▪ Anal sex (in homo & heterosexuals).
▪ Childbirth.

• Clinical features:
o Posterior midline (90%) is the most common location (due to low blood supply), if
found in another location, suspect CD.
o Symptoms: Triad of chronic fissure
▪ Painful bowel movement. (1) Fissure.
▪ Bright red blood on toilet paper (or directly in toilet). (2) Sentinel (pile) tag.
(3) Hypertrophied papilla.
o Signs & examinations:
▪ Inspection:
• Fissure may be seen on external exam.
• Sentinel tag/pile represents chronic fissure (thickened skin at distal end
of anal fissure).
• Avoid Anoscopy because it’s painful (you may use it if you are not sure).
▪ DRE >> very painful, avoid it unless you are not sure of diagnosis.
o Investigations & Diagnosis:
▪ Diagnosis is clinical, there is no need for investigations unless you suspect other
DDx.
▪ Main DDx are >> anal abscess, thrombosed Hemorrhoids, early anal cancer.

• Management:
o Lifestyle changes >> high fiber diet, hydration, Sitz bath, & anal hygiene.
o Medications:
▪ Goal is to relieve pressure (decrease tone + soften stool).
▪ Stool softeners (e.g. docusate).
▪ Topical CCB (e.g. nefidipine).
▪ +/- Botox injections.
o Surgical:
▪ Indicated only in chronic fissure refractory to medical therapy.
▪ Done using Prone-Jack knife position.
▪ Lateral internal sphincterotomy (LIS) >> relieve the pressure of
sphincter tone to provides more perfusion & promote healing.

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Ano-rectal abscess (HIGH-YEILD)

• Overview:
o Pathophysiology:
▪ Anal glands found between the internal & external anal sphincters, &
Horse-shoe abscess
communicate by their duct to the anal mucosa as the level of dentate line.
Is a special type of abscess in
which untreated abscess ▪ Infection of these glands (mostly G-ve enteric bacilli) leads to the formation of
(especially ischio-rectal an inter-sphincteric abscess.
abscess) may spread around ▪ Inter-sphincteric abscess can spread into: Note that any abscess above
the anus in a horse-shoe
• Downwards spread >> peri-anal abscess (60%). the peritoneal lining is from
pattern intra-peritoneal source)
• Outwards spread >> ischio-rectal abscess (30%).
• Inwards >> submucosal abscess (5%).
• Upwards spread >> supralevator abscess (below peritoneal lining).
▪ The abscesses may produce a fistula following these communications.

• Clinical features & Diagnosis:

o Symptom:
▪ Severe rectal pain, throbbing, patient cannot sit or
sleep.
▪ Redness without bleeding.
▪ Draining pus or foul-smelling discharge on underwear.
o Signs & examinations:
▪ Spiking fever, patient may be toxic.
▪ Tender swelling (depends on type or location of
abscess):
• Peri-anal (SC, near orifice). DDx of severe anal pain
• Ischiorectal (in ischiorectal fat). (1) Anal abscess (top DDx).
• Submucosal (nothing may be felt (2) Anal fissure (history of constipation).
externally, but very painful DRE). (3) Thrombosed external hemorrhoids
(swelling, +/- bleeding).
o Complications:
▪ Fistula-in-ano (high chance).
▪ Sinus formation (abscess cavity to skin alone).
▪ Deep pelvic infection or sepsis.
o Diagnosis >> diagnosis is made clinically, however, deep abscess may need CT or MRI.

• Management:
o Incision & drainage (all abscess must be drained):
▪ Done under local or general anesthesia.
▪ Cruciate incision to unroof & drain out all the pus (send to culture).
▪ Many doctors use their finger to drain every potential pockets of pus, because
any remained contents can predispose to fistula formation.
▪ Wound is packed deep, but not tightly, daily dressing are arranged, healing is by
tertiary intention.
▪ If incision & drainage is not possible, arrange for surgical drainage.
o IV/oral antibiotics (in selected cases) >> cellulitis, DM, immunocompromised,
prosthetic heart valves.
o Post-op lifestyle changes >> anal hygiene, Sitz bath, stool softeners.

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Anal fistulas (HIGH-YEILD)

• Overview:
o A fistula >> a connection between 2 epithelialize surfaces.
o Anal fistulas >> a connection between anal canal & skin.
o Causes:
▪ Ano-rectal abscess (most common as a complication).
Recurrent fistulas is
associated with CD, ▪ Chronic diseases (CD, TB, anal cancer).
TB, anal cancers ▪ Others (iatrogenic, trauma, radiation).
o Goodsall’s rule )horizontal rule(:
▪ We draw an imaginary line dividing the anal canal in the coronal plane.
▪ Fistulas anterior to this line >> follows a straight course.
▪ Fistulas posterior to this line >> follows a curved course.
o Park’s classification )vertical rule(:
▪ Type I – inter-sphincteric (most common):
• Between anal canal & skin.
• Passes through internal sphincter & into the inter-sphincteric space &
then goes downwards to exit into the skin.
▪ Type II – trans-sphincteric:
• Between anal canal & skin.
• Passes through both the internal & external sphincter.
▪ Type III – supra-sphincteric:
• Between anal canal & skin.
• Passes through internal sphincter, goes upwards above the level of the
pelvic floor muscles & then comes back down through the pelvic floor
muscles & ischio-anal fossa to skin.
▪ Type IV – extra-sphincteric:
• Between rectum & skin.
• Without passing through the anal
sphincter, the fistula goes through
the pelvic floor into the skin.

• Clinical features & Diagnosis:

o Symptoms:
The usual scenario ▪ Recurrent or persistent peri-anal, foul smelling discharge.
A patients of S&S of anal ▪ Peri-anal pain may indicates blocked fistula, when blockage resolve, there is
abscess that drained
spontaneously relieving gush of fluid (soiling of underpants) & resolving of pain.
pain, but now has o Inspection >> you will see the external opening of fistula.
ON/OFF discharge
o Investigations & Diagnosis:
▪ DRE or anoscope >> May reveal internal opening of fistula.
▪ Examination under anesthesia (EUA):
• Done if DRE & anoscope is non-conclusive.
• Don’t probe (don’t examine using hand or instruments).
• Inject distilled H2O2 (hydrogen peroxide) from the external opening &
watch for bubbling in anal canal.
• Other uses methylene blue or other dyes.
▪ MRI >> if both clinical & EUA is non-conclusive.

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• Management (Surgical):
o Fistulotomy:
▪ Represent unroofing of the fistula tract.
▪ Can be used alone for inter-sphincteric fistulas without affecting continence.
o Staged fistulotomy:
▪ Trans-sphincteric fistulas shouldn’t be unroofed because it will result in
incontinence.
▪ A cutting seton suture (non-absorbable) is placed through the fistula & left in
place for 2-3 months.
▪ This elicits a foreign body reaction that slowly allows the suture to be passed
through the sphincter gradually producing an area of fibrosis in the tissue
behind it, maintaining the capacity of continence.
▪ Needs to be intermittently tightened.

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Pilonidal disease (PND) (HIGH-YEILD)

• Overview:
o It’s an inflammatory condition with several opinions as how it occurs.
o It’s not an anal disease, but it presents similarly to anal fistulas.
o Common in middle east.
o Most common location >> cranial edge of the inter-gluteal clef (natal cleft).
o Pathophysiology:
▪ Loose hair from the head or upper back falls into the sacral area.
▪ Because of several factors (i.e. sitting, rolling, sweating, poor hygiene) the hair is
drawn into the skin & SC tissue producing a cyst.
▪ The cyst becomes infected & it can develop into a sinus tract
to produce pus into the skin.

• Clinical features & Diagnosis.

o Symptoms:
▪ Recurrent foul-smelling discharge on underwear.
▪ Local discomfort (pain, swelling, redness).
o Signs & examinations:
▪ A mass is felt near the sinus opening or nearby.
▪ Sinus opening is seen in the high inter-gluteal cleft.
▪ Fluctuant like mass may be palpable.
o Complications >> pilonidal cyst infection or abscess.
o Diagnosis:
▪ Diagnosis is clinical.
▪ Other DDx >> anal fistula, peri-anal abscess, dermoid cyst.

• Management:
o Managemnet is indicated in recurrent PND.
o Excision of sinus & its tract (most cases):
▪ The wound is packed.
▪ Primary intention >> faster healing but higher recurrence.
▪ Secondary/tertiary intention >> slower healing but low recurrence.
o Marsupialization >> laying open the tract & the sinus.
o In cases of large skin deficits >> a reconstructive techniques using flaps is done.
o Antibiotics (in selected cases) >> cellulitis, DM, immunocompromised, prosthetic heart
valves, MRSA infection, endocarditis risk.

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Anal cancer (Nice to know)

• Overview:
o A rare cancer, common in western countries.
o Risk factors:
▪ HPV infection & HIV.
▪ Cigarette smoking.
▪ Multiple sexual partners.
▪ Anal intercourse.
▪ Immunocompromised.
o Types:
▪ Anal margin tumors (can be seen):
• Squamous cell carcinoma (80%).
• Adenocarcinoma.
▪ Anal canal tumors (may be missed).

• Clinical features & Diagnosis:

o Symptoms:
▪ Patients may be asymptomatic (25%).
▪ Anal bleeding (in majority of patients).
▪ Local pain & swelling.
▪ Mucous discharge.
▪ Peri-anal pruritus.
o Signs:
▪ Inspection >> mass may be obvious on gross inspection.
▪ Palpation >> examine the regional LNs (i.e. superficial inguinal LNs).
▪ DRE or anoscope >> inspect anal canal which may hiding a tumor.
o Investigations:
▪ History is very important, if you don’t ask about sexual history you may
misdiagnose this as hemorrhoids.
▪ Diagnosis is confirmed by excision biopsy.
▪ For staging >> CXR, CT abdomen & pelvis, colonoscopy.

• Management:
o Tumors & CIS >> excision of tumor with wide local margins.
o If the tumor is >5cm >> chemotherapy (5-FU, mitomycin C) + radiotherapy.
o Prognosis:
▪ Anal margins tumors have relatively good prognosis.
▪ Anal canal tumors have a poorer diagnosis, especially if melanoma.

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Cases & Questions

• A 31 yo male with history of Crohn disease presents with severe rectal pain that has
progressively increased last night. P/E demonstrates a small, erythematous, well defined,
fluctuant, subcutaneous mass near the anal orficie.
o What is the most likely diagnosis? anorectal abscesses.
o What is the most likely organism? S. Aureus.
o Management? Incision (cruciate incision), drainage, broad spectrum antibiotics.

