General Surgery Syllabus 2

General Surgery Table of Contents 2
Thyroid Surgery ...............................................................2

Parathyroid Surgery ......................................................13
Adrenal Gland Surgery..................................................22
Multiple Endocrine Neoplasia.......................................35
Mediastinum and Chest Wall Disorders .....................47
Pulmonary Surgery Benign and Malignant .................61
Cardiac Surgery (Adult and Pediatric) .........................71
Basic Immunology and Oragan Transplantation ........80
Pancreas Benign and Malignant Disorders .................91
Genitourinary and Gynecology ..................................101
Abdominal Wall and Hernias ......................................112
Selected Bibliographic Sources .................................124
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Surgery Review Course The Osler Institute
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Anatomy
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Matthew Strode, DO FACS

Surgical Oncology
Womack Army Medical
Center, Fort Bragg, NC 28374
Anatomy Benign Thyroid Disease

✱ Isthmus below cricoid
• Goiterà nonspecific enlargement of the thyroid
with many causes
• Most commonly seen in underserved populations

with Iodine deficiencies but can be hereditary or
other dietary factors
• Workup includes TSH, Free T4, T3, exam and U/S

of gland to establish state of thyroid function
• Possible cross sectional imaging
Nontoxic Goiter Hyperthyroidism
• Treatment is usually the #1 modality for

symptomatic large goiters although can
consider RAI, or TSH suppression in poor
candidates
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Thyroid Surgery page 1

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Hyperthyroidism
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Graves Disease: Auto-immune disease

• Treatment-> Antithyroid
medications (PTU and
MMI), RAI, or surgery
• Clinical situation dictates

management
• MMI first line in most

patients choosing
medication except 1st
trimester
• Tx with meds for 18

months at least
Hyperthyroidism (Graves Dz) Hyperthyroidism (Graves Dz)
Agranulocytosis, hepatotoxic, • Successful remission = euthyroid for >12

teratogenic months
Hepatic failure
• 20-30% relapse requiring other treatments
Hyperthyroidism (Graves Dz) Hyperthyroidism (Graves Dz)
• Patient preference
When????
• RAI most utilized modality
• Pregnancy planning
• Stop antithyroid meds stopped 3 days before • Concurrent other neck

and started 3 days after pathology
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• Failed medical therapy

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• Be careful of transient hyperthyroidism

symptoms initially • Compressive symptoms
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• Inability to rule out

malignancy
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Hyperthyroidism Hyperthyroidism
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§ Toxic Multinodular Goiter:

§ Solitary Toxic Nodule:
§ Most common in women over 50
§ Younger females
§ Etiology: most had nontoxic nodular goiter for
years from which enough nodules became § Nodules usually at least 3 cm
autonomous causing hyperthyroidism
§ Hot nodules eventually enlarge, develop
§ Primary treatment is surgery (subtotal central necrosis transitioning to cold nodules
thyroidectomy) after euthyroid state obtained
with medications-> about a month later § Similar treatment to toxic multinodular goiters
§ I-131 good for poor surgical candidates but may § Antithyroid meds only short term
need more than one dose (up to 25%)
§ U/S is key part of workup
Thyroiditis Thyroiditis
§ Hashimoto’s Disease: Auto-immune § Subacute Thyroiditis:
§ Middle aged women § Painful gland

§ Antimicrosomal (90%) and antithyroglobulin (20-50%)
abs, diagnosis made by serum titers and/or biopsy § Young female with antecedent viral URI
with FNA
§ Disease usually self limited, symptomatic relief with
§ Defective hormone synthesis by lack of organification salicylates or possibly steroids
of trapped Iodine
§ Transient toxicosis followed by euthyroidism then
§ May have a period of mild thyrotoxicosis followed by
hypothyroidism and gland burnout hypothyroidism
§ Treatment: observation or thyroid hormone § Total thyroidectomy may be indicated with persistent
replacement-> regression of size, some need surgery painful thyroiditis but very rare to get to that point
Thyroiditis Solitary Thyroid Nodule

§ Riedel Struma:
§ Found on 20-76% of all adults on ultrasound
§ Goiter with woody or fibrous component involving
adjacent strap muscles and carotid sheaths. § Women 4x’s more likely to have nodules
§ Cause unknown, assoc. with other fibrous processes

like sclerosing cholangitis § Malignancy suggested by adenopathy, extremes of age, male
gender, h/o radiation, aerodigestive symptoms, firm nodules
§ Diagnose with biopsy with irregular outlines or fixation of nodule to surrounding
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structures, microcalcs, PET avid lesions

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§ High dose steroids, tamoxifen may help § Large, hypoechoic, taller than wide, rapidly growing
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§ Surgery for debulking often needed with airway § FNA standard for tissue diagnosis with Bethesda classification
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compression, even tracheostomy in severe driving treatment

circumstances
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Solitary Thyroid Nodule Solitary Thyroid Nodule

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When to
FNA???
Thyroid Cancer types Staging Systems
• Papillary § MACIS-mets, age, completeness of resection, local invasion,

extent of disease
• Follicular (includes Hurtle Cell) Differentiation
• Medullary § TNM-standard AJCC staging, age based <45 (Highest stage is II),
45 or older
• Anaplastic
• Lymphoma MACIS and TNM most accurate
• Metastasis
§ AMES-age, mets, extent of disease and size
Preoperative Evaluation Papillary Carcinoma
• Focused history and exam • Females 3 fold increase in incidence to men
• Ultrasound of neck • Controversial link to autoimmune disease
• +/- Laryngoscopy • Clear association with radiation exposure and

hereditary non-medullary thyroid cancer, FAP,
Cowden disease
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• Routine thyroid function tests, calcium

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• Variants include follicular, tall cell, columnar cell,

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• +/- Genetic testing diffuse sclerosis variant, solid variant

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Papillary Carcinoma Papillary Carcinoma

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BIG PICTURE!!—STRONGLY CONSIDER

TOTAL THYROID WHEN THE CHANCE
OF RAI IS HIGHER
• Total thyroidectomy advantagesà TG levels, • Neck Dissection?? Different opinions and

RAI more effective, surveillance, thyroid controversy
homeostasis, eliminates future primary cancer
risk
• Generally only for clinical disease in the
affected aspect of the neck
• Partial thyroidectomy advantagesà no
overnight stay, less surgical risk, less risk of
need for thyroid replacement • If unilateral neck involvement will need
central neck dissection as well

§ Adjuvant Treatment-> RAI selectively recommended for • Surveillance
any of the following
§ 2-4 cm tumor
§ High risk histology (poorly differentiated, tall cell
columnar cell, hobnail variants)
§ Lymphovascular invasion
§ Cervical + nodes
§ Macroscopic multifocal tumor
§ Unstimulated elevated Tg
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§ +Margins
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+ Highly recommended RAI for extrathyroidal extension,

>4cm tumor, and unstimulated Tg >5-10nm/ml, gross
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residual disease, mets

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EBRT for gross disease in poor Iodine concentrating disease

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Papillary Thyroid Cancer Follicular Carcinoma

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• Management of recurrence § Characterized histologically by invasive of capsule or vessels

§ Hematogenous spread, lower node + disease
• Local recurrence- resect nodal or thyroid tissue,
possible RAI § Frozen section not useful
§ 10% of thyroid cancers, 30-50 years old, F>M
• Distant recurrence- RAI, possible surgery, or EBRT
§ Genetics poorly understood
• Targeted therapy- TKI (Sorafenib, Lenvatinib) for

§ Staging usually through TNM
refractory or RAI resistant disease or clinical trial
Follicular Carcinoma Medullary Carcinoma
• Prognosis varies § More aggressive than papillary or follicular, 3-4% of thyroid

cancers, mean age of 50 yo, equal in genders
• Total thyroid versus lobectomy but far less § Arises from para-follicular c-cells mostly located in upper
nodal mets present, highly individualized poles of gland
§ Hereditary 20-25% or sporadic 75-80%, no risk factors
except MEN II or family history of MTC
• Surveillance and RAI similar to papillary
§ Secrete Calcintonin, CEA, ACTH, and occasionally
Somatostatin
• TKI (Sorafenib,Lenvatinib) advanced disease in
non RAI-avid or clinical trial § MTC penetrance in MEN2 95%, and 88% FMTC
§ RET proto-oncogene related
Medullary Carcinoma Medullary Carcinoma
• 50% have nodal disease and 5-10% have distant

mets at presentation
• Dx-> need detailed FH and clinical suspicion

for familial syndromes should be high
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Genetics
• No role for RAI or TSH suppression
• Biochemical cure after thyroidectomy and nodal

dissection is poor 20-30%
• Distant mets more likely if calcintonin levels > 400

pg/mL
• Non-surgical disease same as PTC/FTC
Hurtle Cell Carcinoma Anaplastic Carcinoma
§ Rare subtype of well-diff thyroid cancer

§ Most originate from follicular carcinoma
§ Higher multifocality, F > M, 50-70 yo
§ Most occur in older pts with longstanding
§ 10-25% nodal disease, 10-29% distant disease goiters
§ Risks factors same as for well diff thyroid cancers § Most are rapidly lethal and surgery is not an
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option
§ Follicular and papillary variants
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§ Tracheostomy is often needed and only surgery

§ Can try RAI but not as RAI avid
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they undergo
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§ TX-> total thyroidectomy and consideration for

central neck and clinically + nodes
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Goals of Surgery
Goals of Surgery
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§ Papillary § Medullary Thyroid Cancer (5-10%)

§ Total Thyroidectomy
§ + Central compartment lymphadenectomy § Traditional Rx: Total thyroidectomy +
§ Local extension central compartment dissection
§ Neck dissection if nodes are clinically
§ Preservation of RLN § Lateral dissection of disease if present
§ Follicular: total thyroidectomy or lobectomy
§ Calcitonin, CEA monitoring
§ Hurtle: total thyroidectomy, +/- LND
§ Relatively resistant to XRT
Postop Goals (DTC) Management of Recurrence
§ I-131 for >2.0 cm § Nodal recurrence: Neck dissection or RAI?

§ 100 mCi for ablation of thyroid
§ Soft Tissues (Trachea, Esophogo, Larynx, upper
§ 150 mCi to Rx residual Ca mediastinum etc): Resection if possible
§ Total body scans a 6 mo intervals until no uptake or
500 mCi dose § Medical therapy ?: unresectable tumor
§ Recombinant TSH for stimulation § RAI?
§ Suppression/Replacement § External Beam XRT ?
§ Thyroglobulin
§ U/S??
Radioactive Iodine Complications of Thyroidectomy
§ Used to manage follicular and papillary § Hemorrhage (0.3-1%)

carcinomas, limited or no value in Hurtle cell
or medullary carcinoma § Nerve injury (1-3%)
§ SLN, RLN
§ I-131 or I-123 scan 6 wks after total
thyroidectomy to evaluate for LN and distant § Hypoparathyroidism
mets. Treat with I-131 § Temporary (15-20%)
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§ Permanent (1-2%)
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§ Levothyroxine replacement necessary

§ Respiratory obstruction
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§ Follow up scan within the next year.

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§ Thoracic duct fistula with chyle leak

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Temporary Hypoparathyroidism Temporary Hypoparathyroidism

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§ Represents contusion or temporary alteration of the § Only treated if symptomatic because you want
blood supply to PT with low or absent PTH secretion parathyroid glands to be stimulated
§ PTH – single most important regulator of Calcium § PO Calcium – 1 to 2 g QID (Calcium carbonate – 40%
§ Stimulate Ca resorption Kidneys/Bone elemental calcium – 1 g CaCO3=400mg Ca)
§ Indirectly stimulate GI absortion through hydroxylation of Vit. D
in kidneys § IV Calcium – prefered Calcium gluconate – 1g/10cc
§ Calcium – 50% ionized / 40% protein bound / 10% organic § Rocatrol – Active form Vit. D – 0.25 mcg BID
ion bound
QUESTIONS? QUESTIONS ?
Thyroid: A 42 y/o man presents to PMD with a 3 wk hx of an

Thyroid: A 42 y/o man presents to PMD with a 3 wk hx of asymptomatic neck mass. 2x3 cm and located in left
an asymptomatic neck mass. 2x3 cm and located in lateral neck. Non-smoker, non-drinker and no
left lateral neck. Non-smoker, non-drinker and no prescription meds. No surgical history. FNA returns
prescription meds. No surgical history. FNA returns “Normal thyroid”.
“Normal thyroid”.
1. A congenital lesion?
1. A congenital lesion?
2. FNA returns “normal thyroid”, but is actually well diff
2. FNA returns “normal thyroid”, but is actually well diff pap Ca (correct)
pap Ca
3. Start on thyroid supplementation.
3. Start on thyroid supplementation.
4. Follow-up in six months
4. Follow-up in six months
No such diagnosis as “lateral aberrant thyroid”. It is well
diff pap thyroid ca
QUESTIONS? QUESTIONS?
Recurrent laryngeal nerve damage (permanent) Recurrent laryngeal nerve damage (permanent)
during thyroidectomy should be approx: during thyroidectomy should be approx:
1. 1% or less 1. 1% or less (Correct)
2. 10% 2. 10%
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3. 20-25% 3. 20-25%
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4. 50% 4. 50%
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Permanent RLN damage during

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thyroidectomy should be 1% or less

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Fine needle aspiration biopsy (FNAB) is Fine needle aspiration biopsy (FNAB) is
characteristically inconclusive for: characteristically inconclusive for:
1. Thyroid lymphoma
1. Thyroid lymphoma
2. Papillary Ca
2. Papillary Ca
3. Medullary Thyroid Ca
3. Medullary Thyroid Ca
4. Follicular thyroid Ca (correct)
4. Follicular thyroid Ca
Follicular thyroid cancer is characteristically non-
diagnostic, due to the lack of demonstration of
capsular or lymphovascular invasion.
The Bethesda Diagnostic Category for thyroid The Bethesda Diagnostic Category for thyroid cancer uses
cancer uses a scoring system to: a scoring system to:
1. Quantify risk of thyroid cancer

1. Quantify risk of thyroid cancer
2. Directs diagnostic management of the patient’s
2. Directs diagnostic management of the nodule
patient’s nodule
3. Indicates adequacy of thyroid FNAB
3. Indicates adequacy of thyroid FNAB
4. All of the above (correct)
4. All of the above
5. The Bethesda scoring system indicates a reproducible
risk of cancer, adequacy of specimen and clinical
management for each category
QUESTIONS? References
• Which of the following are condsiderations for • NCCN guidelines 2021

total thyroidectomy in DTC • Current Surgical Therapy
1. Node positivity
• Textbook of General Surgical Oncology
• 2. Size of tumor
• UPTODATE.com
• 3. Vascular invasion
• 4. Excapsular extension
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• 5. All of the above

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Parathyroid Disease Review Historical Background

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1852- Sir Richard Owen performed an autopsy on a rhinoceros and first described
the parathyroid gland
1880- Swedish medical student, Ivar Sanstrom first identifies and names the human
parathyroid gland
1891- Eugene Gley discovered association with tetany with removal
1923- PTH isolated
1926- Parathyroidectomy on Captain Martell at MGH
Matthew Strode, DO FACS

Surgical Oncology
Womack Army Medical Center
Fort Bragg, NC 28374
Anatomy Physiology
The primary physiologic role of the parathyroid gland is the

endocrine regulation of calcium and phosphate
metabolism
Etiology of Hypercalcemia
Physiology
• Hyperparathyroidism
• Malignancy
• Vitamin A or D intoxication
• Thiazide diuretics
• Hyperthyroidism
• Milk–alkali syndrome
• Sarcoidosis and other granulomatous diseases
• Familial hypocalciuric hypercalcemia
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• Immobilization
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• Paget disease
• Lithium therapy
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• Addisonian crisis
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• Idiopathic hypercalcemia of infancy

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Treatment of Hypercalcemia Treatment of Hypercalcemia

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Therapy of Primary Disease

Reduction of Intestinal Calcium Absorption
• Tumor resection (hypercalcemia of malignancy)
• Parathyroidectomy (primary hyperparathyroidism) • Low-calcium diet
• Glucocorticoids
Expansion of extracellular volume
• Infusion of saline solution
• Enhancement of urinary calcium excretion Other Treatments
• Extracellular volume expansion • Dialysis
• Loop diuretics (furosemide and ethacrynic acid) • Mobilization
• Oral phosphate
Inhibition of Bone Resorption
• Calcitonin • Estrogens or progesterone (postmenopausal women with
• Glucocorticoids primary hyperparathyroidism)
• Plicamycin (mithramycin) • Chloroquine (sarcoidosis)
• Bisphosphonates
• Gallium nitrate
Familial Hypercalcemic
Hyperparathyroidism Etiology
Diseases
o Unknown cause
Familial Hyper PTH o 75-85% adenoma, 10-15% hyperplasia
Familial Hypocalciuric Hypercalcemia o 1% carcinoma
MEN I (Menin)àP.P.P. (all 3 p’s)
o XRT exposure associated
MEN IIA (Ret-proto oncogene)àMTC, Pheo, Hyper PTH
o Post-menopausal women 2-3x’s
o Familial MEN I/IIa
Age and Gender-Specific

Incidence of Primary Pathology of Primary
Hyperparathyroidism Hyperparathyroidism rg e
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Diagnosis
Systemic Effects
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o Stones - Hyperparathyroidism in 5-10% of renal colic patients

o Bones - 10-15% symptomatic Chemical diagnosis first !!!!!!!!!!
o Groans - No clear relationship with PUD
o Moans - Fatigability and proximal muscle weakness Can the patient benefit ???
o Psychiatric overtones - depression or anxiety leading to psychosis and
coma
Localization studies
o Arthralgia
o Hypertension
Surgery
Diagnosis Localization Techniques
o Sestamibi Scan
o Personal and family historyà young patients need
attention o 4D CT scan
o Serum calcium, ionized calcium, intact PTH, 25-OH vitamin o High resolution ultrasound
D, 24hr urinary calcium, volume status, creatinine levels o CT imaging MRI +Angiography
o Malignancy? o Venous Sampling
o MEN??
Sestamibi Scan (+) Mediastinal Adenoma

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Surveillance
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Indications for 4 Gland Options for

Exploration versus Single Parathyroidectomy
Adenoma Removal Technique
Absolute indications: MEN syndrome, Failure of PTH to drop, failure o Traditional 4-gland exploration
to find diseased gland, more than one enlarged gland, negative
o Sestamibi guided unilateral exploration
imaging, multiple suspected diseased sites, thyroid disease that
requires a total thyroidectomy o Scan guided surgery with ‘quick’ PTH
o Under local anesthesia
o Scan directed parathyroidectomy with
Advisable indications: lithium induced disease, familial non-MEN intraoperative gamma probe
disease (physiologic approach)
Options for
Parathyroidectomy Parathyroidectomy
Technique
o Endoscopic parathyroidectomy o Anatomically and Biologically Sound Treatment

o –Cervical o Reproducible Results
o –Mediastinal o Low Complications (1-2% most published studies)
o –Thoracic o Short Learning Curve
o –Transaxillary o Easy to Teach, Learn, and Practice
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o Video assisted parathyroidectomy o Cost Effective

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o Excellent Cosmetic and Function Results

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Surgical Exploration Surgical Exploration

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Baseline PTH
Limited incision ~2cm If glands are missing or not found-> perform secondary
Subplatsymal flaps parathyroid survey
Open midline raphe TE groove (below main trunk of inf thyroid artery)
Expose the side of gland in interest Thymus
If no localization preop-start with inferior glands Carotid sheath
Stay on gland to avoid RLN Intrathyroidal
Parathyroid glands appear dark brown or orange

Operation depends of single versus multi-gland disease
Surgical Exploration Hyperparathyroidism

Special circumstances
o Recurrent/Persistent hyperparathyroidism
Intraoperative monitoring of PTH:
o Usually gland in neck/mediastinum
o Inferior glands from styloid to aortic arch
Miami protocol-> 4mL whole blood pre-incision, pre-excision
o Superior glands usually in TE groove
after dissection, 5 and 10 min after removal and 20 minute if
not dropping at 10 minutes o Repeat preop localization!!!
o Angiographic/Percutaneous ablation? 66% @ 4yrs
o Hypercalcemic crisis – Lasix and saline
Need decrease of 50%
o Emergent parathyroidectomy may ne needed
o Pregnancy - Rare
Accuracy of 98% normocalcemia post-op
o High morbidity and mortality
o Newborns at risk for neonatal tetany
o Parathyroidectomy in 2nd trimester
Secondary/Tertiary
Hyperparathyroidism Treatment Calciphylaxis
o Usually consequence of chronic renal disease
o Control hyperphosphatemia – dietary restrictions,
phosphate binding, gels
o Calcium supplementation
o Dec. aluminum intake
Surgery - Persistent symptoms not controlled medically
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or transplant in secondary
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o Bone pain, fractures, calciphylaxis

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4 gland excision with brachioradialis autotransplant

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MIRP (minimally invasive

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radioguided parathyroidectomy)
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Parathyroid Carcinoma
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o 1-2% of parathyroid pathology o Sestamibi (Cardiolyte) found to concentrate in PTH adenoma

o High serum calcium levels o Gamma Probes become readily available due to
o Failure by local/regional recurrence melanoma/breast sentinel node biopsy
Sestamibi persists in PTH adenoma mitochondria and washes
No large studies
o
o
out in surrounding (thyroid) tissues
o Treatment o Norman et. al. popularize gamma guided Parathyroidectomy
o Wide resection (~1996)
o Lobectomy on affected side
o Ipsilateral lymphadenectomy for clinical
disease, +/- total and BL neck dissection
Nerve Integrity Monitoring

(NIM) Goal of Monitoring
o Locate and Identify RLN at risk

o Continuously observe EMG activity to minimize trauma
due to manipulation
o Verify Integrity of nerve prior to closure
“Endoscopic”
Parathyroidectomy
o Video-assisted
o “Endoscopic”
o “Skin Lifting”
o Trans-axillary
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o NOTES Parathyroidectomy???
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Parathyroidectomy Has Become So Easy,
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Why Aren’t We All Doing It?