• A 25 yo female with history of IBS with constipation presents with severe pain with passing
stool. She notes that the pain is so severe and is afraid to have a bowel movement. The stools
are hard and covered with blood streaks.
o What is the most likely diagnosis? Anal fissure.
o What is anal fissure? Painful tears in the anal mucosa below the dentate line induced by
constipation or excessive diarrhea. Patients will present with painful defecation, bright
red PR bleeding, laceration on 6 and 12 o’clock position. Patients with chronic anal
fissure will have hypertrophy of the surrounding skin and sentinel pile or skin tags.
o What are the options for treating anal fissure?
▪ Sitz bath.
▪ Topical nitroglycerin or CCB or injection of botulinum toxin into the anal
sphincter.
▪ Fiber supplements.
▪ Bulking agents.
▪ Lateral internal sphincterotomy or dilation for chronic case.

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Breast
Diseases

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Anatomy of breast (Review)

• Overview:
o The breast is considered as modified sweats glands.
o Location:
▪ Extends from the lateral border of sternum to the anterior axillary line & from
2nd to the 6th ribs.
▪ 2/3 of the breast lies on pectoralis major fascia, while 1/3 on serratus anterior
muscle fascia.
o Retromammary space >> Space that lies in between the breast tissues & pectoralis
muscle fascia. It allows the breast to move somewhat freely over the pectoralis muscle.
o Breast development (milk line):
▪ Breast is developed on this line.
▪ The line extends from the axilla across the chest,
abdomen & into the perineum & groin.
▪ Any extra breast (polymastia) or nipples (polythelia)
can arise along this line.

• Breast tissues:
o Glandular tissue )males don’t have it(:
▪ Prolactin stimulates milk production in alveoli.
▪ Oxytocin stimulate splitting out of the milk (stimulates myoepithelial cells to
contract the alveoli for milk let down).
o Fibrous tissue (Decrease as one ages, mammographs more difficult to interpret) :
▪ The breast shape is supported by fibrous tissues condensations that stretch
from the deep fascia to the superficial dermal fascia (Cooper’s ligaments or
suspensory ligaments of the breast).
▪ When the cancer invade these structures, they get fibrosed further, resulting in
classic signs of dimpling & nipple retraction
▪ The breast should be nearly symmetrical in mature adults, asymmetrical breasts
in adolescence may be considered normal.
▪ Note that the breast shape is different in individuals, symmetry is the key.
o Adipose tissue (increase as one ages, mammographs are more easy to interpret):
▪ The most abundant of all breast tissues.
▪ Found between fibrous & glandular tissues.

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• Quadrants of the breast:

o Upper outer quadrant:
▪ Contains the tail of Spence (lateral most extension of the breast).
▪ 50% of breast masses occur here (because it contains most of glandular tissue).
o Upper inner quadrant >> 10% of breast masses found here.
o Lower outer quadrant >> 10% of breast masses found here.
o Lower inner quadrant >> 10% of breast masses found here.
o Subareolar >> it not considered as quadrant, but 20% of masses are found to be
subareolar.

• Breast ductal system:

o A group of alveoli forms a breast lobule (total 15-20 lobules), each 3-5 lobules form one
lobe.
o Each lobes drains into a lactiferous duct that reach underneath the nipple as a
lactiferous sinus (this area is known as the nipple areolar complex).
o Each lactiferous sinus opens into the nipple as pores (there are up to 20).
o Nipple areolar complex (NAC):
▪ Grossly, the nipple can be variable in its condition,
Remember!! generally, we assume it to be at the level of 5th intercostal
(1) Estrogen promotes ductal space.
development.
(2) Progesterone promotes
▪ The areola is hyper-pigmented & contains Montgomery’s
lobular development. tubercles.
▪ Underneath the areola, a disc of tissue is felt (represents a
portion of glandular tissue).
▪ The center of areola is raised to form the nipple, however,
some individuals have retracted nipples (thus, you must
ask about any new retractions).

• Breast vasculature:
o Arterial blood supply:
▪ Internal thoracic artery (branch from subclavian artery).
▪ Lateral thoracic artery (branch from axillary artery).
▪ Posterior & anterior intercostal arteries (lateral & perforating branches).
o Venous drainage:
▪ Veins correspond to the arterial supply.
▪ Majority of breast veins drains into axillary veins.
▪ Baston’s vertebral venous plexus is connected with the venous drainage of the
breast (important route for metastasis of breast cancer to the spine).

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o Lymphatic drainage:
▪ Axillary LNs (receive 97% of breast drainage):
• LNs Groups >> anterior (pectoralis), posterior (subcapulatis), lateral
(humeral), central, apical.
• Anterior, posterior, & lateral groups drains into central group, then to
the apical group.
• Apical group drains into:
o (1) Supra & infra-clavicular LNs.
o (2) Right lymphatic duct or the thoracic duct.
o (3) +/- Cervical LNs.
• Note that breast lymphatic may drain to the contralateral axillary LNs
too.
▪ Internal thoracic LNs (Parasternal LNs) >> bad sign in TNM staging (will be N3).
▪ Rotter’s LNs >> lies in between the pectoralis major & minor muscles.
▪ Subareolar lymphatic plexus >> drains the nipple, areola, some lobules & then
into the axillary LNs.
o Surgical levels of axillary LNs:
▪ Axillary LNs are classified from lateral to medial, in relation to the pectoralis
minor muscle.
▪ I (lateral) >> lateral border of pectoralis minor (anterior, posterior, lateral LNs).
▪ II (deep) >> deep to the pectoralis minor muscle (central & apical LNs).
▪ III (medial) >> medial border of pectoralis minor muscle (supra & infra-
clavicular, internal thoracic LNs).

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History & Breast Examinations

(important for clinical exam)

• History (highlighted):
o Chief complaint:
▪ Breast pain.
▪ Mass or swelling.
▪ Nipple discharge.
▪ Skin changes (dimpling, inverting nipple, eczematous nipple, erythema,
ulceration).
▪ Size changes (deviation, asymmetry).
o History of present illness (all symptoms of breast diseases must be evaluated):
▪ Pain >> SOCRATES, relation of pain to menstrual cycle.
▪ Lump questions:
• When did you first notice the mass?
• What did make you noticing it (swelling or pain)?
• Progression of the mass (rapid enlargement may suggest cancer).
• Painful or not.
• Any other swelling?
▪ Nipple discharge >> unilateral or bilateral, color, amount.
▪ Skin changes >> ask about erythema, ulcerations.
▪ Constitutional symptoms >> fever, weight loss.
▪ Symptoms of metastasis >> bone pain, SOB, confusion, back pain.
▪ First time or happened before, other breast is fine?
▪ History of trauma or recent breast feeding.
▪ Does the patient do breast self examination or have done recent breast tests.
o Identify all risk factors of breast cancer:
▪ Past history:
• Medical illnesses (HTN, DM, SCD).
• Previous history of breast diseases & other cancers.
• Previous breast tests.
• Medications history (OCPs & HRT).
▪ Menstruated & obstetric history:
• Age of menarche (& menopause if applicable).
• Current cycle status.
• Age of first pregnancy.
• Breastfeeding.
▪ Family history >> History of Breast cancer (especially 1st degree) if yes ask about
(1) who is the relative, (2) when she develop it, (3) if there is a history any other
hormonal dependent cancers (e.g. ovarian cancer).
▪ Social history >> smoking.
o Ideally, we must ask about fears, concerns & expectations >> breast surgery may have
a tremendous effects on a women’s life.

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• Physical examinations of the breast:

o Initial steps:
▪ Introduction, ask for permission, ask for chaperone.
▪ Wash hand, close the curtains.
▪ +/- Do general exam (vitals & inspection).
o Exposure & position:
▪ Expose both breasts down to the umbilicus.
▪ Initial position >> seated on edge of the bed with hands on her lap.
o Inspection:
▪ Breast shape & symmetry >> assess symmetry & breast contour.
▪ Nipple & areola >> is it at same levels, inverted or everted, assess any skin
changes (eczematous, ulcerated), any discharges.
Normally, the nipples are ▪ Skin changes:
pointing superiorly & laterally.
• Assess any erythema, obvious swelling, dimpling, ulceration.
Don’t forget to check for • Infra-mammary folds should ideally inspected.
accessory nipples. • Raised edges ulcers suggest malignancy.
▪ Inspection in specific positions:
• Hands behind the head or raising arms.
• Hands on hip (to contract pectoralis major muscle to note fixation to
muscle).
• Leaning forward (assess the breast as they are pendulous).
o Palpation:
▪ Before starting palpation:
Breast Examination • Position >> patient is supine.
[Link] • Ask for any pain & leave that site for the end.
MhCE
• Use one hand to support the breast & the other to palpate.
• Assess the normal breast first.
▪ Palpate with the tips of your fingers in a circular pattern, going clockwise from
areola outwards to the tail of spence & axilla (don’t keep removing your hand
because you might miss a spot).
▪ Go back & palpate the nipple areolar complex.
▪ Ask the patient to compress her nipple to assess any discharge (try to figure out
which duct is spilling).
▪ Do the same for the other breast.
▪ Go back to assess any swelling or masses.
▪ Comments on a mass:
• Site (which quadrant or use clock pattern).
If a mass is found, ideally • Size (estimate it, e.g. around 3cm).
metastasis examination
• Shape (circular, irregular).
should be done also such
as liver & bone palpation + • Margins & surface (smooth, nodular).
lung auscultation • Mobility and fixation.
• Consistency (hard as forehead, firm as nose, soft as ear lobule).
It’s very painful to the • Tenderness.
patient & doesn’t really • Overlying skin changes (dimpling, ulcerations, peau d’orange).
help in examinations • Special characters (fluctuations).

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• Approach to a breast mass:

o Triple assessment:
▪ History & examinations.
▪ Imaging investigations (US & mammogram).
▪ Histological investigations (biopsy).

o Initial imaging:
▪ Women older than 30ys >> mammogram > US.
▪ Women younger than 30ys >> US > mammogram.
▪ Why? Because there is far more fibrous tissue in younger breasts which distorts
the mammogram (false +ve).
▪ In general, mammograms are still the best tool got screening for breast cancer.
▪ Mammograms must be done before biopsies (except FNAB), because biopsies
may alter mammogram findings.
▪ Important mammogram findings:
• Mass that distort the normal breast architecture.
• Stellate mass.
• Micro-calcifications (could be benign or malignant).
o Types of Biopsy:
▪ Closed biopsy:
• Fine needle aspiration cytology (FNAB).
• Truecut core needle biopsy.
▪ Open (surgical) biopsy with frozen section:
• Incisional biopsy >> take part from the mass.
• Excisional biopsy:
o Take the whole thing.
o Done intra-op (we send frozen section to histopathology & wait
for results to proceeds to further operative management).

Indications for tissue biopsy

(1) Highly suspicious mass on examinations (solid mass, The biopsy will give us the following
irregular, immobile, skin changes). information:
(2) Highly suspicious mass in US & mammogram. (1) Cytology (Benign or malignant).
(3) Bloody aspirate or nipple discharge. (2) Grading (poor or well differentiated).
(4) Residual mass following aspiration. (3) Receptors (ER, PR, HER2)
(5) Recurring clear cystic fluid.
(6) Persistent breast abnormalities.
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• DDx of breast mass:

o Young age:
▪ Fibroadenoma (smooth, circular, mobile).
▪ Fibrocystic changes (tender, bilateral & fluctuate with menstrual cycle).
▪ Breast abscess or chronic granulomatous mastitis.
▪ Fat necrosis.
▪ Mammary duct ectesia.
▪ Malignancy (very rare).
o Old age >> breast cancer is number one DDx.

• DDx of nipple discharge:

o Bloody discharge:
▪ Intraductal papilloma.
▪ Fibrocystic changes.
▪ Paget’s disease or inflammatory breast cancer.
▪ Intraductal carcinoma.
o Yellowish or greenish discharge:
▪ Breast abscess.
▪ Fibrocystic changes.
▪ Mammary duct ectesia.
▪ Galactocele.
▪ Chronic granulomatous mastitis.
o Milky discharge:
▪ Physiological (bilateral, occur due pregnancy & lactation, stress, excessive nipple
stimulation).
▪ Pituitary prolactinoma.
▪ Hypothyroidism (rare).

• DDx of breast pain:

o Fibrocystic disease. Mondor’s disease is a superficial
o Mastitis. thrombophlebitis of lateral thoracic vein.
o Breast abscess. The patient will present with acute pain in
the axilla & superior aspect of lateral
o Fat necrosis. breast. Diagnosis is confirmed with US
o Inflammatory or advanced breast cancer.
o Mondor’s disease.

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Inflammatory Breast Diseases (HIGH-YIELD)

• Acute mastitis:
o Causes >> S. aureus > streptococcus.
o Clinical features:
▪ Typical patient is a breastfeeding women (improper breast feeding technique
result in nipple cracking, thus, invasion of skin & baby mouth bacteria).
▪ Symptoms >> unilateral breast pain, swelling, localised tenderness + fever.
▪ Signs >> unilateral breast erythema, swelling, warmth.
▪ Complications >> breast abscess.
o Diagnosis >> diagnosis is done clinical, other investigations may be ordered to R/O other
conditions.
o Management:
▪ (1) Patient education:
Periductal mastitis is a • Proper breastfeeding technique.
form of mastitis that • Continue breastfeeding using the unaffected side.
occur due to vitamin A
deficiency which results
• Decompress affected breast by using breast pump.
in squamous cells ▪ (2) Oral Analgesia >> paracetamol.
metaplasia leading to ▪ (3) Oral antibiotics >> amoxicillin/clavulanate OR 1st generation cephalosporins
blockage of lactiferous (cephalexin) OR ciprofloxacin.
ducts. It’s common in
▪ (4) Follow-up >> important to R/O abscess, possible inflammatory cancer
smokers.
(especially in non-lactating or older women).

• Breast abscess:
o A known complications of acute mastitis or mammary duct ectasia.
o Clinical features:
▪ Patients usually presents with a similar picture of acute mastitis, but most of
them with have a previous history of mastitis that is refractory to treatment.
▪ Symptoms >> Throbbing breast pain + purulent nipple discharge + fever.
▪ Signs >> localised area of breast inflammation, fluctuant tender breast mass
(don’t do fluctuation exam because it’s very painful).
o Investigations >> CBC (assess leukocytosis) + US.
o Management:
▪ (1) Incision & drainage OR US-guided percutaneous drainage (send pus for
culture & sensitivity testing).
▪ (2) Empirical oral antibiotics for 14 days & change according to culture &
sensitivity results.
▪ Followup >> R/O inflammatory breast cancer (especially in non-lactating or
older women).

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• Fat necrosis:
o Occur after trauma of the breast, however, 50% of patients don’t remember history of
trauma (because it’s trivial).
o Some clue may lead you to history of trauma, e.g. if the patient is gymnast, boxer or
they have a minor car accident.
o Clinical features:
▪ Symptoms >> painful breast lump.
▪ Signs >> irregular, firm breast mass, +/- tenderness.
o Investigations:
▪ Mammogram >> show calcification (cannot be distinguished from other DDx).
▪ Biopsy >> partially necrotic adipose tissues with foamy macrophages & multi-
nucleated Giant cells + lymphocytic infiltration.
o Management >> excision (usually done anyway). Usually this mass will be
observed or treated & we
• Mammary duct ectasia: won’t know it’s a fat necrosis
o A dilated & inflamed duct due to obstruction, usually occur in the until after biopsy results
distal ducts near the nipple.
o Clinical features:
▪ Non-cyclic, painful, subareolar mass.
▪ Sticky yellowish nipple discharge.
▪ Affected duct must be identified on physical examination.
o Investigations >> mammogram will show dilated duct.
o Management >> surgical excision of affected duct only.

• Gynecomastia:
o Defined as enlarged male breast or girls before age of puberty.
o Causes:
▪ Physiological (puberty, old age, neonates).
▪ Iatrogenic (spironolactone, antipsychotics).
▪ Liver failure (high estrogen).
▪ Prolactinoma.
o Presentation >> enlargement of breast, subareolar disc of tissue.
o Management:
▪ Physiological >> reassurance or cosmetic surgery (subcutaneous mastectomy).
▪ Pathological >> treat underlying cause if possible.

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Benign Breast Conditions (HIGH-YEILD)

• Fibroadenoma:
o A benign breast tumor in which there is a proliferation of the fibrous stroma & duct
epithelium (considered as Biphasic tumor).
o It’s a well-encapsulated tumor & estrogen sensitive (size & tenderness may increase
during pregnancy & lactation).
o It’s the most common breast lesion in adolescence & young females (15-30ys).
o Clinical features:
▪ Symptoms >> most patients are asymptomatic & the lump is found during
Juvenile giant fibroadenoma screening (e.g. Breast Self exam).
(1) A fast growing tumor that
distorts the normal
▪ Signs:
development of breast. • Smooth, firm, well circumscribed, round, very mobile breast mass.
(2) Occur mostly in teenagers. • It could be solitary or multiple.
(3) Must be excised surgically.
• Usually described as mouse of the breast (very mobile).
▪ Note that fibroadenoma has a very low chance for becoming malignant.
o Investigations:
▪ Imaging >> US.
▪ Mammogram & FNAB >> done only is the lump is suspicious or age >40.
o Management:
▪ Close observation >> if young (<30ys) & <2cm, it may regress with it own.
▪ Surgical excision:
• Done if patient is old or the mass is big (>3cm), or if symptomatic.
• In general, surgical excision is preferred to confirm the pathological
diagnosis (however, the presence of it isn’t harmful).

• Phyllodes tumor (Cystosarcoma Phyllodes):

o A biphasic tumor in which there is proliferation of breast parenchyma & epithelial
tissue.
o Types:
▪ Benign.
▪ Intermediate (means that there is local destruction of healthy tissues, but with
no metastasis).
▪ Malignant (<10%).
o Clinical features:
▪ Presents at 30s-40s (much later than fibroadenoma).
▪ Symptoms >> breast lump (large or fast growing).
▪ Signs >> large, freely mobile breast mass that distort the breast shape.
▪ There is a risk of developing cancer compared to fibroadenoma.
o Investigations:
▪ US & mammogram >> depending on patient age.
▪ Core biopsy >> diagnostic method of choice.
o Management:
▪ Surgical wide local excision with >1cm margins (can reoccur more aggressively).
▪ If very large >> simple mastectomy may be offered.
▪ LNs dissection is not needed because metastasis occur by blood (lung is the
most common site).

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• Fibrocystic changes:
Fibrocystic changes
o A common condition that is developed clinically in only 10% of (1) Adenosis.
patients, however, majority of women have some form of FCC. (2) Epitheliosis (atypical
o It involves changes in fibrous tissue of the breast + cyst formation. epithelial hyperplasia).
o Clinical features: (3) Fibrosis (sclerosing
adenosis resembling cancer).
▪ Occur usually between 30s & 50s (pre-menopausal women).
(4) Cyst formation.
▪ Symptoms:
• Pre-menstrual breast pain (hallmark).
• Multiple tender lumps that is associated with menstrual cycle.
• +/- nipple discharge that is clear, yellow, or even brown/straw in color.
▪ Signs:
• Multiple, tender breast nodularities.
• Could be bilateral or unilateral.
• Most common location is UOQ.
▪ Generally speaking, FCC is not associated with increase risk of breast cancer
(except in sclerosing adenosis).
o Investigations:
▪ US & mammogram >> R/O malignancy.
▪ FNAB of dominant cyst (if possible):
• Straw-colored or green fluid is typical.
• If the biopsy show atypia or lobular/ductal hyperplasia, there is a
possibility of developing cancer (thus, must be excised).
o Management:
▪ If patient is <30, no bloody aspirate, no residual mass, surveillance:
• Patient education about breast self exam.
• Avoidance of caffeine.
• Pain control (NSAIDs, Vitamin E, Danazol or OCPs may have some role).
• Follow-up visits.
▪ If bloody aspirate, recurrence or suspicious cases >> open excisional biopsy.

• Intra-ductal papilloma:
o Small, benign fibro-epithelial papillary tumor within the lactiferous ducts (subareolar
duct epithelial cells).
o It’s the most common cause of serous or bloody discharge from female breast (other
important DDx is papillary carcinoma).
o Clinical features:
▪ Symptoms >> bloody or blood-stained nipple discharge.
▪ Signs >> Subareolar breast mass.
▪ Patients has increased risk of developing breast cancer.
o Investigations:
▪ US & mammogram >> not very useful (small duct are not visible).
▪ Galactogram >> most specific imaging method.
▪ Microdochectomy >> excision of affected lactiferous duct (diagnostic &
therapeutic – biopsy is needed to R/O papillary carcinoma).
o Management >> excision of the affected duct.

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Pre-Malignant Diseases

• Ductal carcinoma in situ (DCIS):

o Occur due proliferation of inner layer of ductal epithelial cells.
o They spread along the duct, but not beyond the basement membrane.
o Occur in old age >50s, 50% of patients are post-menopausal.
o Can occur also in males (Compared to LCIS, because males don’t have glands).
o Clinical features:
▪ Almost always asymptomatic, discovered incidentally on mammogram
screening.
▪ Some patients may present with palpable mass.
o Investigations:
▪ Mammogram >> micro-calcifications.
▪ Biopsy >> malignant cells within the ducts, but not invading the basement
membrane.
▪ Interpretation:
• DCIS is considered as the anatomic precursor of invasive ductal
carcinoma.
For 5 years, shown to lower • IDC typically will occur in the ipsilateral breast & same quadrant (vs
risk of breast cancer from LCIS).
development (however, it
▪ Management (surgical removal):
increase the risk of
potentially developing • lumpectomy with 1cm margin + radiotherapy.
endometrial cancer & • If diffuse or contraindication to radiotherapy >> simple mastectomy.
thrombosis) • Estrogen-receptor +ve >> tamoxifen.