Re-Do Parathyroidectomy
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o Relaxed Indications
o Improved Imaging
o Gamma Guidance/Videoscopic Assistance
o NIM
o Intra-operative PTH
o Low Morbidity
o Success in excess of 96%, in abundance of published studies
Question #1 Question #1
The most common histologic diagnosis for Primary

The most common histologic diagnosis for Primary Hyperparathyroidism is:
Hyperparathyroidism is: 1. A parathyroid cyst .
2. Four gland parathyroid hyperplasia.
1. A parathyroid cyst 3. Solitary parathyroid adenoma (correct)
2. Four gland parathyroid hyperplasia. 4. Calciphylaxis
3. Solitary parathyroid adenoma Solitary parathyroid adenoma is the histologic cause of
4. Calciphylaxis primary HyperPTH in approx 75-85% of case studies. Four
gland Hyperplasia ~20% and double adenoma ~6%.
MEN: The primary tumor marker for Multiple

MEN: The primary tumor marker for Multiple Endocrine Endocrine Neoplasia Type IIa (MCT, Pheo, PTH), is;
Neoplasia Type IIa (MCT, Pheo, PTH), is;
1. CEA 1. CEA
2. AFP 2. AFP
3. CA125 3. CA125
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4. Ret Proto Oncogene

4. Ret Proto Oncogene (correct)
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Menin is the marker for MEN I and Ret-proto

oncogene for both MEN Type IIA and Type IIB
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Secondary and Tertiary Hyperparathyroidism is most commonly

Secondary and Tertiary Hyperparathyroidism is most commonly associated with:
associated with:
1. Ulcerative colitis
1. Ulcerative colitis
2. Renal failure (correct)
2. Renal failure
3. Osteoporosis
3. Osteoporosis 4. Pancreatitis
4. Pancreatitis Untreated renal failure for Secondary and frequently
autonomous HyperPTH after renal transplant for Tertiary.
The most common cause of hypercalcemia in a hospitalized

The most common cause of hypercalcemia in a hospitalized population is:
population is: 1. Primary hyperparathyroidism
1. Primary hyperparathyroidism 2. Secondary hyperparathyroidism
2. Secondary hyperparathyroidism 3. Tertiary hyperparathyroidism
3. Tertiary hyperparathyroidism 4. Malignancy (correct)
4. Malignancy General population: HyperPTH, Hospitalized population:
malignancy
Questions References
Parathyroid glands receive blood supply from what artery??
NCCN guidelines 2021

Current Surgical therapy
Textbook of General Surgical Oncology
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Uptodate.com
What are the embryological origins of the parathyroid glands ?
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Adrenal Gland Review The Adrenal Gland

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Adrenal hormones control many important functions in the

body such as:
Maintaining metabolic processes managing blood sugar
levels and regulating inflammation
Regulating the balance of salt and water
Controlling the "fight or flight" response to stress
Maintaining pregnancy
Matthew Strode, DO FACS Initiating and controlling sexual maturation during childhood
and puberty
Surgical Oncology
Fort Bragg, NC 28374
Background Embryology
1563 described by Eustachius Cortex and Medulla have separate embryonal

origins
1855 Addison Disease Bilateral suprarenal glands
1886 Fraenkel termed 3.5 - 5 grams in weight
Pheochromocytoma Three arteries typically
Superior suprarenal (inferior phrenic)
1932 Cushing’s Syndrome Middle suprarenal (aorta)
1955 Conn’s Syndrome Inferior suprarenal (renal)
Right vein to drain to IVC, Left vein drains
to renal vein
Anatomy of Adrenal Gland Physiology
Mineralocorticoids, glucocorticoids, and androgens (MGA)

Mineralocorticoids à outer glomerulosa à aldosterone à fluid
Cortex
and electrolyte balance (RAAS system)
Lipid laden
Glucocorticoidsà inner fasiculata and reticularis à cortisol
Bright yellow
Regulated by ACTH and CRH
Three Zones (glomerulosa, fasiculata, reticularis)
Anti-inflamatory and immunosuppressive
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Medulla
Elevate blood glucose
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Dark gray
Contain chromaffin cells that secrete sympathetic hormones Adrenal sex steroids à reticularis à male and female sex
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hormones
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Blood flow from cortex to medulla then exit via central medullary
venous system Release regulated by ACTH
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Adrenal Cortex
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Aldosterone Secretion
Hormone Production
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Regulated by ->
Decreased afferent arteriolar pressure in renal cortex
Decrease Na, increase K content in renal tubule
ACTH secretion much lesser degree but some effect
Renin converts angiotensinogen to Angiotensin I in kidney
Angiotensin converting enzyme (ACE) converts AT I to AT II in the
lung
AT II simulates aldosterone production
Aldosterone stimulates Na-K exchange, dumps H+ as well
Aldosterone Secretion Cortisol Secretion Pathway
Neural control stimulus

ex. Stress, fear, pain, hypoglycemia
Corticotropin releasing hormone from hypothalamus
stimulates
-> ACTH from Anterior Pituitary which then has its effect on
cortisol
Cortisol has negative feedback on CRH
Cortisol Secretion Cortisol Effects
Permissive effect on glucagon

Memory, learning & mood
Gluconeogenesis
Skeletal muscle breakdown
Lipolysis, calcium balance
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Immune depression
Circadian rhythms
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Steroid Physiology
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Diseases of the Cortex

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Cortisol binds to specific plasma proteins

Unbound forms pass freely through cell membrane to target receptors
in nucleus
Steroid Receptor Site
cortisol almost all tissues
androgens, estrogens breast, prostate, genitalia
Cushing’s syndrome or disease (elevated exogenous cortisol, or
aldosterone renal tubule, salivary ACTH mediated)à Central obesity, hirsutism, humpback,
gland, colonic mucosa
glucose intolerance
Hyperaldosteronism (adenoma versus hyperplasia, primary

versus secondary)
Hyperaldosteronism Hyperaldosteronism
Less common cause of HTN

Primary
Autonomous-> unilateral or bilateral SHOULD BE SUSPECTED IF !!!
Can be familial genetic disorder with overactive Hypertension + Hypokalemia + Metabolic alkalosis =
gland or glands
Hyperaldosteronism
Ectopic tumors
Primary malignancy
Secondary
Increase renin production secondary to RAS,
cirrhosis, CHF, etc
Paraneoplastic tumors secreting renin
Hyperaldosteronism
Who should be screened ?

Hypertension Hypokalemia
Adrenal mass
Sleep apnea
FH of young CVA
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Any FH of the disease

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Atrial Fibrillation
Refractory HTN
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Hyperaldosteronism Hyperaldosteronism
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Screening
1. Plasma aldosterone AND renin levels upright position
2. A:R ratio >20-25 mg/dL with aldosterone >15mg/dL and
Interfering drugs: renin less than 0.5 is suggestive

3. Confirmation testing with 24 hour urine aldosterone, sodium,
Cr and K+ while on high salt diet or saline infusion
4. 24 hour aldosterone levels SHOULD be greater than 12ug/dL
after infusion or high salt diet
5. BEFORE adrenalectomy-> adrenal vein sampling for Bl
adrenal nodularity, nodule 1cm or less, normal appearing glands or
age >35
Hyperaldosteronism
Adenoma (Conns syndrome) versus Hyperplasia

Medical treatment with Spironolactone
Inhibits Na-K exchange in distal renal tubule
Gynecomastia with long-term use
Surgical treatment
Removal of adrenal gland with bilateral hyperplasia
seldom is seldom curative
Must treat hypokalemia and dehydration pre-op
Hyperfunctioning adenoma or unilateral hyperplasia
-> lap adrenalectomy
Hypercortisolism Hypercortisolism
Who should be tested->

Unexplained osteoporosis or HTN in young pt
Adrenal masses
Clinical appearance of typical features
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Take a GOOD history for medications!!!

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Hypercortisolism
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Subclinicial Cushing’s
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Screen Subclinical Cushing’s syndrome (SCS) à suggested

Low Dose Dexamethasone suppression (primary testing) by failure to suppress cortisol with DMST and
absence of obvious symptoms
If fail to suppress less than 1.8ug/dl then further testing with ACTH
levels May have HTN, DM, obesity
24 hour cortisol 24 hr urine cortisol slightly elevated and low or
PM salivary cortisol suppressed ACTH
High Dose Dexamethasone suppression Risk of progression to clinical CS is 12.5% at one year
Should suppress the pituitary axis in Cushing’s disease
Superior outcomes with surgery c/w conservative
ACTH in AM should be low mgt
IF ACTH very high despite this, might be paraneoplastic origin of
ATCH
Treatment of Cortex Disease Pituitary Anatomy
Cushing syndrome secondary to adenoma-> Unilateral Adenohypophysis (anterior)

adrenalectomy with steroid replacement or stress dosed with TSH, ACTH, GH, LH, FSH, DA (inhibits Prolactin)
taper
Neurohypophysis (posterior)
ADH (vasopressin), oxytocin
Cushing’s Disease (pituitary

Pituitary Mass Work-up source of cortisol)
ACTH producing pituitary adenoma

MRI depicts intrasellar masses as small as 5mm Cause of 80% of cases presenting as Cushing’s
CT better depicts calcification Syndrome (HTN, moonfacies, hirsutism, striae, buffalo
hump, etc.)
Often useful for craniopharyngioma (can present with
High Dose Dexamethasone test
optic chiasm compression)
Often no tumor identified with imaging (75%
Obtain baseline hormone levels
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microadenoma)
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Can use petrosal sinus sampling for ACTH for

hemiresection
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Radiation indicated with failed surgery

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Nelsons Syndrome Nelson’s Syndrome

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Functioning pituitary adenoma (ACTH) after bilateral

adrenalectomy for hypercortisolism
Presentation:
Progressive hyperpigmentation
Visual file loss (bi-temporal hemi-anopsia)
Amenorrhea
Symptoms secondary to excess ACTH production
Treatment: Surgery or radiation
Adrenocortical Carcinoma Adrenocortical Carcinoma
2 cases per one million persons per year

F:M = 2:1
5 year survival 32-50% for surgical disease
With metastatic disease-> one year median survival
Adrenocortical Carcinoma Adrenocortical Carcinoma
Diagnosis
Age bimodal, 5 and 60 yrs old
Suspected with rapid onset Cushing’s syndrome
Most commonly presents with stage III, IV disease (75%)
> 6 cm ion diameter, heterogenous, lymphadenopathy, local
Present with Mets in 40% and 85% recur locally or distant
invasion
40-60% are hormonally active
T2 MRI with higher signal intensity and T1 heterogenous
R>L enhancement
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CAP CT, +/- brain MRI

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Clinical Characteristics Clinical Characteristics

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Incidental detection versus tumor-related symptoms

Local symptoms: abdominal fullness, back pain, nausea and
vomiting.
Systemic / metastatic features: Anorexia, anemia, asthenia and
weight loss and features of metastasis.
Hormone secreting ACC
Role of biopsy Adrenocortical Carcinoma
Percutaneous needle biopsy is generally not performed prior to Management

surgical excision
Bad malignancy
Clinically unacceptable risk of needle tract seeding
Aggressive resection = en bloc if possible, >90%
Biopsy only when it will change to plan disease can be removed
Chemo = platinum based+ etoposide+/-
doxorubicin +/-Mitotane
Adjuvant radiation after resection?
Most need lifelong steroid replacement
Surgical Management ACC MEDICAL THERAPY
Mitotane is most commonly used

chemotherapeutic agent in the treatment of
adrenal cortical carcinoma.
Benefit in the adjuvant setting following surgical
resection and in patients with metastatic disease
A significant increase in disease free survival and
overall survival was noted in patients receiving
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Adrenal Insufficiency Adrenal Insufficiency

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Circulatory collapse in acute setting

Usually due to chronic steroid use
Symptoms: hypotension, unresponsiveness to resuscitation
Dx: ACTH stimulation test after obtaining baseline ACTH
and cortisol levels
Adrenal Insufficiency Adrenal Insufficiency
Treatment-> fluid replacement and steroid

administration
Diagnosis is 3 part process: Prevention is key!
1. Demonstrate low levels -Establish chronicity of steroid use and dose,
2. Determine contribution from ACTH and careful history of previous surgeries
concurrent Aldosterone levels -ANY DOSE LESS THAN 3 weeks DOES NOT REQUIRE
3. Primary/secondary/tertiary reason STRESS DOSES
-> 20 mg of prednisone or equivalent for >3 weeks
needs stress does steroids.
Pheochromocytoma Pheochromocytoma
Catecholamine secreting tumors (less than 0.2% of pts with HTN

M = F, 4th - 5th decade, most sporadic, can be hereditary Symptoms-> HTN paroxysmal or sustained, headache,
Rule of 10’s
sweating or asymptomatic entirely
Bilat 10%, NE and Epi production primarily affect alpha receptors for
vasoconstriction
Extra-adrenal 10%
+ Screen but no mass, consider venous sampling, then
Familial 10%, unilateral adrenalectomy
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Multicentric 10% 10% bilateral, unless associated with MEN II where 70%
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Malignant 10% bilateral=>pre-op MIBG can be helpful

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Children 10%
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MEN II 10%
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Diagnosis Pre-op Management:

Alpha-adrenergic blockade with
Plasma fractionated metanephrines first selective (Terazosin, Doxazosin,
etc) or non-selective
If mildly elevatedà 24 hours urine catecholamines or Phenoxybenzamine (alternative
metanephrines should be performed phentolamine used intrap)à 7-
14 days before
VMA (least specific and not recommended any longer) Can add Ca channel blocker if
needed
Imaging
Beta-adrenergic for tachy,
98% found in abdomen, 2 % thorax, 1% neck dysrhythmia or epi-secreting
tumors
CT, MRI 87-100% sensitive Volume repletion and high salt
diet
I131-MIBG 77-87% sensitive
Treatment of Treatment of
Intraoperatively->use nitroprusside to lower BP Anterior approach

Treat post-operative hypotension with Levophed and fluids Posterior approach
Arrythmias-> Esmolol or Lidocaine Laparoscopic/Robotic approach (up to 10cm diameter)
Goal in surgery is to ligate adrenal vein quickly and avoid Minimal handling of tumor
manipulation
Early isolation of vein
If BP does not decrease, then look for second
Avoid capsular rupture
pheochromocytoma
Pheochromocytoma Overview
Adrenal Incidentaloma
0.35 - 5% of abdominal CT
10% Functional
5% pheo (10% of pheos are incidentalomas)
7% aldosterone
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0.06 carcinoma
All patients with incidentaloma should BE SCREENED
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How it Happens in the Real

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Adrenal Incidentaloma World

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Most are nonfunctional Size matters

CT performed for some other reason that finds an
adrenal massà Gets sent to you? What do you do?
When to operate?
Appearance matters
Incidentaloma
What kind of imaging do your order to better

characterize?
What characteristics are important
Biochemical workup
Patient history ?
Incidentalomas of the Adrenal should be surgically treated if:
1. Less than 3 cm in greatest diameter and stable in size
2. Asymptomatic
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3. Non-functional
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4. Functional
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Incidentalomas of the Adrenal should be surgically treated if:

Cushing’s Syndrome exhibits:
1. Less than 3 cm in greatest diameter and stable in size
1. Hyperaldosteronism
2. Asymptomatic 2. Hypokalemia
3. Non-functional 3. Renal calcinosis
4. Hypercortisolism
4. Functional (correct)
Any adrenal incidentaloma greater than 4cm or growth of 0.5cm

in 6 months and any functional neoplasm
Cushing’s Syndrome exhibits:

1. Hyperaldostrone Adrenal Incidentalomas are:
1. Never functional
2. Hypokalemia
2. Always functional
3. Renal calcinosis
3. Variably functional
4. Hypercortisolism (correct)
4. Unnecessary to evaluate functionality
Cushing’s Syndrome is hypercortisolism and Cushing’s
disease is pituitary mediated hypercortisolism (pit. adenoma)
Adrenal Incidentalomas are: The usual arterial supply to the adrenal gland include all
but the following?
1. Never functional
1. Superior suprarenal (inferior phrenic)
2. Always functional
3. Variably functional (correct)
2. Middle suprarenal (aorta)
4. Unnecessary to evaluate functionality
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3. Inferior suprarenal (renal)

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Approx. 10% of incidentalomas are functional (think

pheo).
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4. Gastroduodenal
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References
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1. Superior suprarenal (inferior phrenic) NCCN guidelines 2021

Current Surgical therapy
2. Middle suprarenal (aorta)
Textbook of General Surgical Oncology
https://www.annalsthoracicsurgery.org/article/S000
3. Inferior suprarenal (renal) 3-4975(11)01916-3/fulltext
4. Gastroduodenal (correct)
The arterial supply to the adrenal usually comes from

three arteries. The veins, however do not parallel the
arteries.
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MULTIPLE ENDOCRINE NEOPLASIA

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& MEDULLARY THYROID CANCER MULTIPLE ENDOCRINE NEOPLASIA

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§ Prevalence 1/10,00 to 1/100,000

§ Autosomal dominant syndromes
§ Tumors in multiple endocrine and non-endocrine tissues
§ Genotype – phenotype relationships*
Matthew Strode, D.O.