• Lobular carcinoma in situ (LCIS):

o Lobule cells proliferation without invading the ducts (acinar cells).
o Most common in pre-menopausal females.
o It never occur in males.
o Considered as a marker of impending cancer:
▪ LCIS it self is not precancerous (rarely cross the basement membrane to form
ILC).
▪ It’s usually found bilateral (50% will found LCIS in other breast).
▪ Both breasts is at risk (30% in 20ys to come).
▪ 75% will develop IDC.
o Clinical features >> most patients are asymptomatic & almost never present as a breast
mass.
o Investigations >> it’s not detectable by mammogram (don’t have calcifications) but it
recognized by US & almost found as an incidental findings on biopsy.
o Management:
▪ High risk patients are offered prophylactic bilateral mastectomy.
▪ Intensive close follow up is done.
▪ If estrogen-receptor +ve >> tamoxifen can help reduce the risk of cancer.

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Breast Cancer (HIGH-YIELD)

• Overview:
o Breast cancer is defined as uncontrolled growth of epithelial cells in the breast.
o Epidemiology:
▪ Breast cancer the most common cancer in women & the most 2nd cause of
Men have 1% risk for cancer death in women (after lung cancer).
breast cancer, it
mostly will be ER +ve ▪ 1 in 8 women will develop breast cancer.
▪ 75% have no risk factors.
o Pathophysiology:
▪ Estrogen & progesterone promotes breast cells to grow & divide, thus exposure
Genes that are related to to them for a long time increase the risk of breast cancer.
breast cancer
(1) BRCA-1 & 2. ▪ Also, breast cancer is associated with some mutations:
(2) K-167. • Tumor suppressor genes (e.g. BRCA1, BRCA2, TP53) which prevent cell
(3) B10 & B51. division.
Note that only 5-10% of all • ERBB2 gene mutation increases HER2 which promotes cell division.
breast cancer are associated
with an inherited mutations. • +ve estrogen-receptor (ER) or progesterone-receptors (PR) which
promotes cancer cells to divide faster.
o Risk factors:
▪ Gender & age (female >50ys).
Pregnancy & lactation ▪ Nulliparity, late first pregnancy >30ys, lack of breast feeding.
has a protective effect ▪ +ve Family history (1st degree relative).
against Breast Cancer ▪ Early menarche <11ys & late menopause >54ys.
▪ Personal history (breast cancer, breast procedures, LCIS, DICS, atypia).
▪ Hormonal replacement therapy (more estrogen).
▪ Exposure to radiations.
▪ Lifestyle (obesity, HTN, DM, smoking).

• Screening of Breast cancer:

o Breast self examination proper technique:
▪ Starts at age of 20 and done every month.
▪ Best time is a week after menstruation ends or anytime in post-menopausal.
Can screen mainly for benign ▪ (1) Stand in front of a mirror and notice any changes (skin, asymmetry, nipple).
breast diseases rather than
▪ (2) Lie down & use one hand to examine the breast on the opposite side
cancer (because most cancer
patient are asymptomatic) (palpate all quadrants of the breast).
▪ (3) Do the same for the other breast.
o Clinical breast exam:
▪ Offered to patients >40ys, done annually.
▪ Goal >> identify any risk of cancer before the cancer develops clinically.
▪ When cancers are felt as masses on clinical exam, it’s already too late.
o Mammography (the best we got):
▪ Low radiation dose, that offered to patients >40ys.
▪ 40-49ys >> annually.
Mammography view ▪ 50-74ys >> every 2 years.
CC = Cranicaudal.
MLO = Mediolateral oblique
▪ Young patients (<40ys) with +ve family history of breast cancer should be
screened every 5-ys earlier than the age when the relative develop it.

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• Histological types of Breast Cancer:

o Invasive ductal carcinoma (IDC):
▪ Most common type (80%).
▪ Occur in peri- & post-menopausal women.
▪ Subtypes >> Comedo, scirrhous, medullary, papillary, tubular.
▪ Metastasis to >> bone (most common), lung, liver, brain, adrenals.
DDx of Paget o Invasive lobular carcinoma (ILC):
disease ▪ 10% of breast cancers.
(1) Eczema. ▪ Has a high likelihood of being bilateral.
(2) Allergic reaction.
(3) Mastitis.
▪ Metastasis >> generally LNs, serosal surface, meninges.

• Clinical types (rare, not very common):

o Paget’s disease of the nipple:
▪ Usually secondary to underlying IDC.
▪ The cancer climb up the duct & into the areola, resulting
in a weeping NAC.
▪ Presentation:
• Pruritic, tender, eczematous (weeping) nipple.
• NAC can be completely destroyed.
• +/- subareolar mass.
▪ Investigations >> skin punch biopsy show Paget cells.
o Inflammatory carcinoma (rare 2-3%):
▪ Rare, but aggressive (most lethal form of breast cancer).
▪ 75% of patients have metastasis .
▪ Occur due to invasion of breast subcutaneous lymphatic system resulting in
breast edema while the sebaceous glands remains pitted (peau d’orange).
▪ Presentation:
• Classic history of patient with mastitis unresponsive to antibiotics.
• On examination (no lump):
o Inflammation signs (diffuse erythema, swelling, tenderness,
We do punch biopsy to
warmth).
involve the skin & the
subcutaneous tissue o Peau d’organe.
o Nipple retraction.
o Axillary lymphadenopathy in advanced disease.
▪ Investigations >> punch biopsy will show subdermal lymphatic blockage.
▪ Management (discussed later) >> it’s the one of the breast cancer that we use
neoadjuvant chemotherapy.

• Clinical features of Breast cancer:

o Symptoms:
▪ Asymptomatic until metastasis.
Locations of Breast cancer ▪ Painless Breast mass (most common presentation).
50% UOQ. ▪ Nipple discharge, retraction, or eczema.
20% subareolar. ▪ Skin dimpling or ulceration.
10% UIQ,10% LOQ, 10% LIQ.
▪ Inflammatory features (e.g. peau d’orange).
▪ Symptoms of metastasis >> bone pain, fractures, liver disease features.

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o Signs:
▪ Asymmetrical breast shape & contour.
▪ Palpable breast mass (non-tender, hard or firm, irregular margins, fixed).
▪ Nipple discharge (any color, but serous) or nipple retraction.
▪ Skin changes (dimpling, ulcerations inflammation signs).
▪ Lymphadenopathy (axillary, supra & infra-clavicular, cervical, contralateral
axillary).

• Approach to a patients with suspected breast cancer: Tumor markers of Breast cancer
o Steps of assessing a suspected breast cancer: (non-specific) >> CA-125 & CA-15-3
▪ (1) Triple assessment:
Cytology report following • US (<30ys) >> differentiate solid & cystic lumps.
FNAB or Core biopsy
C1 = unsatisfactory.
• Bilateral mammography (>30ys) >> Radical star/stellate, spinculated
C2 = benign. opacity, micro-calcifications.
C3 = atypical. • Breast-MRI >> useful in patients with breast prosthesis or if
C4 = suspicious.
C5 = malignant. mammogram is not useful.
(Note, if C4 do Core biopsy • Biopsy:
if FNAB, or just repeat it if
already done)
o Fine needle aspiration (assess cytology).
o Core biopsy (assess histology, ER, PR, & HER2).
▪ (2) If the 3 component is suggestive of cancer >> sufficient to proceed to
staging investigations.
▪ (3) If the 3 are not sufficient >> do open biopsy (excisional biopsy).
o Pre-Op staging workup:
▪ Baseline >> CBC, RFTs.
Breast cancer bone ▪ To assess bone metastasis:
metastasis can be • Bone profile; Ca, PO4, Mg, ALP (assess bone metastasis).
osteolytic or osteoblastic
• Bone scan or bone MRI.
▪ To assess lung metastasis >> chest X-ray or CT.
▪ To assess liver metastasis >> LFTs, abdominal CT.
o Intra-Op staging:
▪ Frozen section excisional biopsy:
• Done initially if closed biopsies were not sufficient.
• Sent immediately for histopathology analysis for histology, ER, PR,
HER2/NEU.
▪ Sentinel LN biopsy (know the concept):
• Done if no palpable LNs were detected on examinations or seen on
imaging.
• Goal is to find the primary draining LN, excise it, & send it for pathology
to assess invasion.
• Process >> Blue dye is injected or technetium labeled sulfur colloid into
lymphatics. The first LNs to drains to is the Sentinel node. Then we
excise that node & send it for pathology.
• If sentinel node is +ve >> proceed with axillary dissection.
• If sentinel node is -ve >> no need for axillary dissection.

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• Breast Cancer Staging (by CT abdomen & chest + bone scan):

o TNM Staging >> the nodal component is the most important for prognosis in addition to
the number of LNs.
o T = Tumor size:
▪ Tis >> in situ.
▪ T1 >> <2cm
▪ T2 >> 2-5cm.
▪ T3 >> >5cm.
▪ T4 >> any size + skin involvement (ulceration, nodules, peau d’orange) OR fixed
to muscle.
o N = nodal involvement:
▪ N0 >> none.
▪ N1 >> ipsilateral I & II axillary LNs + Mobile.
▪ N2 >> ipsilateral I & II + Fixed.
▪ N3 >> far LNs (supra or infra-clavicular, parasternal, inferior mesenteric LNs).
▪ Remember that if LNs are not obvious clinically or radiologically, do Sentinel
node biopsy.
o M = Metastasis:
▪ M0 >> no distant metastasis.
▪ M1 >> with distant metastasis (radiologically, clinically, or histologically).
o Numerical staging (not really needed ☺ to memorize):
▪ Stage I >> T1, N0, M0 (tumor is <2m no LNs or distant metastasis).
▪ Stage II-A >> T1 + N1 OR T2 + N0.
▪ Stage II-B >> T2 + N1 OR T3 + N0.
▪ Stage III-A >> T3 + N1 OR any size + N2 (fixed node).
▪ Stage III-B >> T4 (fixed to skin or muscle).
▪ Stage III-C >> N3 (went to far LNs).
▪ Stage IV >> M1 (anything, but with distant metastasis).
o Examples:
▪ A patient with 4cm mass, 2 palpable mobile axillary LNs, no evidence of skin
involvement or metastasis.
• 4cm = T2.
• Mobile LNs = N1.
• No metastasis = M0.
• Stage II-B.
▪ A patient with 5.2cm mass, fixed to the muscle, 1 fixed ipsilateral axillary LN, no
metastasis.
• 5.2cm, fixed to the muscle = T4.
• Fixed node = N2.
• No metastasis = M0.
• Stage III-B.

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• Principles of management:
o Management methods:
▪ Surgical (e.g. modified radical mastectomy, lumpectomy).
▪ Radiotherapy.
▪ Chemotherapy (e.g. CMF, CAF).
▪ Hormonal therapy (e.g. tamoxifen).
▪ Targeted receptor therapy (e.g. trastuzimab/Herceptin).
o Surgical treatment:
▪ Done in almost all cases (usually surgical management +/- reconstruction is
offered for cosmetic reasons).
▪ Breast conservative surgery (lumpectomy):
• At the risk of recurrence, eligible patients (stage I & II) are given the
option to conserve their breast.
• Lumpectomy + post-op radiotherapy + chemotherapy.
• LNs dissection is done only if sentinel node biopsy is +ve.
• Contraindications:
o Small breast (no advantage of lumpectomy).
o Diffuse disease (extensive DCIS).
o Pregnancy (we cannot do radiotherapy).
o Previous exposure radiation.
▪ Modified Radical mastectomy:
• Removal of all breast tissue + NAC.
• Level I & II axillary dissection, then axillary drain is inserted to drain
lymph because of lymphedema risk (kept for 14 days or until <30cc of
drainage).
prolonged lymphedema increase • Complications:
the risk of developing infection & o Cosmetic.
malignancy (Stewart-Treves o Lymphedema of arm.
syndrome) o Long thoracic nerve injury (winged scapula).
o Infection, skin graft necrosis, hematoma, seroma.
• Breast reconstruction:
o Can be done during initial surgery or later.
o Implants >> autologous or prosthetics (saline or silicone).
o TRAM flap >> transverse rectus abdominis myocutaneous flap.
o Latissimus dorsi flap.
o Chemotherapy:
▪ Can be done neoadjuvant or adjuvant.
▪ CMF >> cyclophosphamide, methotrexate, 5-FU.
▪ CAF >> cyclophosphamide, adriamycin, 5-FU.
▪ Indications:
• +ve LNs. High risk patients
(1) >2cm.
• Metastatic cancer. (2) ER/PR -ve.
• High risk patients. (3) Lymphatic or vascular invasion.
• Inflammatory breast cancer. (4) High nuclear grade.
▪ Complications (most important): (5) HER2/NEU +ve.
• BM suppression.
• Risk of developing non-solid tumors (leukemias, lymphoma).

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Tamoxifen is o Hormonal therapy (ER/PR +ve):

contraindicated in
pregnancy (category
▪ Aromatase inhibitors (aanastrazole) >> in postmenopausal women.
D), thus patients must ▪ Selective estrogen receptor modulators (SERM):
be on contraception • Tamoxifen (-ve breast, +ve bone, +ve endometrium). ADRs of tamoxifen (high
(which type??) • Raloxifen (-ve breast, +ve bone, -ve endometrium). estrogen)
o Targeted therapy (HER2/NEU +ve): (1) Endometrial cancer risk
(screen while therapy).
▪ Trastuzamab (Herceptin) >> main ADRs is heart failure.
(2) DVTs/PE (thrombosis
risk).
• Management decisions: (3) Hot flashes, diaphoresis,
o Stage I & II (early invasive): mood swings.
▪ Lumpectomy + post-op radiotherapy + chemotherapy. (4) nausea & vomiting.
▪ LNs dissection is done only if sentinel node biopsy is +ve.
▪ +/- tamoxifin (if ER/PR +ve) & trastuzimab (if HER2 +ve).
o Stage III (locally advanced): Prognosis
5-10% local recurrence
▪ Modified radical mastectomy + axillary LNs dissection (with drain). within 10 years.
▪ Radiotherapy or chemotherapy. 5-year survival rate:
▪ +/- tamoxifin (if ER/PR +ve) & trastuzimab (if HER2/NEU +ve). (1) Stage I >> 95%.
o Stage IV (metastatic): (2) Stage II >> 75%
(3) Stage III >> 50%.
▪ Systemic & palliative care.
(4) Stage IV >> 18%.
▪ Poor prognosis (median survival is 2ys).
▪ May need mastectomy for palliation (severe pain & discharge).
o Inflammatory breast cancer >> Neoadjuvant chemotherapy + palliative care & surgery.
o Pregnant women:
▪ Radiotherapy is contraindicated during pregnancy.
▪ If 3rd trimester >> do lumpectomy now, then radiotherapy postpartum.
▪ If 2nd trimester >> modified radical mastectomy.

• Complications of axillary dissection: Male Breast Cancer

IDC (never ILC) that is usually diagnosed later
o (1) Lymphedema. because it usually not suspected (tumor
o Nerves injury: already invade chest wall.
▪ (2) Long thoracic nerve: Risk factors >> Klinefelter syndrome, Estrogen
Arm lymphedema • Source >> C5, C6, C7. therapy, previous radiation exposure.
• Supplies serratus anterior.
Causes & DDx:
(1) Iatrogenic (post axillary • It’s the most common of injury in breast surgery.
LNs dissection). • Injury >> winging of scapula (ask the patient
(2) Massive lymphatic push the wall with arm extended).
channel obstruction. ▪ (3) Thoracodorsal nerve:
(3) Lymphoma.
(4) Filariasis.
• Source >> posterior cord of brachial plexus.
• Runs within the subscapular artery.
To decrease lymphedema • Supplies latissimus dorsi.
risk after LNs dissection: • Injury >> can’t push self up from sitting
(1) Don’t use the arm too
much. position.
(2) No blood collection or ▪ (4) Medial & lateral pectoral nerves >> Supplies
BP measurement of the pectoralis minor & major.
affected arm.

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Neck &
Thyroid

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Anatomy of the Neck (Review)

• Neck triangles:
o The neck is divided into 2 large triangles by the sternocleidomastoid (SCM) muscle, they
are:
▪ Anterior triangle:
• Carotid triangle.
• Submandibular (digastric) triangle.
• Submental triangle.
• Muscular triangle.
▪ Posterior triangle:
• Occipital triangle.
• Supraclavicular (subclavian) triangle.
o Anterior triangle:
▪ Bounded by the SCM posteriorly, the mandible superiorly, & the midline of the
neck anteriorly.
▪ Carotid triangle:
• Lies below the digastric muscle & above the omohyoid muscle.
• Contains (1) Carotid sheath (carotid artery, internal jugular vein, &
vagus nerve), (2) Ansa cervicalis (groups of nerves that innervates the
infrahyoid muscles except for thyrohyoid).
▪ Muscular triangle:
• Lies anterior to omohyoid muscle superior belly & posterior to the
midline.
• Contains the infrahyoid muscle (deep to this is the thyroid gland).
▪ Submandibular triangle:
• It lies between the 2 bellies of the digastric muscle inferiorly & the
mandible superiorly.
• Contains the submandibular salivary gland & LNs.
▪ Submental triangle:
• Lies anterior to the digastric muscle & right to the side of the midline
(both on each side of the neck meet to form a true triangle).
• Contains submental LN & sublingual salivary gland.

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o Posterior triangle:
▪ Bounded by trapezius muscle posteriorly, SCM anteriorly, clavicle inferiorly.
▪ The omohyoid’s inferior belly divides it into (1) Large occipital triangle
superiorly, (2) Smaller subclavian triangle inferiorly.
▪ Occipital triangle:
• The floor contains the scaleni muscle, through which the phrenic nerve
passes & which the accessory nerve (CN11) crosses transversely to
supply trapezius & SCM.
• The roof contains the external jugular vein & above that is the platysma
muscle (the most superficial muscle).
• Contain the posterior cervical LNs.
▪ Subclavian triangle:
• Contains the 3rd part of the subclavian vessels + suprascapular &
transverse cervical vessels.
• Contains the brachial plexus & supraclavicular LNs.
o Infrahyoid muscles:
▪ Located in the muscular triangle in the anterior triangle.
Structures deep to it are ▪ Components:
considered in the anterior neck • Sternohyoid.
(this includes the thyroid gland) • Sternothyroid.
• Thyrohyoid.
• Omohyoid.
The thyro- part is reflected
to its attachment to thyroid
▪ All the muscles (except for the thyrohyoid) are attached to the thyroid gland.
cartilage ▪ All the muscle (except for thyrohyoid) are innervated by ansa cervicalis.
▪ Thyrohyoid is innervated by hypoglossal nerve.

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• Fascia of the neck (cervical fascia):

o Superficial fascia >> contains platysma muscle.
o Deep fascia:
▪ Investing layer of deep fascia (contains SCM & trapezius).
▪ Pre-tracheal fascia:
• Contains the thyroid gland, trachea, esophagus & recurrent laryngeal
That’s why the thyroid nerve.
moves with swallowing • It’s attached superiorly to the hyoid bone, limiting structures like the
thyroid from extending above.
• It’s continuous with the anterior mediastinum inferiorly (allow thyroid
to grow retrosternally (retrosternal goiter).
▪ Carotid sheath:
• Contains the common carotid artery, internal jugular vein, & vagus
nerve.
• The right common carotid artery arises from the brachiocephalic artery
on right side, but the left common carotid artery arises from the arch of
aorta.
• The internal jugular vein joins the subclavian vein to produce the
brachiocephalic veins, the left one is longer because it crosses to join
the other to form the SVC.
• The vagus nerve arise from the medulla & descends into the thorax &
give back the right & left recurrent laryngeal nerves.
o The left recurrent laryngeal nerve hooks around ligamentum
arteriosum.
o The right recurrent laryngeal nerve hooks around the right
subclavian artery.
▪ Pre-vertebral fascia >> this fascia encases the vertebra & the surrounding para-
vertebral muscles.

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Thyroid gland anatomy (Review)

• Thyroid gland development:

o Thyroid gland develops from the foramen cecum (the base of the tongue).
o Then it descends following a path in the anterior neck (anterior, through, or posterior
the mid-anterior hyoid bone).
o Then it rest in front of the cricoid cartilage & tracheal rings.
o Throughout its path, it’s remains connected to the foramen cecum through the
thyroglossal duct, which is normally obliterates.
o Abnormalities of thyroid development:
▪ Lingual thyroid (failure of descending):
• Presents as posterior tongue mass.
• It’s important to not excise the mass before doing a thyroid scan.
▪ Ectopic thyroid >> aberrant migration.
▪ Retrosternal thyroid >> descends far down.
▪ Thyroglossal cyst or sinus (discussed later) >> failure of complete obliteration.

• Thyroid gland structures:

o The thyroid gland lies in the anterior neck, within the para-tracheal fascia, deep to the
infrahyoid muscles in the muscular triangle (clinically, it moves with deglutition).
o It’s attached to cricoid cartilage & superior tracheal rings, located at the level of C5-T1
vertebra.
o Parts:
▪ Right & left lobes >> ascends up to the level of the thyroid cartilage, the most
lateral part is known as the Tubercle of Zuckerkandl.
▪ Isthmus >> located on the midline of the neck, covers 3rd, 4th, & 5th tracheal
rings.
▪ Pyramidal lobe >> found in 50-80%.