Surgical Oncology
Fort Bragg, NC
WHICH OF THE FOLLOWING MAY WHICH OF THE FOLLOWING MAY

OCCUR WITH MULTIPLE ENDOCRINE OCCUR WITH MULTIPLE ENDOCRINE
NEOPLASIA(MEN) TYPE I SYNDROME ? NEOPLASIA (MEN) TYPE I SYNDROME ?
§ A. Pancreatic Islet Cell Tumors § A. Pancreatic Islet Cell Tumors
§ B. Medullary Thyroid Cancer § B. Medullary Thyroid Cancer
§ C. Pheochromocytoma § C. Pheochromocytoma
§ D. Papillary Thyroid Cancer § D. Papillary Thyroid Cancer
§ E. Follicular Thyroid Cancer § E. Follicular Thyroid Cancer

NEOPLASIA (MEN) TYPE IIA NEOPLASIA (MEN) TYPE IIA
SYNDROME? SYNDROME?
§ A. Pancreatic Islet Cell Tumors
§ A. Pancreatic Islet Cell Tumors
§ B. Medullary Thyroid Cancer
§ C. Pituitary Tumors
§ C. Pituitary Tumors
§ D. Papillary Thyroid Cancer
§ D. Papillary Thyroid Cancer
§ E. Follicular Thyroid Cancer
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§ E. Follicular Thyroid Cancer

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NEOPLASIA (MEN) TYPE IIB NEOPLASIA (MEN) TYPE IIB

SYNDROME ? SYNDROME ?
§ A. Marfanoid Body Habitus
§ A. Marfanoid Body Habitus
§ C. Pheochromocytoma
§ C. Pheochromocytoma
§ D. Cutaneous Neuromas
§ D. Cutaneous Neuromas
§ E. All of the above
§ E. All of the above
MULTIPLE ENDOCRINE NEOPLASIA MULTIPLE ENDOCRINE NEOPLASIA

Each MEN type is associated with the occurrence of specific tumors.
Multiple endocrine neoplasia (MEN) is characterized by the
occurrence of tumors involving two or more endocrine glands § MEN1
within a single patient. § Parathyroid, pancreatic islet and anterior pituitary tumors (and
§ Major forms of MEN, which are all autosomal dominant others)
disorders, are recognized and referred to as:
§ MEN2a
§ Medullary thyroid carcinoma (MTC) develop in 90% develop
§ MEN1 - Menin mutations - Chromosome 11q13 § Pheochromocytoma unilateral or bilateral in 50%
§ Primary hyperparathyroidism in 15-30%
§ MEN2a due to mutations of a tyrosine kinase receptor § MEN2b

encoded by the Rearranged during Transfection (RET) § MTC-> develop MTC very early infancy
protooncogene (includes FMTC) § Pheochromocytoma -> develop around puberty in 50%
§ Marfanoid habitus, mucosal neuromas, medullated corneal
§ MEN2B due to RET mutation fibers and intestinal autonomic ganglion dysfunction, leading to
megacolon
9
MEN-1 TUMORS MEN – 1: CLINICAL DEFINITION

Pituitary adenomas (anterior)
Enteropancreatic tumors
Primary hyperparathyroidism
Foregut carcinoids
§ 2 of the following:
Cutaneous manifestations
§ Primary hyperparathyroidism
Adrenal tumors
§ Enteropancreatic neuroendocrine tumor
95% of patients develop clinical symptoms by the 5th decade of life (youngest 5
§ Pituitary adenoma
years)
OR
Endocrine Lesions Non-Endocrine Lesions
§ At least 1 of the above PLUS a first-degree relative with MEN-
Parathyroid hyperplasia Facial angiofibroma 85%
1
90%- early age
OR
Endocrine pancreatic tumors Collagenomas 70%
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30-80% § Known germline MEN-1 mutation

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Anterior pituitary adenomas Lipomas 30%

40% Thakker RV, Newey PJ,Walls GV, et al. Clinical practice guidelines for multiple
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Adrenocortical lesions 20-50% Leiomyomas 10% endocrine neoplasia type 1 (MEN1). J Clin Endocrinol Metab 2012;97:2990-
3011.
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Foregut carcinoids 15% Meningiomas 5%

Ependymomas 1%
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MEN -1: GENETICS

§ MEN-1 gene identified in 1997
§ Chromosome 11q13
§ The protein product is menin
§ Highly conserved among species
§ Expression is ubiquitous
§ Believed to be a tumor suppressor
§ Over 1133 different germine mutations and 203
somatic mutations identified
Lemos MC, Thakker RV. Multiple endocrine neoplasia type 1 (MEN1):

analysis of 1336 mutations reported in the first decade following
identification of the gene. Human mutation 2008;29:22-32.
MEN -1: GENETICS MEN -1: GENETICS

§ Autosomal dominant inheritance pattern
§ Men and women equally affected
§ All racial groups
§ A single inactivated copy of the MEN-1 gene is present in all
cells of the patient.
§ A second inactivation (second “hit”) results in clonal expansion
(i.e. neoplasia).
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§ 70-90% of MEN-1 kindreds have a mutation identified

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§ 10% of cases are believed to be de novo

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MEN – 1: MEN – 1:
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PRIMARY HYPERPARATHYROIDISM PRIMARY HYPERPARATHYROIDISM

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§ Most frequent and earliest onset § Disease course similar to sporadic primary hyperparathyroidism
§ Penetrance 90-99% § Osteopenia by age 35
§ Age of onset 20-25 years old § Nephrolithiasis in 50%
§ Discovered on routine labs, renal stones, or vague § Surgical indications similar to sporadic primary hyperparathyroidism
abdominal pain
§ Localization studies or imaging rarely helpful and often misleading
§ Asymmetric 4 gland hyperplasia
§ largest gland usually 10x bigger than the smallest gland
MEN – 1: MEN – 1:
PRIMARY HYPERPARATHYROIDISM ENTEROPANCREATIC LESIONS
§ Subtotal parathyroidectomy or total parathyroidectomy with § Penetrance 30-80%
autotransplant in forearm § Age of onset 30-40
§ Utilize cryopreservation when possible
§ Usually multiple small lesions
§ Transcervical thymectomy
§ Frequently malignant – most common cause of death and
§ Supernumerary glands 6%
morbidity in MEN-1
§ 50% of missing glands are in thymus
§ Thymic carcinoid 8% § Functional and non-functional
§ Recurrence rate after subtotal parathyroidectomy = 40-60% at 10

yrs and total parathyroidectomy with autotransplant >50% at 10
years
§ Hypoparathyroidism = 10-30%
MEN – 1: PANCREATIC NET - SCREENING

ENTEROPANCREATIC LESIONS § Annual plasma biochemical evaluation of a fasting gastrointestinal tract
§ Gastrinoma hormone profile
§ 60% of MEN1 patients have gastrinoma or asymptomatic § gastrin
elevation in gastrin
§ glucagon
§ Causes Zollinger-Ellison Syndrome
§ Usually small and multiple in duo or single type II § vasointestinal polypeptide (VIP)
carcinoid in stomach § pancreatic polypeptide (PP)
§ Usually malignant (60-90%) § chromogranin A
§ 50% are metastatic at diagnosis
§ Fasting insulin and glucose
§ Usually located in duodenal submucosa (80%)
§ Only 20% of gastrinomas are related to MEN 1, with the
rest 80% sporadic. Therefore, the lack of a MEN 1 tumor
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family history does not rule out the diagnosis of § A consensus for optimum radiological screening has not been established.
gastrinoma. A suggested minimum imaging protocol includes annual pancreatic and
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§ Insulinoma duodenal visualization with magnetic resonance imaging (MRI), computed

§ Second most common functional neuroendocrine tumor tomography (CT), or endoscopic ultrasound.
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in MEN1
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§ 10-33% malignant Thakker RV, Newey PJ, Walls GV, et al. Clinical practice guidelines for multiple endocrine
§ Often multiple neoplasia type 1 (MEN1). J Clin Endocrinol Metab 2012;97:2990-3011.
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PANCREATIC NET - TREATMENT

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§ Medical therapies include proton-pump inhibitors and somatostatin

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analogs to suppress hyperacidity. Periodic gastroscopic surveillance

§ The main aim is to maintain patients disease- and is indicated in those with hypergastrinemia for the identification of
peptic ulcer disease and gastric carcinoid.
symptom-free for as long as possible and to keep a
good quality of life. § The role of surgery for nonfunctioning pancreatic tumors is
controversial. We suggest considering surgery for tumors that are
§ The aim of treatment for individuals with symptomatic more than 1 cm in size and/or demonstrate significant growth over 6–
12 months.
functioning pancreatic NET including insulinoma is to
§ Treatment of nonresectable tumor mass includes somatostatin
achieve cure, if possible, by surgery. analogs, biotherapy, targeted radionuclide therapy, locoregional
§ The extent of disease should be evaluated fully before treatments, and chemotherapy .
planning specific therapy. § Chemotherapy may be used for inoperable or metastatic pancreatic
NET. Sunitinib and everolimus may be considered for patients with
advanced (inoperable or metastatic) progressive well-differentiated
pancreatic NET.
Thakker RV, Newey PJ, Walls GV, et al. Clinical practice guidelines for multiple endocrine Thakker RV, Newey PJ, Walls GV, et al. Clinical practice guidelines for multiple endocrine
neoplasia type 1 (MEN1). J Clin Endocrinol Metab 2012;97:2990-3011. neoplasia type 1 (MEN1). J Clin Endocrinol Metab 2012;97:2990-3011.
MEN – 1:
ANTERIOR PITUITARY TUMORS
§ Age of onset 30-40
§ Usually macroadenomas (85%)
§ Prolactinoma - galactorrhea
§ GH - Acromegaly
§ Non-functional
§ ACTH – Cushing’s Disease
§ Mass effect
§ Optic nerve compression
§ Headache
§ Hypopituitarism
§ 1/3 are invasive
MEN – 1: MEN – 1:
ANTERIOR PITUITARY TUMORS ADRENAL LESIONS
§ Treatment Surgery vs Pharmacologic
§ Prolactinoma: Cabergoline
§ Penetrance 15-20%
§ Acromegaly: Somatostatin analogs
§ Non-functional: Surgery
§ Bilateral
§ Cushing’s: Surgery § Often non-functional, usually Indolent
§ Failure to pharmacologically inhibit
§ Transsphenoidal hypophysectomy § Hypercortisolism, hyperaldo - rare
§ Surgical failure § Pheochromocytoma – very rare
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§ Radiation therapy
§ ACC – very rare
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§ Surgery for functional tumors, 4 cm size

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Screening Guidelines for MEN-1

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MEN – 1:
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MALIGNANT LESIONS
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§ Biochemical screening is recommended yearly

§ 50% of MEN-1 patients develop a syndrome related cancer with tumor imaging beginning once carrier status
§ Endocrine pancreas
§ Duodenum
is established, or beginning before age 10 if
§ Thymus already established, and continuing for life.
§ Most common cause of death is endocrine pancreas tumor – usually
non-functional and metastatic
Thakker RV, Newey PJ, Walls GV, et al. Clinical practice guidelines for
multiple endocrine neoplasia type 1 (MEN1). J Clin Endocrinol Metab
2012;97:2990-3011.
MEN-2A
FAMILIAL MTC (FMTC)
§ Medullary Thyroid Cancer: 90-100%
§ MTC is the first endocrinopathy to develop
§ Multigenerational transmission of MTC in which no family member
§ Multifocal and bilateral
has PHEO or PHPT.
§ Usually the cause of death
§ The typical age of onset of this condition is later in life than MEN 2A
§ Primary Hyperparathyroidism: 15-30%
§ Asymmetric hyperplasia § The penetrance of MTC is lower
§ Pheochromocytoma: >50% § Hirschsprung's disease 2-5%

§ Unilateral or bilateral
§ Considered by most to be MEN2A
§ Cutaneous Lichen Amyloidosis (634 mutations)
§ Hirschsprung's disease 2-5%
MEN-2B MEN-2B
§ Medullary Thyroid Cancer: 100%
§ Gastrointestinal abnormalities: 90%
§ Early age of onset – infancy <1 year
§ Vomiting
§ Highly aggressive – nodal metastases <3 years § Dehydration
§ Pheochromocytoma: 50% § Constipation: 60-100%*
§ Unilateral or bilateral § Megacolon: 67-100%
§ No Hirschsprung's
§ Mucosal Neuromas: 100%
§ Proliferative lesions of nerves and Schwann cells § Inability to cry tears: >85%*
§ Lips, tongue, and conjunctivae most common § Markedly enlarged peripheral nerves
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§ Marfanoid Habitus
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§ Skeletal abnormalities
§ Slipped capital femoral epiphyses, and club foot
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*Brauckhoff et al. Surgery. Dec 2008;144(6):1044-1050

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MEN-2B MEN 2 SYNDROMES ARE CAUSED BY GERMLINE

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ACTIVATING MISSENSE MUTATIONS IN THE RET

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ONCOGENE.
§ RET gene first identified in 1985
§ MEN2A, FMTC, and MEN2B linked to germline RET mutations in 1993 1
and 1994
§ Somatic RET mutations have been found in 40-50% of sporadic MTC.
§ Genotype-phenotype relationships
1Donis-Keller et al. Hum Mol Genet. Jul 1993;2(7):851-856.
RET = REARRANGED DURING TRANSFECTION
RET encodes a tyrosine kinase on chromosome 10q11.2
FACTS ABOUT RET RET TESTING

§ Most common MEN2 is MEN2A § At risk family members (at birth if possible)
§ Most common MEN2A is due to mutation § Preimplantation testing
affecting cysteine residues in RET codon 634
§ Adults with medullary thyroid cancer or
§ About 20% of apparently sporadic MTC are new
index cases of MEN2A pheochromocytoma
§ >95% of MEN2B are due to M918T mutation § Infants with Hirschsprung's Disease
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§ >50% of MEN2B are de novo germline mutations

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§ Germline RET mutations have been implicated

in 10–40% of cases of Hirschsprung’s disease.
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MEN 2 TUMORS PHEOCHROMOCYTOMA

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§ Pheochromocytoma (MEN2a and MEN 2b) § Pheochromocytoma (MEN2a and MEN 2b)
§ 40-50% of MEN 2 patients develop
§ Hyperparathyroidism (MEN2a) pheochromocytoma
§ Medullary thyroid cancer (MEN 2a, FMTC, § Present at a younger age (30-40 years)
MEN2b) § Classic symptoms in only 50%
§ Commonly bilateral (>50%)
§ Screening begins if suspected or proven mutation
Interventions are based on the results of § Positive or borderline results lead to imaging
screening studies, biochemical tests and codon
mutation
MEDULLARY THYROID CANCER

HYPERPARATHYROIDISM
§ Medullary thyroid cancer, (MTC), is a tumor of the parafollicular c-
cells of the thyroid gland. These cells are derived from the embryonic
neural crests and make up 1% of thyroid cells.
§ Hyperparathyroidism (MEN2a only)
§ 20-35% of MEN 2a patients develop hyperpth
§ Presents later than MTC
§ Less severe than in MEN1
§ 80% due to multigland disease
§ Screening begins at the age when thyroidectomy
would be considered
§ Subtotal parathyroidectomy vs total
parathyroidectomy with forearm autograft
§ C-cells can be found anywhere in the gland but are concentrated in TUMOR MARKERS
the posterior upper poles of the thyroid lobes.
§ Primary tumor markers
§ Calcitonin Doubling time
§ flushing, diarrhea
§ CEA
§ MTC may also secrete

§ Chromogranin A
§ Serotonin
§ Neuron specific enolase
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§ Somatostatin
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§ Gastrin related peptide

§ Substance P
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SURVIVAL
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LYMPH NODE METASTASES

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§ Overall 10-yr survival is 70% to 80%1

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§ Distant metastatic disease10-yr survival < 50%1

§ Lymph node metastases (LNM) from MTC are common in adults
and are a poor prognostic factor.
§ In adult MTC, LNM are present in more than 75% of cases and
in 30% of tumors smaller than 1 cm.
1Roman,S et al Cancer. 2006 Nov 1;107(9):2134-42.

SEER database 1973-2002. N=1252. 29 year follow up.
LOCALLY ADVANCED DISEASE METASTATIC DISEASE

Symptoms associated with local compression § <15 % present with distant disease to:
or invasion are present in up to 15% of § Liver
§ Lungs
patients with MTC. § Bone
§ Brain
§Hoarseness § Subcutaneous tissues
§Dysphagia § Flushing and diarrhea are common complaints with

advanced disease (due to high calcitonin)
§Cough
§Shortness of breath
PROPHYLACTIC THERAPY IN CHILDREN

§ Prophylactic total thyroidectomy for inherited disease
§ Before age 5 in MEN2A and FMTC*
§ Before age 1 in MEN2B
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Wells et al. Thyroid Vol 25, No 6, 2015. p567.

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AGE AND LNM
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YEAR AND LNM
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100%
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100%
90%
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90%
80%
80%
70%
Percent of Patients
70%
Percent of Patients
60%
no LMN 60%
50% LNM no LMN
60%
50%
40% LNM
43.8% 40%
30% 41.5%
32.5% 30%
20% 29.7%
20% 26.2%
10%
12.5% 10%
0%
0%
0 to 6 7 to 12 13 to 18
(n=16) (n=40) (n=89) 1985-1990 1991-1994 1995-1997 1990-2001
1998-2001
Age Categories in years (n=25) (n=41) (n=37) (n=42)
(P = 0.045)
Year Categories
(P=0.03)
Raval MV, Sturgeon C, Bentrem DJ, et al. Influence of lymph node metastases on
survival in pediatric medullary thyroid cancer. Journal of pediatric surgery
2010;45:1947-54.
AMERICAN COLLEGE of SURGEONS AMERICAN COLLEGE of SURGEONS
10-YEAR SURVIVAL BY LNM STATUS SURVIVAL BY AGE GROUP

OVERALL SURVIVAL = 95.3% 1.0-
1.0- 98.4%
99.4%
0.9- 0.9-
91.7%
0.8- 81.5% 0.8-
AMERICAN COLLEGE of SURGEONS AMERICAN COLLEGE of SURGEONS
SYSTEMIC THERAPY
Normal RET Mutation
FDA APPROVED MULTIKINASE INHIBITORS FOR
PROGRESSIVE METASTATIC AND UNRESECTABLE
MTC
•Vandetanib (Caprelsa) April 2011
•Carbozantinib (Cometriq) November 2013

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•EBRT or IMRT
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CONCLUSIONS – MEN 1 CONCLUSIONS – MEN 2 / FMTC

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§ Autosomal Dominant § Autosomal dominant

§ Pit – Pan – Para § Medullary thyroid cancer (all)
§ Cutaneous manifestations § Hyperparathyroidism (2a)
§ Foregut Carcinoids § Pheochromocytoma (2a and 2b)
§ Adrenal lesions § Genotype – phenotype relationships
§ No genotype – phenotype relationships § Genetic screening at birth
§ Annual biochemical screening and imaging begins at age 5 § MTC is the usual cause of death
§ Malignant enteropancreatic lesions
CONCLUSIONS – GENETIC TESTING
§ NCCN guidelines 2019

§ Current Surgical therapy 12th edition 2017
§ Textbook of General Surgical Oncology 2017
§ UPTODATE.com
§ Genetic consult before testing
§ False negative rates are higher in MEN1
gene testing
§ RET testing guides potentially curative
interventions
ANY QUESTIONS? rg e
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Mediastinum &
Chest Wall Disorders
Ahmed Mahmoud, MD
Associate professor of clinical surgery
[email protected]
Incidence
• 60% of Mediastinal masses in adults are: • In children the most common are (80%) are:
– Thymoma – Neurogenic tumors
– Neurogenic tumors – Germ cell tumors
– Benign cysts – Foregut cysts
– lymphadenopathy
Myasthenia Gravis Myasthenia Gravis

• Autoimmune disease • Diagnosed in 30-50% of patients with
– Exertional voluntary muscle weakness Thymoma
– Caused by antibodies to acetylcholine receptor • 50-70% of patients have a drug free
complex of motor end plate remission after Thymectomy
– Bimodal age distribution • Thymoma found in 15% of Myasthenics
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– Women to men ratio of 2:1

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• 10% of patients have other associated

autoimmune disorders
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S}Mahmoud (7/6/2021) Mediastinum and Chest Wall page 1