• Relations of the thyroid gland:

o Parathyroid gland:
▪ Embedded in its capsule or in the thyroid gland itself posteriorly on either sides
of its lobes.
▪ Superior parathyroid glands arise from 4th pharyngeal pouch.
▪ Inferior parathyroid glands arise from 3rd pharyngeal pouch.
o Recurrent laryngeal nerve:
▪ Runs near the posterior part of the gland in the tracheosophageal groove.
▪ Surgeons are careful to first identify the recurrent laryngeal nerve & move it
aside, its injury is a big medicolegal concern in thyroid surgery.
▪ The recurrent laryngeal nerve supplies:
• (1) All the laryngeal muscles, except for the cricothyroid muscle which is
supplied by the external branch of superior laryngeal nerve.
• (2) laryngeal mucosa below the vocal cords (inferior laryngeal nerve
supplies above the vocal cords).
o Trachea >> located posteriorly to the thyroid.
o Carotid sheath >> located postero-laterally to the thyroid.

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• Thyroid gland vasculature:

o Arterial blood supply:
▪ Superior thyroid artery:
• A branch from external carotid artery.
• Travels with the superior laryngeal nerve far away from the gland (thus,
during ligation, do it near the gland to avoid injury to the nerve).
• Superior laryngeal nerve injury >> patients cannot speak in high pitched
voice (monotonic voice).
▪ Inferior thyroid artery:
• A branch from the thyrocervical trunk of
subclavian artery. Branches of subclavian artery
• Travels with the recurrent laryngeal nerve (1) Vertebral artery.
near the gland (thus, during ligation, ligate (2) Internal thoracic artery.
(3) Thyrocervical trunk (inferior thyroid
far from the gland to avoid nerve injury).
artery & suprascapular artery).
• Unilateral injury >> hoarseness of voice. (4) Costovertebral artery (superior
• Bilateral injury >> respiratory distress. intercostal artery, deep cervical artery).
▪ Thyroid ima artery (in 10% of people) >> not (5) Dorsal scapular artery.
present in all people, a branch from arch of aorta or
brachiocephalic artery.
o Venous drainage:
▪ Superior thyroid vein (drains into internal jugular vein).
▪ Middle thyroid vein (drains into internal jugular vein).
▪ Inferior thyroid vein (drain into brachiocephalic vein).
o Innervation:
▪ Sympathetic (vasomotor) >> from cervical sympathetic
ganglia.
▪ Parasympathetic >> recurrent laryngeal nerve &
superior laryngeal nerve.

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Differential Diagnosis of Neck Lumps (HIGH YEILD)

• (1) Lymph nodes enlargement (lymphadenopathy):

o Inflammatory (lymphadenitis; scrofula):
▪ Infectious:
• Bacterial >> local (dental, tonsils), TB (cold abscess “collar stud”).
• Viral >> EBV (posterior cervical lymphadenopathy), HIV (generalized
lymphadenopathy), syphilis.
▪ Non-infectious >> reactive hyperplasia.
o Neoplastic:
▪ Primary >> lymphoma (e.g. CLL).
▪ Secondary >> metastatic (e.g. thyroid, lung, breast, GI).

• (2) Midline lumps:

o Dermoid cyst (in pediatrics):
▪ Occur in midline structures or lateral ends of eyebrows.
▪ It contains structures from the germ layers (hair, nails, skin glands).
o Thyroglossal cyst:
▪ It’s the most common cervical cystic lump.
▪ Occur due to failure of complete obliteration of thyroglossal duct.
▪ It’s usually connected to the mid-portion of hyoid bone.
▪ Clinical features:
• Patients usually presents within the first 5 years of life.
• Midline neck lump, that moves with the protrusion of the tongue (due to
foramen cecum origin) & swallowing (due to pre-tracheal fascia).
• Complications:
Before removing thyroglossal o Infections.
cyst, make a thyroid scan,
because this may be the only
o Mass effect.
thyroid tissue o Fistulas or sinus formation.
▪ Investigations >> neck US showing echogenic cystic mass.
▪ Management >> Sistrunk operation (remove cyst + anterior-
mid portion of hyoid bone + its tract).
o Thyroid mass:
▪ Diffuse enlargement:
• Physiologic goiter (pregnancy, puberty).
• Endemic goiter (iodide deficiency).
• Hyperhyroidism (graves).
• Hypothyroidism (thyroiditis).
▪ Nodular enlargement:
• Solitary nodule (solitary adenoma, toxic adenoma, colloid cyst, cancer).
• Multiple nodular goiter.
o Ranula (frog-like cyst):
▪ Sublingual cyst or fluid collection or cyst that forms in the mouth under the
tongue.
▪ It is filled with saliva that has leaked out of a damaged salivary gland.
▪ Mainly caused by trauma.

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• (3) Anterior triangle lumps:

o Branchial cyst:
▪ A congenital disorder, remnant of cervical sinus.
Branchial (pharyngeal) arches ▪ Clinical features:
(1) Embryologically, the 2nd. • Patients present at late childhood or even in adulthood.
Branchial arch grows rapidly,
• Anterior neck lump, lateral to midline.
then around the 3rd arch, then
it attaches to the 4th producing • Most common location >> beneath the upper 1/3rd of SCM.
a branchial cleft. • Smooth, mobile, & fluctuant mass.
(2) Normally, this obliterates. If • Doesn’t move with swallowing or tongue protrusion.
persistent = branchial cleft cyst
(can become a sinus).
• Complications >> infections, fistula formation.
(3) Branchial cleft cyst is ▪ Investigations >> US & fine needle aspiration showing cholesterol crystals
usually located in the anterior (rectangular with a missing edge).
neck (compared to cystic ▪ Management:
hygroma).
• Cyst >> excision through transverse neck incision.
• Fistula >> tract should also be excised.
o Vascular-related >> carotid aneurysm, carotid body tumors (chemodectoma).
o Laryngoceles >> mostly in tuba players, worsens by blowing.
o Lymphadenopathy >> with its DDx (discussed above).

• (4) Posterior triangle lumps:

o Cystic hygroma:
▪ Jugular lymph sac that is formed by lymphatic malformations (not LNs).
Cystic hygroma may be ▪ It containing multiple large sacs & smaller vesicles all connected together (the
associated with turner large ones are more superficial).
syndrome ▪ The contents are usually clear lymph.
▪ Common locations:
• Neck (posterior triangle).
• Under mandible.
• Floor of mouth.
• Axilla.
• Thorax.
▪ Clinical features:
• Present at birth or in first few years of life.
• Painless neck mass in posterior triangle.
• Bluish tinge are characteristically seen on skin surface.
• The mass is soft, easily compressible, with ill-defined borders, have +ve
transillumination.
• Complications >> Mainly rapid enlargement (resulting in airway
obstructrion or difficult resection).
▪ Investigations:
• May diagnosed parentally by maternal US.
• US & MRI are useful tools.
▪ Management >> early total surgical excision, which may preceded by injecting
sclerosing agents.
Surgical excision can damage
the accessory nerve (CN11)
leading to loss of shoulder
shrugging

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• (5) Submandibular triangle (near the jaw):

o Lymphadenopathy >> with its DDx.
o Salivary gland enlargement (discussed below):
▪ Infections:
• Viral (bilateral) >> Mumps (check for orchitis & pancreatitis).
• Bacterial (unilateral) >> usually in elderly, dehydrated, ICU patients.
▪ Sialolithiasis >> salivary gland stones, most commonly in submandibular salivary
gland.
▪ Parotid gland tumor >> polymorphic adenoma is the most common.
▪ Other causes >> Sjogren’s syndrome.

• (6) Others (can occur anywhere):

o Lipomas:
▪ Has a slippery edge, soft mass.
▪ Found anywhere except palms, sole, scalp.
▪ It’s a subcutaneous mass, i.e. can be separated from skin (compared to
sebaceous cyst).
o Sebaceous cyst:
▪ It’s an epidermal cyst containing keratin, not sebum.
▪ It’s firm, round, & mobile nodule.
▪ Mainly found in scalp, face, ear lobule, not found in palms or soles.
▪ It has a characteristic central punctum, if infected, pus is coming out through
punctum.
▪ +ve fluctuation & transillumination signs.
▪ Complications:
• Infection, abscess, calcification.
• Ulceration (Cock’s Pecular tumor).
• Horn or malignant formation.
▪ Management >> excision of cyst with a part of the skin to avoid recurrence.
o Hematoma:
▪ Throbbing or expanding mass.
▪ Associated with history of trauma, surgery, or anticoagulant use.

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Salivary glands diseases (HIGH YEILD)

• Anatomy review:
o We have 3 major pairs of salivary glands >> parotid, submandibular, sublingual.
o There is hundreds of minor salivary glands.
o The parotid gland opens in the upper 2nd molar tooth, it’s duct called Stenson’s duct.
o The submandibular gland opens below the tongue.
o Normal amount of salivation >> 0.5-1.5 liter/day.
o Important relation >> the facial nerve (it has 5 branches, temporal, zygomatic, buccal,
marginal submandibular, cervical).

• Sialadenitis:
o Inflammation of the salivary glands.
o Causes:
▪ Viral (most common) >> mumps & HIV (bilateral).
▪ Bacterial infection >> usually secondary to duct blockage by a stone.
o Symptoms >> acute facial swelling & pain.
o Signs >> fever, +/- purulent discharge from duct (Stenson’s or Wharton’s).
o Investigations:
▪ A good start is US (assess the origin of swelling, signs of malignancies,
obstruction, stones, etc..).
▪ Other investigations may be ordered depending on the situation.
o Management:
▪ Viral cases >> no treatment is needed, resolve spontaneously.
▪ Bacterial >> abscess must be drained, oral antibiotics (cloxacillin).

• Sialolithiasis:
o Stone in the salivary gland duct.
o Most common site is submandibular salivary gland (80%), followed by parotid gland.
o Symptoms >> pain & swelling of gland area in relation to meals.
o Signs >> tenderness of involved gland, palpable mass/stone in gland or duct.
o Investigations >> gland US, then Sialogram (not always needed).
o Management:
▪ (1) Reassurance >> resolves spontaneously if small.
▪ (2) Symptomatic >> analgesia, antibiotics (if infected).
▪ (3) If small or near distal duct, spontaneous clearance:
• Massaging area & warm compression.
• Encourage salivation (suck on lemon or orange).
• Sialogogues (lemon wedges, sour lemon candies).
▪ (4) If large or refractory >> surgical removal.

• Complications of parotid removal surgery:

o Marginal submandibular nerve injury >> result in facial palsy, to avoid injuring this
nerve, do the incision 2 fingers below the gland.
o Lingual nerve injury >> result in taste loss in anterior 3rd of tongue.
o Hypoglossal nerve injury >> result in deviation of the tongue to the affected side.