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Myasthenia Gravis Thymoma

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• Optimize medically prior to operation (i.e. • The most common anterior mediastinal mass
plasmapheresis or large steroids doses)
in adults
• Anti choline esterase: neostigmine is medical treatment
• Intraoperatively avoid neuromuscular blocking agents • 50% of thymoma are malignant
– Volatile inhalational agents and short acting narcotics are the • Patients are often asymptomatic but may
best anesthetic choice
present with chest pain, cough, or dyspnea
• Complete thymectomy should be done through a
median sternotomy • Often indolent but can be locally invasive and
• Clinical improvements after thymectomy are not recur at local or distal sites
immediate • Surgical resection is the mainstay of treatment,
including stage III and IV a thymomas
Thymomas Thymomas
• Histologic evidence of malignancy is • Treatment is complete thymectomy through a median
difficult to obtain sternotomy
– Stage I – surgery alone
• Benign and malignant lesions can have
– Stage II and III – post op radiation after complete
similar histologic and cytologic features resection
• Surgical evidence of invasion at the time of – Stage IV – optimal treatment unknown
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resection is the most reliable method of

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• Surgery, chemo, and radiation therapy

differentiating between malignant and – Phase II studies have suggested improved survival
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for pre op chemo-Rtx in stages II, III, and IV a

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benign Thymomas
• Post op follow up for 10 years
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Surgery for Thymus

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• Median sternotomy
• Complete resection entails removal of all
structures attached
• Phrenic nerve is controversial
Lymphoma
• Anterior mediastinal
• Large Mass ++
• Dx: Surgical incisional Bx
• Treatment: non surgical
• T cell = Chemotherapy
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• B cell = Chemo + XRt

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• Hodgkin has better prognosis

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• Surgery only for residual masses

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Germ Cell Tumors Germ Cell Tumor: Seminoma

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• Classification; benign teratoma – Seminoma • Tumor markers, HCG increase in 10% AFP is
– nonseminoma not elevated
• Non seminoma are: teratocarcinoma-yolk • Treatment is non surgical
sac tumor-choriocarcinoma-endodermal • Radiation + Cisplatinum chemo = up to 100%
sinus and embryonal cell cure
• Benign teratoma is entirely benign: • Residual tumor = Salvage chemo
treatment is surgical excision only • Residual tumor may be teratoma especially if
tumors markers normalize after chemo
Non Seminoma Germ Cell Tumor

• Tumor markers are elevated in most cases:
AFP 80% and HCG 20%
• Non surgical ttt
• Chemotherapy: cisplatinum based
• Residual Salvage Chemo
• Follow up by Tumor markers
Thoracic Aorta Pathology

• Ascending aorta are middle mediastinal
structures
• Descending aorta are posterior mediastinal
structures
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Types/Degrees of Aortic Dissection True/False Lumen

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Trachea
Mediastinal Compartments
• Anterior- prevascular compartment
– thymoma, lymphoma, germ cell
– thyroid, parathyroid
• Visceral- central or Middle compartment
– foregut cysts: bronchogenic, esophageal
– lymphoma, pericardial cyst
• Paravertebral- posterior compartment
– neurogenic: neurilemoma, neurofibroma,
ganglioneuroma, neuroblastoma
Thoracic Duct / Chylous Effusion

Posterior Mediastinum
• Structures in post mediastinum are:
– Sympathetic ganglia
– Nerve roots
– Lymph nodes
– Parasympathetic chain
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– Thoracic duct
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– Descending thoracic aorta

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Pathology
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• Most masses in posterior mediastinum are • Neurogenic Tumors

neurogenic in origin. They could arise from – Most common tumors arising in the posterior
sympathetic chain (neuroblastoma) or from compartment.
never roots (schwannoma – neurofibroma) – Includes schwannoma, Neurofibroma,
ganglioneuroblastoma, neuroblastoma,
Pheochromocytoma, and paraganglioma
Neurogenic Tumors
• Posterior mediastinum
• 90% benign
• Commonly asymptomatic
• May extend into vertebral foramina
• Complete surgical excision
• Malignancy needs post op XRT
Middle Mediastinum Posterior Mediastinum

• Following structures: • Enteric duplication cysts arising from
– LNs esophagus
– Trachea
– Esophagus
– Azygos vein
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– Vena cava
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– Posterior heart
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– Arch vessels
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Children (below 15) Chest Wall Tumors

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• Lymphoma are most common anterior mediastinal • Incidence

mass in children with Hodgkin 70% and non – 7-8% of all bony tumors
Hodgkin 30%
– Ribs: 80-90% ( 50% are malignant)
• Germ cell tumors are the second most common
– Sternum: 10-15% (95% are malignant)
anterior mediastinal mass in children
– Male:female = 2:1
• Fat containing tumors in children = teratoma =
benign
• Most Germ cell tumors are benign
• Neurogenic are more malignant in children than
adults
Classification Classification
Benign Malignant
• From Soft Tissue • From bone (ribs, sternum) • Soft tissue • Bone
– Hemangioma (common) – Fibrous dysplasia – Rhabdomyosarcoma – Myeloma
– Lymphangioma – Aneurysmal bone cyst – Ewing Sarcoma – Chondrosarcoma
(Common) – Giant cell tumor – Malignant fibrous – Osteosarcoma
histiocytoma – Ewing sarcoma
– Schwannoma – osteochondroma – Malignant peripheral
– Neurofibroma nerve sheath tumor
– Ganglioneuroma – Dermatofibrosarcoma
– paraganglioma protuberans
Malignant Bony Tumors Chondrosarcoma
• Chondrosarcoma
– General
• most common primary malignant tumor of the chest
wall
• still uncommon (60 per year dx in the US)
• most commonly occurs in the anterior chest wall
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• age = 20-40
• ? After trauma, occ malignant transformation of
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Chondrosarcoma
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Malignant Bony Tumors

Radiology
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• Chondrosarcoma
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– Diagnosis
• X-ray
– lobulated mass arising in the medulla of the bone
– ill defined margin of tumor with extensive
destruction of the bony cortex
– CT important to evaluate extent of invasion
• Pathology
– low grade - hyaline matrix with a few cells
– higher grades have more cellularity
– may combine with other histologic groups
Chondrosarcoma
Malignant Bony Tumors
• Chondrosarcoma
– Treatment
• wide resection
– 5 year survival based on ability to
completely resect the tumor = 67 - 89%
– without complete resection, 50% 5 year
survival
– local recurrence significantly decreases
Clinical Features/Diagnosis
• Metastatic tumors to chest wall are the most • Pain and presence of mass
common of all • Pain more common in malignant tumors
• Breast tumors local recurrences to chest • Asymptomatic in 20-25%
wall • Any age (older more malignant)
• Resection with reconstruction provide the
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• CXR and rib detail films required

best result
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• CT scan-with fine detail

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Malignant Principles of Treatment

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• Chondrosarcoma • Excision rather than incisional biopsy

• Myeloma • Full thickness excision with one rib margin
• Osteogenic sarcoma • Large tumors may warrant incisional biopsy
• Ewing’s sarcoma • Needle biopsy for suspicious metastasis or
myeloma
• Sternal tumors treated by sternectomy
Principles of Chest Wall

Results
Reconstruction
• Defect < 5 cm not reconstructed • Low operative mortality
• Posterior defects do not need reconstruction • Long term survival 50-70%
due to scapula • Survival better with wide excision
• Defects > 5 cm Gore-Tex or • Adjunctive therapy may improve survival
methylmethacrylate
• Soft tissue myocutaneous flaps
– Latissimus dorsi or Pectoralis major
Thoracic Outlet Syndrome (TOS)

• The compression of the subclavian vessels
and brachial plexus at the superior aperture
of the chest
• Most compression factors operate against
the first rib
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• Surgical anatomy
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Etiologic Factors Etiologic Factors

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• Anatomic
– Potential sites of neurovascular compression • Traumatic: rare
• Interscalene triangle – Fractured clavicle
• Costoclavicular space
– Dislocation of head of humerus
• Subcoracoid area
• Congenital – Crushing injury to upper thorax
– Cervical rib and its fascial remnants – Sudden effort of shoulder girdle muscles
– Rudimentary first thoracic rib – Cervical spondylosis; c-spine injuries
– Scalene muscle
• Anterior, middle, minimus
– Other, i.e. enlarged transverse process of C7
Signs and Symptoms Signs and Symptoms

• Depends on the structure that is being compressed • Pain
• Neurogenic (95%) > vascular (5%) – Onset is insidious
• Pain/paresthesias present in 95% of the time
– Involves neck, shoulder, arm and hand
• Motor weakness, atrophy of hypothenar and
interosseus muscles (10% of the time) – Brought on by strenuous physical exercise
• Arm abduction
• Symptoms occur commonly in ulnar nerve
distribution • Neck hyperextension
– Medial aspect of the arm and hand
– 5th finger and lateral aspect of the 4th finger
Signs and Symptoms Diagnosis

• Arterial compression
– Coldness, weakness, easy fatigability of the arm and hand, • H&P
diffuse pain
• Neurologic exam
– Distal emboli
• Post stenotic aneurysm with clot
• Films of chest and cervical spine
• Precursor of arterial thrombosis • Ulnar nerve conduction velocity(UNCV)
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– Raynaud’s phenomenon 7% of pts • Peripheral vascular lab studies

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– Arterial occlusion • Arteriogram /CT angiogram

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• Venous obstruction
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– Effort thrombosis (Paget-Schroetter syndrome)

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Normal Ulnar Nerve Conduction

Differential Diagnosis
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Velocities
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• Cervical spine • > 72 m/sec across the thoracic outlet

– Ruptured disk • > 55m/sec around the elbow
• Brachial plexus • 59m/sec in the forearm
– Superior sulcus tumors • Wrist delay is 2.5-3.5 msec
• Peripheral nerves
– Entrapment syndromes
Ulnar Nerve Conduction Velocity

Therapy
in TOS
• Physical Therapy
• Decreased velocity across the outlet is consistent – UNCV > 60 m/sec – conservative management
with TOS (with following grading) – UNCV < 60m/sec – will most likely need surgery
– < 70 m/sec – neurovascular compression – If PT makes symptoms worse – do surgery
– 66-69 m/sec – slight compression (improve with PT) • Surgical treatment
– 60-65 m/sec – mild compression (improve with PT) – Removal of the first rib and other bony abnormalities
– 55-59 m/sec – moderate compression (surg. Tx) – Division of scalenus anterior muscle (carefully), near by?
– <54 m/sec – severe compression (surg. Tx) – High posterior thoracoplasty (specially in redo cases)
– Anterior approach = supraclavicular approach
– Transaxillary approach
Therapy Therapy
• Subclavian vein thrombosis (Urschel, • Arterial compression
Stoney) – Prompt attention to avoid irreversible ischemia
– Catheter guided thrombolysis and tissue loss
– followed by first rib resection /scalenotomy – Principles of surgical management
promptly in the same hospital admission • Complete removal of anatomic abnormality
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producing subclavian artery compression

– Followed by anticoagulation therapy for 3-6
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• Repair or removal of potentially embologenic

months
arterial lesions
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• Restoration of distal perfusion

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Types of TOS / Treatment Mesothelioma

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• Tumors of pleura with poor prognosis

• Neurogenic à physical therapy • Clear relationship to asbestos exposure. 80% of all
cases are related to exposure
• Vascular (venous) à TPA , SURGERY • Epithelioid is most common type (70%) and the
• Vascular (arterial) à surgery only one where surgery can play a role
• Other subtypes: sarcomatoid and biphasic
• Pleural effusion with pain is almost diagnostic
• Extrapleural pneumonectomy
• Limited role for cytoreductive surgery
• Hard to diagnose it from adenocarcinoma so open
biopsy is commonly required for diagnosis
CME Question 1
• Mediastinal masses: Which of the following
best represent surgeon role?
A. radical curative resection
B. Palliative resection
C. only to make tissue diagnosis
D. standby for radiological tissue sampling
E. resection after chemo
CME Answer 1 CME Question 2

• C • Thymoma and Myasthenia gravis (MG).
– Most mediastinal masses are treated non What is correct ?
surgically because of large size and early A. Thymoma patients 80% have MG
involvement of important structures B. MG patients should have thymus resection
when in thymus crisis
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D. core needle biopsy is diagnostic for thymoma

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CME Answer 2 References

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John Cameron, Jennifer Wilson. Current surgical therapy 12th edition

• C 2017; Pages 861:880
– PHRENIC nerve on the left side is 3 times John Putnam. Sabiston textbook of surgery 20th edition 2017; Pages
more likely injured than right phrenic nerve 1576:1590
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Lung Cancer: Pathology

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• Non small cell lung cancer (NSCLC)

Pulmonary Surgery: • Small cell lung cancer (SCLC)
– In patients with NSCLC: separating adeno cancer
Benign & Malignant from squamous cell cancer is important in treatment
of stage IV tumors (chemotherapy response
Ahmed Mahmoud, MD possible)
Associate Professor of Clinical Surgery • Adeno cancer patients 30% of them have
General Surgery course mutations in EGFR, less commonly ALK
(anaplastic lymphoma kinase) and c ROS
oncogene
Lung Cancer:
Pathological Types
• Adenocarcinoma • Squamous cell carcinoma
– More common in females – Central part of the lung
– Peripheral location – More to obstruct bronchus with distal
– Spread mainly by blood (Brain) atelectasis, cavitation and abscess
– Incidence is increasing (the most common) – Spread more by lymphatics
– Bronchoalveolar is a variant of adeno with the
best prognosis of all when localized
Clinical Presentation
• Small cell (oat cell) • Nonspecific presentation
– Worse prognosis – cough, hemoptysis, loss of weight,
– Arises from neuroendocrine cells • CXR

– any solitary lesion on CXR is cancer Until proved
– Blood and lymph spread early otherwise- compare with a prior CXR done more than
– Positive malignant sputum and –ve CXR 2 years ago (lung tumors may have a very slow rate
of growth)
• Other types
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• SPN (solitary pulm nodule)

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– Large cell, adenosquamous, carcinoid,

– Majority are benign , but could be malignant in up to
adenoid cystic and mucoepidermoid
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50%in patients above 50 with smoking history

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S.P.N.
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Solitary Pulmonary Nodule

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• Less than 3 cm nodule typically found

incidentally in CXR or CT
• CT chest is most recommended test
– Age
– Smoking
– Size
– Calcification
• Pleural effusion
• Hoarseness of voice in left side tumors
(left recurrent laryngeal nerve)
• Superior vena cava syndrome:
– face edema
• Pancoast tumor: thoracic outlet
syndrome with ulnar nerve symptoms,
Horner syndrome
Extra Thoracic Manifestations Screening Lung Cancer

• NON METASTATIC • CMS agree to pay for CT chest for
– Clubbing, osteoarthropathy patients aged 55 to 70 who smoked 30
– Hormonal production: ACTH, ADH (small cell) pack per year if they have quit and done
or PTH (non-small cell) that within 15 years
• METASTATIC • 20% reduction in mortality is possible by
– Liver, adrenal, brain, bone this screening
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– Bone mets (the most common cause of High

cancer in lung cancer)
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Diagnosis
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• CXR • Mediastinoscopy, only for LNS seen on CT,

– CT scan chest and abdomen: look for upper and lower para tracheal, subcarinal
• Mediastinal LNS (> 1 cm), pleural effusion chest
wall involvement, Adrenal (30% malig) • Thoracoscopy for peripheral lesion
– Bronchoscopy: sputum, Bronchus, carina • PET scan, depends on glucose uptake by active
• Percutaneous needle biopsy: peripheral lesion cells. Very sensitive (not specific). small cell has
the highest uptake. Renal cell cancer is false –
ve. Sarcoidosis is a cause of false+ve
Determination of Irresectability
• If all above fail ,Tissue DX is obtained during • ANATOMICAL (Extra or Intra thoracic)
thoracotomy – Extrathoracic mets, (bones, liver, adrenal?)
• >20 % of thoracotomy/thoracoscopy – N.B exceptions are:
are done on –VE Tissue DX (the best • solitary brain met in adeno-
chance of survival) • Hormones production is not a contraindication
• 50% of patients are inoperable when first • Clubbing, osteoarthropathy
seen because of Anatomical (extra or
Intrathoracic invasions) or Physiological Causes
Causes of Inoperability
• ANATOMICAL (Intrathoracic): • Physiological
– SVC Syndrome, Contralateral LN, Recurrent – Post operative FEV1 > 800 CC at least for
Laryngeal N, Malignant effusion, heart, vessels
resection of lung to be successful
• The following are not contraindication,
– MVV(maximum voluntary ventilation) = MBC
– Chest wall, Diaphragm, pericardium
> 50% of predicted
– Ipsilateral mediastinal LN(resect after chemo xrt)
– CO diffusion capacity DCo (best measure for
– Pancoast tumor(resect after chemoradiation)
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survival)
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– Cell type (small cell) (resect, then Chemo)

– Coronary artery disease
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Stages of Lung Cancer TNM

Eight Edition
T1a up to 1 cm • T1 tumor is 3 cm or
T1b 1-2 cm less without invasion
T1c 2-3 cm of pleura and without
invasion more than
lobar bronchus
T2 a >3-4 cm
T2 b > 4- 5 cm
T3 >5-7 cm
T4 >7cm
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STAGE IIIA
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STAGE IV Treatment
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• Any T • M1A • Surgery: for stages I and II and selected IIIA

• Any N • M1B • The minimal is lobectomy + Mediastinal LN
dissection or sampling
• Wedge only when can not tolerate lobectomy
• Preop XRT for pancoast tumor, ipsilateral
mediastinal LNs
• Post op adjuvant Chemo for any positive LN
i.e. stage II and above
Neuroendocrine Lung Tumors

• Carcinoid tumors of lung: • Carcinoid syndrome (tachycardia, flushing,
1. typical (more central) hypotension = serotonin)
2. Atypical (more peripheral) • Cushing
• Characters: • Cell of origin: Kulchitsky cell (endodermal
1. very vascular cell of bronchial epithelium)
2. less commonly than GI to produce carcinoid • LNs involvement
syndrome
• Valve lesions
Benign Lung Tumors Secondary Lung Tumors

• Bronchial adenoma • Criteria for resection of Lung Mets:
• Hamartoma – Primary tumor is controlled
• Hemangioma – No extra pulm mets (except liver in colon
cancer)
• Lymphangioma
– Can resect all mets with some margin
– Can tolerate resection
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– Other ttt are not better (so Germ cell tumor

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mets are better treated with Chemo =

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cisplatinum)
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Pneumothorax
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• Best prognosis is Renal cell solitary met • Primary (spontaneous):

• Next is soft tissue sarcoma (25% 5ys) – Tall, thin young adult less than 40 years,
ruptured apical bleb seen preoperatively in
• When the primary is Squamous cell, the
15% or intraoperatively. Recurrence is
lung lesion is usually a new primary common
• With adeno it is 50% chance of being a • Secondary to:
primary lung versus a met – Bullous disease, COPD, Asthma, Cysts, cystic
• The longer the time between control of 1ry fibrosis, Pneumonia (Anaerobic – Staph)
tumor and the appearance of the met à
better prognosis
Pneumothorax Lung Abscess

• Indications of thoracotomy: (VATS with • Aspiration: posterior segment RUL or
apical bleb resection) superior segment of lower lobe
• Massive air leak preventing lung • Tumors, FBs, or immune deficient persons
expansion are other causes
• Persistent air leak > 5 days • Most are treated with Antibiotics. Very
• Second episode of PNX minimal role of surgery
• Occupational indications after the first
episode: Airline pilots. Scuba Divers
• Previous contralateral PNX
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Lung / Pleural Infection

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• Aspergilloma • Empyema:
• Fungus ball – In early stages: thoracic drainage by
thoracocentesis or chest tube placement
• H/O TB, HIV … previous scar
– In late fibrotic stage: lung entrapment,
• Hemoptysis decortication is the procedure of choice
– Pleural thrombolysis is a mid alternative with
some mixed results
Post Op Complications Lung

Lung Infections
Resection
• Histoplasmosis • Atrial fibrillation
• Coccidiomycosis • Air leak: persistent, large = bronchopleural
fistula
• Hemoptysis: • Empyema
– Vessels • Atelectasis (inadequate pain control and
– Rigid bronch inadequate cough mechanisms)
– Role of embolization • RARE: chylous effusion
Incidence of Post Lung Resection

CME Question 1
Complications
• Which of the following structure
involvement contraindicate lung resection
of lung cancer?
A. carina
B. tumor into 4 ribs
C. tumor into one vertebra
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D. tumor in pericardium
E. tumor in diaphragm
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• C • Screening for lung cancer. Which is

– Spine involvement is a contraindication for correct
curative resection A. MRI may better than CT in screening
B. smoking must be part of the history
C. mortality can be reduced to 40%
D. bronchoscopy is typically next successful
step after positive CT findings

• B Malcolm DeCamp. Mastery of surgery 7th edition.
2019;585:604.
– Smoking was the only risk factor included so
Christiana Wei. Complications in surgery 2nd edition; Pages
far in screening 241:320
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Cardiac Surgery
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(Adult & Pediatric) Adult Cardiac

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n Tumors
n Metastatic malignant tumors 20 times more
Osler General Surgery common than primary
n Primary tumors à 75% benign, 25%
Ahmed Mahmoud malig
n Myxoma is the most common (40%)
n 75% in left atrium near fossa ovalis
n familial in young females, sporadic in old
Myxoma
n Mitral valve obstruction n Rhabdomyoma: most common in infants
n Embolization in 50% with acute ischemia in and children – occurs in ventricles, usually
peripheral circulation multiple – bad prognosis
n Histology of the surgically removed
embolus is diagnostic
n Echo is test of choice
n Treatment is excision
Cardiac Trauma
n 10% of penetrating chest trauma involves
the heart
n Right ventricle is the most commonly
injured in stab wounds
n Diagnosis: Suspect in any injury near the
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epigastrium-superior mediastinum)
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Cardiac Trauma Cardiac Trauma (Diagnosis)

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n Patient may present with hypotension, and n Echocardiogram (FAST): Looks

shock, hemothorax or in tamponade) promising. Should be available in the ER.
n Beck triad (Tamponade): distended neck > 90% sensitivity and specificity
veins- muffled heart sounds – hypotension n Pericardiocentesis : Not a diagnostic test,
n Shock with elevated CVP: only done for temporary relief of blood in
u Tamponade # tension PNX
the way to the OR. Blood is not clotted
u Difference > Air way pressure
Sub Xiphoidal Pericardial Window

Cardiac Trauma (Diagnosis)
n Subxiphoidal exploration
u Definitive diagnostic test in stable patient
u Good test to rule out tamponade in

patients who do not have tamponade
u Positive pericardiocentesis or window =
u Blood = median sternotomy
u Most 95% cardiac injuries are repaired

without Bypass
ER (RESUSCITATIVE ER Thoracotomy, Open Pericardium

THORACOTOMY)
n Indications
u 1) penetrating chest injuries with failure
of aggressive resusc to raise BP > 80 mm
Hg (12% survival)
u 2) penetrating chest or abd injuries who
lost vitals during transfer
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u 3) blunt injuries who had vitals before

arrival (2% survival)
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Blunt Cardiac Injury

ER THORACOTOMY (Steps)
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(Myocardial Contusion)
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n Left anterolateral thoracotomy down to the n Incidence: unknown . Most are asymptomatic
table n May range from benign arrhythmia to fatal
ventricular fibrillation. Myocardial rupture and
n Control obvious source of bleeding e.g. left
death
hilum
n ST, T changes and sinus tachycardia are the most
n Open pericardium, watch phrenic nerve common EKG changes
n If no injury is seen, extend to the right chest n Tests of DX:
n Open cardiac massage. Clamp the Aorta n Stable à EKG monitor for 12-24 h
Traumatic Rupture of Aorta

n Unstable: + Echo à to look for pericardial n Rapid deceleration injury with shearing
fluid or other injuries e.g. valve rupture. force
n Treatment is supportive n Most common site is just distal to the left
subclavian 60%. Followed by distal thoracic
aorta 20%
n 60% die at the scene. 40 % make it to the
hospital, third of which die during initial
resuscitation
Traumatic Rupture Aorta Diagnosis of Ruptured Aorta

n Clinical presentation n CXR: wide mediastinum > 8 cm transverse
u Free rupture, death shortly after injury n Normal CXR does not r/o rupture
(60%)
n Aortography: used to be the gold standard.
u Contained rupture: detected on CXR
Was always needed before surgery
(40%)
n Helical CT / reconstruction views are now
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u Chronic rupture:(rare) chest pain, back

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pain, hoarseness of voice years later standard (virtual angiogram)

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u Examination: shock. Look for associated

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Treatment of Aortic Rupture

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n Transesophageal Echo (TEE): Can be n Preoperative preparation: A line, control the

shearing force( BP /HR): Nipride. If tachy --
done in OR / ICU, only good for typical Esmolol
location. PNX may limit its value n ? Simple clamp and repair
n Partial By pass from left atrium to descending
aorta or to Femoral artery à no need for
oxygenator. No full heparin
n Paraplegia 10% regardless. Ant spinal art
n Clamp time > 30 min
Stents in Thoracic Aorta
Acquired Cardiac Disease Classification Stanford

n Aortic Dissection n Stanford
u Type A: involves ascending aorta, usually
has AI, emergency surgical treatment. If
rupture à fatal pericardial tamponade
u Type B: Descending. Treatment is
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hypertension
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Aortic Dissection (False & True) Lumen

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n Coronary artery disease

u Myocardial revascul could be done by
surgery(CABG) or by Angioplasty(stent)
u CABG is the better choice in the
following
t 1) **left main disease
t 2) 2 or 3 vessel disease
t 3) low EF +/- diabetes
Mechanical Complications of MI
n 1)Ventricular septic defect: n 2) Mitral regurgitation: Worse prognosis
pansystolic murmur. 1 % of MI. than other causes of Mitral regurg- try
u Differentiate from mitral regurgitation: by medical support before surgery
measuring the O2 sat step up at the Right n 3) Ventricular Aneurysm
ventricle: if more than 10 à VSD
u If small (2-3) cm and asymptomatic = no
u Treatment is initial medical support (if
ttt
possible) until scar matures then surgical
closure. Sometimes Emergency closure u Large/symptomatic or false needs surgery
Intra Aortic Balloon Pump

n Significant improvement in cardiac patients
n Balloon is placed at descending aorta, just
distal to the left subclavian
n Inflate at diastole = peak of T wave
= dicrotic notch = aortic valve closure
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n Deflate at systole = before R wave

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Valve Diseases
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n Increase in coronary inflow by increase in n Determination of valve stenosis is based on

diastolic blood flow measurement of pressure and flow across
n Decrease in afterload the valve
n Decrease in myocardial O 2 consumption n Mitral stenosis is significant and requires
surgery if: the valve area is < 1.5 cm2
(normal is 5-7) – the pressure gradient
n Absolute contraindications for IABP is: (LAP-LVED) is 15mmhg (normally: none)
Aortic regurgitation
Congenital Cardiac
n Aortic valve stenosis is significant and n The fetal pulmonary vascular resistance is
requires surgery if high in utero, causing blood to shunt from
right to left through the patent foramen
u The valve area is less than 1 cm (N 2-3)
ovale and also from the pulmonary artery
u The pressure gradient is > 50 mm Hg (N into the descending aorta by the Patent
none) ductus arteriosus
u Aortic stenosis is the most serious of all
and should be always corrected before n After birth, the PVR starts to fall with the
any surgery beginning of ventilation
n The infant PVR becomes equal to the n ACYANOTIC n CYANOTIC (all T)

adult level by 4 weeks u With increase in u With increase in pulm
pulmonary flow: flow TGA- TAPVR
VSD-PDA-ASD u With normal pulm
n Persistent fetal circulation (persistent
u With normal pulm flow: TOF- PS-ASD-
pulmonary hypertension) may be caused by: flow: PS-MS-AS- Eisenmenger
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hypoxia, acidosis or pulmonary hypoplasia

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Coarctation syndrome
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Ventricular Septal Defect

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n Ventricular septic defect n Patent ductus arteriosus

n Most common anomaly, usually at membranous
septum, many will close spontaneously by age of n Associated anomalies in 20 %
4, pansystolic murmur
n Try antiprostaglandins first
n Indications for surgery: infants with severe CHF
or respiratory infections in first 3 months
u Shunt ratio > 2:1 (pulmon to syst)
u pulmonary vascular res up to 8 (>10 is
inoperable)
u Aortic regurgitation
n Atrial septal defect (secundum defect) n ASD (PRIMUM ) = A V CANAL

u Located near the fossa ovalis DEFECT
u Fixed wide splitting of second heart u Earlier presentation than secundum
sound u Part of AV canal defects with valve
u May be associated with anomalies in the lesions

pulmonary venous return u CHF is more common
u Closed by interventional cardiology
n TGA n Tetralogy of Fallot

u Most common cause of cyanosis at birth u Most common cyanotic congenital heart
disease (cyanosis usually occurs not at
u Patent VSD, ASD or PDA are essential
birth but shortly after)
for survival before surgery (switch)
u VSD + PS + OVERRIDDING OF
AORTA = RIGHT VENTRICLE
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HYPETROPHY
u Cyanotic spells, relieved by squatting, no
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emergency surgery
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Coarctation CME Question 1

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n Obstruction at the aorta 2 cm distal to left n Most common congenital heart anomaly is
subclavian u A- ASD primuim
n 2 types: infantile (usually severe CHF) and u B- ASD secundum
childhood u C- VSD
n Repair by a subclavian artery flap or
u D- PDA
extended resection and anastomosis
u E- TOF
n Recurrence is repaired by Angioplasty

n Answer is C n Most likely injured part of the heart by stab
n VSD is the most common anomaly wound is
u A- left atrium
u B – left ventricle
u C- right atrium
u D- right ventricle

n D
Ralph Damiano, Schawrtz ‘s Principles of surgery 11th edition
n Right ventricle because of its anterior 2019; Pages 751:853
location
Charles Fraser, Sabiston textbook of surgery 20th edition
2017;Pages 1632:1648,Chapter 59
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Host defense against infection

Th
BASIC IMMUNOLOGY and

ORGAN is 1-nonspecific or
TRANSPLANTATION
2-specific (immune system)
Ahmed Mahmoud, MD
Osler course
NONSPECIFIC • Phagocytosis occurs mainly by leucocytes,

which is considered to be the most
• Starts in the blood by important cell for phagocytosis
– 1) leucocytes phagocytosis and

• It also occurs by macrophages, but
leucocytes are more efficient and more in
– 2) activation of the complement system
number.
both classic and alternative
• PMNL appear early and the bone marrow

• In tissues, macrophages engulf and responds to IL3 (colony stimulating factor)
phagocytose the bacteria. by releasing more PMNL.
• The secretion of monokines and other • Half life time is 12 hours in the circulation
mediators of inflammation (platelet and 24 hours in the tissues. Because of
activating factor and leukotrienes), quickness of release of PMNL from the
complement activation (classic by IgM and bone marrow, some are still premature and
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IgG) or alternative by endotoxin of Gm-ve have some bands.

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…
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• All these will lead to recruitment of PMNL

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Immunology and Transplantation page 1

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Two types of Phagocytes can be PMNL have 3 functions

e
differentiated
Th
• 1) chemotaxis = migration by many chemotactic

• 1-circulating = granulocytes and monocytes factors the most important is C5A
• 2) Phagocytosis= occurs by adherence then

• 2-fixed = macrophages opsonization. the most potent opsonins are C3B.
IgM is the best immunoglobulin to fix complement
• 3) intracellular killing
SPECIFIC FUNCTION
• PMNL have receptors for IgGs, C3B. • HUMORAL (B CELL)
• CELLULAR (T CELL)
AFFERENT AFFERENT CENTER EFFERENT

-CD8
Antigen presenting CD4 -B Lymphocytes
CENTER cell -NK
EFFERENT
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• The immunoglobulins ( IgG, IgM ….)

Humoral released by the B cells act as receptors for
e
B Lymphocytes
Th
the B cells and link them to the Antigen.

• B lymphocytes will originate and grow in
the Bone marrow. IL7 for early
development
• The Antigen then becomes opsonized by the
• They produce Immunoglobulins in response
to antigens. B cells.
• The B cells when activated are called
Plasma cells (have more condensed Golgi
apparatus).
• The Antibody bound surfaces also activates a

destructive enzymatic cascade known as the
Complement system. • B cells (unlike T cells) do not need MHC
to recognize antigen.
• The activation of the Complement causes
multiple effects e.g. opsonization, chemotaxis,
membrane attack complex, Stimulation of factor
XI of coagulation, fibrinolysis, Kallikrein. .
• Immunoglobulins (IgG, IgM….) act
like receptors for B cells, just like T
cell receptors for T cells
• IgM is the first to appear but later changes

to other more specific IgG or IgM. .
• IgA is the mucosal immune antibody • Hyperacute rejection is related to preformed
• IgE for mast cell mediated immunity natural antibody on Donor endothelium
• The cytokines responsible for B cells

activation are IL2, IL 4,IL6 and IL7 for
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early maturation
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Cell Mediated Immunity

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T lymphocytes
Th
• T lymphocytes originates in the bone • The TCR is antigen specific and has alpha, beta
marrow but mature in the Thymus. sub dimer and an essential part is CD3
• Acquire a specific receptor T cell receptor =
TCR. • All TCR have CD3
• T cells can not recognize antigens without a
TCR. The antigen has also to be associated • The TCR also has either CD4 or CD8
with MHC II (HLA II) to be recognized by
the T cell receptor
• Resting (non activated) T cells do not express IL2 • T helper cells (Th1, Th2) have CD4
receptors. • T cytotoxic cells(Tc1,Tc2) have CD8
For CD8 to act on targets, an MHC I has to
• Only when stimulated by a specific antigen with be present
MHC II at the T cell receptor, they then express IL2
receptors and bind the IL2 to become active in
inducing more T-cells to express IL2 receptors. • Interferon Gamma increases the
expression of MHC I (HLA I) on the cells
• This is why IL2 inhibitors e.g. Cyclosporin(mainly to be attacked.
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used in kidney) and (Tacrolimus = Prograf =

FK506)(mainly used in liver) FK506 are
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important.
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Immune Response(Afferent &efferent)
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• Antigen presenting cells

– Are B Cells, macrophages and dendritic cells,
Langerhans cells
– They ingest antigens, process them, then
express them on their surface for TCR, in
association with MHC II (HLA II)
• Major Histocompatibility Complex (HLA)

– transmembrane glycoproteins which are encoded
by the short arm of chromosome 6
– have a high degree of sequence polymorphism
– Type I; A,B,C.
• Present on all nucleated cells, including T cells,
B cells and platelets and are targets for cytotoxic
CD 8 T cells = efferent limb of the immune
response
– Type II; DR, DP, DQ

• present only on B lymphocytes, monocytes,
macrophages and some activated T cells but not
on unstimulated T cells. It is the afferent limb
of the immune response
Why HLA matching is NOT

commonly followed
• HLA matching test takes time. Remember that organ • HLA cross matching is highly
ischemia time (graft is not perfused ) is more important than
HLA matching for the graft to survive and function in the recommended for living related kid Tx. It
recipient. No preservation solution is ideal may also be done for Cadaveric kid since it
• Early long term graft survival is equal in HLA matched or may increase the long term graft survival.
mismatched, long term (> 5 years) graft survival, however, • > 5 mismatching is a relative
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is better in matched transplants

contraindication
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• Necessity of transplantation is more pressing e.g. end stage

liver disease • DR, DQ are the more important
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Graft survival ; HLA matched
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/mismatched Complications of Transplantation

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• Hyperacute rejection; 1%. preformed

antibodies. Occurs immediately after release of
clamp and is irreversible. No treatment available.
• Should be prevented by conducting the Final
Lymphocytotoxic cross match to detect IgG
antibodies directed against class I MHC
• Positive Cross match is a contraindication
• Acute rejection • Chronic rejection seen after 1 or 2 years as

– T cell mediated, treated with steroids initially gradual deterioration of function
with 90% success rate. • Chronic rejection is called;
– Occurs any time after day 5 of Transplantation – Bronchiolitis obliterans in lung
as unexplained function deterioration. – Vanishing Bile duct syndrome in Liver
– Organ is infiltrated with T cells (diagnostic) – Endarteritis obliterans in heart
Complication of transplantation
• Infection • Malignancy
– First month = usual post op infection – Skin tumors SCC > BCC (cardiac transplant)
– 2 to 6 month = opportunistic infection e.g. – B cell Lymphoma (EB virus infection)=
CMV – Pneumocystis- Aspergillosis – Post Transplant Lymphoproliferative Disorders =
– After 6 months = low incidence of infection PTLD - discontinue IL II inhibitors
– give Ganciclovir for EB virus infection
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• Cardiovascular disease
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Early and late mortality after

Question
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Renal TX
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• The most common cause of mortality within • EARLY ( 1st YEAR) • LATE (2-17 YEARS)
the first year after renal Tx is – Sepsis 45% – CVS 35 %
– CVS 35% – Malignancy 20%
• A. Malignant tumors
– Sepsis 19%
• B. Cardiovascular disease
• C. Sepsis
Brain dead Donor Kidney Transplantation

RENAL Transplantation
• Avoid hypotension and hypoxia
• Most common indications are: Diabetes,
• Dopamine, norepinephrine glomerulonephritis
• Thyroxine, insulin, steroids, vasopressin • Cadaveric and Living related TX.
• HLA is used in living related
Complications of Renal Tx • Ultrasonography is the first test

Renal Biopsy for rejection
• US of transplanted kid can detect:
• Arterial or Venous thrombosis. – 1) Vascular anastomosis problems (Artery or
Vein)
• Ureter leak or stenosis – 2) Ureter anastomosis
– 3) Size of kidney(enlarged in rejection) or fluid
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collection around the kidney (lymphocele)

• Lymphocele à 15%
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• Causes of Oliguria after renal Transplantation; • Liver Transplantation

• A- Foley catheter blocked – The recipients are arranged according to the
• B- Arterial thrombosis degree of illness (coma, encephalopathy,
coagulopathy
• C- Rejection (Acute or hyperacute)
• D- Acute tubular necrosis
Veno venous bypass (Anhepatic phase)
• Liver Transplantation
– The recipients are arranged according to the degree of
illness (coma, encephalopathy, coagulopathy,
pulmonary hypertension)
– MELD: Model for End Stage Liver disease (0-40);
less than 17 = no transplant yet
– Creatinine, bilirubin, INR
– Fulminating liver failure = immediate transplant
Adult to children < 5 years
segments 2 and 3 rg e
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• INDICATIONS OF Liver Tx: Liver failure from: • It could be done with incompatible Blood
• 1) Hepatitis C is common groups (results are mixed) and even in the
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• 2) Non Alcoholic hepatic steatosis (NAHS) will be the most presence of preformed antibodies.
common
• 3) Alcoholic Cirrhosis
• 4) Sclerosing Cholangitis
• Hyper acute rejection is rare with Liver TX
• 5)Biliary atresia in pediatric patients
• 6)Tumors ? Fibrolamellar carcinoma (Best prognosis) and • Acute rejection occurs in 50%
some Hepatocellular carcinoma Stage I or II A in cirrhosis.
Milan criteria; if resection is not feasible for HCC à liver
transplant is good option for tumors less than 5 cm or 2
• Chronic rejection (vanishing bile duct
tumors 3 cm each. Patient is given a MELD of 22 syndrome) is also common
Complications of liver TX Pancreas Transplantation