Facial nerve examinations

[Link]
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Clinical approach to Thyroid Mass (HIGH YEILD)

• History Highlights of thyroid history/neck swelling:

o Mass questions:
▪ When did you first notice the mass.
▪ Progression of the mass (rapid enlargement may suggest cancer).
▪ Painful or not.
▪ Any other swellings.
▪ Any associated symptoms (compression symptoms like dysphagia, dyspnea,
voice hoarseness).
o Ask about symptoms of hypothyroidism & hyperthyroidism:
▪ Hyperthyroidism:
• Weight loss & increased appetite.
Causes of thyrotoxicosis
• Heat intolerance & excessive sweating. (1) Grave’s disease.
• Muscle weakness. (2) Toxic multi-nodular goiter.
• Palpitations. (3) Thyroiditis.
(4) Exogenous thyroxine.
• Diarrhea.
(5) Struma Ovarii
• Amenorrhea.
• Insomnia, irritability, hyperactivity.
▪ Hypothyroidism:
• Weight gain.
• Cold intolerance.
• Constipation.
• Hair loss & dry skin.
• Menorrhagia.
• Fatigue, lethargy, muscle weakness.
• Slow mentation, depression, inability to concentrate.
o Ask about constitutional symptoms (to exclude other DDx) >> fever, night sweats.
o Assess risk factors of thyroid diseases:
▪ Radiation exposure & Occupation.
▪ Family history of thyroid diseases and cancers.
▪ Any regular or recent medications.
o If you suspect malignancy (on history) >> Local invasive features (vocal cord paralysis,
change in voice, dysphagia).

• Thyroid & neck examinations (highlighted):

o General inspection:
▪ Appearance (anxious, restless or somnolent).
▪ Built (overweight or underweight).
o General examination:
▪ Hands & arm:
• Clubbing (Graves acropachy).
• Tremors.
• Diaphoretic palms & palmar erythema.
• Pulse (tachycardia or bradycardia).

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Causes of exophthalmos ▪ Face:

(1) Accumulation of • Loss of lateral third of eyebrows (hypothyroidism).
glycoaminoglycans.
(2) Infiltration of retroorbital
• Xanthelesma (hypothyroidism).
space by T cells. • Graves opthalmopathy (stand on side or from above the patient).
(3) Inflammatory edema & • Lid retraction & lid lag (ask the patient to look down).
swelling of extra-ocular muscles.
(4) Fatty infiltration. • Assess any mass at the back of the tongue.
▪ Lower limbs >> assess pretibial myxedema & reflexes.
o Neck examinations:
▪ Ask the patient to sit on chair if present, if not, on the side of the bed (Why?
Because we need to go around the patient & examine from back).
▪ Inspection:
• Assess any swelling of discoloration.
• For swelling >> Site, Size, Shape, Surface or skin overlying, Special
characters (movement with swallowing or tongue protrusion).
• Pemberton’s sign >> ask the patient to raise his hands over the head or
2-3mins, with retrosternal mass, there will be obstruction of the SVC
resulting in face plethora.
▪ Palpation:
Other characters for swelling
• Ask if any pain is present, leave the painful area
description
to the end. (1) Compressible or reducible.
• Stand behind the patient. (2) Indentable.
• (1) Palpate the trachea >> assess any (3) Fluctuating or Paget’s test.
(4) Cough impulse.
deviation.
(5) Pulsating.
• (2) Palpate the swelling >> Site, size, shape, (6) Thrills.
surface, consistency, mobility, tenderness, (7) Fixation (can you move overlying
warmth. skin, does it become more prominent
when contracting neck muscles).
• (3) Palpate the LNs:
o Occipital LNs.
o Post-auricular & pre-auricular LNs.
o Parotid LN & gland.
DDx of cervical lymphadenopathy
o Submandibular & submental LNs.
(1) Metastasized thyroid cancer.
(2) EBV mononucleosis. o Posterior & anterior cervical LNs.
(3) HIV. o Follow the SCM down & palpate for the supraclavicular LNs.
(4) TB lymphadenopathy. o Go back up to the thyroid prominence, follow it down to the
(5) Lymphoma. thyroid isthmus, then move laterally to feel the lateral lobes.
o Ask the patient to swallow to feel the thyroid move up.
▪ Percussion >> sternal percussion (dullness suggest retrosternal goiter).
▪ Auscultation (with Bell) >> carotid artery & over mass to assess bruits.
o Ideally, you must finish you examination by:
▪ Cardiovascular examination.
▪ Neurological examination (reflexes).
▪ Pelvic examination in females (Struma ovarii & trophoblastic disease can cause
hyperthyroidism).
▪ Lower limb examination (assess pretibial myxedema).

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• Investigations in thyroid mass:

o Labs:
▪ CBC >> assess WBCs.
▪ Thyroid function testing (TSH, T4, T3):
• Best initial workup.
• Important to R/O hypo or hyperthyroidism.
▪ Ca levels >> assess any disturbances, if there abnormality, order PTH.
o Thyroid ultrasound (best initial imaging):
▪ Confirm the thyroid mass.
▪ Single or multiple nodules.
▪ Lump features (size, site, shape, cystic or solid).
▪ Presence of micro-calcifications (suggesting malignancy).
▪ Assess vascularity of the nodule.
▪ Assessment of LNs.
o Ultrasound-guided fine needle aspiration (FNA):
▪ Biopsies are taken for histopathology, only follicular cell carcinoma cannot be
diagnosed by FNA.
▪ Benign cysts >> clear aspirate, complete disappearance of cyst, no re-
accumulation, cytology is clear.
▪ Malignant cysts >> aspirate is hemorrhagic, residual lump is present, rapid re-
accumulation of fluid in cyst, cytology shows malignant cells.
o Thyroid scan >> done only in cases of hyperthyroidism.
o CT scan of the neck >> ordered only if there is obstructive symptoms.

Diagnosis of Grave’s Disease Results of FNAC

Approach to a thyroid nodule
Clinical >> hyperthyroidism symptoms, I >> non-diagnostic.
Exophthalmos (50%), pretibial II >> benign. <1cm with no evidence of
myxedema (10-15%) & thyroid bruits III >> Atypia. malignancy >> no need for FNA.
(50-90%). IV >> follicular neoplasm. >1.5cm >> needs biopsy.
Labs >> low TSH & +ve TSI antibodies. V >> suspicious for malignancy.
Thyroid scan >> increased uptake. VI >> Malignant.

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Thyroid cancer (HIGH YEILD)

• Overview:
o Types:
▪ Papillary carcinoma (80% - most common type).
▪ Follicular carcinoma (10%).
▪ Medullary carcinoma (5%).
▪ Hurthle cell carcinoma (4%).
▪ Anaplastic carcinoma (1%).
o General workup:
▪ Labs >> thyroid tests, bone profile (Ca, P, ALK-P), calcitonin levels.
▪ Imaging >> US, +/- thyroid scan.
▪ Cytology >> fine needle aspiration.
▪ Staging >> CXR, bone scan.

• Papillary carcinoma:
o Main risk factor is radiation exposure, occur more in females than males.
o Average age >> 30-40ys.
o Histology >> psammoma bodies.
o Presentation >> painless, dysphagia, dyspnea, hoarseness.
o Spread & metastasis:
▪ Spreads mainly by lymphatics (may result in cervical lymphadenopathy).
▪ +ve LNs doesn’t affect the prognosis.
▪ Most common distal metastasis is to the lungs.
o Management:
▪ (1) Total thyroidectomy, +/- central LN dissection.
▪ (2) Don’t give the patient any thyroid hormone for 3 weeks post-op (Why?
Because we want to starve any residual thyroid tissue).
▪ (3) Then we give radioactive iodine to destroy any residual thyroid tissues.
▪ (4) Put patient on life-long thyroid replacement therapy (main goal is to replace
thyroid hormones + suppress TSH because it’s a hormonal dependent cancer).
▪ Follow up >> by thyroglobulin tumor marker.
▪ 10 years survival rate >> 95% (Best cancer to have).

• Follicular carcinoma:
o Occur in females more than males.
o Cannot be distinguished from follicular adenoma by FNA (needs tissue structure to
identify capsular invasion).
o Presentation >> painless mass (typically rubbery & encapsulated).
o Spread & metastasis:
▪ Spread mainly by blood.
▪ Most common site of distal metastasis is bone.
o Management:
▪ (1) Total thyroidectomy (intra-op lobectomy is done first & sent to
histopathology analysis by frozen section to determine capsular invasion, then
total thyroidectomy is done) + (2) radioactive iodine.
▪ Follow up >> by thyroglobulin tumor marker.

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• Medullary carcinoma:
o Risk factors:
▪ Most are sporadic, occur in females more than male.
▪ MEN2 A&B (patients who found MEN2 must have their family screened &
offered prophylactic thyroidectomy).
o Histology >> amyloid deposits (due to calcitonin hyper-secretion).
o It has poor thyroid scan uptake.
o Presentation >> painful mass, dysphonia, dysphagia, palpable LNs.
o Spread & metastasis >> both lymphatics & blood.
o Diagnosis >> Pentagastrin stimulation test will have high calcitonin level.
o Management:
▪ Total thyroidectomy + central & lateral LN dissection, +/- chemotherapy.
▪ May need modified neck dissection if lateral LNs are involved.
▪ Follow up >> by calcitonin + CEA (carcinoembryonic antigen).
▪ 10-years survival:
• 80% without LN involvement. In medullary carcinoma, there is no rule
• 45% with LN involvement. for thyroid starvation, radio-ablation, or
thyroid hormone replacement, because
parafollicular cells don’t respond to TSH
• Anaplastic carcinoma (undifferentiated carcinoma):
o Occur in elderly >65ys.
o It has poor thyroid scan uptake.
o Histology >> giant cells & spindle cells.
o Spread & metastasis:
▪ Mainly by direct invasion to local structures.
▪ RLN palsy (hoarseness of voice).
▪ Airway obstruction & Dysphagia.
o Management:
▪ Total thyroidectomy + chemotherapy (doxorubicin).
▪ In airways obstruction cases, debulking surgery, tracheostomy, chemotherapy.
▪ 5-years survival rate (very poor) >> 3%, most patients presents late when it’s
already metastasized.

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Principles of thyroidectomy (HIGH YEILD)

• Indications:
o Hyperthyroidism )Grave’s Disease(:
▪ Failed medical therapy for 1-2 years.
▪ Poor candidates for radio-ablation (pregnancy, young patients, large goiters).
▪ Compressive symptoms (very large goiters).
▪ Suspicion of malignancy.
o Thyroid neoplasia:
▪ Solitary adenoma (lobectomy).
▪ Thyroid carcinoma (total thyroidectomy).

• Pre-op preparation:
o Adequate consent for the possibility of complications (discussed below).
o Pre-op thyroid control (make it euthyroid as possible):
▪ Medical management of hyperthyroidism (as best as you can).
▪ Main goal is tp prevent risk of thyroid storm intra-op.
o Indirect laryngoscopy:
▪ Important to check pre-op mobility of vocal cords & take pictures of it (for
medicolegal reasons).
▪ 3% of patients have asymptomatic cord paralysis.