• 1- Bleeding. (portal hypertension, coagulopathy) • indication : Diabetics
• 2- Portal vein thrombosis may go unnoticed
• Methods of TX
• 3- Primary Graft Nonfunction ? 2- 5% à
retransplantation • Drainage of Duodenum into the urinary
• 4- Biliary tract complications bladder. Or into the small bowel
• 5- Sepsis (most common cause of early death ) • Complications:
• 6- Hepatic artery thrombosis typically presents – Vascular thrombosis
with bile duct stricture or leak.. Most require
retransplants – Allograft pancreatitis
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Lung and Heart CME question transplantation

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• Lung transplantation:
• Most common cause of technical failure in
– Bronchiolitis obliterans is the most common
complication pancreas transplant is
– Most lung transplants are unilateral. • A- Pancreatitis
– In cystic fibrosis Bilateral lung transplant is
needed to avoid infection in the new lung
• B- Arterial thrombosis
• Heart transplantation: Atherosclerosis of the new heart • C- venous thrombosis
coronary arteries is the limiting long term
complication • D- pancreatic duct stricture
• E- acute rejection
CME question transplantation References

• Most common cause of technical failure in Nancy Ascher. Sabiston textbook of surgery 20th edition.
2017;640:677
pancreas transplant is
Pierre Alain Clavien. Mastery of surgery 7th edition.
• A- Pancreatitis 2019;156:177.
• B- Arterial thrombosis
• C- venous thrombosis
• D- pancreatic duct stricture
• E- acute rejection
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Benign Pancreas Disorders

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• Pancreatic divisum
Pancreas • Failure of the 2 pancreatic ducts to combine during embryological
development
Benign & Malignant Disorders • Common, but typically asymptomatic
• Most of the pancreas (tail, body and neck) will be drained by accessory small
Ahmed Mahmoud, MD duct
Osler General surgery
Duct of Wirsung (Main pancreatic duct)
Benign Pancreatitis
• Annular pancreas • Biliary
• May present later in life • Most common. CBD stones.
• Majority resolve (90%) within 5 days
• Duodenal obstruction: double bubble sign • Timing of laparoscopic cholecystectomy
• Treated (by pass) • IOC
• Duodenoduodenostomy • MRCP prior to ERCP
• Impacted stone in 2%
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Pancreas: Benign and Malignant page 1

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Pancreatitis
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• Biliary
• 5% develop complications
• Timing of lap cholecystectomy is not related to complications
• Alcoholic, more likely to develop complications
• Metabolic hyperlipidemia, viral, trauma, post op, post ERCP
RANSON criteria are historical value
Pseudo Cysts
• More in alcoholic than biliary
• At least 6 weeks after attack to use the term pseudo cyst
• Acute fluid collection is the term used prior to 6 weeks
Pancreatic Pseudocyst - Treatment

• Timing Pancreatic Pseudocyst - Treatment
• Within 4 wks: acute fluid collection Acute Fluid Collection
• Percutaneous
• > 6-8 wks: pseudocyst
• Failures up to 70%
• ERCP/MRCP • Superinfection risk
• Communicate with duct • Higher infection rate with
• Management catheter placement
• Conservative if asymptomatic • Risk of pancreatic fistula
Pancreatic Pseudocyst
• Intervene if: • Endoscopic
• Symptomatic
• Success in 60 – 90%
• early satiety, GOO, jaundice,
• Complications in 20%
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pain
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• Complications • Surgical
• Hemorrhage, infection, rupture • >90% success rate
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• Enlarging (> 6cm) • Biopsy cyst wall

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• Angio embolization; life saving • Cyst enterostomy

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Pancreatic Necrosis, Infected, CT Guided Drainage

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Necrosis: Role of Antibiotics

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Bleeding in Patients with Pancreatitis Chronic Pancreatitis

• Hemorrhagic pancreatitis • More likely in ETOH patients
• Hard to separate from cancer
• Erosion in splenic artery or vein • Chain of calcifications, dilated and stricture ducts
• Pain is a prominent feature
• Pure gastric varices (splenic vein thrombosis ) • Only surgical option is Peustow operation
Puestow Procedure
(Pancreato Jejunostomy) Pancreatic Cysts
• Pancreatic pseudocysts
• Serous cystadenomas
• Mucinous cystic
neoplasms
• Solid pseudopapillary
tumors
• Intraductal papillary
mucinous neoplasms
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• Main duct
• Branch duct
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• Mixed type
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Cystic Neoplasms
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CEA Levels
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IPMN Any region of pancreas

Old age more male, Incidental Major duct is associated with duct dilatation >5mm
2 types Branch duct is with dilated branches
Pseudocyst Unilocular, encapsulated with well defined walls
Serous cystadenoma Multilocular, microcystic central scar is seen in 30% pathognomonic

More females, old age
Mucinous cystadenoma Multilocular, well encapsulated smooth margin, body tail of pancreas,
Sixth decade, all female internal septations, (calification (16%) = malignancy)
Solid pseudopapillary neoplasm Unilocular encapsulated. Solid and hemorrhagic

Young age female
Mucinous Cystic Neoplasms

Serous Cystadenomas • Premalignant
• Benign lesion • Patients: 40-55yo women
• Patients: 60-70yo women • Ovarian-like stromal layer
• Imaging • Imaging
• Microcystic, septated • Macrocystic
• Honey-combed, lobulated • Thick wall septation
• Central scar in 30% • Peripheral Ca++ (25%) 95% MCNs are located in the body and tail
• No duct communication • No duct communication

• Fluid: • Fluid
• Serous, clear, thin • Mucin
• Glycogen + cells • Amylase ↓
• Amylase ↓ • CEA ↑
• CEA ↓
Solid Pseudopapillary Tumor

Solid Pseudopapillary Tumor • Solid, cellular areas
• 1-2% exocrine pancreatic tumors • Lack gland formation
• Pseudopapillary formations from
• Hamoudi tumor degeneration
• Frantz tumor • Positive for:
• Median size: 8cm • NSE
• Vimentin
• Young women • Alpha-1-antitrypsin Sheets of cells with uniform nuclei
• 2nd & 3rd decade of life • Alpha-1-antichymotrypsin
• Median age: 26yo • Often encapsulated • Fluid analysis:
• Non-Caucasian • PAS + globules
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• Low malignant potential

• Cellular aspirates w/ papillary structures
• Presentation
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• ~5-6% recurrence rate • CEA ↓

• Epigastric mass • 10-15% metastasize • Amylase ↓
• Vague abdominal pain • Amenable to resection
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• Including metastasectomy
Well-encapsulated lesion w/ mixed appearance
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Intraductal Papillary Mucinous Neoplasms

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Neuroendocrine Pancreatic Tumors

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• Premalignant
• Patients: 60-70yo (M=F)
• Non functioning adenoma is the most common
• Imaging (MRCP)
• Main: duct dilation • Insulinoma is the most common of endocrine producing tumors
• Panductal (diffuse) • Insulinoma is mostly benign (90%)
• Segmental • Insulinoma is equally distributed through the glands
• Branched: cluster of
grapes • It is more vascular than all others
• Mixed • In children it is more diffuse and more difficult to treat
• Duct communication • Presents typically with hypoglycemia symptoms; sweating, confusion,
• Fluid Analysis tachycardia
• Mucin • CT scan, no role for OCTERIOTIDE SCAN
• Amylase ↑
• CEA ↑
GASTRINOMA Gastrinoma Triangle

• SPORADIC (80%)
• Pancreas is not the most common site
• Part of MEN I
• Diffuse, more likely metastatic
• Secretin test,
• Localization
Glucagonoma Adenocarcinoma of Pancreas

• Mostly malignant
• More in females
• Diabetics with necrolytic skin rash found in tail, body of pancreas
treated by distal pancreatectomy
• somatostatinoma; most malignant of all, larger in size

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• head tumors are treated by enucleation

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Outcome Pancreatic Cancer Surgery Genetic Background Pancreas Tumors

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• Individuals with two or more blood relatives, and at least one first-
degree relative, with pancreatic cancer
• Carriers of p16, PALB2, or BRCA2 mutations with a first-degree
relative with pancreatic cancer
• All individuals with Peutz-Jeghers syndrome
• Individuals with Lynch syndrome and a first-degree relative with
pancreatic cancer
Pancreatic Cancer – Risk Factors Diagnosis of Pancreatic Cancer

Genetic (10%)
Risk Characteristic Relative Risk Lifetime Risk (Age 70)
• Biopsy is recommended only when imaging results of a pancreatic
No identifiable features 1 0.5% lesion are ambiguous:
BRCA1 2x 1.2% • EUS-guided biopsy is preferred and percutaneous sampling should be avoided
BRCA2 3.5-10X 2%-5%
Lynch syndrome 8.6x 3.86%
FAMMM* 20x-34x 10-17%
Familial PC (3 first degree relatives) 32x 16%
Hereditary pancreatitis 50x-80x 25-40%
Peutz-Jeghers syndrome 132x 66%

* Familial Atypical Multiple Mole Syndrome
www.cancernetwork.com
Diagnostic Work-Up Pancreas Cancer

• Patients should undergo triphasic multidetector CT with thin-slice, cross-
Define Tumors to be Resected
sectional imaging; the difference in contrast enhancement is highest during
the second phase, so a triphasic approach enables a clear distinction • Borderline tumors for resection include the following:
between a hypodense lesion and the rest of the pancreas. • No distant metastases
• Contrast MRI is acceptable when CT is not possible, but MRI has not been
• Involvement of the SMV or PV with distortion or narrowing or
shown to be more effective or accurate in diagnosing and staging
occlusion of the vein with vessel proximal and distal, allowing for
pancreatic cancer; however, MRI can be a useful adjunct in diagnosing
resection and replacement
high-risk patients.
• PET/CT is not a substitute for high-quality contrast-enhanced CT, but may • Gastroduodenal artery encasement up to the hepatic artery, without
be considered after CT to detect small metastatic deposits. extension to the celiac axis.
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• If no mass is evident in the pancreas on CT protocol imaging, EUS is • Tumor abutment to the SMA < 180° of the circumference of the
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recommended before other evaluation options. vessel wall.

• EUS-guided fine-needle aspiration (FNA) offers better safety and lower risk
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of peritoneal seeding than CT-guided FNA

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Surgery Cancer Pancreas Surgical Points

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• Pancreatoduodenectomy (Whipple procedure) is the treatment of • Vascular points:

choice for tumors of the pancreatic head 1. anomaly, replaced Right hepatic artery
• For tumors in the body or tail of the pancreas, distal pancreatectomy, 2. verification of gastroduodenal artery before ligation
including the resection of the body and the tail of the pancreas and 3. creation of plane anterior to portal vein / smv
the spleen, is usually performed 4. what vessels you may occasionally ligate?
• No evidence exists that extended lymphadenectomy is beneficial;
standard lymphadenectomy should involve the removal of ≥ 15 lymph
nodes to allow adequate pathologic staging
• Postoperative gemcitabine or 5-fluorouracil (5-FU) chemotherapy is
recommended
Steps of Whipple: Resection Phase Kocher Maneuver

Pancreaticoduodenectomy
3. Portal dissection 4. Transect stomach

(antrectomy)
5. Transect jejunum and

2. Extended Kocher dissect ligament of
maneuver Treitz, rotating
duodenum under
mesenteric vessels
1. Exposure of 6. Transect pancreas and

intrapancreatic SMV complete retroperitoneal
dissection by removing
specimen from SMV and
SMA
Steps of Whipple: Resection Phase Kocher Maneuver

Pancreaticoduodenectomy
3. Portal dissection 4. Transect stomach

(antrectomy)
5. Transect jejunum and

2. Extended Kocher dissect ligament of
maneuver Treitz, rotating
duodenum under
mesenteric vessels
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1. Exposure of 6. Transect pancreas and

complete retroperitoneal
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intrapancreatic SMV
dissection by removing
specimen from SMV and
SMA
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Steps of Whipple: Reconstruction Phase

Portal Vein Reconstruction
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• Types
• Primary anastomosis
• Vein patch
• Interposition graft
• Saphenous
• Internal jugular
• Right gonadal vein
• Tension free
• Mobilize liver, hilum
• Cattel-Braasch
• Ligate splenic vein
• Impact
• No impact on survival
• 23.4 mo vs 26.5 mo (standard) Tyler DS, Evans DB. Ann Surg. 1994 Feb;219(2):211-21
Reconstruction: Pancreatic Anastomosis

Pancreaticojejunostomy
Role of Adjuvant Chemo in Cancer Pancreas
Pancreaticogastrostomy
• In border line resection cases:

• Neoadjuvant may determine resection versus palliative therapy
• Post op adjuvant is indicated in all except stage I tumors with R0 results

• In the absence of medical or surgical contraindications, patients who did
not receive preoperative therapy should be offered 6 months of adjuvant
chemotherapy with either gemcitabine or fluorouracil plus folinic acid
initiated within 8 weeks of surgical resection.
Two-layer, end-to-side, duct-to-mucosa One-layer, end-to-side
• Effects on overall survival and disease free survival
Post Op Complications Pancreas Resection CME Question 1

• Post op bleeding • Which of the following findings contraindicate resection of head
• Pancreatic fistula pancreas tumor?
A. paraduodenal lymph node positive
• Biliary fistula B. porta hepatis lymph node positive
C. partial SMA involvement
D. tumors positive in pancreatic duct margin
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Answer 1 CME Question 2

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•C • Annular pancreas can be best treated by

• SMA can technically be resected and re constructed but survival is not any A. gastro jejunostomy
better B. duodenojejunostomy
• Neo adjuvant therapy is needed in these cases C. duodenoduodenostomy
D. any of the above
Answer 2 References
•C • William Fisher, Schwartz’s Principles of Surgery 11th edition 2019;
• Gastro jejunostomy is not a good option because of the pylorus Pages 1429:1477
• Keith Lillemore, Mastery of surgery 7th edition 2019; Pages 1471:1550
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Development & Congenital

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anomalies
Th
n Kidney develops in 3 stages:

n Pronephros = disappears
Genitourinary & gynecology n Mesonephros à mesonephric duct à Ureteric bud à
grows up (cephalad) forming ureter, pelvis and
collecting tubules (excretory part of the kidney)
n Metanephros à forms glomeruli, proximal, distal
Ahmed Mahmoud tubules and loops of Henle (secretory part of the
Associate professor clinical surgery kidney)
n Fusion between the 2 completes the development
General surgery course
Congenital anomalies
n Polycystic kidney
n Failure of communication between
mesonephros and metanephros
n So the kidney is producing urine that is not well
drained = multiple cysts not draining into the
ureter
n Infantile Duplex system (Double ureter +/- double

n Adult (autosomal dominant): + cysts in pelvis) is the most common GU anomaly
spleen, liver, pancreas + aneurysms of
intracranial vessels
PUJ obstruction
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More common in females. Intermittent

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Gynecologic and GU Surgery page 1

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Renal cell carcinoma

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Th
n Renal vascular anomalies: 15% of n Arises from proximal tubules

population have multiple renal vessels n Clear cell carcinoma. Rarely bilateral
n Vesicoureteric reflux n Pseudocapsule
n Recurrent UTIS in children n Spreads: local invasion, blood and lymph
n Diagnosed by voiding cystourethrogram
n Tendency to invade renal veins, IVC
“tumor thrombus”, sometimes to Right
atrium
n Clinically: painless, causeless and recurrent

haematuria in a > 40 years old male
n Incidental renal solid mass on CT abdomen
is Renal Cancer à Nephrectomy (no Bx)
n Atypical presentation: Fever unknown
origin- polycythemia-HTN- PTH like
secretion - Varicocele
n CT scan à stage – renal vein involvement n Radical nephrectomy (transabdominal)

n US ? Solid or cystic n Tumor thrombectomy from renal vein or
n MRA à vascular involvement IVC.
n PET scan à look for small lung mets n Right atrium tumor needs Cardiopulmonary
bypass and Hypothermic circulation arrest
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n Role of IL2, Interferon, immunotherapy

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n Lung mets are resectable

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Wilm’s tumor
(nephroblastoma)
n Variable histology: Renal tubular adeno myo n Lungs are the most common sites for mets
sarcoma
n Clinically, abdominal mass which does not
n Most common abdominal tumor in children. 80% cross the midline (rarely haematuria)
occur in children < 4 years
n Associated anomalies: Aniridia – Undescended n Treatment:
testis n Surgery (radical nephrectomy)
n Hematuria is rare and late n Post op Radiation if tumor is outside capsule or
n Most important prognostic sign is Histological spillage during surgery
gradingà n Chemotherapy is effective
n Favorable versus Non favorable
Renal trauma
n Other rare renal tumors n Blunt trauma is managed conservatively

n Hamartoma with success in most of the times
n Angiomyolipoma n Penetrating trauma: If intraoperative, do not
open Gerota fascia unless a large
haematoma is expanding (get vascular
control first) or major urine extravasation
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Bladder tumors
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Th
n Renal vascular injuries: Absent kidney on n Mostly malignant

CT = Angiogram n 90% are epithelial (transitional cell carcinoma).
Superficial tumors tend to recur
n Renal artery thrombosis from blunt trauma
n Clinically: recurrent UTI , haematuria
n First 2 hours, thrombectomy may save the
kidney n Cystoscopy, biopsy, CT scan àresectability
n After 4 hours, no chance, no need for
n Treatment: superficial tumors = TURP, intravesical
nephrectomy since HTN is rare chemotherapy
n Deep tumors: total radical cystectomy, diversion with
ileal conduit
Bladder trauma
n Blunt: 80% extraperitoneal, 20% n Penetrating, always explore, may repair the
intraperitoneal bladder from inside.
n Extraperitoneal à conservative treatmentà
foley catheter
n Intraperitoneal à repaired immediately
n Diagnosis: cystogram (300 cc, AP, Lateral
and post voiding films
Prostate cancer
n Most are adenocarcinoma arising from outer n Bone scan, CT scan

parts of the gland (benign prost hypertrophy n Grading 2-10
arises from inner part of gland) n Treatment
n Multifocal n Very small tumors with good grading in very elderly
n Local spread, blood to pelvic bones patients à no treatment
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(osteoblastic) lymph to pelvic LNS n Radical prostatectomy versus radiotherapy

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n Healthy patients = surgery

n Clinically: rectal exam =hard mass.
n High risks = XRT
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n Trans rectal US to guide Bx. PSA level

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Testicular tumors
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Th
n Advanced tumors n Age 30- 50

n Hormonal therapy to decrease bone pain n Painless scrotal mass, small hydrocele, mass
after trauma is still tumor until proved
n Stilbestrol was the first to be used
otherwise (no haematoma)
n LHRH agonists are the current drugs n Testicular US or Tumors markers
n Rarely orchiectomy à increase LHRH n Testicular Biopsy by inguinal approach
(never trans scrotal)
n CT abd, Chest
Tumor markers
n Most arise from Germ cells, n Alpha feto protein: Elevated in 70% of
n Seminoma or NSGC, when elevated you can rule out
n Nonseminoma germ cell tumor (NSGC) seminoma
n Teratocarcinoma- embryonal-teratoma or n Beta HCG: In choriocarcinoma
choriocarcinoma n LDH
n All spread by lymph, rarely by blood except
choriocarcinoma
Treatment of testicular tumors
n 1- Radical orchiectomy by inguinal approach n 3-if Not Seminoma (NSGC) à

n 2- if seminomaà tumor is very radiosensitive n Retroperitoneal LN dissection and or
chemotherapy
à Radiation is given for para aortic LN or
n No radiation since tumor is not as
one stage ahead of the extent of the tumor.. radiosensitive as seminoma
Add Chemotherapy for mediastinal mets or n Prognosis is excellent
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lung or other mets (CISPLATINUM)

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n 95% 5 years survival in stage 1

n 60% in stage IV
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Testicular torsion
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n Any sudden onset of scrotal pain is torsion until proved

otherwise
n Is torsion of cord not testis with cut off blood supply Gynecologic Surgery
n Emergency. After 5 hours testis is dead
n US and nuclear medicine help but Surgical exploration
is most definitive and almost always needed
n mid line scrotal exploration. Orchidopexy in 4
locations and other non torsion side as well
n Anomaly is bilateral (higher insertion of tunica on the
cord
Vulvar Tumors Other diseases of vulvar area

n Carcinoma is Squamous Cell Carcinoma n Melanoma is second to SCC
n Punch biopsy is recommended for any suspicious
n Paget disease of vulva: post menopausal,
lesion
pruritis. Dx is difficult – WLE
n Treatment:
n Wide local Excision = if tumor is less than 2cm in
diameter, less than 2 mm in depth, no Lymph
nodes, Grade is I or II
n Radical Vulvectomy with unilateral or bilateral
inguinal and femoral LNS dissection. If any above
criteria is not present
Cervix Carcinoma Ovarian tumors
n CIN: Cervical intraepithelial neoplasm n Benign: (Functional and Proliferative)

n Grade I: no risk of cancer n Functional = Graafian Follicle or Corpus
n Grade II: cervical cone excision luteum cyst
n Grade III: controversial n Criteria, Unilateral, Cystic, freely mobile
and less than 5 cm in diameter, seen in
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n Stage I Ca to cervix only or to Corpus (still

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stage 1) = treatment is total hysterectomy ovulating women. OBSERVATION

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n Stage II or III: surgery and RXT are equal

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Benign Ovarian tumors Benign Which can turn

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(proliferative) Malignant
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n **Dermoid Cyst or benign cystic teratoma n Serous Cystadenoma

n Most common ovarian tumor in pregnancy
n Is the most common
n 10 –20 years of age
n Bilateral 10% n 10% can turn malignant
n May reach 20 cm in size n Is the most malignant ovarian tumor =

n 5% turn malignant =SCC serous cystadenocarcinoma
n Treatment: premenopausal = cystectomy
n Postmenopausal = oophorectomy
n ** Solid = Fibroadenoma,
n Mucinous n **Granulosa Theca cell tumor

n 30% can turn malignant n 60% are Benign
n 25% are malignant
n Only 10% of malignant tumors are
n Produce sex hormones
mucinous cystadenocarcinoma
n May cause endometrial hyperplasia or carcinoma
n May reach a large size
n **Dysgerminoma. Most radiosensitive
n **Arrhenoblastoma androgen producing tumors =
hirsutism
Management of Ovarian tumors Management of ovarian Tumors
n Most occur in women above age of 60 n Cystic ovarian enlargement in young females,< 5 cm
and suspected to be physiological e.g. corpus luteum
n If malignant. the classic is Total abdominal
cyst and follicular cyst are treated by close
hysterectomy + BSO + Omentectomy + observation and US
subdiaphragmatic Scrapping. ? Second look n Premenopausal, benign tumors (benign cystic
laparotomy teratoma, most dysgerminoma) can be treated by
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n In advanced cases, debulking is effective cystectomy = simple excision of the cyst and preserve
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especially if tumors left is less than 3 cm the ovary as long as they are cystic less than 5 cm.
Patient requires children. If postoperative pathology
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is not favorable = relaparotomy

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Accidently discovered adnexal

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masses
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n Perform the original operation.. Splenectomy in n Postmenopausal, solid and more than 5 cm then
ITP unilateral salpingo-oophorectomy
n If Open Cholecystectomy; examine both ovaries, n Endometriosis; chocolate ovarian cyst, painful
look for peritoneal nodules, omentum mets or menstrual cycles
subdiaphragmatic mets n Most respond to hormonal suppression cycles e.g.
n Never TAH +BSO androgens or contraceptive pills
n Premenopausal: nothing else now and return to n Rarely: surgery if there is colon obstruction or
OR later(3-4days). You may also remove the solid intraabdominal bleeding
tumor if less than 5 cm or the cyst , but preserve
the tube and ovary
Infections Bartholin cyst, abscess
n Difficult to differentiate from appendicitis n Treatment is:

n Laparoscopy n I and D with placement of word catheter (soft,
n Most tubo ovarian abscess respond to rubber tube with inflatable tip )
antibiotics n OR
n Drainage is rarely indicated n MARSUPIALIZATION
n Salpingo-oophorectomy is rarely indicated,

only if the tube is necrotic or gangrenous or
patient is in septic shock
The pregnant patient in surgical

Appendicitis in pregnancy
practice
n Anemia of pregnancy: (plasma volume n Perforation rate increases with progress of
50%, RBC 25%) pregnancy (20% à 70%)
n COP increase n Clinical picture, affected by appendix
n Mild alkalosis displaced by enlarging uterus
n Lab changes: Alkaline phosphatase, WCC n Laparoscopy is safe, Co2 (avoid acidosis),
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increase, creatinine decrease position of patient, lower pressure, open

technique
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Biliary tract disease Ectopic pregnancy

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n Acute cholecystitis. Try to wait to 2nd trimester n Ruptured is a life threatening emergency
n Recurrence is common with medical treatment n Treatment:
n Lap chole. is safe in 2nd trimester n Salpingostomy if possible
n If not à resection of the tube
n Fetal monitoring during lap chole.
n Tocolytic: Mg, B agonist, Ca blockers
Pelvic infection Breast mass in pregnancy
n Role of laparoscopy n 1st trimester ca breast

n Bacteriology n Can not use XRT
n Treatment of TOA
n Medical – perc drainage- surgery
Thyroid disease in pregnancy

Vascular diseases in pregnancy
parathyroid
n Thyrotoxicosis n DVT: more common, more severe
n Radioactive iodine is contraindicated n Splenic artery
n Surgery after rapid medical treatment n Renal artery
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Q1 CME Answer q1
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n Three years after radical nephrectomy for n C. Resection of lung mets has 40% 5 years
renal cell tumor, patient has 2 lung survival rate
metastatic lesion on right and left lung.
n Best management is:
n A- chemotherapy
n B- radiation therapy
n C- surgery for the 2 sides
n D- immunotherapy
CME q 2 Answer q2
n Most common cause of intra abdominal n A-

bleeding in pregnancy is n Ectopic is the most common
n A- ruptured ectopic n Other causes follow in the same order
n B- hepatic adenoma
n C- splenic artery
n D- renal artery
References
Howard Jones and Michael Coburn. Sabiston textbook of
surgery, 20th edition. 2017;2013:2040
Michael Sourial, Schwart’s principles of surgery 11th edition.

2019:1759-1792
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Objectives
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Abdominal Wall n Review of:

n Types of abdominal wall hernias
& Hernias n Anatomical landmarks
n Hernia terminology
n Treatment and surgical approaches
Ahmed Mahmoud, MD n Common clinical scenarios
Osler n Sample questions
Abdominal Hernias
n GROIN n ANTERIOR WALL
n Inguinal n Umbilical
n Direct n Ventral / Incisional
n Indirect
n Epigastric
n Pantaloon
n Spigelian
n Femoral
n Parastomal
n PELVIC
n POSTERIOR /LUMBAR
n Obturator
n Superior (Grynfeltt’s)
n Sciatic
n Inferior (Petit’s)
n Perineal
Sabiston’s Textbook of Surgery
Common Terminology Inguinal Hernia

n Reducible n Richter’s
n Incidence - 5% of population
n Incarcerated n Intestinal wall
incarceration n Prevalence increases with age
n Irreducible contents
n Strangulated n Littre’s n 700,000 repairs per year (US)
n Blood Supply n Containing a Meckel’s n (M:F) = (25:1)
diverticulum
compromise
n Pantaloon n More common on right
Sliding
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Inguinal direct and n Slower descent of R testicle
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n Sac contains visceral
peritoneum indirect n Barrier of Sigmoid Colon on L side
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Abdominal Wall and Hernia page 1

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Inguinal Hernia Inguinal Anatomy

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Abdominal wall structures:

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n
n Inguinal n Skin
n Indirect (2/3 – most common) n Subcutaneous Fat
n Direct
n Camper’s Fascia
n Pantaloon
n Scarpa’s Fascia
n Treatment is the same for all of the above n Superficial Vasculature
n Mesh repair n Superior Circumflex Iliac
n Primary repair n Superficial Epigastric
n External Pudendal
n External Oblique Aponeurosis
Inguinal Anatomy Inguinal Anatomy

n Inguinal Canal Borders n Inguinal Canal – Between deep and superficial rings
n External Oblique Aponeurosis – superficial
n Inguinal (Poupart’s) Ligament – inferior n Spermatic Cord
n Lacunar Ligament – inferior and medial n Testicular Artery and Vein (Pampiniform Plexus)
n Internal Oblique and Transversus Abdominis – superior n Cremaster Muscle and Vessels (off epig.)
n Transversalis Fascia – deep / posterior (inguinal floor) n Genitofemoral Nerve (genital branch)
n Vas Deferens
n Hasselbach’s Triangle – defines floor of canal
n Inferior Epigastric Vessels – superior / lateral n Lymphatics
n Edge of Rectus Sheath – medial n HERNIA SAC (Indirect)
n Inguinal Ligament - inferior n Nerves
n Ilioinguinal and Iliohypogastric
Inguinal Anatomy
n Ilioinguinal and Iliohypogastric
n Sensation to groin, base of penis, upper medial thigh
n Pierce internal oblique and run along spermatic cord
n Genital Branch of Genitofemoral nerve

n Innervates cremaster muscle and skin of
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scrotum/labia laterally
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n Accompanies the cremasteric vessels

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Inguinal Anatomy
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n Poupart’s (inguinal) Ligament

Femoral Hernia
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n Inferior edge of external oblique aponeurosis

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n Cooper’s Ligament n Boundaries of femoral ring are:

n Pectinineal ligament and periosteum on n Anterior: inguinal (Poupart)ligament
pubis. n Posterior: Pectineal (Cooper)ligament
n Lacunar Ligament n Medial: Lacunar (Gimberant)Ligament
n Inguinal ligament insertion to pubis n Lateral Femoral Vein
n Conjoined Tendon n Femoral hernia are palpated below the inguinal
n Internal obliques and transverse abdominis aponeurosis (5- ligament & lateral to pubic tubercle
10% of pts.)
n Cremaster Muscle
n Internal oblique lower-most fibers
Inguinal Anatomy Etiology

n Acquired - Increased Intra-abdominal pressure
n Femoral Canal n Severe constipation
n Cooper’s Ligament – posterior n Urinary straining

n Pulmonary disease
n Iliopubic Tract – anterior
n Heavy lifting
n Medial border is junction of above structues
n Congenital
n Femoral Vessels - Lateral n Hydrocele
n Patent procesus vaginalis
n Undescended testicle
n Iatrogenic
Differential Diagnosis Femoral Hernia
n Inguinal / Femoral Hernia n More common in women – (M:F) = (1:10)

n Hydrocele / Varicocele n Bulge BELOW inguinal ligament
n Cystic lesion / Lipoma / Hematoma n Can sometimes create bulge above
n Inguinal Adenitis / Epididymitis n Highest rate of strangulation (~20%)
n Inguinal / Psoas Abscess / Hidradenitis
n All should be repaired surgically
n Testicular Torsion / Ectopy
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n Thigh sarcoma / Neoplasm n McVay repair

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n Lymphoma / Metastatic n Laparoscopic mesh repair

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n Femoral Artery (pseudo)-Aneurysm

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Non-operative Management Surgical Options

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n WATCHFUL WAITING n Suture based primary anatomical repairs

n Balance of RISKS vs. BENEFITS n High recurrence rates
n Moribund patients n Cases with simultaneous contamination
n Asymptomatic patients – Fitzgibbons et. al. n Open mesh-based repairs
n Verylow rate of incarceration -0.03% n Lichtenstein, Plug and patch
n Many patients crossed over to surgical group (~25%) n Stoppa, Kugel
n Laparoscopic mesh-based repairs

n TAPP,
n TEP
Primary Anatomical Repairs Tension-Free Repairs

n Bassini – Transversus abdominis and internal n Most universally used
oblique to inguinal ligament
n McVay (Cooper ligament) – Transversus
n Open
abdominis aponeurosis to Cooper’s ligament and n Lichtenstein
iliopubic tract n Plug and Patch
n Shouldice – Multilayer repair of posterior wall of
inguinal canal with continuous sutures
n Laparoscopic
n Iliopubic tract - Transversus abdominis to iliopubic
n TAPP
tract with interrupted sutures n TEP
n Marci – Suture closure of the internal ring
Lichtenstein Repair
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Laparoscopic TEP Laparoscopic Hernia Repair

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n Indications n Advantages
n Bilateral hernias n TAPP vs. TEP
n Recurrent
n Primary?
n Disadvantages
n Complications
n Contraindications
n Learning curve
n Not tolerating GETA
n Extensive PSH(x)
n Radical Prostatectomy
Laparoscopic Repair - Pitfalls
n Triangle of Doom
n Vas deferens, Spermatic vessels, Peritoneum
n Femoral vessels and nerve
n Triangle of Pain / Electrical Zone
n Spermatic vessels, Iliopubic tract, Peritoneum
n Cutaneous nerves in iliac fossa
n Corona Mortis
n b/w obturator and inferior epigastric vessels
“Triangle of Doom” NERVE INJURY

n Triangle of Pain contains:
n Femoral Nerve
n Lateral Femoral Cutaneous
n L2 / L3
n Genitofemoral Branch
n L1 / L2
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n Divides anterior to the psoas muscle

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Colborn GL, et al. Surg Rnds (1995); 223-232.

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Post op pain - Treatment Hernia recurrence

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n 30-40,000 performed per year (~5%)

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n Time — usually effective n Medial recurrence – most common location (open)

n Medical n Major risk factors
n Anti-inflammatory n Poor technique*
n DM
n Anti-depressants
n Obesity
n Anesthetic block
n Steroids
n Surgical n Smoking
n Excise the neuroma n Wound infection
n Repair the recurrence n Connective tissue disorders
n Ascites
n Poor nutrition
n Immunosuppression
“Sports Hernia” “Sports Hernia”

n Differential Diagnosis
n Athletic pubalgia
n Adductor muscle pain
n Groin pain in athletes
n Osteitis pubis
n Misnomer?
n Stress fractures
n Prevalence 5-28% n Avulsion fractures
n Soccer and Hockey n Hernias
n Radiologic studies n Entrapment neuropathy
n Referred pain
n Urogenital conditions
n Appendicitis /diverticulitis
Nam & Brody - Management and Therapy for Sports Hernia Nam & Brody - Management and Therapy for Sports Hernia
J Am Coll Surg: Vol. 206, No. 1, January 2008 J Am Coll Surg: Vol. 206, No. 1, January 2008
Sports Hernia Treatment Which repair is best ???
n Rest and rehabilitation

n Surgical exploration/repair “It is not the technique that eventuates in a
n Laparoscopic repair
well-performed hernia repair; it is the
n Open repair
n Allows visualization/repair of damages muscles

enthusiasm for perfection and the skill of
n +/- Adductor tenotomy the surgeon”
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n +/- ilioinguinal neurectomy

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Nam & Brody - Management and Therapy for Sports Hernia

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Pelvic Hernias Pelvic Hernias

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n Obturator Hernia Sciatic Hernia Perineal Hernia

n Greater Sciatic Foramen n Exceedingly rare
n Herniation through obturator canal (membrane)
n Gluteal /Intragluteal mass n Sac through pelvic
n Howship-Romberg sign (medial thigh pain) n Sciatic nerve pain diaphragms
n Diagnosis n Bowel n Multiparous women
n 50% present with bowel obstruction n Obstruction n APR / Prostatectomy
n Incarceration n Recto-vaginal exam
n CT scan often diagnostic
n Surgical approach n Surgical approach
n Treatment n Transperitoneal n Transabdominal
n Posterior
approach (open or laparoscopic) Transgluteal
n n Perineal
n Mesh used when no contamination occurs Prosthetic mesh repair
n n Combined
Anterior Hernias
n Umbilical
n Ventral
n Incisional
n Epigastric
n Spigelian
n Parastomal
Incisional / Ventral Incisional / Ventral

n Up to 20% of abdominal operations n Etiology
n Obesity
n Smoking
n Most within 2 years of surgery
n Malnutrition
n DM
n Diagnosis n Collagen diseases
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n H&P n Wound infections

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n Emergent procedures
n CT scan
n COPD
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n Technical issues
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Principles of repair
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n
n Open repair
n Various techniques
n Primary
n Mesh (Stoppa)
n Laparoscopic repair
n Advantages? – Does not violate overlying skin
n Technical concepts
n Overlap
n Tacking
n Fixations
Separation of Components
n Used to decrease tension
on abdominal wall repairs
n Contaminated environment
n Loss of domain
n Can be used along with
mesh
n Biologic
n Technique
n Incision of external oblique
aponeurosis
n Incision of posterior sheath
what are the phases in separation

Types of Mesh
of components
n Synthetic n Procedure Classification
n Absorbable n Clean
n Permanent n Clean-contaminated
n Biological n Contaminated
n Human n Dirty / Infected
n Porcine
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Epigastric Umbilical - Adult

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n F>M
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n Between umbilicus and xyphoid n Etiology - Aquired

n M > F (3:1), 20-50 y.o. n Obesity, cough, ascites, pregnancy
n Etiology n Differential Diagnosis

n Urachal cyst, Endometrioma, Lymph Node
n Congenital, Aquired, Iatrogenic
n Diagnostic Modalities
n Diagnostics
n H&P , CT
n Exam, CT scan (obese) n Surgical treatment
n Chronic incarceration n Open vs. Laparoscopic
n Omentum, preperitoneal fat (painful)
Lumbar Hernia Other Rare Hernias

n Spigelian Hernia
n Superior Lumbar Triangle (Grynfeltt) n At semilunar line and through Spigelian fascia
n 12th rib, paraspinal muscles, internal oblique n Absence of posterior fascia
n Most common n Interparietal hernia
n Inferior Lumbar Triangle (Petit’s) n Localized pain with bulge (hernia is behind anterior
fascia)
n Iliac crest, latissimus dorsi, external oblique
n High risk of incarceration – REQUIRES REPAIR
n Repair – Primary or with mesh / open or

n NOT prone to incarceration (extraperitoneal fat) laparoscopic
n Rectus Abdominis Diastasis
n Prosthetic mesh repair is preferred
n Not a true hernia – repair usually NOT indicated
Spigelian Hernia Pediatric Hernias

n Inguinal Hernias
n Suture-closure of internal ring usually sufficient
n Open vs. Laparoscopic
n Contralateral side can be visualized laparoscopically
n Open exploration not indicated (infertility)
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Umbilical - Newborn Umbilical anatomy &defects

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n During fetal development, The midgut communicates with the

n Congenital Yolk sac by the omphalomesenteric duct . This should normally
obliterates
n Most common in African Americans n Failure of obliterationàanomalies;
n 1)Meckel diverticulum
n 2)enterocutaneous fistula. Presents as passage of meconium

n Observation until age 5 in first few days of life. This should be treated promptly to
n Surgical repair indicated if no closure occurs avoid volvulus .
n 3)umbilical polyps ;which fail to be treated with silver nitrate
Congenital Abnormalities
Clinical Scenarios
pediatric
n Gastroschisis n Omphalocele n Patient with infected mesh
n R abd wall defect n 1 in 5000 births
n Enterotomy during repair
n No peritoneal sac n Umbilical ring defect
n Thickened bowel due to n Peritoneal cover n Strangulation and bowel resection
amniotic irritation n 50% have anomalies n Dehiscence with contamination
n Anomalies infrequent n Chromosomal abn.
n Nonrotation (always)
n Loss of abdominal domain
n Liver / GI tract within.
n Post delivery problems n Surgical management
n Fluid loss n Silastic silo
n Surgical management n Closure if < 2cm
Anatomy Anatomy
n Placement of tacks between the vas deferens n Placement of tacks between the vas deferens
and the gonadal vessels during laparoscopic and the gonadal vessels during laparoscopic
hernia repair may lead to: hernia repair may lead to:
n A. testicular atrophy n A. testicular atrophy
n B. hemorrhage n B. hemorrhage (triangle of doom)
n C. lateral thigh pain n C. lateral thigh pain