• Intra-op key points:

o It’s a clean surgery, there is no need for pre-op antibiotics.
o Laryngoscopy may be done multiple times to document changes in vocal cords (at least
once before & after).
o The RLN & parathyroid glands should be identified before thyroidectomy.
o The superior & inferior thyroid arteries + the inferior thyroid vein is ligated (the vein is
ligated to prevent spillage of thyroid hormone in circulation).
o Minimize handling of the thyroid gland as possible.

• Post-op key points:

o Starve the residual thyroid tissue (3-4 weeks), then perform a whole body thyroid scan
to look for an residual thyroid tissues.
o If present, radioactive iodine should be done.
o Patients are routinely started on oral calcium carbonate for 2 weeks.
o Lifelong thyroid hormone replacement is needed.
o Follow up >> order serum Ca, thyroid tests, & thyroglobulin levels.

Tracheomalacia is a well-known complication of long

standing goiter that can cause fatal respiratory arrest.
To diagnosis it before surgery >> thoracic inlet X-ray.
Management >> during surgery keep some tissue to
hold the tracheal rings

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• Complications of thyroid surgery:

o General >> anesthesia complications, MI, PE, atelectasis, pneumonia.
o Local >> hematoma, seroma, wound infection.
o Thyroid storm:
▪ Occur due to release of thyroid hormone to the blood.
▪ Presentation:
• Intra-op >> tachycardia (early), fever, shaking.
• Post-op >> sweating, agitation, confusion, diarrhea.
▪ Managed by:
• IV fluids, O2 supplements, cooling blankets.
• PTU & beta-blockers.
• Adrenal support with steroids (decrease peripheral conversation of T4
to T3 + prevent relative adrenal insufficiency due to hyperthyroidism).
• Iodine (Wolff-Chaikoof effect).
o Hemorrhage (expanding hematoma):
▪ Slipped ligature result in bleeding into a closed cervical space leading to airway
obstruction & carotid vessels compression.
▪ It’s an emergency & need rapid intervention.
▪ If airway control is unable to be obtained prior to operating room, the wound
should be opened at the bedside.
▪ Prevention >> put a drainage after surgery.
o Respiratory obstruction:
▪ Laryngeal edema (extensive manipulation of larynx intra-op or due to ETT).
▪ Expanding hematoma.
▪ Bilateral RLN injury.
o RLN paralysis: Note that most patients
may have a transient
▪ May be unilateral or bilateral, transient or permanent. voice hoarseness after
▪ Unilateral >> voice hoarseness, dyspnea on excretion. surgery, due to stress of
▪ Bilateral >> aphonia, respiratory obstruction. surgery, not RLN injury

o Superior laryngeal nerve injury >> result in monotonic voice.

o Hypocalcemia (hypoparathyroidism):
▪ It may be transient or permanent.
▪ First sign of hypocalcemia is paresthesia of face (peri-oral numbness).
▪ Signs >> Chvostek sign & Trouseau sign.
▪ Transient hypocalcemia occur 25-48h post-op (we usually give Ca supplements
post-op).
▪ In severe hypoglycemia symptoms, IV calcium gluconate is given.

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Parathyroid gland

• Anatomy & physiology (review):

o Anatomy review:
▪ The parathyroid glands (PTG) are 2 pair of glands that is located in posterior to
the thyroid gland, either within the capsule or outside it.
▪ It’s supplied by inferior thyroid artery.
▪ Contains chief cells that produce parathyroid hormone (PTH).
▪ Superior parathyroid glands developed from 4th pharyngeal pouch.
▪ Inferior parathyroid glands developed from 3rd pharyngeal pouch.
o Physiology review:
▪ PTH function in increasing net Ca in the blood.
▪ Ca-sensing receptors (CaSR) in PTG will sense drop in Ca & eventually promotes
PTH secretion (low Mg will prevent this step).
▪ PTH functions:
• (1) Promotes PO4 excretion & Ca reabsorption in kidney.
• (2) Activates vitamin D2 to D3 (Calcitriol) in the kidney.
• (3) Osteoclast activation in order to break down bone to release Ca.
o Important points:
▪ Ionized Ca is the active form, while the inactive from is bound to albumin.
▪ Total Ca in blood = Ca attached to albumin (40%) + Ca attached to minerals
(15%) + ionized Ca (45%).
▪ Corrected Ca = Ca + {0.02 + (40-albumin in mg/dl)}
▪ Normal total Ca level = 8.5-10.5 mg/dL.
▪ Normal ionized Ca level = 4.8-5.7 mg/dL.
▪ Normal serum phosphate levels >> 2.5-4.5 mg/dL.

• Primary hyperparathyroidism:
o One or more glands produce inappropriately high amounts of PTH relative to the serum
Ca levels.
o Causes of hypercalcemia (Ca >10.5 mg/dL):
▪ PTH-dependent:
Familial hypocalciuric
• Primary hyperparathyroidism (most common).
hypercalcemia (FHH) is an AD
disorder characterized by a • Tertiary hyperparathyroidism (in chronic renal failure patients).
defect in Ca sensing receptors • Familial hypocalciuric hypercalcemia (FHH).
in parathyroid gland. Lab
▪ PTH-independent:
result are low Ca in urine &
high serum Ca. • Cancers (especially squamous cell cancers).
• Multiple myeloma.
• Granulomatous diseases (sarcoidosis & TB).
• Vitamin D toxicity.
o Causes of primary hyperparathyroidism:
▪ Adenomas (80%), majority involving only one gland.
▪ Hyperplasia (20%), all 4 glands are affected.
▪ Carcinoma (<1%).
o Risk factors >> history of radiation exposure, family history (MEN1 & MEN2).

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o Clinical features of hypercalcemia:

▪ Patients can be asymptomatic in mild cases.
▪ Stones >> nephroliathiasis, nephrocalcinosis.
▪ Bones >> Bone aches, Osteitis fibrosa cystica (brown tumors) predisposes
patient to pathologic fracture.
▪ Groans >> Muscles pain, pancreatitis, peptic ulcer disease, gout, constipation.
▪ Other symptoms >> polydipsia, polyuria, HTN, shortened QT interval.
▪ Malignancy features >> hoarseness of voice, dysphagia, neck pain, palpable
neck mass.
o Investigations & Diagnosis:
▪ Check albumin levels & calculate corrected C levels to exclude
If PTH are high, primary pseudohypercalcemia.
hyperparathyroidism is ▪ PTH & total Ca levels >> high.
suspected, check Cr, eGFR, ▪ Serum phosphate >> low, high in tertiary hyperparathyroidism.
24-h urinary Ca excretion to
calculate risk of renal ▪ Urinalysis >> hypercalciuria, hypocalciruia in FHH.
complications ▪ Chloride/phosphorus ratio >> Ratio >33 is diagnostic or primary
hyperparathyroidism.
▪ Radiological studies:
• CXR >> may show subperiosteal bone resorption.
• Neck US >> done if there is a lump.
• Sestamibi scan >> diffuse uptake suggest hyperplasia, while single
uptake suggest adenoma.
• DEXA scan >> measure bone density (primary hyperparathyroidism
decreased bone density & increase risk of pathological fractures).
o Management:
▪ Management of hypercalcemia:
• If corrected Ca levels >14 mg/dL (severe):
o (1) IV isotonic saline (200-300 mL/hour to maintain urine output 100-150
mL/hour).
o (2) Furosemide (loop diuretics) & (3) IV bisphosphonate
(zoledronic acid) is given to lower Ca levels.
o In severe cases (>18 mg/d), hemodialysis can be done.
• If corrected Ca levels <14 mg/dL >> Adequate hydration + avoid
medications that can increase Ca levels such as thiazide diuretics &
lithium + decrease dietary Ca intake to <1g/day.
▪ Surgical removal of parathyroid glands:
• The only definitive treatment, however, not all patients requires it.
Relative indications for surgery in • In hyperplasia >> neck exploration, removal of all 4 PTG.
primary hyperparathyroidism • Adenoma or carcinoma:
1. Age <50 ys. o Neck exploration & excision biopsy of affected gland.
2. Marked decrease in bone mass.
3. Nephroliathiasis & renal
o If carcinoma, ipsilateral thyroidectomy + modified radical neck
insufficiency. dissection for LN metastasis.
4. Severe hypercalcemia.
5. Urine Ca >400mg in 24h.

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• Hypoparathyroidism:
o Causes of Hypocalcemia (Ca <8.5 mg/dL): Pseudohypoparathyroidism is an end-
▪ Primary hypoparathyroidism (iatrogenic). organ resistance to the action of PTH,
laboratory findings include
▪ Hypomagnesemia (cause resistance of PTH). hypocalcemia, hyperphosphatemia, high
▪ Renal failure & Vitamin D deficiency. PTH, low urinary cAMP
▪ Low albumin (result in a decrease in total Ca level).
▪ Others >> acute pancreatitis (saponification), loop diuretics.
o Causes of hypoparathyroidism:
▪ Accidental removal of glands during head & neck surgery (e.g. thyroidectomy,
radical surgery for head & neck).
▪ Non-surgical hypoparathyroidism are very rare.
o Clinical features of hypocalcemia:
▪ Patients with mild hypocalcemia can be asymptomatic.
▪ Increased neuromuscular irritability:
Chvostek sign • Numbness & tingling (perioral, fingers, toes).
([Link] • Hyperactive deep tendon reflexes.
/watch?v=2tV4J2DxjNM)
• Grand mal seizures.
Trousseau sign • Chvostek sign (tapping facial nerve elicits contraction of facial muscles).
([Link]
/watch?v=SBuquydjZDc) • Trousseau sign (inflating the BP cuff to a pressure higher than the
patients systolic BP for 3 min elicits carpal spasm).
▪ Cardiac arrhythmias & palpitations (prolonged QT interval).
o Investigations & Diagnosis:
▪ First blood tests are serum Ca & albumin, calculate corrected Ca levels.
Normal albumin >> 3.5-5.5 ▪ Total Ca >> low.
mg/dL ▪ Serum phosphate >> high.
Normal PTH >> 10-65 pg/mL.
▪ Serum PTH >> low, if high suspect pseudo-hypoparathyroidism or secondary
causes.
▪ If PTH is normal of high, check Vitamin D & Mg to rule out other causes for
hypocalcemia .
o Management:
▪ If corrected Ca >7.5 mg/dL >> oral Ca is given.
▪ If corrected Ca <7.5 mg/dL >> IV calcium gluconate is given.
▪ In vitamin D deficiency >> Vitamin D supplementation.
▪ Note that in cases of hypomagnesemia, Ca supplementation won’t be effective
until hypomagnesemia is corrected (give IV magnesium sulfate).

Note that both vitamin D & Ca

replacement can increase urinary Ca
excretion precipitating kidney stones.
Thus, administration must be with
caution to avoid hypercalciuria

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