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n D. bladder perforation n D. bladder perforation

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n E. none of the above n E. none of the above

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Questions Questions
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During exploratory surgery of the abdomen, an incidental finding During exploratory surgery of the abdomen, an incidental finding
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was a herniation of bowel between the lateral edge of the rectus was a herniation of bowel between the lateral edge of the rectus
abdominis muscle, the inguinal ligament and the inferior epigastric abdominis muscle, the inguinal ligament and the inferior epigastric
vessels. These boundaries defined the hernia as a(n): vessels. These boundaries defined the hernia as a(n):
a. Congenital inguinal hernia a. Congenital inguinal hernia

b. Direct inguinal hernia b. Direct inguinal hernia (Hasslebach’s triangle)
c. Femoral hernia c. Femoral hernia
d. Indirect inguinal hernia d. Indirect inguinal hernia
e. Umbilical hernia e. Umbilical hernia
Questions Questions
The superficial inguinal ring is an opening in which structure?
The superficial inguinal ring is an opening in which structure?
a. External abdominal oblique aponeurosis
a. External abdominal oblique aponeurosis
b. Falx inguinalis
b. Falx inguinalis
c. Internal abdominal oblique muscle
c. Internal abdominal oblique muscle
d. Scarpa's fascia
d. Scarpa's fascia
e. Transversalis fascia
e. Transversalis fascia
References
Kristine Makiewicz. Rush University review of surgery, sixth
edition. 2019;226:235
Thank You
Scott Kizy. Schwatrz textbook of surgery 11th edition.
2019:1549-1570
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GS-W202107ROR Bibliographic Sources
Selected references are listed below. Additional bibliographic sources are provided in the recorded presentations.
Pediatric Trauma and Emergencies

● Advanced Trauma Life Support (ATLS), 9th Ed. 2012, American College of Surgeons Pub. Chapter 10 on Pediatric
Trauma.
● Ashcraft’s Pediatric Surgery, 6th Ed. Holcomb, Murphy & Ostlie Eds. Elsevier Pub. 2014, Chapters 14-19 (Trauma),
Chapter 31 (malrotation), Chapter 33 (necrotizing enterocolitis), Chapter 38 (intussusception).
Pediatric Tumors
● Ashcraft’s Pediatric Surgery, 6th Ed. Holcomb, Murphy & Ostlie Eds., Elsevier Pub. 2014, Section VII (neoplasms).
● Sabiston Textbook of Pediatric Surgery, 20th Ed., Townsend Ed. Elsevier Pub. 2017, Chapter 66 on Pediatric
Surgery, pp. 1858-1899.
Congenital GI Disorders
● Ashcraft’s Pediatric Surgery, 6th Ed. Holcomb, Murphy & Ostlie Eds., Elsevier Pub. 2014.
● Sabiston Textbook of Pediatric Surgery, 20th Ed., Townsend Ed. Elsevier Pub. 2017, Chapter 66 on Pediatric
Surgery, pp. 1858-1899.
Ethics and Palliative Care Medicine

● Ashcraft’s Pediatric Surgery, 6th Ed. Holcomb, Murphy & Ostlie Eds., Elsevier Pub. 2014, Chapter 80 (Ethics in
Pediatric Surgery).
● Current Surgical Therapy, 12th Ed. Cameron & Cameron Eds. Elsevier Pub. 2017, Chapter on Surgical Palliative
Care, pp. 1361-1368.
Minimally Invasive and Metabolic Surgery

● Cameron JL. Current Surgical Therapy. 12 edition. El Sevier. 2017.
● Brunicardi FC and Andersen DK. Schwartz’s Principles of Surgery. 11th edition. 2019.
● Division of Education. SESAP 16. American College of Surgeons. 2014.
● Ngyen NT. et al. The ASMBS Textbook of Bariatric Surgery. 1st edition. Springer. 2015.
Shock and Multiple Organ Failure

● Cameron JL. Current Surgical Therapy. 12 edition. El Sevier. 2017.
● Division of Education. SESAP 16. American College of Surgeons. 2014.
● Moore EE et al. Trauma.8th edition. Mcgraw-Hill Education. 2017.
Aortic and Carotid Disorders

● Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery
stenosis. N Engl J Med. 2010 Jul 1;363(1):11-23.
● http://emedicine.medscape.com/article/1979501-overview#a0156
● Life Science Intelligence LSI-PV-US118SU: U.S. Surgical Procedure Volumes from 2007-2014 (12/2011)
● http://www.findtheaaanswers.org/get-the-facts/what-is-aaa/
● Stenting versus Endarterectomy for Treatment of Carotid Artery Stenosis. Brott, TC, et al. N Engl J Med
2010;363:1-23
Peripheral Artery Diseases

● Egorova N et al. Analysis of gender-related differences in lower extremity peripheral arterial disease, J Vasc Surg.
2010 Feb;51(2):372-8.
● Jaff MR et al. An Update on Methods for Revascularization and Expansion of the TASC lesion Classification to
Include Below-the-Knee Arteries: A Supplement to the Inter-Society Consensus for the Management of
Peripheral Arterial Disease (TASC II). Ann Vasc Dis 2015;8:343-357.
● Vouyouka AG et al. Lessons learned from the analysis of gender effect on risk factors and procedural outcomes of
lower extremity arterial disease. J Vasc Surg. 2010;525:1196-1202.
Venous and Thromboembolic Disorders

● PREPIC Study Group. Eight-year follow-up of patients with permanent vena cava filters in the prevention of
pulmonary embolism: the PREPIC (Prevention du Risque d'Embolie Pulmonaire par Interruption Cave)
randomized study. Circulation 2005;112:416-22
● Hann CL, Sreiff MB. The role of vena caval filters in the management of venous thromboembolism. Blood Rev.
2005;19:179-202.
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Med J Aust 2019; 210:516-524.
Stomach and Duodenum – Malignant Disorders

● Gold JS, et al. Development and validation of a prognostic nomogram for recurrence-free survival after complete
surgical resection of localized primary gastrointestinal stromal tumor: a retrospective analysis. Lancet
Oncol.2009;10:1045-1052.
● Yonemura et al. Operative morbidity and mortality after D2 and D4 extended dissection for advanced gastric
cancer: a prospective randomized trial conducted by Asian surgeons. Hepatogastroenterology; 2007
● Valentini V et al. Survival after radiotherapy in gastric cancer: systematic review and meta-analysis. Radiother
Oncol. 2009 Aug;92(2):176-83.
● Cameron JL. Current Surgical Therapy. 12 edition. Elsevier. 2017.
Oncology and Tumor Biology

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● Schwartz Principles of Surgery, 11th Edition
● ASCRS Textbook, 3rd Edition
● National Comprehensive Cancer Network guidelines (NCCN.org)
Thyroid Surgery
● NCCN guidelines 2019
● Current Surgical Therapy 12th Ed. 2017 (JL Cameron and AM Cameron, eds) Endocrine Gland Section. pp 767-786.
● Textbook of Complex General Surgical Oncology 2017 (S Morita and C Balch, eds) Endocrine Section. pp 333-386.
Parathyroid Surgery
● Lowney JK, Weber B, Johnson S, et al. Minimal incision parathyroidectomy: cure, cosmesis, and cost. World J
Surg. 2000;24:1442-1445.
● Bilezikian JP, Brandi ML, Eastell R, et al. Guidelines for the management of asymptomatic primary
hyperparathyroidism: summary statement from the Fourth International Workshop. J Clin Endocrinol
Metab. 2014 Oct;99(10):3561-9.
● Current Surgical Therapy 12th Ed. 2017 (JL Cameron and AM Cameron, eds) Endocrine Gland Section. pp
787-801.
● Textbook of Complex General Surgical Oncology 2017 (S Morita and C Balch, eds) Endocrine Section. pp
333-386.pp 409-416.
Adrenal Surgery
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749-759.
Multiple Endocrine Neoplasia
● Wells SA et al. Revised American Thyroid Association Guidelines for the Management of Medullary Thyroid
Carcinoma: The American Thyroid Association Guidelines Task Force on Medullary Thyroid Carcinoma Thyroid Vol
25, No 6, 2015. p567.
● Raval MV, Sturgeon C, Bentrem DJ, et al. Influence of lymph node metastases on survival in pediatric medullary
thyroid cancer. Journal of pediatric surgery 2010;45:1947-54.
749-759.
● UpToDate
Mediastinum and Chest Wall Disorders

● Cameron J, Wilson J. Current surgical therapy 12th edition 2017; Pages 861:880
● John Putnam, Sabiston textbook of surgery 20th edition 2017; Pages 1576:1590
Pulmonary Surgery: Benign and Malignant

● Malcolm DeCamp, Mastery of surgery 7th edition 2019;Pages 585:604
● Christiana Wei, Complications in surgery 2nd edition; Pages 241:320
Cardiac Surgery: Adult and Pediatric

● Ralph Damiano, Schawrtz ‘s Principles of surgery 11th edition 2019; Pages 751:853
● Charles Fraser, Sabiston textbook of surgery 20th edition 2017;Pages 1632:1648,Chapter 59
Immunology and Transplantation

● Ascher N. Sabiston textbook of surgery 20th edition 2017; Pages 640:677
● Clavien PA. Mastery of surgery 7th edition 2019;Pages 156:177
Pancreas – Benign and Malignant Disorders

● Tyler DS, Evans DB. Ann Surg. 1994 Feb;219(2):211-21.
● William Fisher, Schwartz’s Principles of Surgery 11th edition 2019; Pages 1429:1477
● Keith Lillemore, Mastery of surgery 7th edition 2019; Pages 1471:1550
Gynecologic and GU Surgery

● Howard jones and Michael Coburn, Sabiston textbook of surgery 20th edition 2017;Pages 2013:2040
● Michael Sourial, Schwartz’s Principles of Surgery 11th edition 2019:1759-1792
Abdominal Wall and Hernias

● Sabiston Textbook of Surgery, 20th edition 2017. Section 10 Abdomen pp. 1088-1140.
● Colborn GL, et al. Surg Rnds (1995); 223-232.
● Nam & Brody - Management and Therapy for Sports Hernia. J Am Coll Surg: Vol. 206, No. 1, January 2008
● Kristine Makiewicz, Rush University Medical Center Review of Surgery Rush University review of surgery , sixth
edition 2019; Pages 226:235
● The Surgical Critical Care Handbook: Guidelines for Care of the Surgical Patient in the ICU:1549-1570
Breast – Benign Disorders

● http://ultrasoundregistryreview.com/BreastTrial4.html
● AAFP journal, When You Have Breast Pain. Am Fam Physician. 2000 Apr 15;61(8):2385.
● Dupont, WD page, DL, parl, FF, et al. Long term risk cancer in women with fibroadenoma. NEJM 1994;331:10
● Michael S Sabel. Overview of benign breast disease. UptoDate 2008, November 14
● Sabiston Textbook of Surgery, 20th ed. Ch. 36: Diseases of the Breast and Ch. 37: Breast Reconstruction.
● Robbins and Cotran Pathologic Basis of Disease. 9th Ed. (V. Kumar et al., eds) Chapter 23 The Breast.
Breast – Malignant Disorders

● Sabiston Textbook of Surgery, 20th ed. Ch. 36: Diseases of the Breast and Ch. 37: Breast Reconstruction.
● Robbins and Cotran "Pathologic Basis of Disease. 9th Ed. 2014 (V. Kumar et al., eds) Chapter 23 The Breast.
Sarcoma
● Sabiston Textbook of Surgery, 20th ed. Ch. 33: Soft Tissue Sarcomas
● Pinchus LB and Fox LP. The Stewart–Treves Syndrome. N Eng J Med 2008; 359:950
● Robbins and Cotran Pathologic Basis of Disease. 9th Ed. 2014 (V. Kumar et al., eds) Chapter 26 Bones, Joints and
Soft Tissue Tumors
Skin and Melanoma

● Sabiston "Textbook of Surgery"
● Robbins and Cotran Pathologic Basis of Disease. 9th Ed. 2014.(V. Kumar et al., eds). Chapter 25 The Skin.
Anorectal and Colorectal – Benign Disorders

● Bordeianou L, et al. Dis Colon Rectum. 2017;60(11):1121-31..
● ASCRS Textbook, 3rd Edition
● Current Therapy in Colon and Rectal Surgery (Fazio, et al), 3rd edition
Anorectal and Colorectal – Malignant Disorders

● National Comprehensive Cancer Network guidelines for colon, rectal, and anal cancer (https://www.nccn.org/)
● ASCRS Textbook, 3rd Edition (chapters on colon cancer, rectal cancer, anal cancer)
Small Bowel, Appendix and Spleen

● Shankar S1, Ledakis P, El Halabi H, Gushchin V, Sardi A. Neoplasms of the appendix: current treatment
guidelines. Hematol Oncol Clin North Am. 2012 Dec;26(6):1261-90.
● Gastrointestinal Carcinoids: Imaging Features with Clinicopathologic Comparison 1.Angela D. Levy, COL, MC,
USA and Leslie H. Sobin, MD January 2007 RadioGraphics, 27, 237-257.
● Liang PS, Shaffer K. Metastatic gastrointestinal carcinoid tumor with unknown primary site. Radiology Case
Reports. 2007;2:90.
● Rubin LG, Schaffner W. Clinical practice. Care of the asplenic patient N Engl J Med. 2014 Jul 24;371(4):349-56.
Clinical practice. Care of the asplenic patient.
● ASCRS Textbook of Surgery, 3rd Edition
● National Comprehensive cancer network guidelines (NCCN.org)
Head and Neck Trauma

● Mattox KL, Moore EE, Feliciano DV. Trauma. 7th Edition. McGraw-Hill. New York. 2013.
● Cameron JL, Cameron AM. Current Surgical Therapy. 10th Edition. Elsevier Saunders. Philadelphia. 2011
Thoracic Trauma
Abdominal Trauma
Pelvic Trauma
Pulmonary Critical Care

● Marino PL. The ICU Book. 4th Edition. Wolters Kluwer/Lippincott Williams & Wilkins. Philadelphia. 2014.
● Parrillo JE, Dellinger RP. Critical Care Medicine. 4th Edition. Elsevier and Saunders. Philadelphia. 2013.
Head and Neck Surgery

● Bailey Otolaryngology-Head & Neck Surgery, 5th ed. Volume 2, Ch. 1: Head and Neck Surgery
● Sabiston Textbook of Surgery, 20th ed. Ch. 33: Head and Neck
Burn and Inhalation Injuries

● Cameron JL, Cameron AM. Current Surgical Therapy. 10th Edition. Elsevier Saunders. Philadelphia. 2011.
● Parrillo JE, Dellinger RP. Critical Care Medicine. 4th Edition. Elsevier Saunders. Philadelphia. 2013
Esophageal Disorders – Benign and Malignant

● Vakil N, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global
evidence-based consensus. Am J Gastroenterol. 2006;101:1900-20.
● Shah, Nigam H., et al. “Proton pump inhibitor usage and the risk of myocardial infarction in the general
population.” PLoS One 10.6 (2015): e0124653.
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paraesophageal hernia repair: long-term follow-up from a multicenter, prospective, randomized trial. J Am Coll
Surg. 2011 Oct;213(4):461-8. doi: 10.1016/j.jamcollsurg.2011.05.017. Epub 2011 Jun 29.
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Biomarkers Prev. 2010 Jun;19(6):1468-70
Gastrointestinal Bleeding
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Stomach and Duodenum – Benign Disorders

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Ashley). McGraw Hill.
Nutrition and Metabolism

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Cardiac Critical Care

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Preoperative Evaluation and Perioperative Care
Fluids, Electrolytes, and Acid-Base

● Parrillo JE, Dellinger RP. Critical Care Medicine. 4th Edition. Elsevier Saunders. Philadelphia 2013.
Infection and Antimicrobial Therapy

● Parrillo JE, Dellinger RP. Critical Care Medicine. 4th Edition. Elsevier and Saunders. Philadelphia 2013
Evidence Based Medicine

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systematic review of randomised controlled trials. BMJ. 2003 Dec 20;327(7429):1459-61.
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Patent Safety and Quality Improvement

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Transfusion and Disorders of Coagulation

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Hepatobiliary/Portal Hypertension I & II
● Current Surgical Therapy 12th Ed. 2017 (JL Cameron and AM Cameron, eds) Section: The Liver pp. 335- 386
and Section: Portal Hypertension pp.387-426.
● Sabiston textbook of surgery: the biological basis of modern surgical practice. 20th ed., 2017. Chapters 53 and
54 – The Liver and Biliary Systems.

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General Surgery Table of Contents 2

Thyroid Surgery ...............................................................2

Matthew Strode, DO FACS

Anatomy Benign Thyroid Disease

• Most commonly seen in underserved populations

• Workup includes TSH, Free T4, T3, exam and U/S

• Possible cross sectional imaging

Nontoxic Goiter Hyperthyroidism

• Treatment is usually the #1 modality for

Thyroid Surgery page 1

Graves Disease: Auto-immune disease

• Clinical situation dictates

• MMI first line in most

• Tx with meds for 18

Hyperthyroidism (Graves Dz) Hyperthyroidism (Graves Dz)

Agranulocytosis, hepatotoxic, • Successful remission = euthyroid for >12

• 20-30% relapse requiring other treatments

Hyperthyroidism (Graves Dz) Hyperthyroidism (Graves Dz)

• Stop antithyroid meds stopped 3 days before • Concurrent other neck

• Failed medical therapy

• Be careful of transient hyperthyroidism

• Inability to rule out

Thyroid Surgery page 2

§ Toxic Multinodular Goiter:

§ Hashimoto’s Disease: Auto-immune § Subacute Thyroiditis:

§ Middle aged women § Painful gland

Thyroiditis Solitary Thyroid Nodule

§ Cause unknown, assoc. with other fibrous processes

structures, microcalcs, PET avid lesions

compression, even tracheostomy in severe driving treatment

Thyroid Surgery page 3

Solitary Thyroid Nodule Solitary Thyroid Nodule

Thyroid Cancer types Staging Systems

• Papillary § MACIS-mets, age, completeness of resection, local invasion,

Preoperative Evaluation Papillary Carcinoma

• Focused history and exam • Females 3 fold increase in incidence to men

• Ultrasound of neck • Controversial link to autoimmune disease

• +/- Laryngoscopy • Clear association with radiation exposure and

• Routine thyroid function tests, calcium

• Variants include follicular, tall cell, columnar cell,

• +/- Genetic testing diffuse sclerosis variant, solid variant

Thyroid Surgery page 4

Papillary Carcinoma Papillary Carcinoma

BIG PICTURE!!—STRONGLY CONSIDER

Papillary Carcinoma Papillary Carcinoma

• Total thyroidectomy advantagesà TG levels, • Neck Dissection?? Different opinions and

Papillary Carcinoma Papillary Carcinoma

+ Highly recommended RAI for extrathyroidal extension,

residual disease, mets

EBRT for gross disease in poor Iodine concentrating disease

Thyroid Surgery page 5

Papillary Thyroid Cancer Follicular Carcinoma

• Management of recurrence § Characterized histologically by invasive of capsule or vessels

• Targeted therapy- TKI (Sorafenib, Lenvatinib) for

Follicular Carcinoma Medullary Carcinoma

• Prognosis varies § More aggressive than papillary or follicular, 3-4% of thyroid

Medullary Carcinoma Medullary Carcinoma

• 50% have nodal disease and 5-10% have distant

• Dx-> need detailed FH and clinical suspicion

Thyroid Surgery page 6

Expose the side of gland in interest Thymus

If no localization preop-start with inferior glands Carotid sheath

Stay on gland to avoid RLN Intrathyroidal

Parathyroid glands appear dark brown or orange

The most common histologic diagnosis for Primary

MEN: The primary tumor marker for Multiple

4. Ret Proto Oncogene

Menin is the marker for MEN I and Ret-proto